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• CHEST PAIN
• ANGINA (ISCHEMIC CARDIAC PAIN): Squeezing, crushing, strangling, constricting pain in center of chest. Pain may radiate to left shoulder, left arm, right shoulder, jaw.
• Stable (Typical) Angina: Angina upon effort, or angina induced by increased blood pressure or increased heart-rate. 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.
• Characteristic ECG findings can help distinguish variant angina from typical angina.
• Nitroglycerin will probably still relieve pain, as it relaxes coronary arteries.
• Myocardial Infarct: Typical presentation = Unstable angina lasting longer than 15 minutes, that is not relieved by nitroglycerin.
• Silent MI's and MI's with atypical presentation do occur.
• NON-ISCHEMIC CARDIAC PAIN:
• Mitral Valve Prolapse: Usually asymptomatic, but may present with an intermittent, sharp, sticking pain over left precordium.
• Pericarditis: The patient feels relief by shallow breathing and by sitting up and leaning forward.
• Dissecting Aneurysm: Sudden, severe tearing pain, radiating to the abdomen, neck, or back, depending on where the aneurysm is going.
• PLEURITIC (PULMONARY) CHEST PAIN: Also see pulmonary study guide.
• Pulmonary Embolism: May be asymptomatic, or the patient may feel a dull tightness if the embolus is large enough.
• Paroxysmal Dyspnea is the most common symptom of pulmonary embolism.
• Pleurisy: Pain upon breathing. May be caused by pulmonary embolism, pneumonia, bronchitis, or pleural effusion.
• Pulmonary Hypertension: Dyspnea is a more common symptoms than pleuritic pain.
• Pneumothorax: Pain may be confused with pain of an MI.
• 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.
• GASTROINTESTINAL CHEST PAIN:
• Esophageal Spasm: Substernal chest pain and dysphagia.
• Esophageal Reflux (GERD): Chest pain relieved by antacids.
• Gallstone Colic: Colicky RUQ pain radiating to back and to right shoulder. Occasionally it may be confused with angina.
• CHEST WALL PAIN:
• TIETZE'S SYNDROME (COSTOCHONDRITIS): Inflammation of Costochondral joints. Pain is often localized and can be elicited by palpating the sternum over the involved ribs.
• HERPES ZOSTER: Pain may precede the appearance of the rash. Both pain and rash follow dermatomal distribution.
• DACOSTA'S SYNDROME: Psychogenic pain usually localized to the cardiac apex. May be associated with anxiety.
• May also see palpitations, hyperventilation, dyspnea, weakness, depression, or other signs of anxiety.
• Vertebral Column Disease: It may occasionally lead to anterior chest pain.
• DYSPNEA: Air hunger or difficulty breathing may be associated with cardiac diseases.
• EXERTIONAL DYSPNEA: Dyspnea on exertion is a common symptom of mild or severe Congestive Heart Failure.
• DYSPNEA at REST:
• Pulmonary causes of dyspnea (PE, COPD, pneumothorax) often occur at rest. With cardiac problems, dyspnea usually does not occur at rest, or it is overshadowed by angina.
• Anxiety Dyspnea: Difficulty breathing due to anxiety occurs only at rest.
• ORTHOPNEA: Dyspnea occurring with patient in the supine position. Orthopnea is a sign of Congestive Heart Failure that is more severe than that associated with exertional dyspnea.
• CAUSE: Supine position increases pulmonary blood flow ------> exacerbate pulmonary congestion and pulmonary edema. The problem is relieved by resuming a more upright position.
• Two-Pillow, Three-Pillow Orthopnea: Terms to describe the severity of the orthopnea. Three pillow is worse than two-pillow.
• PAROXYSMAL NOCTURNAL DYSPNEA (PND): Similar to orthopnea, except it has sudden onset and occurs only after the patient has been lying down at rest for at least an hour.
• Unlike orthopnea, It is not relieved immediately by sitting up.
• Patient is usually able to return to sleep, eventually.
• PULMONARY EDEMA: Pulmonary edema is usually a manifestation of left-ventricular heart failure. Peripheral edema associated with CHF is a manifestation of right-sided heart failure (Cor Pulmonale).
• SYMPTOMS: Severe symptoms. Extreme anxiety, dyspnea, air hunger, cold sweats, fear of impending death.
