The History takingAndPhysical Examination

Data from the history, physical examination, chest roentgenogram, electrocardiogram, and other routine laboratory tests,when integrated properly, facilitate an accurate diagnosis and appropriate decisions regarding therapy in many patients at a relatively low cost.

THE HISTORY

The complete history requires information pertaining to:

SymptomsTraditional cardiovascular risk factors,A general medical history, Occupation, Habits, Family history,Systems review

The major symptoms associated with cardiac disease include :

•Chest discomfort•Dyspnea• Fatigue• Edema• Palpitations•Syncope•Cough• Hemoptysis•Cyanosis

•Claudication •Limb pain• Edema •Skin discoloration

Usually indicate a vascular disorder

Chest Pain

The differential diagnosis of chest pain is extensive. In addition to angina pectoris and myocardial infarction, other cardiovascular diseases, gastrointestinal diseases, psychogenic diseases, neuromuscular diseases, and diseases of the pulmonary system must be considered

Differential Diagnosis of Chest Pain

1. Angina pectoris/myocardial infarction2. Other cardiovascular causes  a. Likely ischemic in origin    (1) Aortic stenosis    (2) Hypertrophic cardiomyopathy    (3) Severe systemic hypertension    (4) Severe right ventricular hypertension    (5) Aortic regurgitation    (6) Severe anemia/hypoxia  b. Nonischemic in origin    (1) Aortic dissection    (2) Pericarditis    (3) Mitral valve prolapse3. Gastrointestinal  a. Esophageal spasm  b. Esophageal reflux  c. Esophageal rupture  d. Peptic ulcer disease4. Psychogenic  a. Anxiety  b. Depression  c. Cardiac psychosis  d. Self-gain5. Neuromusculoskeletal  a. Thoracic outlet syndrome  b. Degenerative joint disease of cervical/thoracic spine  c. Costochondritis (Tietze syndrome)  d. Herpes zoster  e. Chest wall pain and tenderness6. Pulmonary  a. Pulmonary embolus with or without pulmonary infarction  b. Pneumothorax  c. Pneumonia with pleural involvement7. Pleurisy

Angina pectoris

The quality of the chest discomfort is usually described as "tightness," "pressure," "burning," "heaviness," "aching," "strangling," or "compression

Classically, the discomfort is induced by exercise, emotion, eating, or cold weather.

Anginal pain is ordinarily retrosternal.

The chest pain of myocardial ischemia tends to radiate bilaterally across the chest into the arms (left more than right) and into the neck and lower jaw. Occasionally, radiation to the back or occiput is noted.

Chest pain at rest can occur only as nocturnal angina.

Angina is usually relieved within 5 to 20 minutes by rest, with or without the use of vasodilator drugs such as nitroglycerin (TNG), although sublingual TNG or TNG spray characteristically hastens relief.

Occasionally, angina will dissipate despite continued exercise (the walk-through phenomenon) or will not occur when a second exercise effort is undertaken that previously produced chest discomfort (warmup phenomenon).

Both circumstances can be attributed to the opening of functioning coronary arterial collaterals during the initial myocardial ischemia.

Myocardial infarction

Pain associated with acute coronary syndrome (ACS) is usually more severe and longer-lasting than anginal pain and is often associated with nausea, vomiting, and diaphoresis

Canadian Cardiovascular Society Functional Classification of Angina Pectoris

I. Ordinary physical activity, such as walking and climbing stairs, does not cause angina. Angina results from strenuous or rapid or prolonged exertion at work or recreation.

II. Slight limitation of ordinary activity. Walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, in cold, in wind, or when under emotional stress, or only during the few hours after awakening. Walking more than two blocks on the level and climbing more than one flight of ordinary stairs at a normal pace and under normal conditions.

III. Marked limitations of ordinary physical activity. Walking one to two blocks on the level and climbing more than one flight under normal conditions.

IV. Inability to carry on any physical activity without discomfort—anginal syndrome can be present at rest

Pericarditis

It is most often sharp and penetrating in quality; patients often obtain relief by sitting up and bending forward .

The cardinal diagnostic feature of pericardial pain is its frequent worsening by changes in body position, during deep inspiration, and occasionally on swallowing.

The chest discomfort can radiate to the shoulders, upper back, and neck because of irritation of the diaphragmatic pleura.

Aortic dissection

The pain is usually of sudden onset

Patients frequently characterize the pain as having a tearing quality, and commonly localized to the interscapular area.

The discomfort can radiate widely into the neck, back, abdomen, flanks, and legs and can migrate, depending on the location and progression of the aortic dissection

Respiratory Symptoms

1.Dyspnea is defined as difficult respiration or the unpleasant awareness of one's breathing.

Dyspnea on effort, a frequent symptom, is usually caused by congestive heart failure, chronic pulmonary disease, or physical deconditioning

Chronic dyspnea can be caused by heart failure, pulmonary disease, anxiety, obesity, poor physical fitness, pleural effusions, and asthma.

Acute dyspnea can occur with acute pulmonary edema, pneumothorax, pulmonary embolism, pneumonia, and airway obstruction.

2.Orthopnea results from an increase in hydrostatic pressure in the lungs that occurs with assumption of the supine position. It consists of cough and dyspnea in some patients with LV failure or mitral valve (MV) disease and necessitates the use of two or more pillows on lying downlie flat comfortably.

