Clinical Cardiology OVerview By Ragab abd elsalam ( MD) Prof. of Cardiology Approach to Patient with Heart Disease 1- Symptoms of Heart Disease = 2 myocardial ischemia = disturbances of the contraction
system / and or relaxation of myocardium = obstruction of blood flow = disturbances of the contraction = abnormal cardiac rate 2- Symptom Relationship to Etiology - ischemia = manifest as chest pain - disturbance contraction or relaxation = weakness / fatigue Severe cyanosis, hypotension, syncope, increased intra-vascular pressure
CHEST PAIN Two categories: Recurrent, often paroxysmal pain, which is mild or moderate in intensity. Prolonged & severe pain which is commonly asscoiated with clinical evidence of acute, serious illness. (1) Recurrent chest pain:
(a) Angina pectoris: Characteristics of anginal pain: It is visceral pain: poorly localized and squeezing, oppressive, burning or heavy in quality. Duration: brief, usually it is lasting 2 to 10 min. & it is rarely longer or shorter. Usually it is mild or moderate in intensity. Site: it is typicaly retrosternal, but it may occur in other locations. Even then at least a portion of the pain is commonly beneath the sternum.
The pain may be referred to precordium, neck, lower jaws, shoulders, arms, back and epigasterium. Radiation to the left shoulder and arm is especially common. Precipitations: effort or emotional stress, after meals, exposure to cold air or wind. N.B.: Anginal pain may be excluded under the following circumstances: If it can be localized with one finger. If it consistently last less than 30 sec. or longer
than 30 min. If it is sticking, jabbing or throbbing. If it occurs exclusively at rest with two exceptions: Pre-infarction angina. Variant form of angina, described by prinzmetal, vasospasm of coronaries usually is the leading cause.
If the intensity of the pain is consistently severe. Musculoskeletal chest pain: Characteristics: Radicular in nature. The pain usually occurs at night. It is usually precipitated by fatigue, incorrect posture and movement of the involved segments but not movement of the body as a whole.
It may be intensified with coughing or sneezing. The discomfort is usually dull and aching, and may be sharp. The pain usually lasts for hours at time. It is usually relieved by rest, analgesics postural exercises and local heat. Tioetzes syndrome: - Costochondral and chondrosternal pain, or swelling or both.
- The pain is usually well localized, but may radiate across the chest and over to the arms. -Tenderness on palpation over the involved articulations. Rib pain: may be due to trauma. Rib tumour causes pain if it is metastatic in origin. -Pain is usually described as sharp or burning and reproduced by local pressure. Fleeting, jabbing, lancinating or sticking pains are common in many normal individuals.
The thoracic outlet syndromes (e.g. the scalenus anterior, costoclavicular hyperabduction cervical rib-syndrome), may cause chest pain. Symptoms depend on whether neural or vascular structures are compressed at the thoracic outlet. - Nerve compression is the common cause of pain
and paresthesia. It may be associated with a demonstrable weakness. - Vascular compression is quite rare, as venous obstruction by thrombosis. Shoulder disorders: 1. May cause pain that is referred to chest. 2. Careful analysis usually reveals that pain is aggravated by shoulder movement, not the body motion.
3. There is local tenderness and pain. Passive movement and limitation of motion are commonly present. Less common causes: herpes zoster and Mondor disease (superficial phlebitis of thoracic wall and chest). Psychogenic pain : The discomfort of angina may be mimicked by anxiety states.
It may take various forms : Intermittent sharp, knifelike pains. Persistent precordial aching unrelated to effort. Tight sensations in chest. It is commonly associated with sighing respiration and
symptoms owing to hyperventillation. There is an important statement, that is mentioned by the patient, the pain is coming from the heart DACOSTA'S SYNDROME: - Psychogenic pain usually localized to the cardiac apex. May be associated with anxiety. - It May be also associated
palpitations, hyperventilation, dyspnea, weakness, depression, or other signs of anxiety. Pain due to pulmonary hypertension: -The cause of pain may be: -Right ventricular ischemia - Enlarged right ventricle & pulmonary artery may compress
on chest &sternum. Pain associated with valvular diseases: (a) mitral valve prolapse: The pain may be due to : tension on base of the redundant leaflet. Tension on chordae tendinae and papillary muscle. Friction effect of redundant leaflet on
myocardium. Associated with syndrome X. Associated with gastrointestinal cause of pain. Coincidental chest pain. Aortic Regurgitation: The pain usually nocturnal. (Nocturnal Angina). It is termed Angina of Lewis. May be related to baradycardia occurs
at night and marked decrease in the diastolic pressure. Prolonged chest pain Prolonged, severe, protracted chest pain may be the result of serious underlying disease, such as myocardial infarction, therefore, immediate hospitalization of patients for proper diagnosis and therapy is
mandatory. (a) Acute myocardial infarction: (b) Pain due to Aortic Dissection: (c) Acute pericarditis: Three types of pain may occur in acute pericarditis: Pleuritic pain is the most common type. Steady, severe retrosternal pain of sudden onset, simulating pain of acute myocardial infarction. The rarest type is pain at the cardiac apex felt
synchronously with each heart beat. Characteristics: The pain is commonly sharp increased by breathing deeply, swallowing and lying supine. It is sometimes relieved by sitting-up and leaning forward. The pain is most commonly located in the precordial region and may radiate to the neck or left shoulder Mediastinal Emphysema: Free air in the mediastinum produces chest
tightness and dyspnea. ** Hamman's Sign: Crunching, rasping sound heard synchronous with the heartbeat, indicative of mediastinal emphysema. Reminders Angina pectoris: angina is a discomfort in chest or adjacent area that is associated with myocardial ischemia without necrosis. It is due to an imbalance in myocardial
oxygen supply and demand. Stable (Typical) Angina: Angina upon effort, or angina induced by increased blood pressure or increased heartrate. Angina is relieved by nitroglycerin, although nitroglycerin is not specific to this type of angina. * Levine's Sign: Patient makes fist and holds it up to his chest, to describe the pain. Second-wind Phenomenon: If patient repeats same activity after the attack,
he may not feel the attack again the second time. Walk-through Angina: The pain subsides as patient continues the activity. Atypical Angina: Atypical presentation of typical angina. Atypical Symptoms: Sharp or stabbing pain, rather than crushing pain. Atypical Causes: Angina with change in position, for example, rather than angina strictly upon effort.
Angina Equivalents: Other symptoms that are caused by myocardial ischemia. > Exertional dyspnea. > Nausea, indigestion. > Dizziness, sweating. Unstable Angina: Angina even at rest, or angina that has recently gotten worse. It is associated with sharply increased risk for myocardial infarct within 4 months.
Angina Decubitus is a specific term for angina occurring at rest. Variant Angina (Prinzmetal Angina): Paradoxic angina occurring during rest but usually not during exercise. It is caused by coronary artery spasm. It can be hard to spot because it can coexist with typical angina. Clinical presentation of patients with chest pain:
It can be divided into three subsets: Typical angina pectoris. Atypical angina pectoris. Non-anginal chest pain. Dyspnea Definitions : It is the patient complaint of: - shortness of breath.
or - he cant get enough breath. or - awareness of respiration. It is subjective distress complaint of difficult breathing. It is one of the most common distressing symptom in cardiovascular disease. Types: - Dyspnea on effort (exertional dyspnea).
- Orthopnea. - Paroxysmal nocturnal dyspnea. - Acute pulmonary edema. - Cheyne-Stokes Breathing. - Dry non-productive cough. * According to the cause, dyspnea may be: Cardiac causes of dyspnea.
Non-cardiac causes of dyspnea. Lung diseases. Anxiety. Anemia. Thyrotoxicosis. False-dyspneas in: Pregnancy huff and puff Compansatory hyperpnea associated with metabolic acidosis due to diabetes mellitus and uremia.
(a)Dyspnea on effort: it is a common complaint. It is usually due to congestive heart failure or chronic pulmonary disease. * It is necessary to establish the degree of activity requiring to produce dyspnea. - What is about the daily activity of the patient? - When the patient began to notice increasing dyspnea? * When dyspnea is associated with wheezing: If the patient is an adult especially over 40 years old, heart failure
is the foremost in the mind of the physician. If there is a history of periodic wheezing and dyspnea since childhood, bronchial asthma and lung disease is more likely to be the cause of dyspnea. It is important to remember that long standing pulmonary disease may develop heart disease and heart failure. Also heart failure may precipitate more bronchial asthma. Orthopnea: It implies that the patient has more dyspnea when he is
lying down. The patient relates that he must use two or three pillows in order to have a restful night. Orthopnea is often associated with congestive heart failure, but may also be associated with severe lung disease. The fatigue associated with the exertion of breathing seems to be less when dyspnea is due to pulmonary disease than when it is due to heart failure. Ask the patient:
1. Does the dyspnea occur whether the patient lies on back, left or right side?. 2. Is it improved with digitalis & diuretic?. 3. Does it being within a half minute of lying flat? 4. Is the patient not completely free of dyspnea at any chest elevation (severe mitral stenosis). 5. Is the dyspnea developed rapidly and for less than one minute in supine position and then feels no dyspnea? (suggest pulmonary hypertension).
(c) paroxysmal Nocturnal Dyspnea: Characteristically, the patient goes to bed and has little difficulty going to sleep in the recumbent position. One or two hours later he is awakened from sleep with acute shortness of breath. He seeks relief by sitting upright, perhaps on the side of the bed, or he even sits in a chair. He occasionally goes to the open window searching for air. After a time he becomes comfortable and returns to bed.
He may then sleep comfortably the remainder of the night. It is almost specific for left side heart failure. The only other causes for this unusual sequence of events are: - Hyperventillation syndrome due to anxiety. Pulmonary emboli. (1) For pulmonary emboli: it would be most unusual for pulmonary emboli to occur for very many nights at the
same hour. (2) For hyperventilation syndrome due to anxiety: It is not so clearly relieved by sitting-up and is associated with other signs suggesting this syndrome, such as tingling of arms and hands and other evidence of anxiety. ASK about: 1. How long after sleeping does it occur? (Redistribution of fluid takes 2-4 hours to raise left atrial pressure). 2. Does the patient angle legs to get relief?.
3. Duration? (10-30 minutes). 4. Is it associated with cough, wheezing or frothy, pink sputum? 5. Obstructive sleep apnea? History of heavy snoring? 6. Paroxysmol nocturnal dyspnea usually occure in patients who are suffering also from exertional dyspnea and orthopnea. 7. The precipitating factors of the attack is uncertain and probably variable. Cough, bad dreams, slipping position, turning to side on which he is ordinary dyspneic and abdominal distension are among those suggested factors.
(d) Acute Pulmonary Edema: The patient experiences the sudden development of dyspnea and cough and he may produce frothy blood-tinged sputum. This symptom may occur without previous warning as in myocardial infarction, or its may be preceded by cardiac asthma or dyspnea on effort. (e) Cheyne-Stokes breathing: Periods of hyperpnea which alternate with periods of apnea.
This type of breathing occurs in: 1. Older patients with heart failure, hypertension or cerebrovascular accident 2. It is associated with: Hypoventillation syndrome of obesity (pickwickian syndrome) the breathing is periodic in nature, but it is not typical as chyne-stoke breathing. 3. Rarely occurs in children or in patients with core pulmonale. (f) Dry non-productive cough: 1. Cough may on occasion the earliest symptom, the most
prominent symptom or the only apparent symptom of left ventricular failure. 2. * Cough is an important symptom in certain forms of cardiovascular diseases, even in absence of heart failure : 3. Aortic aneurysm with compression on bronchus or trachea. 4. Mitral stenosis with aneurysmally dilated left atrium. 5. Markedly dilated pulmonary artery. 6. Congenital double aortic arch forming a vascular compression ring around the trachea.
Trepopnea: Dyspnea that occurs in only one of several recombent positions not due to congestive heart failure: (a) Cardiomegally. (b) Musculoskeletal. Platypnea: It is the dyspnea provoked by sitting-up.