• SIGNS: Pink, frothy sputum, and bubbly breath sounds.
• VALVULAR HEART DISEASE: Mitral Stenosis is associated with dyspnea.
• CONGENITAL HEART DISEASES:
• Tetralogy of Fallot: Exertional dyspnea is common.
• Ventricular Septal Defect: Tachypnea and sweating. Late cyanosis.
• CARDIAC -vs- PULMONARY DYSPNEA:
• OTHER CAUSES OF SHORTNESS OF BREATH:
• Kussmaul Respiration: Intense hyperventilation (respiratory alkalosis) occurring with Diabetic Ketoacidosis, as a compensatory mechanism to relieve the metabolic acidosis.
• PALPITATIONS: An unpleasant awareness of one's own heart-beat. Often described as fluttering, or skipping a beat.
• Paroxysmal Atrial Tachycardia: May cause palpitations with an instantaneous onset.
• Premature Ventricular Contractions (PVC's): May be experienced as palpitations or a skipped beat. The premature contraction is followed by a compensatory pause, to allow for ventricular filling.
• FATIGUE: Non-specific finding often found with heart disease.
• FATIGUE CAUSED BY HEART DISEASE: It usually occurs later in the day or in the evening. Fatigue early in the morning is usually not associated with heart disease, unless the patient was aroused from REM sleep.
• The heart disease gets worse, as the patient experiences onset of fatigue earlier in the day.
• OTHER CAUSES OF FATIGUE: Lots. Chronic illness of many types, anemia, psychological causes.
• SYNCOPE: Fainting, transient loss of consciousness.
• VASOVAGAL EVENTS: Most common cause of syncope, it is caused by excessive stimulation of the Vagus nerve ------> excessive bradycardia and reduced blood-flow to the brain.
• Anxiety: It is usually associated with acute anxiety or excessive emotion. The Vagal hyperactivity is thought to be a hypersensitive response to sympathetic outflow.
• CARDIOVASCULAR CAUSES:
• Arrhythmias:
• STOKES-ADAMS SYNDROME: Syncope caused by reduced cardiac output secondary to an arrhythmia.
• Both severe tachycardia and bradycardia can reduce cardiac output, leading to syncope. Severe tachycardia reduces cardiac output by reducing ventricular filling time.
• Cardiac Outflow Tract Obstruction:
• Aortic Stenosis may lead to syncope.
• Myxomas, benign myocardial tumors, may cause outflow obstruction and lead to syncope.
• Tetralogy of Fallot is associated with fainting attacks.
• Myocardial Ischemia
• Carotid Sinus Syncope: Hypersensitivity of the Carotid Sinus in elderly men is common cause of syncope.
• Impaired Vasomotor Reflexes: Impairment of Baroreceptors. Syncope is associated with orthostatic hypotension.
• Decreased Blood Volume
• FLUID REMOVAL:
• Micturition Syncope: Syncope occurring with micturition but at no other time. Associated with removal of fluid from the body.
• POST-TUSSIVE SYNCOPE: Syncope after a bout of coughing, or after the Valsalva maneuver, may occur in patients with COPD.
• HEMOPTYSIS: Mitral Valve Stenosis is a cardiac disease that may cause hemoptysis. Mitral Stenosis ------> pulmonary venous congestion ------> may lead to hemoptysis.
• EDEMA:
• Pitting Edema is a common sign of Congestive Heart Failure.
• Presacral Edema may be found in bed-ridden patients, and may lead to decubitus ulcers.
• Anasarca: Severe generalized edema and ascites, as seen in severe CHF, liver cirrhosis, or nephrotic syndrome.
• Lymphedema may be caused Filariasis or a tumor obstructing a lymphatic vessel.
• CYANOSIS: Presence of excessive deoxygenated hemoglobin in the blood. It becomes visible when the concentration of deoxygenated hemoglobin exceeds 5 g / dL -- a higher rate of desaturation than is found in the venous blood of normal people.
• Central Cyanosis: Visible in the lips, face, conjunctivae, tongue. It is caused by primary systemic hypoxia due to impaired oxygenation of blood. EXAMPLES:
• Tetralogy of Fallot or the late stages of other congenital heart defects
• Venoarterial shunt
• Peripheral Cyanosis (Acrocyanosis): Visible in the fingers and toes, earlobes, nose. It is caused by localized hypoxia due to poor circulation, reduced blood-flow, CHF, shock.