3.Paroxysmal nocturnal dyspnea (PND) is the occurrence of dyspnea during sleep, commonly 2 to 3 hours after going to bed, which is relieved by assuming the upright position. The probable mechanism for this relatively specific symptom of left-sided heart failure is the increase in central blood volume in the supine position

4.A dry, unproductive cough, occurring with effort or at rest, can be related to the pulmonary congestion associated with heart failure.

The cough that accompanies acute pulmonary edema is often associated with frothy, pink-tinged sputum.

Cough also can be caused by angiotensin-converting enzyme inhibitors.

5.Hemoptysis occurs in many cardiac disorders.

Bright red pulmonary venous blood from rupture of submucosal pulmonary venules can be expectorated by patients with pulmonary venous hypertension caused by mitral stenosis (MS) or severe left ventricle failure.

Darker blood or clots often occur with pulmonary emboli.

Pink, frothy sputum can be produced during acute pulmonary edema

Massive hemoptysis with exsanguination can follow rupture of an aortic aneurysm into the bronchial tree.

Edema and Ascites

Edema is a common symptom or finding in patients with right- or left-sided heart failure. A patient can detect edema of the ankles and lower legs during the day and note that it diminishes during the night.

Cardiac edema rarely involves the face or upper extremities.

Persistent edema in the legs from which veins were harvested at the time of bypass surgery is common.

The calcium antagonists can produce bilateral edema of the lower legs

Other causes of edema—such as varicosities, obesity, tight girdle, renal insufficiency, or cirrhosis with hypoproteinemia—must be considered.

Patients with severe edema caused by congestive heart failure can develop ascites; however, ascites is particularly common in patients with constrictive pericardial disease, sometimes occurring before peripheral edema becomes obvious .

Palpitation

The patient can complain of a "pounding," "stopping," "jumping," or "racing" in the chest.

Most normal individuals are intermittently aware of their heart action, particularly at the time of physical and emotional stress..

Simple premature beats can be perceived as a "floating" or "flopping" sensation in the chest caused by the more forceful beat that occurs after the pause following the premature beat.

Rapid heart action of a paroxysmal tachycardia usually begins and terminates abruptly and causes a pounding sensation in the chest.

Syncope

Cardiac syncope (fainting) is defined as the transient loss of consciousness caused by inadequate cerebral blood flow secondary to an abrupt decrease in cardiac output .

Brief, unsustained seizure activity can occur with syncope caused by a cardiac arrhythmia. The patient can be incontinent during cardiogenic syncope

An aura, sustained tonic-clonic movements, tongue biting, and confusion or drowsiness after the event are more characteristic of syncope caused by central nervous system disease.

In contrast, return of consciousness to the alert state is prompt after reversal of the arrhythmia causing cardiac syncope.

The common faint (vasovagal syncope) results from bradycardia and hypotension caused by excessive vagal discharge. It is often associated with some precipitating event such as a heavy meal in a warm room and has brief premonitory signs and symptoms such as nausea, yawning, diaphoresis, and sometimes the feeling of decreased hearing or vision. Following a fainting episode, the patient can be pale and diaphoretic and have a slow heart rate

A hypersensitive carotid sinus can cause syncope. A history of episodes during an activity such as shaving, wearing of a tight collar, or extreme turning of the head can occur

Syncope following urination (micturition syncope) can occur at the time of rapid decompression of a distended bladder, which typically occurs after a period of sleep.

Paroxysms of coughing, usually in patients with underlying pulmonary disease, can result in syncope.

Stokes-Adams syncope is caused by intermittent complete heart block, sinus arrest, or ventricular tachyarrhythmias . It is characterized by abrupt loss of consciousness without warning, a variable period of unconsciousness (seconds to minutes), and then a rapid return of normal mental status without amnesia or a postictal state.

In the presence of severe LV outflow obstruction (aortic stenosis or hypertrophic cardiomyopathy), loss of consciousness with effort can occur

Postural hypotension usually occurs when the individual is upright and often just after rising from a supine or sitting position. Possible causes include peripheral neuropathy, autonomic dysfunction, volume depletion, aging or drug side effect.

Cyanosis

Cyanosis is a bluish color of the skin or mucous membranes caused by excess amounts of reduced hemoglobin.

A distribution of cyanosis involving the mucous membranes as well as the periphery (central cyanosis) is caused by the admixture of venous blood at the level of the heart or great vessels.

A patient or a family member can detect that the cyanosis is more intense in the feet than in the hands. This differential cyanosis suggests a right-to-left shunt through a patent ductus arteriosus in a patient with Eisenmenger physiology.

Peripheral cyanosis does not involve the mucous membranes but is the result of slow peripheral flow with in the setting of circulatory failure, shock, or peripheral vasospasm

Table 3- The Old New York Heart Association Functional Classification

Class 1 No symptoms with ordinary physical activity.

Class 2 Symptoms with ordinary activity. Slight limitation of activity.

Class 3 Symptoms with less than ordinary activity. Marked limitation of activity.

Class 4 Symptoms with any physical activity or even at rest.

Classification of Cardiac Disability

Assignment of symptom severity contributes importantly to risk assessment,clinical decision-making and patient outcome

The portion of the classification New York Heart Association that concerns functional capacities in heart failure is commonly used .

Although the Canadian Cardiovascular Society's grading system for angina is more widely used for patients with chest pain

The Cardiovascular Examination

Jugular Venous Pressure and Wave Form

Examination of the Jugular Venous Pulse

The two main objectives of the bedside examination of the neck veins are estimation of the CVP and inspection of the waveform.