1. Left atrial myxoma. 2. Ball-valve thrombus of left atrium. 3. Orthostatic hypotension. N.B.: Some patient with angina pectoris, may complaint of dyspnea rather than chest pain. This is termed (Angina equavelent). Clinical significance of orthopnea:
1. It is usually the result of heart disease (as many as 95% cases). It reflects, a severe lung congestion on lying supine in patients with left sided heart disease. 2. In about 5% of causes, are related to lung diseases: 3. Chronic obstructive lung disease (COLD) with apical bullae, where the sitting position, not only improves the gas exchange but also, lung mechanics. N.B.: 1. patients with COLD, usually have a sitting-up and either clasping the
side of the bed or pushing over their thighs, producing the formation of two patches of hyperpigmented callus immediately above the knees (Dahls sign.). 2. Orthopnea in asthmatic patient is usually a sign of severity. If it is observed at time of emergency, it is a good predictor of poor outcome. Paroxysmal Nocturnal dyspnea (PND). It is sought to be specific for Left sided heart disease and failure, but: Patient with chronic obstructive lung disease (COLD) may
have PND due to excessive secretion upon lying down. Asthmatic patients also may have PND due to night worsening bronchospasm. Orthopnea: Occurs in patients with heart failure, but also may occur in patients with COLD due to partial loss of diaphragmatic and accessory muscle function when supine. Palpitation
It is a disagreable awarness of the heart beat. The patient may use some other terms and report as pounding, stopping, jumping, or racing in the chest. The patient may complain when the heart beat is slow, fast or irregular. If there is a history of palpitations: 1. 2.
1. 2. 3. 4. 5. 6. 7. 8.
(a) Orientation: When did they begin? Ask about: shortest, and longest duration and the length of time between attacks. (b) Types and rate: ask about. Regular or irregular. Sustained or occasionally, strong beats. Onset and offset. gradual sinus tachycardia. sudden ectopic tachycardia.
Rest or exercise. Associated symptoms. Maneuvers or medications that stop it. Hemoptysis Definition : It means coughing-up blood. Brisk bleeding: is commonly associated with specific focal ulceration of the bronchus, such as (bronchogenic carcinoma, foreign body, or bronchiectasis).
Slow bleeding: Strongly suggest venous bleeding and is more likely to be the result of increased pulmonary vascular resistance, with secondary increase in flow through the bronchial venous system such as may occur as a result of mitral stenosis or bronchiectasis. It is also helpful to notice whether the expectorated blood is admixed with sputum or pus. This is valuable, as the site of origin of the bleeding could be determined. Intimate admixture of blood and pus are signs pointing to a deep-seated site of pulmonary suppuration such as pyogenic lung abscess.
Three conditions must never be overlooked as causes of hemoptysis: (1) Mitral stenosis: 1. It is frequently induced by physical exercise, sexual intercourse, or marked excitement. 2. It may be the first symptom, and may occur during pregnancy. 3. The blood comes from a break in the pulmonary veins, which rupture under high pressure.
4. Apoplexy: occurs in 10% of cases with reversible pulmonary hypertension due to rupture of broncho-pulmonary venous varicosities. This type tend to subside as the vein adapt to high pressure and as pulmonary arteriolar disease develops. 2) Pulmonary infarction: Frank hemoptysis occurs in the minority of instances. When hemoptysis occurs in a patient with heart failure, pulmonary infarction is likely. The bloody sputum usually appears from a few hours
to a day after the embolus. (3) Eisenmenger physiology: 1. 2. 3. 4. Patients with severe pulmonary hypertension
associated with atrial septal defect, or patent ductus arteriosus, may have hemoptysis, secondary to rupture of pulmonary capillaries. Four additional rare causes of hemoptysis: Rupture of a pulmonary arteriovenous fistula. Rupture of aortic aneurysm into the trachea or bronchus. Pulmonary hemosiderosis. Bronchial ulceration due to foreign body.
Cyanosis Definition : Bluish coloration of skin and mucous membrane. Cyanosis cannot occur when the hemoglobin is less than 33 percent of normal since reduced hemoglobin cannot be produced in an amount sufficient to cause the bluish color (Five grams of reduced hemoglobin is needed for cyanosis to occur). When the hemoglobin is normal, about one-third of it must be in the reduced form for the bluish color to appear.
* Clinical significance of history of cyanosis: If cyanosis is present only during the neonatal period the possibility of an atrial septal defect with temporarily reversed flow (right-to-left shunt) during the neonatal period is suggested. However, the most common causes of neonatal cyanosis are, atelectasis, pneumonia,
or even occasionally from cerebral damage. Persistent and severe neonatal cyanosis suggests a right-to-left shunt often with marked impairment of pulmonary blood flow: 1. 2. 3. 4.
Tetralogy of Fallot with pulmonary atresia. The hypoplastic left ventricular syndrome. Tricuspid atresia. Sometimes transposition of great vessels. Cyanosis that develops after a few years of life suggests a less severe form of tetralogy of Fallot, in about of 75% or more. Cyanosis often appeas
following delayed closure of a patent ductus arteriosus, or when child begins to walk. Cyanosis occuring later in life of childhood is suggestive of Eisenmenger complex (N.B. Occasionally cyanosis may be present early in life with this disorder, but not common). Patients with trialogy of Fallot (atrial septal
defect and pulmonary stenosis), usually describe history of cyanosis, late in (childhood or adolescence). A history of squatting with severe cyanosis (Hypoxic spells), are most suggestive of:
Tetralogy of Fallot. Trialogy of Fallot. - tricuspid atresia.
N.B. Squatting seldom occur in Eisenmenger syndrome. The squatting usually occur to relieve dyspnea and spells of unconsciousness, with severe cyanosis. In adults cyanosis and digital clubbing may be caused by right- to-left- shunting. Such shunting is most often the result of the Eisenmenger syndrome and occasionally of tetralogy or trialogy of fallot or Ebsteins anomally, or partial transposition of the great
vessels. Adult cyanosis also may result from chronic or acute pulmonary disease. Adult cyanosis also may result from chronic or acute pulmonary disease. Chronic disease as: Chronic obstructive lung disease. Hypoventillation syndromes.
Pulmonary infiltrative diseases as Hamman-Rich syndrome, sarcoidosis, metastatic cancer or severe bronchiectasis. Acute disease: Pneumonia. Pulmonary embolism. But the patient seldom complains of cyanosis in these problems.
Cyanosis due to stagnant hypoxia: Distal parts of extremities usually cyanosed in advanced heart failure. Cyanotic hands may be due to local stagnation called (Acrocyanosis). Rarely, cyanosis is caused by chronic or acute methemoglobinemia, or apparent cyanosis by argyria, which causes a bluish-gray discoloration of the nail beds and mucosae associated with prolonged use of nose drops containing silver.
Acute cyanosis in patients with chronic heart failure, should suggest the possibility of associated pulmonary embolism. Very specific physiologic implication can be made when differential cyanosis is found: (1) Cyanosis of the fingers greater than that of the toes suggests complete transposition of great vessels with either a preductal coarctation or complete interruption of
aortic arch and pulmonary hypertension with reversed shunt through a patent ductus arteriosus delivering oxygenated blood to the lower extremities. N.B. If the left arm is slightly less cyanotic than right arm, the coarctation of aorta is suggested. On the other hand if both arms are intensely cyanosed, complete aortic interruption is suggested. (2) Cyanosis and clubbing of the toes associated with pink finger nails of right hand and minimal cyanosis and clubbing of left hand
are suggestive of pulmonary hypertension with reversed shunt through patent ductus arteriosus with normally related great vessels. (3) If the right hand is pink and the left hand and lower extremities are intensely cyanosed, this suggest, that the right subclavian artery arises proximal to aortic obstruction, plus patent ductus arteriosus and pulmonary hypertension. On the other hand, if the right subclavian artery originates anomalously from the descending aorta, then both hands are cyanotic.
Syncope Definition: It is a complete and transient loss of consciousness due to inadequate cerebral blood flow. The physician should bear in mind that the commonest variety of syncope (vasodepressor syncope) is not caused by organic heart disease, or by organic disease of the circulation.
Clinical significance: Syncope that occurs in a threatening situation, such as venipuncture suggests simple vasodepressor syncope. A history of syncope since childhood when associated with organic heart disease, may suggest the possibility of congenital aortic stenosis. Syncopal spells occur with tetralogy of Fallot, in
such a case, it is associated with dyspnea & cyanosis. In children syncope rarely occurs in primary pulmonary hypertension. Syncope seldom occurs in congenital complete atrioventricular (AV) block since the heart rate is usually greater than 55/min. and the cardiac output reasonably well maintained. In older patients a history of syncope may be related to one of several variaties of organic heart diseases:
If the patient is thought to have mitral stenosis, a history of syncope may be very significant, it seldom occurs with uncomplicated mitral stenosis. Such a history suggests the possibility of a left atrial myxoma, or ballvalve thrombus with intermittent obstruction to left ventricular filling. Syncope in patient with ESM &
LVH : If typically occurs with exercise suggests aortic stelosis. If it occurs after stopping exercise suggests HOCM. A history of syncope in patient with angina should raise the possibility of aortic valvular stenosis. Syncope rarely occurs in patient with ischemic heart disease, although occasionally it occurs at the outset of acute myocardial infarction. Syncope may occur in patients who have paroxysmal
tachycardia. Syncope may be the initial symptom of massive pulmonary embolism. Syncope that occurs while shaving or while suddenly turning the head, especially when wearing a tight collar, suggests carotid sinus syncope. It is important to have a history of the position in which syncope occurs. The patient may become light-headed or giddy when first
arising in the morning and becomes more able to tolerate the upright posture during the day. This history suggests orthostatic hypotension. Syncope, which is associated with memory defects, temporary hemiparesis, paraplegia, vertigo or tinuitus in an older patient suggests that vertebrobasilar artery insufficiency may be responsible.
It is a heterogeneous symptom, including sensations of vertigo, presyncope, disequilibrium and light-headedness. It is one of the most complaint in general medical clinics. It is often selflimiting and only rarely relates to lifethreatening events, even in elderly patients. *Common causes include: Peripheral vestibular vertigo, labyrinthitis, Menieres disease
Central vestibular cerbellovascular tumor. Psychiatric disorders and hyperventilation usually in younger patients. Multicausal. ** Blurring of vision and even petit mal epilepsy may be revered as dizzy spells Giddiness: blurring of vision associated with altered consciousness and swaying sensation. Vertigo:
Literally it means sense of turning rotation either of the ones body or of the surroundings. ** The history is an easy pointer to vertigo: Patient reports objects in his environment spun around Or his body was turning. Or his head was spinning. Sometimes he may state that the floor or walls seemed to undulate or sank or rose-up toward him or he was feeling of to and fro or up-and down movement of the body, usually head. The symptoms of vertigo are usually paroxysmal and of short duration but may
be chronic following acute attack. It is accompanied by varying degrees of nausea and vomiting, nystagmus headache and ataxia, as well as by the need to avoid movement of the head. Edema Definition: It is an increase in the volume of interstitial fluid (i.e., the extravascular portion of the extracellular compartment). The plasma volume may or may not be increased.
** Interstitial fluid volume may increase considerably before it is clinically appreciated. ** Edema is considered a symptom and a sign. It is important to ascertain whether edema of the extremities preceded or followed dyspnea on effort. Edema of cardiac origin is usually preceded by dyspnea, and usually associated with dyspnea except
with tricuspid stenosis. Edema of one leg: 1. - Varicose veins. 2. - Thrombophlebitis. 3. - Lymphedema. Periorbital edema: 1. It is common in children than adult.
