Cardiovascular Disorders
AORTIC ANEURYSM
Athoracic aortic aneurysm is an abnormal widening of the ascending, transverse, or descending part of the aorta. Aneurysm of the ascending aorta is the most common type and has the highest mortality. An abdominal aneurysm generally occurs in the aorta between the renal arteries and the iliac branches.
Causes
Aneurysm commonly results from atherosclerosis, which weakens the aortic wall and gradually distends the lumen. The exact cause is unknown, but there are factors that contribute which are included here:
age and family history
fungal infection (mycotic aneurysms) of the aortic arch and descending segments
bicuspid aortic valve
congenital disorders, such as coarctation of the aorta or Marfan syndrome
inflammatory disorders
trauma
syphilis
hypertension (in dissecting aneurysm)
tobacco use.
AGE ALERT
Ascending aortic aneurysms, the most common type, are usually seen in hypertensive men under age 60. Descending aortic aneurysms, usually found just below the origin of the subclavian artery, are most common in elderly men with hypertension. They may also occur in younger patients after traumatic chest injury or, less commonly, after infection.Pathophysiology
First, degenerative changes create a focal weakness in the muscular layer of the aorta (tunica media), allowing the inner layer (tunica intima) and outer layer (tunica adventitia) to stretch outward. The outward bulge is the aneurysm. The pressure of blood pulsing through the aorta progressively weakens the vessel walls and enlarges the aneurysm. As the vessel dilates, wall tension increases. This increases arterial pressure and dilates the aneurysm further.
Aneurysms may be dissecting, a hemorrhagic separation in the aortic wall, usually within the medial layer; saccular, an outpouching of the arterial wall; or fusiform, a spindle-shaped enlargement encompassing the entire aortic circumference.
A false aneurysm occurs when the entire wall is injured, with blood contained in the surrounding tissue. A sac eventually forms and communicates with an artery or the heart.
COMPLICATIONS
Cardiac tamponade if aneurysm ruptures
Dissection
Rupture
Signs and Symptoms
Ascending Aneurysm
Pain, the most common symptom of thoracic aortic aneurysm
Bradycardia
Murmur of aortic insufficiency
Pericardial friction rub (caused by a hemopericardium)
Unequal intensities of the right carotid and left radial pulses
Difference in blood pressure between the right and left arms
Jugular vein distention
Descending Aneurysm
Pain, usually starting suddenly between the shoulder blades; may radiate to the chest
Hoarseness
Dyspnea and stridor
Dysphagia
Dry cough
Abdominal Aneurysm
Although abdominal aneurysms usually don’t produce symptoms, most are evident as a pulsating mass in the periumbilical area. Other signs include:
systolic bruit over the aorta
tenderness on deep palpation
lumbar pain that radiates to the flank and groin.
CLINICAL TIP
Pain caused by a dissecting aortic aneurysm:
may be described as “ripping” or “tearing”
commonly radiates to the anterior chest, neck, back, or abdomen
usually has an abrupt onset.
Diagnostic Test Results
Echocardiography shows the aneurysm and its size.
Anteroposterior and lateral abdominal X-rays show aortic calcifications present in abdominal aortic aneurysms; posteroanterior and oblique chest X-rays will show widening of the aorta and mediastinum in thoracic aortic aneurysms.
Computed tomography scan shows the effects on nearby organs.
Aortography shows the size and location of the aneurysm.
Complete blood count reveals decreased hemoglobin levels.
Abdominal ultrasound can detect and monitor the progression of AAA.
Treatment
A dissecting aortic aneurysm is an emergency that requires prompt surgery and stabilizing measures. Treatment includes:
antihypertensives such as nitroprusside
negative inotropic agents to decrease force of contractility
beta-adrenergic blockers
oxygen for respiratory distress
opioids for pain
I.V. fluids
possibly, whole blood transfusions.
Treatment of stable AAA focuses on surveillance and tight BP control to prevent enlargement.