Usually, the right internal jugular vein (IJV) is superior for both purposes because the EJV is valved and not directly in line with the superior vena cava (SVC) and right atrium (RA.

In most normal subjects, the maximum pulsation of the IJV is observed when the trunk is inclined by less than 30 degrees.

Simultaneous palpation of the left carotid artery aids the examiner in deciding which pulsations are venous.

The venous pressure is measured as the vertical distance between the top of the venous pulsation and the sternal inflection point, where the manubrium meets the sternum (angle of Louis). A distance of >3 cm is considered abnormal.

In patients suspected of RV failure but with a normal resting venous pressure, the abdominojugular test is useful.

The abdominojugular reflex is performed using pressure over the right upper quadrant, for at least 10 seconds. A sustained rise of >3 cm in the venous pressure for at least 15 seconds is a positive response.

Normal Venous Pulse The normal jugular venous pulse (JVP) reflects phasic pressure changes in the right atrium and consists of three positive waves and two negatives troughs

In order to time these pulsations, feel the left carotid artery with your right thumb or listen to the heart simultaneously

The positive presystolic a wave is produced by right atrial (RA) contraction and is the dominant wave in the JVP, particularly during inspiration.

Following a wave, the JVP contour declines, forming the normal negative systolic wave, the x wave. The x descent is caused by a combination of atrial relaxation, the downward displacement of the tricuspid valve during RV systole, and the ejection of blood from both ventricles

The positive, later systolic v wave in the JVP results from the increase in blood volume in the venae cavae and right atrium during ventricular systole when the tricuspid valve is closed

Following the summit of the v wave, there is a negative descending limb, referred to as the y descent or diastolic collapse, which is caused by the tricuspid valve opening and the rapid inflow of blood into the RV.

The a wave precedes the first heart sound (S1).

A prominent a wave is seen in patients with reduced right ventricular (RV) compliance from any cause.

A cannon a wave occurs with A-V dissociation and RA contraction against a closed tricuspid valve .

The a wave is absent with AF.

Abnormal Venous Pulse

The x descent

its obliteration or even replacement by a positive wave caused by tricuspid regurgitation

In patients with constrictive pericarditis, the x descent wave is often more prominent than the early diastolic y wave

The v wave follows just after S2.

• The v wave is smaller than the a wave because of the normally compliant right atrium.

•In patients with atrial septal defect (ASD), the a and v waves may be of equal height;

•In tricuspid regurgitation (TR), the v wave is accentuated.

The y descent•If there is resistance to ventricular filling in early diastole, the y descent will be blunted, as is the case with pericardial tamponade or tricuspid stenosis.

•The y descent will be steep when ventricular diastolic filling occurs early and rapidly, as with pericardial constriction.

Schematic representation of the normal jugular venous pressure (JVP), four types of abnormal JVP, and the JVP in three arrhythmias. AV, atrioventricular; ECG, electrocardiogram; S1, first heart sound; S2, second heart sound

Elevated Venous Pressure

The most common cause of an elevated jugular venous pressure is an increased RV pressure such as occurs in patients with PS, PH, or RV failure secondary to left-sided heart failure or RV infarction.

The venous pressure also is elevated when obstruction to RV inflow occurs, as with tricuspid stenosis (TS) or RA myxoma, or when constrictive pericardial disease impedes RV inflow. It also can result from vena cava obstruction and, at times, an increased blood volume.

The normal venous pressure should fall by at least 3 mm Hg with inspiration.

A rise in venous pressure (or its failure to decrease) with inspiration is known as the Kussmaul sign,and is classically associated with: •Constrictive pericarditis,•Restrictive cardiomyopathy,• Pulmonary embolism, •RV infarction•Advanced systolic heart failure.

Measuring the Blood Pressure

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•For the noninvasive evaluation of arterial BP, a pneumatic cuff with a mercury or aneroid manometer is the most frequently used technique .

•The mercury manometer is the gold standard; the aneroid manometer should be calibrated against the mercury manometer at least every 6 months.

Phases of the Korotkoff Sounds

Phase I  The pressure level at which the first faint, consistent tapping sounds are heard. The sounds gradually increase in intensity as the cuff is deflated. The first of at least two of these sounds is defined as the systolic pressure.

Phase II  The time during cuff deflation when a murmur of swishing sounds are heard.

Phase III  The period during which sounds are crisper and increase in intensity.

Phase IV  The time when a distinct, abrupt, muffling of sound (usually of a soft blowing quality) is heard. This is defined as the diastolic pressure in anyone in whom sounds continue to zero.

Phase V  The pressure level when the last regular blood pressure sound is heard and after which all sound disappears. This is defined as the diastolic pressure unless sounds are heard to zero.

The Korotkoff sounds have been divided into five phases occurring in sequence as the occluding pressure declines .

(1)The auscultatory gap is a period of silence occurring during Korotkoff phases I and II. This disappearance of sound is temporary and is usually short, but the gap can occur over a 40 mmHg measurement.

(2) An absent Korotkoff phase V occurs when sounds are heard to 0. When this is the case, phase IV should be recorded along with phase V. In this case, phase IV is the best reference for diastolic pressure.