2. It is common due to renal causes, but may occur in heart failure. 3. ** Rare causes of periorbital edema: (superior vena caval obstruction, and trichinosis). Ascitis: It is recognized by the patient as an increase in girth or swelling of the abdomen. Ascitis due to heart failure is uncommon to day and
usually follows peripheral edema. A local factor such as cirrhosis is also suggested when ascitis associated with heart failure, seem to be out of proportion to peripheral edema. Constrictive pericarditis and endomyocardial fibrosis are rare causes of cardiac causes of ascitis. In children: 1. Hepatomegally and ascitis are the first symptoms & sign of cardiac
edema than peripheral edema due to: 2. Portal circulation of children is less complaint. 3. Systemic circulation in children is more complaint. Edema is a symptom and also it is a sign. 1. On examination it can be elicited as follows: 2. Press on the skin over a bony area with 3 fingers spread
apart for 10-30 seconds. 3. Feel and look of at the valleys produced. It is of two types. 1. Slow edema: the pitting remains for more than 60 seconds, and it is usually due to congestion. 2. Fast edema: the pitting remains less than 40 seconds, and it is usually due to hypoalbuminemia. Fatigue
Definition: It is a sense of weakness, described by the patients variously as exhuastion, tiredness, lack of interest, low vitality or a feeling of being all in. It is often accompanied by a subjective sensation of weakness and a strong desire to rest and sleep. When a patient with heart disease is water-logged or when there is pulmonary congestion due to heart disease, the patient is likely to complain of
dyspnea. Fatigue in a cardiac patient may be due to: 1. Heart failure. 2. The complain of fatigue may occur just before, during or following myocardial infarction. 3. Fatigue may be the main complaint of patient with myocardial ischemia. 4. Cardiovascular drugs:
Diuretics. B-Blockers. Antihypertensives that cause postural hypotension. Hoarseness of voice 1. It is usually unrelated to cardiovascular disease.
2. It may occur in patients with: 3. Aortic aneurysm that involves the recurrent laryngeal nerve. 4. Mitral stenosis, occasionally may cause hoarseness (Ortners syndrome). 5. Pericardial effusion, may be related to myxoedema which may produce a coarse, lowpitched voice. 6. Sometimes in patients with larger ductus arteriosus.
Intermittent claudication Intermittent pain of the skeletal muscles due to temporary ischemia that is usually (but not always) caused by atherosclerosis of the artery or arteries that supply a particular anatomic part of the body. It is produced by effort and relieved by discontinuing the effort. It is never related to emotional stress. The arterial obstruction is located proximal to the site of claudication.
Leriche syndrome; Intermittent claudication of the thighs and buttocks, is caused by obstructive disease of the iliac arteries or the terminal aorta. Intermittent claudication of the masseter muscles suggests takayasu disease. The blue toe syndrome is caused by cholesterol emboli of the toes from proximal atherosclerotic lesions of the arteries proximal to the feet.
Acute and persistent pain in the calf, thigh or other muscle group suggests an embolus to the artery or acute thrombosis of an obstructive lesion. Cardiac cachexia Mechanisms: 1. Poor eating and digestion: due to gastrointestinal congestion and anorexia. 2. Poor absorption also due to gastrointestinal congestion.
3. Deficit metabolism: liver congestion. 4. Tumor necrosis factors, play an important role in initiation and prolonged cardiac cachexia . All of these factors lead to caloric, protein and vitamin malnutrition. Significance Of The History As a pointer to the Diagnosis
Cardiomyopathy Hypertrophic cardiomyopathy: 1. Family history of sudden death 2. Younger or middle-aged patient. 3. Anginal pain or syncope, after but not during exertion. 4. Recurrent attacks of palpitation. 5. Worsening of the symptoms on digitalis therapy. Dilated cardiomyopathy:
Influenza-like illness, followed by symptoms & signs of heart failures. Short-term, history of dyspnea. History of drug-intake that is known to cause myocardial depression. Peripartum symptoms & signs of HF suggestive of Peripartum CM. Restrictive Cardiomyopathy 1. History of frequent blood transfusion, skin color
changes, recurrent arthritis, impotence with diabetes mellitus may suggest hemochromatosis. 2. Recurrent attacks of bronchial asthma in young patient with history of embolic manifestations may suggest esinophilic restrictive cardiomyopathy. 3. History of attacks of postural hypotension, with skin bleeding and scratching may suggest amyloidosis. 4. Recurrent eye symptoms (uveitis), history of kidney stone and renal problems and recurrent attacks of syncope may suggest sarcoidosis.
Cardiopulmonary disease Chronic obstructive lung Disease (COLD) 1. Heavy smoking history. 2. History of seasonal asthmatic attacks. 3. History of repeated asthmatic attacks since childhood, helped with bronchodilator. 4. The patient may give a history of easier breathing on leaning forward.
5. Chronic cough and wheezing. 6. Occupational history e.g (coal-miner workers). Pulmonary emboli with corepulmonale: 1. 2. 3. 4. 5.
History of long sitting after surgery. Pregnancy & delivery. Trauma. Phlebitis and oral contraceptives. History of deep venous thrombosis. History suggestive of Rheumatic fever : Polyarthritis:
Fleeting or migrating arthritis. Redness, hotness & swelling. Associated with complete loss of mobility. Self-limited.
Shows a dramatic response to Aspirin therapy. No permanent deformity. History of fever with murmur. long-acting of penicillin taking history. Family history. History of murmur during school examination, insurance or military service. Cyanosis:
Time of appearance: 1. Since birth: (transposition, Fallots tetralogy.) 2. Childhood: (Eisenmengers syndrome or Ebsteins anomaly) 3. Adult with pulmonary hypertension may suggest ASD. 4. During infancy associated with crying or feeding,
may suggest Fallots tetralogy. Squatting: may suggest. 1. Fallots tetralogy. 2. Pulmonary atresia. 3. Eisenmenger syndrome. Differential cyanosis: suggests ductus with Eisenmenger syndrome.
Stroke in cyanotic patient, considers cerebral abscess e.g. in Fallots tetralogy. Cyanosis & hemoptysis may suggest congenital arteriovenous fistula. History suggestive of pericardial diseases: 1. 2.
3. 4. 5. 6. Medical history: Uremia Metastatic carcinoma, lymphoma, leukemia. Connective tissue disorders as rheumatoid arthritis. History of skin rash after direct sun exposure
(systemic lupus) History of tuberculosis. Recent viremia. 1. 2. 3. 4. 5. 6.
7. Medicinal history: Chest radiation (recurrent). Chemotherapy. Isoniazid, or minoxidil. Patient symptoms: Chest pain: increased on lying flat and relieved on leaning forward. Epigastric pain 1-3 days before chest pain.
Abdominal swelling before lower limb edema and just before beginning of dyspnea or simultaneous with dyspnea on exertion. Position and Expose. First position the patient at 45 degree angle. Get comfortable with your surroundings, make sure the patient and area is well lit, and make sure
that the patient is comfortable. General Inspection (must be 1. 2. 3. 4. performed from the end of the patients bed)
(if the examiner are standing at the end of the bed, ask them to move!) Look for: Dyspnea. Cachexia (referred to as cardiac cachexia). Irritability. Obesity&... Elfen facies: It is characterized by 1. Short and upturned nose.
2. Widely spaced eyes. 3. Full checks. 4. Wid mouth with patulous lips. Deep husky voice, and friendly personality. It is often associated with: 1. Hypercalcemia. 2. Supravalvular aortic stenosis.
3. Mental retardation. Corvisarts facies: It is characterized by: Puffy, purplish and cyanotic & swollen eyelids. Shiny eyes. * It is observed in patients with: -Aortic regurgitation. -Heart failure.
DeMussets facies: It is the bobbing motion of the head, synchronous with hear tbeat. Significance: 1. 2. 3. 4.
5. It is first characterized as a typical facies of patient with AR. It is neither sensitive nor specific. In fact it is usually observed in hyperkinetic states (large stroke volume). There is a variant of DeMussets sign, seen in severe tricuspid regurgitation but the bobbing of the head, tend, to be more lateral as a result of the regurgitant column of blood rising along the superior vena cava.
It may be observed in patient with massive left pleural effusion. Mitral facies: It is the face of mitral stenosis. It is characterized by pink and slightly cyanoticcheeks. When patients with mitral stenosis develop right-sided heart failure and tricuspid regurgitation as a result of long-standing pulmonary hypertension, the overall skin color
becomes sallow and often overty icteric. This appearance contrasts quite well with persistently cyanotic cheeks. Facies of lupus erythematosus: It is characterized by: A classic malar, butterfly-like-rash, and often involving the bridge of the nose. Acromegally.
1. Excessive growth of facial bones. 2. Broad forehead. 3. Protruding mandible. Hypothyroidism: 1. 2. 3. 4.
5. 6. Dull face with distorted thick skin. Coarse features. Dry hair. Puffy eyelids. Enlarged tongue. Loss of outer 1/3 of eye brows.
Butterfly Rashs: Systemic lupus erythematosus is associated with libman-sacks endocarditis. Malar flash, without Rash: may be seen in patients with severe mitral stenosis. Edematous lids, loss of outer brow hair & sleepy appearance hypothyroidism.
Oculomotor palsy may suggest association of complete heart block. Ectopia lentis,. Iridodonesis Marfans syndrome or Homocystinurea. Blue sclerae may be found in: 1. Mafrans syndrome. 2. Ehlers-Danlos syndrome. 3. Osteogenesis imperfectae: Usually associated with AR & MR.
Arcus senilis in patients under 40 years hyperlipidemia. A coloboma (fissure) of iris and choroid is a major sign of the Cat eye syndrome is associated with: total anomallous pulmonary venous drainage. Cataract: 1. Marfans syndrome. 2. Downs syndrome.
3. Homocystinurea. Bacterial endocarditis: may lead to infected emboli. 1. May present with severe ophthalmitis. 2. Subconjunctival hemorrhage. 3. Petechiae. Jaundice: It is not often seen with cardiac problems.
It may be seen in: 1. High output states due to hepatic cirrhosis and alcoholic hepatitis & may be associated with cardiomyopathy. 2. Cardiac cirrhosis due to advanced and long-standing heart failure. 3. Pulmonary embolism and infarction. 4. Red-cell hemolysis due to prosthetic valves. N.B.: The serum billirubin level seldom rises above 6 mg/100 ml, even in severe heart failure. If it is above 6 mg/100 ml, additional problem plus heart failure is
suspected. Clubbing and cyanosis: These are typical of congenital heart disease or pulmonary arteriovenous fistula with a right to left shunt. Differential cyanosis and clubbing: It has a specific physiologic implication: Cyanosis of fingers is greater than that of the toes; suggests transposition of great vessels with either a
preductal coarctation or complete aortic arch interruption with pulmonary hypertension, and reversed shunt. In this case, if the left arm is less cyanotic than right, coarctation of aorta is suggested. On the other hand, if the cyanosis is intense and symmetrically, aortic arch interruption is suggested. Cyanosis and clubbing of the toes, associated pink fingernails of right hand and minimal cyanosis of left hand: this suggests
patent ductus arteriosus with normally related vessels and pulmonary hypertension with reversed shunt. Cyanosis & clubbing of the toes and left hand while the right hand is not cyonatic, this suggests, the right subclavian artery arises proximal to coarctation of aorta. Reversed differential cyanosis:
Hands are cyanotic and clubbed, but the feet are normal. This occurs when there is right ventricular origin of both great vessels, with concomitant disorder including VSD, PDA & pulmonary hypertension oxygenated blood from LV enters the pulmonary trunk through VSD, or from PDA into descending aorta so the feet are normal. While the oxygendesatrurated blood from RV enters the ascending aorta and brachiocephalic vessels so the upper extremities are cyanosed and clubbed.
* Unilateral clubbing: Aneurysm of aorta, or innominate/subclavian arteries. Pancosts tumour and lymphangitis. Remember : DD of clubbing : C = Cyanotic heart diseases L = Lung diseases U = Ulcerative colitis , Crohn,s diseases B= Birth defect .
B=Biliary cirrhosis I = Infective endocardits N = Neoplasm ( es. Hodgkins) G= Gastrointestinal malapsorption. Red fingertips, tuft erythema: it may signify small or intermittent right to left shunts with only slight reduction in oxygen saturation. Acute painful clubbing or hypertrophic osteoarthropathy is a manifestation of
bronchogenic carcinoma, which may invade or metastasize to the heart and pericardium. Quinkes pulsations: it is flushing of nail beds, synchronously with heart beats. It is a sign of high output states as aortic regurgitation. Splinter hemorrhage; they are: Longitudinal, black and splinter shaped. Usually located in the distal third of the nail. * Differential diagnosis: remember (SPLINT)
S= Sepsis P= PAN /SLE/ RA
L=Limey ( Vit.C deficiency) I = Infective endocarditis N = Neoplasm T = Trichomonas, trouma. Oslers nodes: They are reddish purple, raised, tender nodules in the distal
pad of fingers or toes. They suggest infective endocarditis Janeway lesions : small non-tender raised erythematous or hemorrhagic leasions of palms or soles: They may suggest infective endocarditis.