GENERAL PHYSICAL EXAM: Many congenital disorders are associated with various heart defects. See Table 4-5, page 150 for complete list. Also see Table of Physical Findings for a complete list of physical findings.

• THE FACE:
• THE EYES:
• THE MOUTH:
• THE SKIN:
• Rheumatic Fever: Characteristically you will see Erythema Marginatum and Subcutaneous Nodules.
• THE THORAX:
• THE ABDOMEN:
• THE EXTREMITIES:
• Clubbing of fingers and toes is a classic finding of Cyanosis. May also be seen with infective endocarditis or other conditions.

BLOOD PRESSURE:

• PALPATION:
• AUSCULTATION (Korotkoff Sounds):
• Phase 1: Clear tapping sounds representing systolic pressure.
• Phase 2: Softer tones
• Phase 3: Louder once again.
• Phase 4: Muffled Tones.
• Phase 5: Tones cease. Diastolic Pressure. Diastolic pressure may actually be higher than estimated by auscultation.
• INTERPRETATION:
• Auscultatory Gap: Period of silence that may occur between Phase 1 and Phase 2. The beginning and end of the Auscultatory Gap may be mistaken for Diastolic or Systolic blood pressure, respectively.
• CAUSES: Venous distension or severe Aortic Stenosis.
• Orthostatic Hypotension: Upon standing, normal decrease in systolic blood pressure is 5-15 mm Hg; anything more is Orthostatic Hypotension. Diastolic pressure normally remains constant or increases slightly.
• Obese Patient: Use a large cuff.
• Hypertension:
• Coarctation of the Aorta will result in a systolic pressure that is quite high in the arm, but much lower in the leg.

JUGULAR VENOUS PULSES:

• Central Venous Pressure (CVP): Use the right Internal Jugular to estimate CVP because it is straighter.
• MEASUREMENT:
• With patient sitting up, clavicles are 10 cm above right atrium, thus CVP = jugular venous distension above clavicles + 10 cm.
• With patient elevated 30, sternal Angle of Louis is normally about 5 cm above right atrium, and Internal Jugular should be visible about 3 cm directly vertical (use a ruler), above the sternal Angle of Louis.
• RESPIRATION: CVP should decrease with inspiration and increase with expiration.
• KUSSMAUL'S SIGN: Paradoxical change in CVP during inspiration (and increase instead of decrease), caused by a restriction in filling of the right ventricle, such as pericardial effusion.
• HEPATOJUGULAR REFLEX: Normally, it should only show a transient increase in CVP. With Cor Pulmonale, the increased CVP is maintained throughout.
• JUGULAR VENOUS WAVES:
• a-Wave: Right atrial contraction, corresponding to peak filling of the jugular vein.
• A large a-wave is characteristic of pulmonary hypertension.
• A giant a-wave is characteristic of a total heart block.
• No a-wave is characteristic of atrial fibrillation.
• x-Descent: Follows a-wave, as atrium relaxes. Decreased jugular vein filling.
• First heart sound is heard during the
• c-Wave: Occurs with contraction of the ventricles. Usually not visible at bedside.
• CAROTID PULSE occurs during this, which is right after the a-wave and also during the x-descent.
• v-Wave: Passive phase of atrial filling during ventricular systole.
• y-Descent: Brief decreases in jugular vein pressure after the Tricuspid valve opens (beginning of Systole).

