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.
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).
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.)
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.
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.
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.
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.