Rheumatoid arthritis: There is ulnar deviation of the fingers, thickening of the middle interphalangeal joints, boxing of the wrists and subcutaneous nodules. Jacouds artheritis: 1. Marked ulner deviation at the metacarpophalangeal joints. 2. It is almost always due to repeated attacks of rheumatic fever activity. 3. * The deformity is due to periarticular fascial and tendon
fibrosis, rather than synovitis. So the fingers can be moved freely into correct alignment. Nail Color: a) Leukonychia : White as in hypoalbuminemia . b) Wellow color : - Nicotine stains - Wellow Nail Syndrome ( Peripheral edema , brochiactasis & pleural effusion)
c) Blue nail: as in cyanosis , ochonosis , Bluered polycythemia . d)Cherry red : CO poisoning. e) Terry,s nails : the distal half is brow-red , while the proximal part is white-pink occurs in - liver & in chronic renal failure . f) Metanonychia : Multiple brownishlongitudinal streaks. Occurs in - Black person (normal) - White person: melanoma
under fingernails Obesity Obesity may be central or peripheral. In fact its location correlates strongly with its effect on health. (a) Central obesity: Involves primarily the trunk and it is characterized by: A bihumeral diameter is greater than bitrochanteric
diameter. Subcutaneous fat has a descending distribution and is concentrated primerily in the upper half of the body (neck, cheeks, shloulder, chest and upper abdomen). b) Peripheral obesity: Involves primerily the extremities, and it is characterized by: A bitrochanteric diameter is greater than the bihumeral diameter. Subcutaneous fat has an ascending distribution and is concentrated primerily in the lower half of the body (lower
abdomen, pelvic girdle, buttocks, and thighs). ** Central obesity is more common in men, while peripheral obesity is more common in women. ** Central obesity carries a much worse prognosis because of its higher association with hypertension,diabetes, atherosclerotic cardiovascular diseases, dyslipidemia and lower extremity venous stasis diseases. * Body Mass Index (BMI):
1. It is the federal governments standard for body weight. 2. It is calculated as a ratio between weight and height and provides a better measurement of body fat than the traditional height and weight charts. According to old standards: Men were considered overweight if they had BMI 27.3.
Women were considered overweight if they had BMI 27.8. Revised guideline: Any one with BMI 25 is considered abnormal Skin signs Amyloidosis: 1. Recurrent purpura; purpura in response
to minimal trauma to skin as gentle pinch. This is due to fragile vascular wall, yellow or reddish brown papules. 2. Amyloidosis may be primary or secondary. 3. * Amyloidosis may be associated with: 2) Sarcoidosis: - It is a granulomatous disease of unknown cause. Sarcoid skin lesions:
1. Red, painful, tender nodules, of anterior portion of lower extremity. 2. Sarcoid papules with atrophic centers, around the nose and mouth. 3. May be diffuse with serpiginous borders. 4. In some cases, plaques may develop and simulate psoriasis. (3) Thyroid dysfunction: (a) Hyperthyroidism:
1. 2. 3. 4. Skin is warm and smooth. Palms are pink and moist. Nails may show oncholysis. Pretibial myxoedema flesh-colored plaques.
(b) Myxoedema: 1. Skin is puffy, dry and swollen but does not pit with pressure. 2. Slightly yellow color to the skin (as the carotene is metabolized poorly by the liver). 3. Outer part of eyebrows may disappear and scalp hair may become brittle. 4. Axillary and pubic hair become sparse. Systemic lupus erythematosus: (a) Skin is highly sensitive to sunlight:
1. Persistent flush & urticaria. 2. Descoid lesion scaly, reddish areas with follicular plugging. 3. Ulcers may develop. (b) Malar rash: 1. A reddish macular eruption, but may be urticarial. 2. Usually, found over, nose & cheeks butterfly or bat wings appearance. 3. (c) Telangiectasis, purpura, Raynauds phenomenon, subcutaneous nodules and paniculitis may develop.
Scleroderma (Progressive systemic sclerosis): It is a connective tissue disease. 1. * Skin: It is tight, thick associated with vasculitis. 2. Raynauds phenomenon and ulcerations or scars of finger digits. 3. Skin of the face may be affected expressionless & immobile skin around mouth. 4. Telangectasia and hyperpigmentation.
CREST syndrome: 1. 2. 3. 4. 5. There are 4 out of 5 features are skin lesion: Calcinosis C.
Raynauds phenomenon R Esophageal dysfunction E Sclerodactyly S Telangiectasia T Diabetes mellitus: 1. Diabetic dermopathy: pigmented atrophic scars in the pretibial areas. 2. Bullous diabeticorum: large bulous filled with blood, heald without scars, in the hands, forearm, feet, & lower legs.
3. Eruptive xanthomas: small pinkish yellow papules with a red base erupt on the buttocks and extensor surface of forearms (Diabetes & hypertriglyceridemia). 4. Lipodystrophy: at the site of injection of insulin. 5. Necrobiosis lipoidica diabeticorum: Small red papules over tibias gradually increase in size atrophic with red border and yellow center. 6. Infant with diabetic mother may develop hypertrophic cardiomyopathy.
Hyperlipidemia: 1. -Xanthomatous lesions: localized infiltration of lipid-containing macrophages, that are located within the tendons and skin. 2. Eruptive xanthomas. 3. Soft tuberous xanthomas. 4. Eye-lid xanthomas. Hyperesinophilic syndrome:
1. Red hyperpigmented papules or macules. 2. Uriticaria & angioedema. 3. Perifollicular papules. 4. Skin itches and scratch markers. Endocarditis: 1. Skin lesions such as infected wounds or furuncles that serve as a source for bacteremia and subsequent endocarditis.
2. Skin lesion secondary to endocarditis: 3. Petechial hemorrhage of skin and mucous membrane. 4. Oslers nodes. 5. Janeway lesions. 6. Splinter hemorrhage. 7. Finger clubbing. Hemochromatosis: may be primary (genetic) or secondary:
Excessive iron that deposits in tissues can cause cirrhosis, diabetes mellitus, artheritis, hypogonadism and cardiomyopathy. Skin: 1. May has a bronze color due to hypermelanosis. 2. May be a salte-gray color due to hemosiderin. 3. The skin may become dry and scaly. 4. The hair may become sparse and spooning of nails may occur.
Malignant Melanoma: It is a cutaneous mole that changes in color, size, shape, or consistency, or mole that itches or become painful. Cardiovascular lesions: 1. 2. 3.
4. 5. 6. Cardiac metastasis. Charcoal heart. Pericarditis & effusion tamponade. Arrhythmias. - Conduction defects. - Heart failure may occur.
Rheumatic fever: 1. Subcutaneous nodules: non-tender, non-movable nodules occur on elbows, the forehead and bony prominences. 2. Erythema marginatum: is a pin-black, with clear center, and occurs on abdomen, trunk and proximal parts of legs & arms. * N.B.: Other causes of subcutaneous nodules &
erythema marginatum. 1. Rheumatoid arteritis. 2. Lupus erythematosus. 3. Annular erythema may occur in glumerulonephritis, drug toxicity & sepsis. Rheumatoid arthritis: Early: transient rash of pink macules & papules on the face, palms & soles in association with, low gradfever, months or years before artheritis.
Late: in adults there are rheumatoid nodules, these are firm, movable subcutaneous nodules, (one to several centimeters in size) & are painless. They are found on the bony prominances. Palmar erythema, purpura ulceration of skin due to arteritis. Raynauds phenomenon may occur. ER.MARGINATUM
(i) Enlarged liver due to engorgement with venous blood that is not able to return to the failed right heart and (ii) impaired intestinal absorption due to congested intestinal veins secondary to congested liver -Look for morphological features of Marfans Syndrome, Downs Syndrome, Turners Syndrome
(each of which has cardiovascular sequelae). -Look for any pacemaker, holter monitor, or telimetry leads in situ. Also look for GTN patches, Nicotine patches, etc. -Now peruse the bedside and look for iv fluids, GTN spray or GTN patch, O2
prongs, TEDS, ECG pads, etc. (3) Examination of the Hands. Ask the patient to put both of his hands, palms down, onto a pillow Proceed to get down on your knees (a position you will grow accustomed to as a medical student) and inspect the hands of the patient, you may ask the patient to lift the hands off the pillow to better view the fingers especially, but it is important not to
touch the hands at this stage. Once you proceed to touch the patients hands, make sure to inquire first if there is any pain in the hands. Clubbing - look for the following stages (which occur in this order) (i) increased fluctuance (2 ways to assess this (a) place one thumb at the root of the nail
just at the end of the skin before the cuticles arise, and place the other thumb at the very end of the nail and see-saw the pressure between the two thumbs or (b) place one thumb on the lateral most portion of the nail, and the other thumb on the opposite lateral portion of the nail and see-saw the pressure between the thumbs.
Increased fluctuance feels boggy. (ii) Loss of angle - this can be assessed using Shamroths sign. * This is performed by placing the patients two index fingers together so that the nails are face to face, and the most distal index interphalangeal joints are touching (like forming the M shape with your two index fingers). * In this position, normal patients have a
diamond shaped space between the two nails, however in patients with second stage clubbing, there will be no space in this position and thus loss of angle can be pronounced. (iii) Increased AP diameter - this is a qualitative assessment, compare with your finger AP diameter
(iv) Drumstick appearance of the pulps of your fingers (v) Hypertrophic Pulmonary Osteoarthropathy NOTE: make sure to look at the toes as well for clubbing. -Cyanosis (peripheral) which is due to
vasospasm -Splinter Haemorrhages - which are visible on the nail bed. -If these are distal, they are most likely due to manual labour. -If they are proximal, they are likely to indicate a vasulitic process. -If they are proximal and tend to be linear and parallel to the long axis of the nail this may well
be vasculitis due to infective endocarditis Now look for Tendon Xanthomata (not xanthelasma which occurs around the eye). This is a yellow or orange deposition of lipid in tendons which occurs in Type II Hyperlipidemia XANTHELASMA
(increased LDL). This causes deposition over tendons in the arms, hands and legs/feet .-At this stage, kindly ask the patient to turn their hands over so that you may observe the palmar aspect of the hands .-Oslers nodes - (O is for Osler as O is for Ouch) these are painful red raised nodules on the pads of the fingers and/or toes which occur due to vasculitis
.-Janeway lesions -these are non-tender erythematous maculopapular lesions which contain bacteria and occur on the palmar aspect of the hands and feet Palmar xanthomata may occur but they indicate a different abnormality to tendinous xanthomata. Palmar xanthomata and Tuberoeruptive xanthomata (yellow/orange maculopapular rash which occur over
the elbow and/ or knee joints) both indicate Type III Hyperlipidemia (increase in VLDL) -Look for palmar crease pallour which may signify anaemia. * Examination of the Face: Eyes: Corneal arcus - donot call it arcus sinilis, it implies the patient is senile and it is
a dated term. This is a yellow ring around the iris which occurs in patients with hypercholesterolemia. However, if it it occurs in the elderly > 65yrs old, then it is insignificant. Sclerae - look for icterus (yellowing) which may occur with (1) severe congestion of the liver in heart failure and (2) prosthetic valve induced haemolysis due to
excess turbulence. Also look for blue sclerae which occurs in Marfan, s Syndrome and Ehlers Danlos Syndrome and has implications in terms of aneurysms and dissections. Facial Tissue * Mitral Fascies - rosy cheeck with bluish tinge of dilatation of malar capillaries due to pulmonary hypertension secondary to
mitral stenosis) * This can be distinguished from the Malar Butterfly rash that occurs in Systemic Lupus Erythematosus because in SLE the rash doesnot spare the bridge of the nose, in mitral fascies it does. Mouth: Shine a pen torch onto the roof of the patients mouth.
A high arched palate signifies Marfan s syndrome (genetically predisposed to Aortic root dilatations, Mitral Valve Prolapse, Aortic Dissections and Aneurysms.) Enlarged tongue: 1. Amyloidosis. 2. Glycogen storage disease. 3. Hurlers syndrome.