 TYPES OF AORTIC ANEURYSMS |
CARDIAC ARRHYTHMIAS
Abnormal electrical conduction or automaticity changes heart rate and rhythm. Arrhythmias vary in severity — from mild, producing no symptoms, and requiring no treatment (such as sinus arrhythmia, in which heart rate increases and decreases with respiration), to catastrophic ventricular fibrillation, which mandates immediate resuscitation. Arrhythmias are generally classified according to their origin (ventricular or supraventricular). Their effect on cardiac output and blood pressure, partially influenced by the site of origin, determines their clinical significance. (See the appendix “Types of cardiac arrhythmias.”)
Causes
Each arrhythmia may have its own specific cause. Common causes include:
congenital defects
myocardial ischemia or infarction
organic heart disease
drug toxicity
degeneration or obstruction of conductive tissue
connective tissue disorders
electrolyte imbalances
hypertrophy of heart muscle
acid-base imbalances
emotional stress.
AGE ALERT
Electrocardiogram changes that occur with age include:
longer PR, QRS, and QT intervals
lower amplitude of QRS complex
leftward shift of QRS axis.
Pathophysiology
Altered automaticity, reentry, or conduction disturbances may cause cardiac arrhythmias. Enhanced automaticity is the result of partial depolarization, which may increase the intrinsic rate of the sinoatrial node or latent pacemakers or may induce ectopic pacemakers to reach threshold and depolarize.
Ischemia or deformation causes an abnormal circuit to develop within conductive fibers. Although current flow is blocked in one direction within the circuit, the descending impulse can travel in the other direction. By the time the impulse completes the circuit, the previously depolarized tissue within the circuit is no longer refractory to stimulation; therefore, arrhythmias occur.
Conduction disturbances occur when impulses are conducted too quickly or too slowly.
COMPLICATIONS
Impaired cardiac output
Cardiac arrest in certain arrhythmias
Stroke in prolonged atrial arrhythmias
Signs and Symptoms
Signs and symptoms of arrhythmias result from reduced cardiac output and altered perfusion to the organs and may include:
dyspnea
hypotension
dizziness, syncope, and weakness
chest pain
cool, clammy skin
altered level of consciousness
reduced urinary output
palpitations.
Diagnostic Test Results
Electrocardiography (ECG) detects arrhythmias as well as ischemia and infarction by showing prolonged or shortened intervals, elevated or depressed T waves, premature contractions, or absence of waves.
Blood tests reveal electrolyte abnormalities, such as hyperkalemia or hypokalemia and hypermagnesemia or hypomagnesemia, as well as drug toxicities.
Arterial blood gas analysis reveals acid-base abnormalities, such as acidemia or alkalemia.
Holter monitoring, event monitoring, and loop recording show the presence of an arrhythmia.
Exercise testing detects exercise-induced arrhythmias.
Electrophysiologic testing identifies the mechanism of an arrhythmia and the location of accessory pathways; it also assesses the effectiveness of antiarrhythmic drugs, radiofrequency ablation, and implantable cardioverter-defibrillators (ICDs).
Treatment
Follow the specific treatment guidelines or protocols for each arrhythmia. Treatment generally focuses on the underlying problem and may include:
antiarrhythmic medications
electrolyte correction
oxygen
correction of acid-base balance
cardioversion
radiofrequency ablation
ICD
pacemaker
cardiopulmonary resuscitation.
 SITES OF COMMON CARDIAC ARRHYTHMIAS |
CARDIAC TAMPONADE
Cardiac tamponade is a rapid, unchecked rise in pressure in the pericardial sac that compresses the heart, impairs diastolic filling, and limits cardiac output. The rise in pressure usually results from blood or fluid accumulation in the pericardial sac (pericardial effusion). Even a small amount of fluid (50 to 100 mL) can cause a serious tamponade if it accumulates rapidly.