1. Blood pressure should be measured in the seated position with the arm at the level of the heart

2. The patient should be relaxed for 5 to 10 minutes.

3. In the supine position, the arm should be raised to bring it to the level of the mid-RA (i.e., elevated on a pillow).

4. The length and width of the cuff's bladder should be 80 and 40 percent of the arm's circumference, respectively

5. The cuff should be placed 1 to 2 cm above the antecubital fossa to allow for placement of the stethoscope over the brachial artery.

6. The cuff should be inflated to 30 mm Hg above the systolic pressure and the pressure should be released at 2 to 3 mm Hg per second

The BP should be taken with the subject upright as well as supine.

Measurement of the BP in both arms is recommended, especially in the elderly.

The systolic pressure be recorded as the point at which the first tapping sounds occur (phase I) and that the diastolic pressure in adults be recorded as the point at which sounds become inaudible. In children and in adults with a hyperkinetic circulation, the diastolic pressure should be recorded as the point at which muffling of the sounds occurs (onset of phase IV). The arterial pressures at both the onset of muffling (phase IV) and the disappearance of sound (phase V) should be recorded.

The mean BP can be estimated by the addition of one-third the pulse pressure (systolic pressure minus diastolic pressure) to the diastolic pressure.

Patients with atrial fibrillation can have a significant beat-to-beat variation in their arterial pressure. Accordingly, the indirect BP should be measured several times and the average noted.

The arterial pressure can be underestimated if the cuff is deflated too rapidly, or if inadequate inflation does not result in complete arterial occlusion.

When the cuff is deflated too slowly or is immediately reinflated for multiple pressure determinations, the resulting venous congestion can elevate the diastolic pressure artificially and falsely decrease the systolic pressure by decreasing the intensity of phase I or phase II sounds to an inaudible level

Studies correlating direct and indirect BP measurements have, in general, shown a good correlation between indirect and direct measurements of BP in the arm.

The indirect method tends to underestimate systolic pressure by several millimeters of mercury, to overestimate diastolic pressure by several millimeters of mercury when phase IV is used as an endpoint, and to slightly underestimate diastolic pressure in normal individuals when phase V is taken as the endpoint

Korotkoff sounds may be heard all the way down to 0 mm Hg in patients with:

chronic severe AR, children, pregnant patients, in the presence of a large (AV) fistula

In these cases, both the phase 4 and 5 pressures should be noted.

Blood pressure should be measured in both arms either in rapid succession or simultaneously; normally the measurements should differ by <10 mm Hg, independent of handedness.

Systolic leg pressures may be as much as 20 mm Hg higher than arm pressures;

Leg blood pressure should be measured using large thigh cuffs with auscultation at the popliteal artery or using a standard large arm cuff on the calf with simultaneous auscultation at the posterior tibial artery

Normal pressures have been defined on the basis of values included within two standard deviations of the mean of pressures obtained in a large population of apparently healthy individuals.

The normal BP range varies with age, sex, and race

The normal BP limits for adults are approximately 100 to 140 mmHg systolic and 60 to 90 mmHg diastolic

Factor contributing to variations in an individual's BP during daily activities include: (1) body posture; (2) state of muscular, cerebral, or gastrointestinal activity; (3) emotional or painful stimuli; (4) environmental factors such as temperature and noise level; and (5) the use of tobacco, coffee, alcohol, and other drugs with direct or neurally mediated vasomotor properties.

The average diurnal pattern of BP consists of an increase throughout the day and early evening and a significant, rapid decline to a low point during the early, deep stage of sleep.

With normal respiration, the peak systolic BP is greater during expiration than during inspiration by as much as 10 mmHg

Increased Pulse Pressure

This usually is caused by an increase in stroke volume and ejection velocity, often with a decrease in peripheral resistance.

Fever, anemia, hot weather, exercise, pregnancy, hyperthyroidism, or arteriovenous fistulas can produce this change. Several cardiac diseases, such as AR, patent ductus arteriosus, and truncus arteriosus, also can result in a widened pulse pressure. An increased pulse pressure caused by a large stroke volume can occur with complete heart block or marked sinus bradycardia.

Atherosclerosis of the large arteries often reduces arterial compliance and results in an elevated systolic pressure with a normal or even decreased stroke volume.

The increased pulse pressure associated with systemic arteriovenous fistulas is less common; a relative tachycardia can be the only clinical clue. Compression of a systemic arteriovenous fistula can produce a prompt slowing of the heart rate (Branham sign).

Reduced Pulse Pressure

A narrow pulse pressure is uncommon in normal subjects but can result from an increased peripheral resistance (increased circulating catecholamines in heart failure), decreased stroke volume (severe as in arteriosclerosis [AS]), and/or markedly decreased intravascular volume (diabetic ketoacidosis).

Unequal Pulse Pressures

The diagnostic importance of BP differences between the right and left arms can occur as a result of supravalvular AS and the subclavian steal syndrome

A difference in arm and leg pressures can occur because of coarctation of the aorta or acquired disease, such as aortic dissection, aortic arch syndrome, or the subclavian steal syndrome.

Pulsus Paradoxus

A normal person can exhibit a 10 mmHg drop in systolic pressure during normal inspiration.

A greater decline can be identified in patients with acute cardiac tamponade, constrictive pericarditis, severe obstructive lung disease, and restrictive cardiomyopathy.