4. Downs syndrome. 5. Hypothyroidism. Orange, large lobulated tonsils occurs in Tangier disease (type of hyperlipidemia.) Petechiae on buccal mucosa, occurs in bacterial endocarditis.
A high arched palate can be observed in Marfans syndrome. Cleft palate is associated with 1. 2. 3. 4. a high incidence of different types
of congenital heart disease: Atrial septal defect. Patent ductus arteriosus . Dextrocardia. Coarctation of aorta. * Xanthelasma which are yellow lipid deposits around the eyes and which occur in type II or type III hyperlipidemia.
* Look for blood vessels on the iris of the patient (called Rubeosis)and it occurs in poorly controlled diabetic patients. Look for cataracts which occur in poorly controlled diabetic patients (it occurs due to high levels of blood glucose being converted
to sorbitol by aldose reductase in the eye which deposits as cataracts Look for Hypertensive changes: (1) Silver Wiring due to hardening of retina (2) arteries (2) Arterio Venous (AV) Nicking or Nipping (where the hardened arteries indent the softer veins). (3)Exudates
(4)Papilloedema - enlarged optic nerve insertion due to increased pressure CSF pressure which occurs with hypertension (Papilloedema is required to be present for malignant hypertension to be pronounced) ** Taking of the Pulse It is important to turn the patientshand palm side up
for taking the pulse, or else the exainer will not be able to view what it is you are doing. @Assess the Rate: Normal is 60 - 100 beats per minute. Bradycardia is < 60 and Tachycardia is >100. Assess the Rhythm: (i) Regular (consistent predictable beat),
(ii) Irregularly irregular (inconsistent unpredictable beat which occurs in atrial fibrillation), and (iii) Regularly irregular (inconsistent but predictable pattern to the beat which occurs in Second Degree Mobitz Type I (Wenckebach) Heart Block which is increasingly prolonged PR
intervals (on ECG) followed by a dropped QRS at which point the PR shortens and then lengthens progressively again until QRS is dropped again, and so on) or Sinus arrhythmia which is increased pulse on inspiration due to increased venous return, and
decreased pulse on expiration (it is normal). @Assess the character of the pulse: Note that the character of the pulse is poorly assessed by the radial pulse. Rather, the carotid or brachial pulse should be used to assess the brachial pulse. Water Hammer Pulse: this is checked by
raising the patients arms while assessing the pulse. The pulse bolus can be felt to fall back towards the patient and this is significant of Aortic Regurgitation (you are in effect creating a hydrostatic pressure increase into the valve by raising the arm and so the pulse which is a blood ejection bolus impinges on the incompetent valve)
(ii) Slow Rising Plateau Pulse: This is a pulse that has a slow rising bolus under your finger, but then the bolus itself lasts for a long time before it slowly comes down. It can be likened to feeling a long worm sliding past your finger as you feel the pulse. This signifies aortic stenosis. (iii) Pulsus Alterans: This is a pulse that is strong
one minute,then weak the next. This signifies Left Ventricular Failure. @Assess the volume of the pulse: > The volume is increased in aortic regurgitation, and decreased in aortic stenosis. It can be best described as the loudness of the pulse under your finger. > And it is a qualitative measure of the pulse pressure. Since in aortic regurgitation the diastolic pressure is so low
(as blood slips back into the left ventricle from the aorta), then the ejection of the over-filled ventricular blood in systole will cause a dramatic increase in pressure. >This will feel like a loud pulse under the examiners fingers. @Assess Radio-Radial Delay: Feel for the radial pulses in both arms simultaneously. If any delay is detected, this may signify
a large arterial occlusion by large atherosclerotic plaque or aneurysmal process Look at the Tongue and Lips for central cyanosis (defined as > or equal to 5mg/dl of deoxyhemoglobin in the blood. This is interesting because it is more difficult for patients with anaemia to reach this concentration of deoxyhemoglobin and so more difficult for them
to become centrally cyanosed, even though they may have greater difficulty oxygenating their blood) Look at the mucosa (inner part of the lips) for petechiae (which isvasculitic and may signify infective endocarditis) Look at the tongue and note any enlargement which may occur due to amyloidosis
(amyloidosis can cause restrictive cardiomyopathy). (7) Examination of the Neck: Carotid Arteries Inspect the neck area for carotid endarterectomy scars Palpate the carotid arteries. NEVER palpate both carotids simultaneously, you may occlude the
majority of the cerebral perfusion and thus cause your patient to faint ....and a big fat fail to ensue as your exam mark. Palpate for the character of the pulse which can be as follows: Also, on palpating the carotid artery, it is important to evaluate the -
presence of systolic thrill, that may be produced by: Carotid atherosclerosis. Kinking of carotid arteries. Valvular aortic stenosis. Carotid shudders in severe aortic regurgitation. * Anacrotic - means small volume, slow uptake, notched wave on upstroke indicative of
aortic stenosis. * Plateau - means a prolonged but diminished upstroke, is also indicative of aortic stenosis. * Biferiens - is the term used for anacrotic and collapsing pulse which occurs when the patient has both aortic stenosis and regurgitation simultaneously.
* Alterans - strong and weak beats interchanging irregularly - indicative of Left Ventricular Failure * Jerky pulse - strong and spike of a pulse wave - indicative of Hypertrophic Cardiomyopathy. Abnormalities of Arterial Pulse: I.
- General Abnormalities: The size of the arterial pulse is determined by: Left ventricular stroke volume. Rate of ejection. Distensibility of the systemic arterial bed. Peripheral resistance. Systolic and diastolic pressures. The distance between the heart and the palpated
artery. * There are two clinical abnormalities of the pulse size: a) Hypokinetic Small, weak pulse. b) Hyperkinetic large, strong pulse. So on palpation of an artery, one should obtain an impression of both the height of pulse pressure and the rate of pressure pulse change.
Hypokinetic Pulse Weak and small pulse Occurs in conditions with: 1. Low stroke volume of left ventricle 2. A narrow pulse pressure. 3. Increased peripheral vascular resistance. Common causes:
Left ventricular failure. Constrictive pericarditis and tamponade. Valvular stenosis (aortic, mitral, tricuspid or pulmonary) - Shock, tachycardia...). Hyperkinetic Pulse The pulse pressure shows a rapid rates of rise.
It may be a) Rapid rates of rise with normal size: This is termed: (Jerky or Brisky Pulse). Occurs in: Double way of left ventricular ejection, as in: Mitral regurgitation.
Ventricular septal defect (VSD). Hypertrophic obstructive cardiomyopathy (HOCM): where there is no obstruction until the outflow tract contracts and approximates the thickened septum to mitral valve. The hypertrophied muscles of LV ejects about 80% of blood before obstruction. b) Pulse of rapid rate rise with increased pulse pressure.
1- Bounding pulse: rapid rates of rise with increased pulse pressure, but with normal contour. 2- Collapsing or water hummer pulse, sometimes termed Corrigans pulse: Exaggeration of bounding pulse, where there is a short and sharp peak, with contour change, as the wave is transmitted peripherally. The rapid upstroke and downstroke tend to be exaggerated as the pulse wave is transmitted peripherally. So these abnormalities are often better appreciated by palpating the brachial and radial arteries than palpating carotid
arteries Hyperkinetic pulse is usually associated with: 1. 2. 3. 4. Increased stroke volume of left ventricle
Wide pulse pressure. Decrease in peripheral resistance. Hyperkinetic circulatory states, may be considered in three main categories: 1- Hyperkinetic states with NORMAL hearts: 1. Fever. 2. Pregnant females secondary to arteriovenous shunt in the placenta
3. Hyperthyrodism, anemia..., etc 2- Hyperkinetic states due to abnormally rapid run-off of blood from arterial system: -Shunting of blood from aorta: (patent ductus arteriosus, aortopulmonary septal defect, rupture of a sinus of valsalva into the right atrium or right ventricle). - Large peripheral arterio-venous fistula: (Congenital, traumatic, mycotic etc).
- Small multiple arterio-venous fistula: (Pajets disease of bone, cirrhosis of the liver). - Aortic regurgitation moderate to severe. - Occasionally severe mitral regurgitation. 3) Complete Heart Block with bradycardia, increased strok volume. (II) Specific abnormalities:
A) Pulsus Parvus et Tardus: It describes a small pulse with a delayed systolic peak. - This pulse has a delayed peak, so it is termed (plateau) pulse. - When the aortic stenosis is severe the anacrotic notch is easily observed in the ascending limb, so it is also termed (anacrotic) pulse. - This type of pulse is characteristic of aortic stenosis of at least moderate severity.
N.B. Systolic thrill is usually palpated over carotids & usually occurs between anacrotic notch and the peak. The character of this pulse may be disappeared in patients with left ventricular failure, and in patients with concomitent mitral stenosis. Some elderly patients with calcific aortic stenosis may have nearly normal carotid pulse inspite of severe
obstruction due to rigid aorta, as a result of atherosclerotic changes, so the aorta is unable to expand. In supravalvular aortic stenosis, also the patient has a plateau pulse, but can be differentiated by: Difference in pulse volume between both arms. Right sided carotid thrill. Blood pressure is higher in the right arm than the
left. Characteristic facies (Elfen Face). B) Double Beat = Twice -beating pulse: This term is applied when two waves are palpated during each cardiac cycle. The second wave may be palpated either during systole or diastole. Dicrotic Pulse. The Second wave is palpated during diastole.
It is produced by accentuation and palpable dicrotic wave following the second heart sound. Palpated in both carotid and peripheral arteries. The dicrotic wave becomes palpable when there are: Low cardiac output. Soft and elastic aorta. High peripheral resistance
The most common causes of palpable dicrotic wave are: Severe congestive heart failure as in (DCM). Tamponade. The low output state following open heart surgery, especially aortic valve replacement. Fever.(typhoid fever) Anacrotic Pulse: Exaggeration of anacrotic notch gives palpable two wave
during systole as in aortic stenosis (Severe). Pulsus Bisferiens: Bis = twice & feriens = beating: Causes and Mechanisms HOCM: > Upstroke or ascending limb rises initially very rapidly and forcefully. (an initial systolic wave (Percussion
Wave). > Systolic dip: due to sudden decrease in the rate of left ventricular ejection, as the obstruction becomes significant. > Tidal wave: Follows the systolic dip, and produced by continued but slower decelerated ventricular ejection, and reflected wave from periphery. > The percussion wave is usually higher than
the tidal wave. Significance: It is characteristic of Hypertrophic obstructive cardiomyopathy and it may be the first clinical clue of HOCM. It may be possible to bring out the characteristic bisferiens pulse by performing valsalva maneuver or by exercise. In combined Aortic stenosis (AS) and Aortic
regurgitation (AR) The aortic regurgitation should be at least of moderate severity. The bisferiens pulse may be palpated in pure Aortic Regurgitation which should be severe. Also bernouli effect is the underlying mechanism.
** There is an important feature that can differentiate the bisferiens pulse in HOCM from other causes of pulsus bisfierience; which is the character of pulse following extrasystoles: - In HOCM, the pulse is very small following extrasystoles, where more contraction causes more obstruction.
- In other causes, in normal the pulse wave is strong after extrasystole (post-extrasystolic potentiation) =(pulse is exaggerated than normal). Pulsus Alternans There is a regular alternation of the height of the pressure pulses, but the beats occur at a regular intervals. Frequently, may be more readily detected while taking the arm blood pressure.
There is alternation of left ventricular contractile force. Alternation of LV end-diastolic volume and stroke volume. Sometimes alternation of LV end-diastolic pressure ** mechanisms Sudden critical change in diastolic filling period. Alternation in the number of cardiac fibres contributing to each systole. Significance: - May be associated with third heart sound (S3)
- May be observed after premature ventricular contraction or tachycardia in heart failure without pulsus alternans. - Latent pulsus alternans: in some patient with heart failure, without apparent pulsus alternans, the characteristic pulse can be exaggerated by: > Upright position. > Nitroglycerine therapy. > Exercise.
D) Pulsus Bigeminus: It is the most common cause of peripheral arterial pulsations that alternate in size from beat to beat: The strong pulsation occurs after long diastolic filling phase following the premature beat. The weak pulse occurs due to weak premature beat. Significance: It is commonly associated with digitalis toxicity.