ARTERIAL PULSES:

• Normal Pulses: Radial, Brachial, Carotid, Femoral, Popliteal, Posterior Tibial, Dorsalis Pedis.
• Rhythm Abnormalities:
• Sinus Arrhythmia: The pulse accelerates with inspiration.
• Premature Contractions:
• Atrial Premature Contractions (APC): Normally do not disturb the cycle.
• Ventricular Premature Contractions (PVC): They are followed by a compensatory pause, and a new rhythm is established.
• Pulse Deficit: With Atrial Fibrillation + Tachycardia, the radial pulse may not be equal to the cardiac apical pulse. Two rapid beats in a row may not allow sufficient ventricular filling for the systole to be transmitted to the periphery. The lapse between apical and radial pulse is the pulse deficit.
• Bigeminal Pulse: Two consecutive heartbeats closely coupled, with subsequent pause before the next beat.
• Volume Abnormalities:
• Hyperkinetic Pulse: Quick up stroke and full volume, seen with hypertension, anxiety.
• Corrigan's Pulse: A brisk pulse with large volume, or "Collapsing" pulse, seen in Aortic Regurgitation.
• Duroziez Murmur should be heard across the femoral artery simultaneous with the collapsing pulse.
• Quincke's Pulse: Visible capillary pulsations in the nail-bed. Another sign of Aortic Insufficiency.
• Pulsus Bisferiens: Bifid pulse. Two distinct impulses with each heartbeat. Seen in:
• Aortic Regurgitation
• Hypertrophic Cardiomyopathy.
• Pulsus Alterans: One pulse feels large, the next one small. Due to decreased cardiac contractility and carries a poor prognosis.
• Pulsus Paradoxus: Weakening of the pulse with inspiration more than normal.
• Systolic pressure normally decreases by less than 10 mm Hg. Paradoxical pulse occurs when decrease is greater than 10 mm Hg.
• Indicative of constrictive cardiac disease: Pericardial effusion, constrictive pericarditis.
• Grading Pulses: Scale of 0 to 4
• Scale:
• 0 = no pulse
• 3 = normal pulse
• 4 = bounding pulse
• Intermittent Claudication: Temporary weakening of lower extremities due to arterial insufficiency.
• Leriche's Syndrome: Atherosclerosis of abdominal Aorta, reducing flow to lower extremities and leading to impotence.
• Takayasu's Disease: Pulseless disease -- no pulse in arms, due to progressive obliterative arteritis.

THE PRECORDIUM:

• Aortic Valve: Second right interspace (upper right -- on the opposite side because the Aorta bends over toward the right side).
• Pulmonic Valve: Second left interspace (upper left -- on opposite side because the Pulmonary arteries bifurcate behind the Aorta.)
• Tricuspid Valve: Lower parasternum (centrally located)
• Mitral Valve: Apex
• Erb's Point: Place to listen to right-sided pathologies, at the third left interspace.

PALPATION / PERCUSSION:

• Point of Maximal Impulse (PMI): Should be at the apex.
• If it is located more centrally and down, that is indicative of COPD due to barrel chest and constantly inflated lungs, displacing the heart centrally (right-sided shift).
• Right Ventricular Hypertrophy can shift the PMI posteriorly, as the right-ventricular mass masks the left-ventricular PMI, making it difficult to palpate.
• Shock: An impulse of a heart sound transmitted to the examining hand.
• Heave / Lift: Forceful, systolic thrust that moves the palpating hand up a little.
• Thrill: A palpable murmur. A palpable vibration that by definition is accompanied by an audible murmur.

STETHOSCOPE: Get a good one. The shorter the tube, the better. Double-barreled tubes are better than single-barrel.

• DIAPHRAGM: High-pitched (primarily systolic) sounds, and press firmly.
• BELL: Low-pitched (primarily diastolic) sounds, and press lightly.