Pulsus paradoxus is best detected by inflating the BP cuff above systolic pressure and then slowly releasing it. As the cuff pressure is gradually reduced, the BP sounds become audible during expiration. The difference in pressure between the first audible sound heard on expiration and the pressure level at which the sounds are heard during all phases of respiration gives a measurement of magnitude of pulsus paradoxus

The Ankle-Brachial Index

The ankle-brachial index (ABI) is the ratio of the systolic blood pressure at the ankle divided by the higher of the two arm systolic blood pressures.

It reflects the degree of lower-extremity arterial occlusive disease, which is manifest by reduced blood pressure distal to stenotic lesions.

An arm systolic pressure of 120 mmHg and an ankle systolic pressure of 60 mmHg yields an ABI of 0.5 (60/120).

The ABI is inversely related to disease severity.

A resting ABI <0.9 is considered abnormal.

Lower values correspond to progressively more severe occlusive peripheral arterial disease (PAD) and disabling claudication.

An ABI <0.3 is consistent with critical ischemia, rest pain, and tissue loss.

Assessing the Pulses

The arterial pulse occurs at the same frequency as the heartbeat.

Ejection of blood with every cardiac contraction is converted to pulsations in arteries throughout the body.

Examination of the Arterial Pulse

All pulses should be examined for symmetry, timing, and strength. Concomitant palpation of the brachial or radial pulse with the femoral pulse should routinely be performed; The carotid pulses should not be examined simultaneously or before auscultation for a bruit; light pressure should be used

A pulse in the foot should not be considered absent unless examined with the foot in a dependent position. Otherwise, the arterial pulses usually are examined with the patient supine and with the trunk of the body slightly elevated

The usual technique for palpating the arterial pulse is to press with the examining fingers until the maximum pulse is sensed

Arterial pulses compared using a scale such as the following:

0 = complete absence of pulsation; 1+ = small or reduced pulsation; 2+ = normal or average pulsation; and 3+ = large or bounding pulsation

The carotid artery pulse The carotid pulse is usually best examined with the sternocleidomastoid muscles relaxed and the head rotated slightly toward the examiner. The carotid pulse should be palpated in the lower half of the patient's neck to avoid carotid sinus compression.

Use the index and middle fingers or thumb of your opposite hand.

Cup your hand under the patient’s elbow and feel for the pulse just medial to the biceps tendon.

The patient’s arm should rest with the elbow extended, palm up.

With your free hand, you may need to flex the elbow to a varying degree to get optimal muscular relaxation.

Brachial pulse

Palpate the radial pulse with the pads of your fingers on the flexor surfaceof the wrist laterally. Partially flexing the patient’s wrist may help you feel this pulse.

The femoral pulse.

Press deeply, below the inguinal ligament and about midway between the anterior superior iliac spine and the symphysis pubis.

The popliteal pulse.The patient’s knee should be somewhat flexed, the leg relaxed. Place the fingertips of both hands so that they just meet in the midline behind the knee and press them deeply into the popliteal fossa.

The dorsalis pedis pulse.

Feel the dorsum of the foot just lateral to the extensor tendon of the great toe.

The posterior tibial pulse.

Curve your fingers behind the medial malleolus of the ankle.

Allen testThe integrity of the arcuate system of the hand can be assessed using the Allen test.

1. Ask the patient to make a tight fist with one hand;

2. Compress both radial and ulnar arteries firmly between your thumbs and fingers.

3. Ask the patient to open the hand into a relaxed, slightly flexed position. The palm is pale.

4. Release your pressure over the ulnar artery.

5. If the ulnar artery is patent, the palm flushes within about 3 to 5 seconds.

Normal Pulse countor

Normally, the incident (or percussion wave) begins with systolic ejection (just after S1) and is the predominant monophasic pulse appreciated at the bedside .

Percussion wave is caused by arrival of the impulse generated by LV ejection

Schematic diagrams of the configurational changes in the carotid pulse

Normal Anacrotic pulse Pulsus bisferiens In aortic regurgitation

Pulsus bisferiens in hypertrophic obstructive cardiomyopathy

Dicrotic pulse

A bounding pulse

Large, bounding arterial pulses usually indicate the rapid ejection of an increased volume of blood from the left ventricle.

Commonly, the arterial pulse pressure is increased, and the peripheral arterial resistance diminished .

It Caused by:

Fever AnemiaThyrotoxicosis, Severe bradycardia ARArteriovenous fistula.

Bisferiens Arterial Pulse

The bisferiens (from the Latin twice beating) pulse has a waveform characterized by two positive waves during systole .

The pulse wave upstroke rises rapidly and forcefully, producing the first systolic peak (percussion wave). A brief decline in pressure is followed by a smaller and somewhat slower-rising positive pulse wave (tidal wave).

The bisferiens pulse is sometimes more easily palpable in a brachial or radial artery.

A bisferiens pulse often occurs in patients with pure AR and in patients with combined AS and severe AR. It also occurs in association with the rapid ejection of an increased stroke volume from the left ventricle (e.g., exercise, fever, patent ductus arteriosus).

The bisferiens pulse often is present in patients with hypertrophic cardiomyopathy, many of whom have a pressure gradient in the LV outflow tract. In this syndrome, the midsystolic negative wave usually coincides with a marked decrease in the rate of LV ejection.