E) Pulsus paradoxus: Normally the systolic blood pressure usually declines (5-10 mm.Hg) during inspiration. ** Best observed by careful measurement of blood pressure. ** It is due to relative pooling of
blood in the pulmonary vasculature during inspiration, as a result of lung expansion and of the more negative intrathoracic pressure. In addition transmission of the negative intrathoracic pressure to aorta and great vessels. ** So pulsus paradoxus is exaggeration of the normal: the declines in the systolic pressure during inspiration is more than 10 mm.Hg.
Significance: * Pulsus paradoxus may be produced by conditions which: - Limit the inspiratory increase in blood flow to right ventricle and pulmonary artery. - Cause a greater than normal amount of inspiratory pooling of blood in the lungs. - Cause the intrathoracic pressure to have very wide extremes of pressure during inspiration and expiration.
- Interfere with venous return to either atrium relatively more during inspiration, e.g abnormal inspiratory increase in pericardial pressure. ** Several clinical conditions are associated with pulsus paradoxus: > Superior vena cava obstruction. > Asthma, emphysema and airway obstruction. > Pulmonary embolism. > Severe heart failure
> Cardiac tamponade due to pericardial effusion. > Constrictive pericarditis. > May occur in patients with severe hypotension shock. N.B: Patients with cardiac tamponade have pulsus paradoxus. - Also may have kussmauls sign (a truly paradoxic finding), which is an increase in peripheral venous distension during
inspiration. - Mechanism: change in the pericardial shape rises the intrapericardial pressure obstructs venous return to the heart. In contrast to this the pulsus paradoxus that occurs with pulmonary diseases (asthma, emphysema... etc) have marked
exaggeration of the normal expiratory increase in venous pressure. *So this is of great diagnostic importance that differentiate pulsus paradoxus in patient with pericardial diseases from that in patients with pulmonary disease Blood Pressure Measurement: =First make sure that the blood pressure cuff you are
utilising is the right size for the patient (this is done by placing the width of the cuff around the arm , for it to be accurate, the width of the cuff needs to be approximately of the circumference of the arm. This is significant because a cuff that is too large for the patient over estimates blood pressure and a cuff that is too small for the patient under estimates the blood pressure. =Sit the patient down or keep them lying in the bed but sit
them up at 45 degree angle. * Too-narrow and too-large cuff: * A too-narrow cuff may give false higher reading in systolic pressure up-to 50 mmHg, due to higher inflation pressure is needed to inflate the cuff. * A too- large cuff may give false low blood pressure.
* On begining deflation of cuff the release should be slowly to avoid spasm of artery at the begining. =First find the systolic pressure by inflating the cuff while feeling for the radial pulse. (Do not use the stethoscope yet). The pressure at which the pulse first disappears is the systolic pressure. This is done first because it allows you to estimated what range you; d expect the systolic pressure to be in this
patientbefore commencing auscultation. .. =Deflate the cuff. Now position the stethoscope over the brachial artery, and inflate the cuff again until the pulse sounds are no longer heard. ..Now deflate the cuff at about
3-4mmHg per second until the first pulsation is heard again (this is the first Karatkoff sound). ..Continue to deflate the cuff until absolutely no more sounds are heard anymore (the very last turbulent sound will be that of the 5th Karatkoff sound). =Repeat the process in the other arm. Note that the BP can
vary between arms by up to 10mmHg and still be normal. =Now Repeat the Blood Pressure in the patient while theyare standing. If systolic blood pressure falls by >15mmHg or diastolic pressure falls >10mmHg then one can pronouncethe patient has postural hypotension (the gold standard test is the Tilt Table Test where the BP and ECG is taken at 3 minute intervals while the patient is
Tilted in a special table from the horizontal position To the vertical in increments of 15 degrees * Auscultatory gap: > It is the silence caused by the disappearance of korotkoff sounds after the first appearance of the true systolic pressure, and reappearance of pressure (some 10-20 mm.Hg lower ). > It requires venous distension of the forearm and concomitant low flow.
-To avoid it: Determine the systolic blood pressure first by palpitory method. Routinely ask the patient to clench his first 10 times and inflate the cuff rapidly. * Pseudo-hypertension: > Misleadingly high systolic, diastolic or mean blood pressure measured by cuff compared with
the pressure measured directly by intra arterial needle. > Observed in medial necrosis of brachial artery (Monckeberg arteriosclerosis). --- Pipesteam calcified brachial artery. * Pseudohypertension is suspected in elderly: > Disproportionate elevation of blood pressure to clinical findings: (no ECG. evidence of LVH, no
cardiomegaly in X-ray). > A palpable radial pulse after the brachial pulse has been eliminated by inflation of the cuff above systolic pressure. (Oslers sign maneuver) Subclavian Steal: > the use of a vertebral artery as a collateral circulation to feed the subclavian artery (usually
on the left). > Blood from a vertebral artery flows retrogradely into the distal subclavian, thus stealing blood from the brain causes vertibrobasilar insufficiency and the blood pressure is lower in one arm than other. Pulse pressure: It is the difference between systolic and diastolic blood pressure: ( thus in patient with systolic
blood pressure of 120 mmHg, and diastolic blood pressure of 80 mmHg, the pulse pressure is 40 mmHg ). -Abnormally narrowed pulse pressure: The pulse is considered abnormally narrowed if it is
less than 25% of the systolic value. (For example, a patient with systolic blood pressure of 100 mmHg and diastolic pressure of 90 mmHg has a pulse pressure of 10 mmHg ( Causes: a- The most common cause is a drop in left ventricular stroke volume, as in patients with obstruction to left ventricular filling or left ventricular emptying (e.g.: tamponade, constrictive pericarditis
or aortic stenosis(. b- It may be observed in extreme tachycardia, in which the filling time of ventricle is reduced. c- It may be seen in shock as a result of increased peripheral resistance. -* Reversed pulsus paradoxus: > It is an increase in systolic blood pressure that coincides with inspiration rather than expiration.
> It is observed in : 1- Hypertrophic cardiomyopthy: it is a typical sign due to (stiff septum) & reversed inspiratory movement. 2- Some cases of severe left ventricular failure (stiff & less compliant ventricle). 3- Positive-pressure ventilation reverses the respiratory changes in intra- thoracic pressure. Neck Vein The bedside examination of the pulsations in the
neck veins is the clinical key to the dynamics of the right side of the heart. Two main objectives should be observed: > Study of the wave form of pulsations. > Venous pressure. * Principles of studying the Neck Veins: 1- It is necessary to examine both internal and external jugular veins on both sides as well as venous pulsations
which may be visible in the suprasternal notch or in the supraclavicular fossa. 2-The right IJV is superior for accurate evaluation of venous wave form due to: - Direct continuouty with RA. - Innominate vein may be compressed by the arch of the aorta, making the left sided venous pressure to be abnormally high in normals.
* Position of the patient: > The trunk of the body should be elevated until maximum pulsation is noted. > In most normal subjects the maximum pulsation is usually observed when the trunk is inclined less than 45 (15-30) degree. Sit the patient up at 45 degree angle with their head turned away from you Remember you are always on the
patient,s right side, So you will be viewing the right JVP. Although both can be viewed, the right JVP is actually closer to the right atrium and so functions as a more accurate manometer of right atrial pressures). Look for a pulsation between the two heads of the
sternocleidomastoid muscle (the clavicular insertions). This is the site of the internal jugular vein, and it is the internal jugular vein that is used for JVP because the external jugular vein is too tortuous for good measurement and viewing.
Light should be tangential to illuminate highlights and shadows. Neck should not be sharply flexed. Using a centimeter ruler, measure the vertical distance between the angle of Louis (manubrio sternal joint) and the highest level of jugular vein pulsation. A straight edge intersecting the ruler at a right angle may be helpful.
You will assess the JVP for Height and Character: Height - the height is measured from the sternal angle (of Louis) in a line perpidicular to the floor. * JVP is considered raised if > 3cm (note: some may say it is raised if >8cm and the reason for this is that some people are purists, and so they consider the right atrium as 0cm.
Now since the angle of louis is 5 cm above the right atrium,one simply adds 5 cm to any measurement above the angle of Louis for this method of JVP measurement,so donot let that throw you). A raised JVP indicates a raised Right Atrial Pressure which can be from many conditions ie Fluid Overload
(iatrogenic), Right Ventricular Fialure. * Character of the JVP - The wave form of the JVP is complex and you will not be expected to comment on subtle changes in these wave forms in different patients. * But you will be expected to know the normal wave form
and some pathological manifestations. Technique A: Jugular Venous Pressure Measurement (JVP) **NB: 1-The neck muscles especially sternomastoid should be relaxed because if it is tense it will obscure pulsations so place small pillow under the neck or gentle massage by your hand.
2-The head should not rotated or if necessary for few degrees only to avoid tense of neck muscles. 3-Proper evaluation of venous pulsations is possible only when they are correlated with all events of the cardiac cycle. 4- Carotid pulse may be used to time venous pulse. Heart sounds are preferable for timing. Jugular Vein
Carotid Artery No pulsations palpable. Palpable pulsations. Pulsations obliterated by pressure above the clavicle. Pulsations not obliterated by
pressure above the clavicle. Level of pulse wave decreased on inspiration; increased on expiration. No effects of respiration on pulse. Usually two pulsations per systole (x and y descents).
One pulsation per systole. Prominent descents. Descents not prominent. Pulsations sometimes more prominent with abnominal pressure.
No effect of abdominal pressure on pulsations. The normal wave form is composed of the following in order: A wave, C wave, X - descent, V wave, Y-descent. A wave Atrial contraction, C wave Closure of tricuspid, X - descent , relaXation of atrium, V wave - atrial filling
(Filling), and Y-descent - emptYing of atrium. * (a-wave): Mechanism: > Retrograde transmission of the pressure pulse produced by atrial contraction, where there is a brief backward flow of blood from right atrium to venae cavae. >It is the prominent positive wave in normal.
> It is a presystolic wave begins just before first HS. > Occurs at the moment of (S4) if present * (C-wave): It is a brief positive wave that interruptes the descent of venous pulse from the summit of (awave). Mechanism: > Impact of carotid artery adjacent to vein so it is
termed (carotid impact) > Retrograde transmission of pressure pulse due to bulging of TV into RA during RV systole. * (V-wave): Mechanism: > During ventricular systole the TV is closed, but blood continues to fill the venae cavae and RA leading to increase in the volume and pressure within them. So the pressure rises from the
trough of (x-wave) to the positive (v-wave). > The 2nd HS occurs shortly prior to the summit of v-wave which marks the opening of TV. * (X-wave) = Systolic Collapse: Occurs in late systole, shortly before the 2nd HS. Mechanism: > Downward displacement of the base of the ventricles including TV during ventricular Systole
fall in RA pressure. > Continued atrial Relaxation. * (Y- wave) = Diastolic collapse: Mechanism: V-wave descent caused by opening of TV & rapid rush of blood from RA to RV. Ascending limb of Y-wave is produced by continued diastolic inflow of blood into the great
veins, RA & RV (which are in free communication during diastole). The S3 of right side occurs at the moment of Y trough while the S3 of left side occurs shortly before the trough. Manometer of right atrial pressure. Function at waveform
ASK ME: points: Atrial filling Systole Klosed tricuspid Maximal atrial filling Emptying of atrium Abnormalities of The Venous Pulse:
Abnormalities of (a-wave): a-wave is normally the dominant wave and tends to increase during inspiration inspite of the decrease in venous pressure. Abnormalities involves: their timing & amplitude. Timing: Absent a-wave in atrial fibrillation due to absent atrial contraction.