HEART SOUNDS:

• NORMAL HEART SOUNDS: Normal order of events = M₁, T₁, A₂, P₂
• S1: Closing of Mitral (M₁) and Tricuspid (T₁) valves.
• S1 is loudest near the apex.
• LOUD S1: Occurs with higher cardiac output, such as fever, exercise, thyrotoxicosis.
• SOFT S1: Occurs with impaired myocardial contraction, CHF, mitral regurgitation.
• S2: Closing of Aortic (A₂) and Pulmonic (P₂) valves.
• SPLITTING: Normally, Aortic closes before Pulmonic, due to higher pressure in Aorta.
• Wide Splitting: INSPIRATION normally increases the interval between A₂ and P₂, which is attributed to increased pulmonary blood flow, and decreased pulmonary vascular resistance.
• INTENSITY: A loud S₂ usually is attributed to the Aortic valve (A₂), and often occurs with hypertension.
• THIRD HEART SOUND (S3): Considered normal in infants and children.
• CAUSE: Slowing of velocity of blood, or vibrations from turbulent blood-flow during ventricular filling, especially at the beginning.
• POSITION: Patient should be in left lateral decubitus position for maximal auscultation of S3.
• Gallop: S3 sound plus tachycardia, giving the sound of a galloping horse.
• ETIOLOGIES: Cardiac disease which causes increased ventricular volume, such as:
• Mitral and Tricuspid Regurgitation
• Congestive Heart Failure
• Opening Snap (OS): Brief click heard when mitral valve opens at the beginning of diastole (around S3). Associated with Mitral Stenosis
• Kentucky: S1, S2, S3 together have this approximate rhythm.
• FOURTH HEART SOUND (S4): Always pathological.
• CAUSE: Contraction of the atria at the end of diastole ------> turbulent blood flow which is audible as S4.
• Decreased ventricular compliance is the most common etiology of S4 sound.
• ETIOLOGIES:
• Left-Sided: hypertension, aortic stenosis, angina pectoris.
• Right-Sided: pulmonary hypertension, pulmonic stenosis.
• Tennessee: S4, S1, S2 sounds together have this approximate rhythm.
• SUMMATION GALLOP: S3 + S4 + Tachycardia, as seen in chronic hypertension leading to CHF.
• SYSTOLIC SOUNDS and CLICKS:
• Ejection Sounds: Can be innocent, or caused by abnormal Aortic valves or a dilated Aorta.
• Mitral Valve Prolapse (MVP): Will result in a mid or late systolic click, as the mitral leaflet protrudes back into the atrium during ventricular contraction.
• NON-VALVULAR SOUNDS:
• Precordial Knock: Results from constrictive pericarditis and can be heard over the internal jugular at the base of the neck.
• CAUSE: thickened pericardium limits expansion of ventricles during rapid filling phase of diastole, resulting in backup of blood.
• Pericardial Friction Rub: Caused by pericardial effusion, and can be heard over a limited area in left parasternal space.
• More extensive pericardial effusion may eliminate the rub, as the pericardium gets completely separated from the epicardium.,

HEART MURMURS: General Properties

• Timing
• Location
• Configuration: Crescendo / Decrescendo
• Intensity:
• Grade I: Barely audible by an expert.
• Grade III: Moderately loud with palpable thrill.
• Grade VI: So loud it can be heard without the stethoscope making complete contact with the skin.
• Frequency
• Quality
• TRANSMISSION: Where does the sound transmit to? This is characteristic for certain pathologies and can be diagnostic.

SYSTOLIC MURMURS: Cardiac disorders and their associated findings.