Dicrotic Arterial Pulse

The dicrotic (from the Greek dikrotos, "double beating") pulse is a twice-peaked pulse with one peak in systole and the second in diastole

The dicrotic pulse is most common in young or middle-aged patients with impaired LV performance

Rarely, the dicrotic wave can be palpated in young, febrile patients

pulsus paradoxus

A >10 mm Hg fall in systolic pressure with inspiration

In patients with cardiac tamponade, fluid accumulation in the pericardium increases intrapericardial pressure, and the heart's filling capacity is reduced. During inspiration, the expected augmentation of venous return to the right side of the heart occurs despite the elevated intrapericardial pressure. The diminished thoracic pressure also causes a pooling of blood in the pulmonary veins and capillaries and diminishes pulmonary venous return to the left atrium. This produces a decline in LV stroke volume and systolic BP during inspiration.

Pulsus paradoxus is not specific for pericardial tamponade, and has been described with:

Massive pulmonary embolus Hemorrhagic shockSevere obstructive lung diseaseTension pneumothorax

Pulsus alternans

Defined by the beat-to-beat variability of the pulse amplitude. Generally seen in severe heart failure

pulsus parvus et tardus

Severe aortic stenosis may be suggested by a weak and delayed pulse.

Arterial bruits

Created by turbulent flow through narrowed arteries.

The absence of a bruit does not rule out significant luminal compromise.

Palpation of the Precordium

Palpation of the precordium is also best performed from the right side, with the patient supine and the upper trunk elevated 30 degrees

Patients should be examined in the left lateral decubitus position, rotated 45 to 90 degrees. In this position, the normal LV impulse can be displaced several centimeters leftward and can appear more prominent and sustained.

The pads of the fingers are most useful for detecting LV motion, whereas the palm and proximal metacarpals are usually best used for palpating the parasternal systolic lift of RV hypertrophy.

Thrills are palpable vibrations from murmurs or bruits ordinarily associated with grade 4/6 murmurs or louder. Thrills are palpated most easily using either the palm of the hand or the proximal metacarpals

The normal apex (apical) impulse usually is located within 10 cm of the sternal midline, at or within the left midclavicular line in the fifth intercostal space, when the patient is supine. It can be located lateral to the midclavicular line when associated with a high diaphragm, pregnancy, marked pectus excavatum, or other conditions that displace a normal heart to the left.

The normal apex impulse is less than 3 cm in diameter. The outward movement of the apical impulse is normally not excessively forceful and is felt only during the first third of systole.

Apical Area Pulsations

In general, a greatly sustained apex impulse indicates either marked LV hypertrophy or depressed LV systolic function, whereas LV dilatation displaces the apex impulse laterally and inferiorly.

A late systolic bulge at the cardiac apex can be caused by a functional LV aneurysm, occasionally resulting in a bifid apex impulse

A bifid apex impulse during systole also can be caused by marked LV dilatation and hypertrophy in patients with both AS and regurgitation or in patients with hypertrophic cardiomyopathy.

Systolic retraction of the apical impulse usually indicates either constrictive pericarditis or severe TR with marked RV dilatation .

Auscultation of the Heart

Cardiac AuscultationThe Stethoscope

has only a short segment of flexible tubing, and is equipped with a diaphragm and a bell.

The rubber tubing should be as short as possible; experience indicates that tubing approximately (30 cm) long is the best compromise. Thick-walled tubing approximately 3 mm in diameter is best suited to transmit sounds and murmurs. A stethoscope requires both a diaphragm and a bell, and each must be applied to the chest wall with optimal pressure. The diaphragm, which is fairly rigid, brings out the high frequencies and attenuates the lows. When it is used to accentuate high-pitched sounds, the diaphragm should be pressed very firmly against the skin. The bell tends to accentuate the low-frequency sounds and to filter out the high-pitched tones.; in these situations, the stethoscope is placed very lightly on the skin, with just enough pressure to seal the edge at the point of maximal impulse.

Examination of the Patient

Usually, the physician will examine from the right side.The patient should be lying on his or her back, and each area should be surveyed with both chest pieces.

There are four primary areas of cardiac auscultation: (1) the primary and secondary aortic areas in the second right interspace and the third left interspace adjacent to the sternum, respectively, (2) the pulmonary area in the second left interspace, (3) the tricuspid area in the fourth and fifth interspaces adjacent to the left sternal border, and (4) the mitral area at the cardiac apex.

With the bell applied lightly to the skin at the apex, the patient is instructed to roll onto the left side, and the clinician selectively tunes in to diastole and the low-frequency range. This allows the physician to determine the presence or absence of diastolic filling sounds or diastolic rumbles arising from the AV valves.

The examination is continued with the patient in the sitting position.With the patient's breath held in deep expiration, the physician examines the aortic and pulmonic areas with the diaphragm firmly pressed against the chest wall, selectively tuning in to the high-frequency range in an effort to hear the faint blowing diastolic murmur of AR or, if the clinical situation warrants, the presence of a pericardial friction rub.

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HEART SOUNDS

FIRST HEART SOUND (S1)

The normal first heart sound (S1) comprises mitral (M1) and tricuspid (T1) valve closure.

The first high-frequency component of S1 coincides with the complete coaptation of the anterior and posterior leaflets of the mitral valve.