Venous pulsation in AF: Absent a-wave. Decreased or obliterated X-descent or even systolic expansion. The predominant wave is Y-descent. Irregularity of the pulsations. In sinus tachycardia a-wave may be fused with the preceding v-wave & so be
diminutive or even absent. * When a discrete a-wave with ascending and descending limbs is clearly seen to be completed prior to the first HS it occurs in prolonged P-R. (First Degree HB). Amplitude:
1- Prominent a-wave: Observed when the right atrium contracts against decreased compliance of RV as in pulmonary hypertension & acute pulmonary Embolism. 2- Giant a-wave: Observed when RA contracts against obstruction: - Tricuspid stenosis, Tricuspid atresia - Severe pulmonary stenosis
3-Cannon-wave: Occurs when the RA contracts against closed TV during RV systole So the resulting wave is the fusion of (a,c & v) waves. * Significance > Regular connon waves:
AV-junctional Rhythm. > Irregular Cannon waves: Most common type & it is of great diagnostic importance observed in: Ventricular premature beats. Complete HB in this type the wave may be longer than arterial pulse. Ventricular tachycardia. Abnormalities of the systolic
collapse (x-wave): In tricuspid regurgitation this collapse may be: Decreased or Obliterated or even replaced by a positive wave. This depends on the degree of tricuspid regurgitation (TR): > Mild TR decreases the systolic collapse.
> Moderate TR causes obliteration or small regurgitant (r-wave). > severe TR systolic expansion large r-wave. ** in this case S wave or what is called Arterialization of neck vein, or, ventricularization of neck vein. ** In constrictive pericarditis : The predominant wave is sharp deep Y-descent.
X-descent is shallow. N.B : X-descent may be prominent & deep than Ydescent if it is associated with active pericaiditis. Abnormalities of the diastolic collapse (Ywave). The down slope of the Y descent or V-wave depends on: Height of RA & great venous pressure Pressure -volume relation between RA & great veins Rate of venous return.
Resistance to forward flow across TV. Ventricular compliance. RV. impedance. Slow & shallow Y descent tricuspid stenosis. Sharp, deep & rapid Y-descent is observed in Constrictive Pericarditis Patients with severe HF.
* They are differentiated by the Lancisis Sign Lancisis Sign : large regurgitant systolic wave (systolic expansion) characteristic of severe TR in HF, not in constrictive pericarditis. Jugular Venous Pulse (JVP): The JVP has the following characteristics remembered by : MOPHAIR >>
M - Multiple Wave Form, O - Occludable, P - Positionally dependent , H - Hepatojugular reflux is present, A - Above (fills from Above), I - Impalpable, R - Respiratory changes ). IV- Venous Pressure: > Normally the internal Jugular vein is collapsed except
in its lower part. > The degree of congestion of the neck veins reflects the pressure in the right atrium. > The venous pressure is said to be elevated when the venous column in the neck is more than 4 cm above the zero reference point. ** The angle of lewis is the zero reference. *** Clinically the medial end of the clavicle in 45 inclined position is the best clinical reference
where the angle of lewis and medial end of the clavicle at the same level. so examination on 45 is the best. ** The level of the clavicle in sitting position is above the angle of lewis whereas in 45 position, the sternal Angle is at the same level of clavicle. Estimation of central venous pressure:
>First position the patient to get a good view of the internal jugular and its oscillations. > Identify the highest point of pulsation, which usually occurs during exhalation and coincides with the peak of the a and v waves. > Find the sternal angle of lewis ( junction of the manubrum with the body of the sternum). > Measure the vertical distance from the sternal angle to the top of the jugular
pulsations in centimeters. This distance represents the jugular venous pressure (JVP). >This method relies on the that fact that the center of the right atruim (in which venous pressure is by convention zero) is approximately 5 cm below the sternalangle of lewis. > This relationship occurs in peoples of normal
size, shape, regardless of body position. > Thus, using the sternal angle as the reference point (the vertical distance in centimeters to the top of the column of the blood in the Jugular vein) provides an adequate measurement of JVP. ** JVP in turn is 5 cm lower than central venous pressur (CVP). Thus CVP=JVP+5. ** Causes of congested
Neck veins. - Right ventricular failure > The most important cause. - Raised intracardiac pressure: - Constrictive pericarditis - Pericardial effusion. - Resistance to flow as in tricuspid stenosis, tricuspid Atresia, pulmonary hypertension.
- SVC obstruction: Congested non-pulsating neck veins. - Thrombus. - Bronchogenic carcinoma. - Retrosternal hugely enlarged thyroid gland. Dominant v wave [easily heard]. Tricuspid regurgitation Absent x descent
Atrial fibrillation Exaggerated x descent Cardiac tamponade Constrictive pericarditis Sharp y descent Constrictive pericarditis Tricuspid regurgitation Slow y descent Right atrial myxoma
Causes of elevated JVP - Bradycardia - Fluid overload [esp. IV infusion] - RVF - Constrictive pericarditis - Pericardial effusion - SVC obstruction - Tricuspid stenosis or regurgitation - Hyperdynamic circulation
- Raised Intra-thoracic pressure: > Pleural Effusion > Emphysema. > Increased Blood volume: > Acute nephritis. > Large IV infusion. > Pregnancy. - High output states as in: > Anaemia.
> Fever. > Thyrotoxicosis. > Arterio-vnous fistula. > Beri-beri....etc. *Hepatojugular (Abdominojugular Reflux): it is termed the one-minute Abdominal compression tests: firm pressure over the right upper quadrant of
the abdomen for 60 seconds. Abnormal elevation of the internal jugular pressure indicates that the right ventricle cannot accept the increased venous return caused by abdominal compression. **Kussmauls sign: Paradoxic increase in jugular venous distension during inspiration. Observed in:
> Severe right sided heart failure. > Constrictive pericarditis. > Right ventricular infarction. > Restrictive cardiomyopathy. > Tricuspid stenosis. > Superior vena cava syndrome. The external Jugulars are less suited for venous pulsations examination due to:
> They often become compressed while going through the various fascial planes of neck. > They have valves that may prevent adequate transmission of right atrial pulsation. > They are so constricted, in patients with increased sympathetic activity. > They are not in straight line with right atrium. Jugular venous findings of a right ventricular Infarction:
> The mean JVP is increased. > Prominent a-wave. > Prominent X and Y descents. > Positive abdominojugular reflux. > Concomitant tricuspid regurgitation, gives additional findings (such as giant V-waves and right earlobe bobbing ) . Significance of neck veins in differentiating the type of pericardial
disease: * In tamponade: there is an X-descent but little or no Y descent, where there is much restriction from the begining of diastole. * Constrictive pericarditis: there is a shallow Xdescent and deep Y descent, when the restriction occurs only after the opening of tricuspid valve. * Effusive -constrictive pericarditis: the Xdescent is more or less equal to the Y- descent.
* Bernheim Effect: left ventricle bulge into RV during diastole prevents good RV filling, but does not prevent the RV outflow (SO it is a type of inflow obstruction, not an outflow obstruction). -Prominant a-wave. -Decrease in Y-descent. -Increase in X-descent.
** Occurs in: > Chronic mitral regurgitation with dilated left ventricle. > Chronic LV hypertrophy: > Aortic stenosis. > Hypertrophic cardiomyopathy. > Severe hypertension. * Reversed Bernhiem: in severe acute RV dilation,
interventricular septal bulge toward the LV in diastole and reduce the LV stroke volume causes: > Palsus paradeoxicus. > Lung congestion if it is severe causes dyspnea. * Sustained apex: > It is the apex that remains outward throughout systole and begins to fall a way only with second beart sound.
*Significance: a- A significant finding of aortic stenosis. b- May be due to ventricular aneurysm involving apex. c- If the apex is palpated in axilla and it is sustained it may be due to complete absence of pericardium. d- In HOCM sustained apex means severe left ventricular hypertrophy or in absence of LVH, it means decrease in ejection fraction.
Palpable presystolic impulse at the apex: > Atrial hump due to strong left atrial contraction & it rounded in contour, it is usually felt in systolic dysfunction. Palpable 4th heart sound: the palpable atrial hump is termed palpable 4th heart sound. It is sharp and associated with auscultated 4th heart sounds. It is observed in patients with impaired diastolic
function and with normal systolic function as in HOCM & in hypertension. * Presystolic impulse is commonly observed in HOCM, more than aortic stenosis... How? In HOCM, although the interventricular septem is very thick, where the strong atrial kick can easly expand the rest of LV, which is not hypertrophied as
the septum. In AS: The entire LV is equally hypertrophied and therefor resists expansion of left atrial contraction. *Tracheal Tug: (to diagnose aortic aneurysm of aortic arch): Stand behind the seated patient. Apply steady upward pressure on the
cricoid cartilage by one finger you will readily detect the downward pull on trachea with each aortic pulsation. * Left parasternal pulsations: a) A slight precordial lift may occur in children normally. b) Bulging of the precordium in children denotes longstanding right ventricular enlargement. c) A localized, sustained heaving lift in the lower
left parasternal region denotes right ventricular hypertrophy due to pressure overload. (PS.) d) A hyperdynamic impulse denotes right ventricular volume overload as in (ASD) . e) A left parasternal lift due to enlarged left atrium. * Continuous thrill: > Infraclavicular patent ductus arteriosus. > Root of neck venous hum. > Back:
- localized: arterio-venous fistula - Posterior intercostal, spaces & apex of scapulae enlarged collaterals of coarctation. * Thrill on carotids: - Bilateral systolic thrill (AS). - Bilateral vibrations (carotid shudders). - Unilateral:
- Right side; > Supravalvular AS. > Right sided kinking & atherosclerosis of carotids. - Left side; > Pulmonary stenosis (transmitted). > Left sided arteriosclerosis. * Pulsations of the right sternoclavicular Joints and right
sternum. a) Pulsation of right joint may indicate rightsided aortic arch. b) Aortic dissection or aneurysm. c) Aneurysmally dilated RA & RV. d)Dextrocardia. * Auscultate the Carotid arteries for any bruits. It is important to know physically why a bruit is
produced in any artery. * There is an equation from physics which describes the parameters necessary to produce a bruit. * In effect a bruit is the sound made from turbulent flow. The following is the equation which you
should commit to memory if you want high honours: (1) Either the flow is laminar or (2) The carotid is completely 100% stenosed thus producing no flow whatsoever. This can be confirmed because in a completely stenosed carotid artery, the carotid pulse cannot be felt. Abnormal waveform causes
* Dominant a wave Pulmonary stenosis Pulmonary hypertension Tricuspid stenosis * Cannon a wave Complete heart block Paroxysmal nodal tachycardia Ventricular tachycardia (8) EXAMINATION OF THE
PRECORDIUM: Inspection: -Look for scars: midline sternotomy is CABG or valve repair, left or right sided lateral thoracotomy scars (check under female pendulous breasts) which may indicat previous closed mitral or tricuspid valvotomy. -Look for abnormal rib cage: (i) Pectus
excavatum (ii) Pectus carnatum (iii) Kyphoscoliosis. * These can be caused by Marfan,s syndrome which may result in distortion of the position of the great vessel and displacement of the apex beat.
* If severe, it can cause Pulmonary Hypertension (secondary to a reductionin pulmonary function). -Look for pacemaker (under the right or left pectoral muscle) -Look for a visible apex beat -Look for a visible pulmonary artery pulsation due to severe pulmonary hypertension.
* Palpation: > Apex beat: always begin your palpation of the apex beat from the axillae towards the midline. > Once you can palpate it (the size of a 2 euro coin) count dow the number of spaces with the left hand while maintaining position of the apex with the right hand.