• AORTIC STENOSIS: Diamond-shaped systolic ejection murmur.
• Location: Over the Aortic valve, at the second right intercostal space.
• Transmission: to the carotids bilaterally.
• PULMONIC STENOSIS: Diamond-shaped systolic ejection murmur.
• Location: Second or third left parasternal interspace.
• HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY: Diamond-shaped midsystolic murmur.
• PATHOLOGY of DISEASE:
• Septal region of left ventricle is thickened ------> Left Ventricular Hypertrophy.
• During systole, anterior leaflet of mitral valve is abnormal.
• Impaired relaxation of the left ventricle during diastole.
• SOUND: Similar to Aortic Stenosis, but it does not transmit to the Carotids.
• EXAMINATION TECHNIQUES: The murmur becomes louder as left ventricular volume is reduced. This is paradoxic behavior as compared to most murmurs
• Handgrip ------> increase in left ventricular volume ------> decreased murmur. This occurs because the septal obstruction is relatively less significant.
• Valsalva Maneuver: Murmur becomes louder in the late-stage of the Valsalva Maneuver, rather than softer as in most murmurs.
• Murmur becomes quieter when the patient squats -- also paradoxical behavior.
• MITRAL VALVE PROLAPSE: If it occurs with mitral regurgitation, a late systolic murmur will be heard after the midsystolic click.
• Examination Technique: Like cardiomyopathy, reduce left ventricular volume ------> louder murmur (and an earlier click).
• HOLOSYSTOLIC MURMURS: They indicate that blood is flowing down a pressure gradient when it shouldn't be, as in insufficiencies.
• CAUSES: Mitral regurgitation, Tricuspid regurgitation, Ventricular septal defect.
• MITRAL REGURGITATION: The most common cause for Holosystolic Murmur.
• Causes: Anything that makes the mitral valve incompetent, or mitral leaflets damage:
• Vegetations
• papillary muscle dysfunction
• shortened chordae tendineae
• Concurrent features of Mitral Regurgitation:
• Left Ventricular Hypertrophy ------> Shifted PMI
• S3 gallop
• VENTRICULAR SEPTAL DEFECT: Best heard at lower left parasternal border (Erb's point)
• TRICUSPID REGURGITATION: Holosystolic murmur
• May result from IV drug use ------> endocarditis, or Rheumatic valvular disease.
• OTHER MURMURS:
• STRAIGHT BACK SYNDROME: Systolic ejection murmur.
• Innocent Murmurs
• Venous Hum: Heard above the clavicles in normal individuals.
• Mammary Souffle: High pitched continuous flow heard over base of heart in pregnancy.

DIASTOLIC MURMURS: Cardiac disorders and associated findings.

• AORTIC INSUFFICIENCY: Blowing or Decrescendo diastolic murmur.
• Many causes: infectious, rheumatic, dissecting aortic aneurysm.
• CHF makes the murmur softer.
• Associated findings:
• Corrigan's Water Hammer Pulse: Collapsing pulse, with little up stroke or downstroke.
• de Musset's Sign: to and fro head movement synchronous with the heartbeat.
• Quincke's Pulse: capillary pulsation of fingertips.
• Duroziez's Sign: Femoral artery systolic and diastolic bruits.
• Hill's Sign: Blood pressure in the legs being higher than it is in the arms.
• Normal difference = 20 mm Hg
• Aortic Insufficiency = 40-60 mm Hg.
• PULMONIC INSUFFICIENCY: Decrescendo diastolic murmur.
• GRAHAM STEELL'S MURMUR: Pulmonary Hypertension as the cause of pulmonic hypertension (due to dilation of pulmonic leaflets).
• Prominent a-wave is found concurrent with the murmur.
• Paradoxical Splitting also occurs.
• MITRAL STENOSIS: Middiastolic murmur
• CAUSE: Chronic Rheumatic Heart Disease is most common cause.
• TRICUSPID STENOSIS: Middiastolic murmur
• RHEUMATIC FEVER:
• Carey Coombs Murmur is the characteristic murmur occurring during the acute stage of Rheumatic Fever. It is a blubbering middiastolic murmur heard at apex. The murmur disappears after acute disease has subsided.
• Middiastolic murmur of mitral stenosis might then remain as a sequel.
• PATENT DUCTUS ARTERIOSUS:
• Continuous Murmurs: Murmurs occurring throughout the cardiac cycle, caused by blood continually flowing from higher pressure to lower pressure. Can be heard with Patent Ductus Arteriosus.