Causes
Idiopathic
Effusion (due to cancer, bacterial infections, tuberculosis, or, rarely, acute rheumatic fever)
Traumatic or nontraumatic hemorrhage
Viral or postirradiation pericarditis
Chronic renal failure requiring dialysis
Drug reaction (procainamide, hydralazine, minoxidil, isoniazid, penicillin, or daunorubicin)
Heparin- or warfarin-induced tamponade
Connective tissue disorders
Postcardiac surgery
Acute myocardial infarction (MI)
Pericarditis
Pathophysiology
In cardiac tamponade, the progressive accumulation of fluid in the pericardial sac causes compression of the heart chambers. This compression obstructs filling of the ventricles and reduces the amount of blood that can be pumped out of the heart with each contraction.
Each time the ventricles contract, more fluid accumulates in the pericardial sac. This further limits the amount of blood that can fill the ventricular chambers, especially the left ventricle, during the next cardiac cycle.
The amount of fluid necessary to cause cardiac tamponade varies greatly; it may be as little as 50 to 100 mL when the fluid accumulates rapidly or more than 2,000 mL if the fluid accumulates slowly and the pericardium stretches to adapt. Prognosis is inversely proportional to the amount of fluid accumulated.
COMPLICATIONS
Decreased cardiac output
Cardiogenic shock
Death if untreated
Signs and Symptoms
Elevated central venous pressure (CVP) with jugular vein distention
Muffled heart sounds
Pulsus paradoxus (decreases systolic blood pressure with inspiration)
Diaphoresis and cool, clammy skin
Anxiety, restlessness, and syncope
Cyanosis
Weak, rapid pulse
Cough, dyspnea, orthopnea, and tachypnea
CLINICAL TIP
Cardiac tamponade has three classic features, known as Beck’s triad, that include:
elevated CVP with jugular vein distention
muffled heart sounds
pulsus paradoxus.
Diagnostic Test Results
Chest X-rays show a slightly widened mediastinum and possible cardiomegaly. The cardiac silhouette may have a goblet-shaped appearance.
ECG detects a low-amplitude QRS complex and electrical alternans, an alternating beat-to-beat change in amplitude of the P wave, QRS complex, and T wave. Generalized ST-segment elevation is noted in all leads.
Pulmonary artery catheterization detects increased right atrial pressure, right ventricular diastolic pressure, and CVP.
Echocardiography reveals pericardial effusion with signs of right ventricular and atrial compression.
Treatment
Supplemental oxygen
Continuous ECG and hemodynamic monitoring
Pericardiocentesis
Pericardectomy
Resection of a portion or all of the pericardium (pericardial window)
Trial volume loading with crystalloids
Inotropic drugs, such as isoproterenol or dopamine
Posttraumatic injury: blood transfusion, thoracotomy to drain reaccumulating fluid, or repair of bleeding sites may be needed
Heparin-induced tamponade: heparin antagonist protamine sulfate to stop bleeding
Warfarin-induced tamponade: vitamin K to stop bleeding
 CARDIAC TAMPONADE |
CARDIOMYOPATHY
Cardiomyopathy is classified as dilated, hypertrophic, or restrictive.
Dilated cardiomyopathy (DCM) results from damage to cardiac muscle fibers; loss of muscle tone grossly dilates all four chambers of the heart, giving the heart a globular shape.
Hypertrophic cardiomyopathy (HCM) is characterized by disproportionate, asymmetrical thickening of the interventricular septum and left ventricular hypertrophy.
Restrictive cardiomyopathy (RCM) is characterized by restricted ventricular filling due to decreased ventricular compliance and endocardial fibrosis and thickening. If severe, it’s irreversible.
Causes
Most patients with cardiomyopathy have idiopathic disease, but some are secondary to these possible causes:
viral infection
long-standing hypertension
ischemic heart disease or valvular disease
chemotherapy
cardiotoxic effects of drugs or alcohol
metabolic disease, such as diabetes or thyroid disease.
Pathophysiology
In DCM, extensive damage to cardiac muscle fibers reduces contractility in the left ventricle. As systolic function declines, stroke volume, ejection fraction, and cardiac output fall.
COMPLICATIONS
Heart failure
Emboli
Syncope
Sudden death
In HCM, hypertrophy of the left ventricle and interventricular septum obstruct left ventricular outflow. The heart compensates for the decreased cardiac output (caused by obstructed outflow) by increasing the rate and force of contractions. The hypertrophied ventricle becomes stiff and unable to relax and fill during diastole. As left ventricular volume diminishes and filling pressure rises, pulmonary venous pressure also rises, leading to venous congestion and dyspnea.