> Comment on the (i) Position of the apex beat and (ii) Character of the Apex beat (i)Position - the normal position of the apex beat is 5th intercostal space on the left, and 1 cm medial to midclavicular line. > If the apex beat is lateral or inferior to this, it can indicate cardiac enlargement, chest wall deformity, or
pleural/pulmonary disease. (ii)Character - is described by the following: * Left vent. Thrust =Normal apex. * Pressure Loaded - a sustained beat pressing against your hand indicative of aortic stenosis or hypertension. * Volume Loaded - increased area of the palpated beat which is indicative of left ventricular failure
(LVF). ** Therefore, the size of the apex beat is larger than the normal 2 euro size. . Double Impulse (or triple) - indicative of HOCM, this occurs because the atria contract into hardened ventricles causing a loud S4
sound that is palpable. This loud S4 is palpable just before the tapping of the ventricle that is the apex beat thus giving rise to a double impulse Tapping Apex - A palpable S1 (mitral or tricuspid stenosis) with a normal apex beat which follows. The S1 is palpable in these stenoses because the atria arestill trying to squeeze
blood passed the stenosed valve when the ventricle contracts thus slamming the valve shut (if you are trying to close a door while someone on the other side is pushing it open, when you finally close it....its gonna slam shut.....same idea here). Absent Apex - can be a finding if the chest wall of the patient is thick, if they have emphysema,
pericardial effusion, shock (or death), or Dextrocardia from Kertagener,s syndrome. Parasternal Heave - felt left of sternum (interdigitate your fingers in the intercostal spaces and feel for any heaves)
this is indicative of Right Ventricular Enlargement or Severe Left Atrial Enlargement Feel for a palpable P2 which is indicative of Pulmonary Hypertension Feel for any thrills over the relevant valve areas (if felt,see if it
corresponds with apex beat, if it does it is a systolic thrill, if not then it is diastolic) Auscultation: Hunt for a Murmur -(always listen for HS I and II while listening in all the areas) -First place the bell of your stethoscope over the mitral area
-Remember to apply the bell of your stethoscope to the chest wall very lightly or else a diaphragm is created by the stretched skin and this defeats the purpose of using the bell -The low pitched sounds that you would expect to hear over this area are that of mitral stenosis or the 3rd heart sound. -Second place the diaphragm of your
stethoscope over the mitral area (to listen for high frequency sounds). -Thirdly place the diaphragm at the tricuspid area (5th intercostal space, left sternal edge) and auscultate any murmurs. -Next place the diaphragm at the pulmonary area (2nd intercostal space, left sternal edge) and auscultate any murmurs. -Next place the diaphragm at the aortic area
(2nd intercostal space, right sternal edge) and auscultate any murmurs. -Next ask the patient to sit forward and place the diaphragm of your stethoscope between both shoulder blades, -Whenever you hear a murmur, make sure to simultaneously listen to the murmur and feel for a radial or
carotid pulse todetermine if the murmur is systolic (occurs with each beat of your pulse) or diastolic (occurs in between each beat of your pulse). * Heart Sounds I,II, III, IV and the Split: The following is the sort of abnormalities you may hear when listening to the heart sounds: Heart Sound I (which is the closure of the
tricuspid and mitral valves) Loud HS I = occurs whenever the flow from the atria to the ventricles is still high pressure and high volume when the ventricles start contracting thus closing these valves despite the continued high pressure and high volume flow). Soft HS I = occurs whenever the pressured volume of flow from atria to ventricles is long gone (the flow is
complete) , yet the ventricle has not started contracting yet. As a result, the closure of the valve simply closes softly, donot coapt * Loud A2 = if there is systemic hypertension or aortic stenosis * Loud P2 = in pulmonary hypertension * Soft A2 or P2 = Aortic (pulmonary)
regurgitation or calcification * Splitting: ** If you think you hear a split second heart sound , note that normally the aortic valve closes before the pulmonary valve due to greater diastolic pressure pushing back on the aortic valve. Logically then, since inspiration causes
increased venous return to the right side of the heart which causes larger amount and stronger ejection of venous blood pressing open the pulmonary valve to gain access to the pulmonary artery, thus the closing of the PV is delayed further on inspiration in relation to the closure of the AV.
** As a result, splitting of the two heart sounds (I & II) is increased on inspiration. First heart sound (S1) 1.Louder than normal 2.Variable in intensity 3.Diminished in
intensity 1.Mitral stenosis, short PR interval 2.Atrial fibrillation, complete heart block 3.Mitral regurgitation, severe aortic regurgitation, long PR interval, calcified mitral valve Second heart sound (S2)
1.Fixed splitting 2.Wide, physiologic splitting 3.Paradoxical splitting 4.Increased intensity of A2 5.Increased intensity of P2 6.Decreased intensity of A2 7.Decreased intensity of P2
1.Atrial septal defect 2.Right bundle branch block, pulmonic stenosis 3.Left bundle branch block, aortic stenosis 4.Severe hypertension 5.Pulmonary hypertension 6.Calcific aortic stenosis 7.Pulmonic stenosis
Increased Splitting:occurs in pulmonary stenosis, Right bundle branch block, and Ventricular septal defects (because l pressure is greater than R. pressure, the right side becomes fluid overloaded). Fixed Splitting:occurs in Atrial Septal Defects and this occurs because of equalisation of the 2 atrial pressures and volumes and thus inability for change in volume to occur on inspiration.
Paradoxical Splitting:occurs in aortic stenosis, aortic coarctation, hypert. and a large Patent ductus arteriosus which increases the flow to the left atria/ventricles and thus keeps aortic V open longer thus delaying the A2 component of the second heart sound). When one hears a splitting of the second heart
sound, it is impossible for you to ascertain whether the split is a regular split (A2 followed by P2) or a paradoxical split (P2 followed by A2). The only way you can tell is by auscultating while asking the patient to inspire. If the splitting is increased, then it is a normal split. If the splitting is decreased, then it is a paradoxical split (note that a paradoxical split occurs when there is aortic stenosis).
Extra Heart Sounds: NOTE: the extra heart sounds can only be heard if the atria are contracting appropriately, as a result dont say that you can hear the S3 sound right after saying that the patient has Atrial Fibrillation, because this is impossible. Remember this is the order or pattern of the heart sounds (note the relative distance between the sounds): 4th---------1st----------------------------------------2nd--------3rd
S3: a low pitched sound arises from the l or R ventricles. It represents rapid ventricular filling (ie AR or mitral regurgitation) This sound can be normal in young patient <40 yrs old and in pregnant patients. It occursbecause the ventricle is already filled with fluid to the brim, so an extra push of fluid
from the atrium causes the ventricle to balloonout causing a low pitched 3rd HS. When it is present, the rhythm that is heard is Ken----------Tucky. The Ken representing HS1, Turepresenting HS2, and ckyrepresenting HS3. S4: a high pitched sound arises from the L or R ventricles. This sound occurs due to the atria contracting
fluid into a non-compliant ventricle. This heart sound is always pathological if heard and it may be due to anything which hardens the ventricle be it hypertrophy or fibrosis (ie aortic stenosis, hypertension, mitral regurgitation, ischaemic heart disease (this heart sound may present during angina or MI). If HS3 and HS4 are present at the same time, the sound is referred to a quadruple
gallop and it is representative of severe ventricular dysfunction. If the patient becomes tachycardic (HR > 100bts/min) while having HS3 and HS4 simultaneously, these two sounds can become superimposed which is referred to as a summation gallop. Extra heart sounds 1.Third heart
sound (S3) 2.Fourth heart sound (S4) 3.Opening snap 4.Ejection sound 1.Markedly diminished left ventricular diastolic function 2.Modestly diminished left
ventricular diastolic function 3.Mitral stenosis 4.Bicuspid aortic valve, pulmonary valve stenosis Additional Sounds: Opening snap- occurs in mitral stenosis or tricuspid stenosisand it occurs because of difficult of these valves in first opening.
Ejection Systolic Click - occurs in aortic or pulmonary stenosis (due specifically to bicuspid congenital valves) Non-Ejection Sytolic Click - occurs if there are redundant mitral valve leaflets or an ASD Tumour Plop (diastolic) - occurs when one has an atrial myxoma (which occurs in the atria thus the name) and so on diastole,
when the mitral or tricuspid valves open, the tumour plops down into the tricuspid or mitral valve opening. Pericardial knock (diastolic) is a sudden cessation of ventricular filling b/c of inability of the ventricle to expand any further due to some restrictive extrinsic boundary. Thus, it tends to occur in constrictive
pericarditis. Prosthetic Heart Valves - you should have some idea of the differencesbetween ball-cage valves and disc valves (both prosthetic), xenograft tissue valves (porcine valves) do not have a differentsound to them because they are tissue! Pacemaker Sound - is a late diastolic high pitched click due to the contraction of the chest
wall muscle on pacemaker firing just before ventricular contraction. * Systolic murmurs: The very vast majority of murmurs are systolic When soft they are usually early in systole and disturb the end of S1. S1 often appears slurred in these cases as opposed to ending abruptly as is normally the case
* Mid-late systolic murmurs. The careful clinician focuses on the end of S1 for soft systolic murmurs. Holosystolic murmur: refers to a systolic murmur that begins during or immediately after S1 and ends with the onset of S2 Pansystolic murmur: refers to a systolic
murmur that begins during or immediately after S1 and continues into and obscures S2 (note that left ventricular pressure ) continues to be greater than left atrial pressure after aortic valve closure during isovolumetric contraction). Systolic murmurs 1Early systolic
1-Acute, severe mitral regurgitation, low-pressure tricuspid regurgitation 2-Aortic sclerosis, aortic dilatation, aortic stenosis, 2Midsy pulmonic stenosis, hypertrophic cardiomyopathy, stolic increased aortic valve flow (can also be caused by Diastolic murmurs: - Less commen than systolic murmurs - Low frequency
-Rather low intensity and so are graded out of 4, not 6 -Best identified with the bell of the stethoscope -My be early diastolic , mid0diastolic or late ( presystolic) murmurs. Diastolic murmurs 1. 1Early
diastolic 2. 1.Aortic regurgitation, high-pressure pulmonary regurgitation 2.Mitral stenosis, tricuspid stenosis, severe mitral regurgitation 3.Mitral stenosis, severe aortic 2regurgitation (Austin Flint murmur), Mid-diastolic
left atrial myxoma 3. Continuous murmurs: -Common -Typically associated with a PDA, but also arteriovenous fistulas -Usually vary in intensity throughout the cardiac cycle, however the murmur is detected at all times -The continuous nature of the murmur may only be
noted at the PMI, while at other locations it may only be systolic, for example. To and Fro murmurs: The name for the situation when a systolic murmur and a diastolic murmur (due to different physiologic etiologies) coexist. Continuous murmurs
1.Peaks before and after S2 2.Rough, noisy, or high-pitched, louder during diastole 3.Louder during systole 1.Patent ductus arteriosus 2.Normal venous hum 3.Mammary souffle Intensity:
The intensity of the murmur at its origin is related to (Blood flow velocity) x (Rate of flow). * Overall, the intensity of a heart murmur is not related to the severity of the lesion; however for some diseases there is a rough correlation between the intensity of the murmur and the severity of the lesion such as: Mitral valve insufficiency Aortic / subaortic valve stenosis Pulmonic valve stenosis
The intensity of a murmur is graded on a scale of 1 to 6: Grade 1 = a very soft, localized murmur detected only after several minutes of listening. Grade 2 = a soft murmur, heard immediately but localized to a small area. Grade 3 = a moderately intense murmur that is readily detected and detected over
more than one location. Grade 4 = a moderately intense or loud murmur, detected over several areas, usually both sides of the chest, however a precordial thrill is not detected in this case. Grade 5 = a loud murmur accompanied by a precordial thrill over the point of maximal intensity.
Grade 6 = a very loud murmur accompanied by a precordial thrill and the murmur is detected when the stethoscope is pulled slightly off the chest wall. Murmur Grades Thrill Volume
Grade no very faint, only heard with optimal conditions 1/6 no
loud enough to be obvious 2/6 no louder than grade 2 3/6
yes louder than grade 3 4/6 yes heard with the stethoscope partially off the
chest 5/6 yes heard with the stethoscope completely off the chest 6/6
** HYPERTENSION EXAMINATION:. Inspection - look for signs of secondary hypertension (Cushing; s, Acromegaly, Polycythemia, Chronic Renal Failure) Take the Blood Pressure (see above for technique) in arms and legs
Palpate for radiofemoral delay (coarctation) and radio-radio delay (dissection of aorta) Examine the Fundi (see endocrine section to note what the hypertensive changes are) Examine the rest of CVS system looking for LVF secondary to hypertension, and look for signs of coarctation of aorta also palpate and auscultate the carotids for bruit because hypertension may lead to damage, dissection, atheromatous change, etc.
4th Heart sound is present if the patients BP > 180/110 Palpate abdomen for renal and/or adrenal mass and look for AAA (which is a complication of HT). Auscultate for renal bruits 2 cm above and lateral to umbilicus on both sides (note however that most bruits heard on the left side of the abdomen are from the splenic artery and are of no significance) Examine the CNS for previous strokes Urinalysis also for evidence of renal disease and
Vanylmendallic Acid and Homovanillic acid (increased in phaechromocytoma)