The primary factors determining intensity of S1 are

(1) integrity of valve closure, (2) mobility of the valve, (3) velocity of valve closure, (4) status of ventricular contraction, (5) transmission characteristics of the thoracic cavity and chest wall

Integrity of Valve ClosureIn rare situations, usually in the setting of severe MR, there is inadequate coaptation of the mitral leaflets to a degree that valve closure is not effective. As a result, abrupt halting of the retrograde blood column during early ventricular contraction does not occur, and S1 can be markedly attenuated or absent

Mobility of the ValveSevere calcific fixation of the mitral valve with complete immobilization will cause a markedly attenuated M1. This is seen most commonly in the setting of long-standing severe MS.

Velocity of Valve Closure

At short PR intervals (30 to 70 ms), the mitral valve leaflets are maximally separated by atrial contraction at the onset of LV systole. With LV contraction, the mitral valve closes at a high velocity with a large excursion. This results in a loud, late M1

The clinical finding of marked variation in the intensity of S1 in a patient with a slow heart rate often will alert the clinician to the diagnosis of complete AV block with AV dissociation.

Variations in the intensity of S1 also occur with atrial fibrillation. The loud S1 occurs at short RR intervals, whereas a softer S1 occurs at longer RR

S1 in Mitral Stenosis

A loud, late M1 is the hallmark of hemodynamically significant mitral stenosis

The closure of the leaflet begins from a domed position within the LV cavity and takes place over a much greater distance following the onset of LV contraction

S1 in Mitral Valve Prolapse

The increased amplitude of leaflet excursion with explains the loud M1 associated with holosystolic prolapse. An alternate explanation can be a summation of a normal M1 and an early nonejection click of valvular prolapse.

S1 and Left Bundle-Branch BlockIn LBBB, M1 is decreased in intensity and is frequently delayed, at times resulting in reversal of sequence of S1. The reason for the delay and the decreased intensity of M1 in this condition is multifactorial. The primary factors involved are (1) delay in onset of LV contraction, (2) degree of LV dysfunction, (3) presence of concomitant first-degree heart block

S1 in Acute Aortic RegurgitationOne of the important auscultatory findings in acute AR is attenuation or absence of M1. Severe regurgitation causes a marked increase in the LV end-diastolic pressure, resulting in premature closure of the normal mitral valve in mid-diastole

SECOND HEART SOUND (S2)

The second heart sound (S2) comprises aortic (A2) and pulmonic (P2) valve closure. A2 and P2 are produced by the sudden deceleration of retrograde flow of the blood column in the aorta and pulmonary. P2 normally occur after A2

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Normal Physiologic Splitting

During inspiration, both components become distinctly audible as the splitting interval widens

On auscultation, splitting of S2 is usually best heard at the second or third left intercostal space;

The normal P2 is softer than A2 and is rarely audible at the apex. When P2 is heard at the apex, either significant PH is present or the apex is occupied by the RV, a situation seen commonly in normotensive ASD.

In younger subjects, maximal splitting during inspiration averages 40 to 50 ms; with age, this value decreases such that a single S2 during both phases of respiration can be normal in subjects older than 40 years of age.

Abnormal Splitting

1.Wide Physiologic Splitting of S2 caused by

Right bundle-branch block

Severe PH and PS

ASD (wide, fixed splitting)

Acute MR.

2.Reversed Splitting of S2

Complete LBBB

Hypertrophic cardiomyopathy

Valvular AS

Chronic AR

Patent ductus arteriosus.

Type B Wolff-Parkinson-White syndrome(early activation of the RV through an accessory pathway has caused P2 to occur prematurely.)

SYSTOLIC SOUNDS

An ejection sound is a high-pitched, early systolic sound and is usually associated with

congenital bicuspid aortic or pulmonic valve disease. aortic or pulmonic root dilation

The ejection sound that accompanies pulmonic valve disease decreases in intensity with inspiration, the only right-sided cardiac event to behave in this manner.

Nonejection clicks, which occur after the upstroke of the carotid pulse, are related to mitral valve prolapse

DIASTOLIC SOUNDS

1. The high-pitched opening snap (OS) of mitral stenosis

Opening Snaps caused by sudden checking of the early diastolic descent of the funnel-shaped stenotic valve when its elastic limits were met.

Usually best heard in the apex.

A loud opening snap is found in mobile stenotic valves with good excursions , whereas the opening snap is absent with severe calcific fixation of the valve.

The opening snap follows A2 by an interval of 0.03 to 0.15 s. In patients with mild MS, the interval is usually long, whereas in patients with more severe stenosis, the A2–opening snap interval is shorter. The A2–opening snap interval in atrial fibrillation can vary with cycle length.

2. A pericardial knock is a high-pitched early diastolic sound in patients with constrictive pericarditis.

3. A tumor plop is rarely heard with atrial myxoma; it is a low-pitched sound that may be appreciated only in certain positions and arises from the diastolic prolapse of the tumor across the mitral valve.

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4.The Third Heart SoundPhysiologic S3

The physiologic S3 is a benign finding commonly heard in children, adolescents, and young adults, but it is rarely present in adults after 40 years

Pathologic S3

Most agree that the pathologic S3 is an exaggeration of the physiologic S3, with a common mechanism of production.

the S3 occurs when the ventricle suddenly reaches its elastic limits and abruptly decelerates the onrushing column of blood.

A third heart sound (S3) occurs during the rapid filling phase of ventricular diastole. An S3 indicates systolic heart failure in older adults and carries important prognostic weight . A left-sided S3 is a low-pitched sound best heard over the LV apex in the left lateral decubitus position.