TECHNIQUES FOR ENHANCING AUSCULTATION:

• INSPIRATION: Normally you should see splitting of S2 with inspiration. P₂ occurs later and moves further away from A₂.
• Paradoxic Splitting: S2 splitting is decreased instead of increased with inspiration.
• Left Bundle-Branch Block causes paradoxic splitting. In this condition, under normal circumstances, A₂ already occurs after P₂ (instead of before), because of the left-sided heart-block. Thus, with inspiration, P₂ actually moves closer to A₂ and you see paradoxic splitting.
• EXHALATION: Can be used to evaluate right-sided heart murmurs.
• The intensity of most right-sided heart murmurs will decrease with exhalation, while left-sided murmurs remain unchanged.
• MÜLLER'S MANEUVER: Have patient pinch the nostrils shut with one hand and suck hard on a finger with the other.
• MECHANISM: This creates prolonged negative intrathoracic pressure. That shift blood from the systemic to the pulmonary circulation, which amplifies and prolongs the murmurs found with inspiration. It makes it easier to hear inspiratory murmurs.
• VALSALVA MANEUVER: Have patient hold breath and bear down for 20 seconds. Can be used to evaluate left-sided heart murmurs.
• MECHANISM: This creates a prolonged positive intrathoracic pressure. That shifts blood from the pulmonary to the systemic circulation -- the exact opposite as Müller's Maneuver.
• TIME COURSE: Most left-side murmurs first grow louder, and then grow softer.
• First 10-15 seconds: Initially, cardiac output increases, and the intensity of left-sided murmurs increase accordingly.
• After 10-15 seconds: Cardiac then begins to decrease, as venous return from the lungs decreases. Most left-sided murmurs then grow softer again.
• EXCEPTIONS: Two conditions show different characteristics than above:
• Hypertrophic Obstructive Cardiomyopathy: Left-ventricular hypertrophy and resultant cardiomyopathy, due to hypertension. With this condition, the late-phase of the murmur actually increases or may be heard for the first time.
• Mitral Valve Prolapse: Late-phase murmur usually increases rather than decreases, and may be heard for the first time.
• STANDING to SQUATTING: Have patient squat down and breathe normally, and then stand. Squatting increases stroke volume, and standing decreases it again.
• Hypertrophic Obstructive Cardiomyopathy: As patient squats, this murmur should be decreased.
• Mitral Regurgitation: Occasionally decreases.
• SQUATTING to STANDING:
• Hypertrophic Obstructive Cardiomyopathy: As the patient stands back, this murmur should increase.
• Mitral Regurgitation: Occasionally increases.
• PASSIVE LEG ELEVATION:
• Hypertrophic Obstructive Cardiomyopathy: Murmur should decrease, as left ventricular volume increases and the left ventricle enlarges.
• ISOMETRIC HANDGRIP: Using a handgrip for 1 minutes increases peripheral vascular resistance.
• DECREASED INTENSITY: Hypertrophic Obstructive Cardiomyopathy, Aortic Stenosis (about 30% of cases).
• INCREASED INTENSITY: Ventricular Septal Defect, Aortic Regurgitation, Mitral Regurgitation.
• CONTRAINDICATIONS: Do not do this test on people with myocardial ischemia, ventricular arrhythmias, or unstable angina!
• TRANSIENT ARTERIAL OCCLUSION: Place blood pressure cuff on both arms and occlude blood-flow for 20 seconds.
• INCREASED INTENSITY: Mitral Regurgitation, Ventricular Septal Defect. Most other murmurs are unaffected.
• AMYL NITRATE: Have patient inhale amyl nitrate ------> decreased TPR. Auscultate sounds 15-30 seconds later.
• DECREASED INTENSITY: Mitral Regurgitation, Ventricular Septal Defect.
• INCREASED INTENSITY: Right-sided murmurs, aortic stenosis, hypertrophic obstructive cardiomyopathy.

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