COMPLICATIONS
Pulmonary hypertension
Heart failure
Sudden death
In RCM, left ventricular hypertrophy and endocardial fibrosis limit myocardial contraction and emptying during systole as well as ventricular relaxation and filling during diastole. As a result, cardiac output falls.
COMPLICATIONS
Heart failure
Arrhythmias
Emboli
Sudden death
Signs and Symptoms
Shortness of breath
Peripheral edema
Fatigue
Weight gain
Cough and congestion
Nausea
Bloating
Palpitations
Syncope
Chest pain
Tachycardia
Diagnostic Test Results
Chest X-rays show cardiomegaly and increase in heart size.
Echocardiography reveals left ventricular dilation and dysfunction or left ventricular hypertrophy and a thick, asymmetrical intraventricular septum. It can also quantify the outlet left ventricular outflow gradient in HCM.
Cardiac catheterization shows left ventricular dilation and dysfunction, elevated left ventricular and, commonly, right ventricular filling pressures, and diminished cardiac output.
Thallium or cardiolite scan usually reveals myocardial perfusion defects.
Cardiac catheterization reveals elevated left ventricular enddiastolic pressure and, possibly, mitral insufficiency.
ECG usually shows left ventricular hypertrophy; ST-segment and T-wave abnormalities; Q waves in leads II, III, and aVF, and in V4 to V6; left anterior hemiblock; left axis deviation; and ventricular and atrial arrhythmias.
Treatment
Treatment of underlying cause
Control of arrhythmias
Angiotensin-converting enzyme inhibitors, diuretics, digoxin (not used in HCM), hydralazine, isosorbide dinitrate, beta-adrenergic blockers, antiarrhythmics, and anticoagulants
Revascularization
Valve repair or replacement
Heart transplantation
Lifestyle modifications, such as quitting smoking; avoiding alcohol; eating a low-fat, low-salt diet; and restricting fluids
Ventricular myotomy or myectomy
Mitral valve repair or replacement
Defibrillator placement with or without biventricular pacing
 TYPES OF CARDIOMYOPATHY |
CONGENITAL DEFECTS
The most common congenital defects of the heart are atrial septal defect (ASD), coarctation of the aorta, patent ductus arteriosus (PDA), tetralogy of Fallot, transposition of the great arteries, and ventricular septal defect (VSD). Causes of all six defects remain unknown, although some have specific clinical associations.
ATRIAL SEPTAL DEFECT
An opening between the left and right atria permits blood flow from the left atrium to the right atrium rather than from the left atrium to the left ventricle. ASD is associated with Down syndrome.
Pathophysiology
Blood shunts from the left atrium to the right atrium because left atrial pressure is normally slightly higher than right atrial pressure. This difference forces large amounts of blood through a defect that results in right heart volume overload, affecting the right atrium, right ventricle, and pulmonary arteries. Eventually, the right atrium enlarges, and the right ventricle dilates to accommodate the increased blood volume. If pulmonary artery hypertension develops, increased pulmonary vascular resistance and right ventricular hypertrophy follow.
COMPLICATIONS
Right-sided heart failure
Heart rhythm abnormalities
Pulmonary hypertension
Signs and Symptoms
Fatigue
Early to midsystolic murmur and low-pitched diastolic murmur
Fixed, widely split S2
Systolic click or late systolic murmur at the apex
Clubbing of nails and cyanosis with a right-to-left shunt
Palpable pulsation of the pulmonary artery
COARCTATION OF THE AORTA
Coarctation is a narrowing of the aorta, usually just below the left subclavian artery, near the site where the ligamentum arteriosum joins the pulmonary artery to the aorta. Coarctation of the aorta is associated with Turner’s syndrome and congenital abnormalities of the aortic valve.