5.A fourth heart sound (S4)

A fourth heart sound (S4) occurs during the atrial filling phase of ventricular diastole. An S4 is especially common with left ventricular hypertrophy or myocardial ischemia.

Pericardial Friction Rub

Inflammation of the pericardial sac with or without fluid can cause a pericardial friction rub.

These friction sounds are very high pitched, leathery, and scratchy in nature.

They seem close to the ear and are auscultated best with the patient leaning forward holding his or her breath after forced expiration.

The pericardial rub can have three components during the intervals of the cardiac cycle—at the time of atrial systole, at the time of ventricular contraction, and during rapid early diastolic filling.

CARDIAC MURMURS

Heart murmurs result from audible vibrations caused by increased turbulence and are defined by their timing within the cardiac cycle.

There is seldom any difficulty distinguishing between systole and diastole, because systole is considerably shorter at normal heart rates. At rapid heart rates, the examiner can usually time the murmur by simultaneous palpation of the lower right carotid artery or can rely on the fact that the S2 is usually the louder sound at the base

Other important attributes, which aid in identification, include frequency, location, radiation, and response to bedside maneuvers

1. Very faint, heard only after listener has “tuned in”; may not be heard in all positions

2. Quiet, but heard immediately after placing the stethoscope on the chest

3. Moderately loud

4. Loud, with palpable thrill

5. Very loud, with thrill. May be heard when the stethoscope is partly off the chest

6. Very loud, with thrill. May be heard with stethoscope entirely off the chest

Gradations of Murmurs

Systolic murmurs are early, mid-, late, or holo-systolic in timing.

Acute severe MR results in a decrescendo, early systolic murmur

Mid-systolic murmurs begin after S1 and end before S2; they are usually crescendo-decrescendo in configuration. Aortic stenosis (AS) is the most common cause of a mid-systolic murmur in an adult.

There are several other causes of a mid-systolic heart murmur, including HOCM, pulmonic stenosis (PS), and increased pulmonary blood flow in patients with an ASD and a left-to-right shunt.

A grade 1 or 2 mid-systolic murmur can often be heard at the left sternal border with pregnancy, hyperthyroidism, or anemia—physiological states that are associated with accelerated blood flow across normal semilunar valves. A murmur of this type is also commonly heard in healthy children and adolescents.

A late, apical systolic murmur usually indicates mitral valve prolapse

Holosystolic murmurs occures in chronic MR and TR and membranous ventricular septal defect (VSD) without pulmonary hypertension.

MR is best heard over the cardiac apex and a VSD at the mid-left sternal border where a thrill is palpable in the majority of patients.

DIASTOLIC MURMURS.

Diastolic murmurs invariably signify cardiac abnormality.

Chronic AR causes a high-pitched decrescendo early to mid-diastolic murmur.

The diastolic murmur is both softer and of shorter duration in acute AR.

The murmur of pulmonic regurgitation (PR) is heard along the left sternal border and is most often due to annular enlargement from chronic PA hypertension (Graham Steell murmur).

Mitral stenosis is the classic cause of a mid- to late diastolic murmur. The murmur is best heard over the apex in the left lateral decubitus position, is low-pitched (rumbling. Presystolic accentuation refers to an increase in the intensity of the murmur in late systole following atrial contraction in patients in sinus rhythm.

The low-pitched mid- to late apical diastolic murmur associated with severe AR (Austin Flint murmur) can be distinguished from mitral stenosis

CONTINUOUS MURMURS

The presence of a continuous murmur implies a pressure gradient between two chambers or vessels during both systole and diastole.

Examples include the murmurs associated with PDA Ruptured sinus of Valsalva aneurysm Coronary, great vessel, or hemodialysis AV fistulas Cervical venous hum Mammary souffle of pregnancy

DYNAMIC AUSCULTATION

Right-sided events, save for the pulmonic ejection sound, increase with inspiration and decrease with exhalation; left-sided events behave oppositely

The intensity of the murmurs associated with MR, VSD, and AR will increase in response to maneuvers that increase LV afterload (handgrip, vasopressors)

Squatting is associated with an abrupt increase in ventricular preload and afterload; whereas rapid standing results in a sudden decrease in preload. In patients with mitral valve prolapse (MVP), the click and murmur will move away from S1 with squatting, because of the delay in onset of leaflet prolapse at higher ventricular volumes. With rapid standing, the click and murmur move closer to S1, as prolapse occurs earlier in systole at a smaller chamber dimension. The murmur of HOCM behaves in a directionally similar

Valsalva Maneuver

When a person strains down against a closed glottis, venous return to the right heart is decreased.

Most murmurs decrease in length and intensity. Two exceptions are the systolic murmur of HOCM and MVP

Prosthetic Heart Bioprosthesis

In the mitral position is usually associated with a mid-systolic murmur (from turbulence created by systolic flow across the valve struts as they project into the LV outflow tract) and a soft, mid-diastolic murmur. Holosystolic apical murmur signifies paravalvular or bioprosthetic regurgitation.

A bioprosthesis in the aortic position is invariably associated with a grade 2 to 3 mid-systolic murmur at the base.A diastolic murmur of AR is abnormal

Mechanical prosthesis

A decrease in the intensity of either the opening or closing sounds of a, depending on its type, is a worrisome finding.

A apical systolic murmur in patients with a mechanical mitral prosthesis, or a diastolic murmur in patients with an aortic prosthesis, indicates prosthetic dysfunction (or dehiscence).