Pathophysiology
Coarctation of the aorta may develop as a result of spasm and constriction of the smooth muscle in the ductus arteriosus as it closes. Possibly, this contractile tissue extends into the aortic wall, causing narrowing. The obstructive process causes hypertension in the aortic branches above the constriction and diminished pressure in the vessel below the constriction.
Restricted blood flow through the narrowed aorta increases the pressure load on the left ventricle and causes dilation of the proximal aorta and ventricular hypertrophy.
As oxygenated blood leaves the left ventricle, a portion travels through the arteries that branch off the aorta proximal to the coarctation. If PDA is present, the remaining blood travels through the coarctation, mixes with deoxygenated blood from the PDA, and travels to the legs. If the ductus arteriosus is closed, the legs and lower portion of the body must rely solely on the blood that circulates through the coarctation.
COMPLICATIONS
Rupture of the aorta
Stroke
Cerebral aneurysm
Signs and Symptoms
Heart failure
Claudication and hypertension
Headache, vertigo, and epistaxis
Blood pressure greater in upper than in lower extremities
Pink upper extremities and cyanotic lower extremities
Absent or diminished femoral pulses
Possible murmur
Possibly, chest and arms more developed than legs
PATENT DUCTUS ARTERIOSUS
The ductus arteriosus is a fetal blood vessel that connects the pulmonary artery to the descending aorta, just distal to the left subclavian artery. Normally, the ductus closes within days to weeks after birth. In PDA, the lumen of the ductus remains open after birth. This creates a left-to-right shunt of blood from the aorta to the pulmonary artery and results in recirculation of arterial blood through the lungs. PDA is associated with premature birth, rubella syndrome, coarctation of the aorta, VSD, and pulmonic and aortic stenosis.
Pathophysiology
The ductus arteriosus normally closes as the neonate takes his first breath but may take as long as 3 months in some infants.
In PDA, relative resistance in pulmonary and systemic vasculature and the size of the ductus determine the quantity of blood that’s shunted from left to right. Because of increased aortic pressure, oxygenated blood is shunted from the aorta through the ductus arteriosus to the pulmonary artery. The blood returns to the left side of the heart and is pumped out to the aorta once more.
Increased pulmonary venous return causes increased filling pressure and workload on the left side of the heart as well as left ventricular hypertrophy and possibly heart failure.
COMPLICATIONS
Chronic pulmonary hypertension
Cyanosis
Left-sided heart failure
 CONGENITAL HEART DEFECTS |
Signs and Symptoms
Respiratory distress with signs of heart failure in infants
Gibson murmur
Thrill palpated at left sternal border
Prominent left ventricular impulse
Corrigan’s pulse
Wide pulse pressure
Slow motor development and failure to thrive
TETRALOGY OF FALLOT
Tetralogy of Fallot is a combination of four cardiac defects: VSD, right ventricular outflow tract obstruction, right ventricular hypertrophy, and an aorta positioned above the VSD (overriding aorta). This defect is associated with fetal alcohol syndrome and Down syndrome.
Pathophysiology
Unoxygenated venous blood entering the right side of the heart may pass through the VSD to the left ventricle, bypassing the lungs, or it may enter the pulmonary artery, depending on the extent of the pulmonic stenosis. The VSD usually lies in the outflow tract of the right ventricle and is generally large enough to permit equalization of right and left ventricular pressures. However, the ratio of systemic vascular resistance to pulmonic stenosis affects the direction and magnitude of shunt flow across the VSD.
COMPLICATIONS
Endocarditis
Stroke
Signs and Symptoms
Cyanosis or “blue” spells (Tet spells)
Clubbing of digits, diminished exercise tolerance, dyspnea on exertion, growth retardation, and eating difficulties
Squatting to reduce shortness of breath
Loud systolic murmur and continuous murmur of the ductus
Thrill at left sternal border
Right ventricular impulse and prominent inferior sternum
TRANSPOSITION OF GREAT ARTERIES
The aorta rises from the right ventricle and the pulmonary artery from the left ventricle, producing two noncommunicating circulatory systems. This defect is associated with VSD, VSD with pulmonic stenosis, ASD, and PDA.
Pathophysiology
The transposed pulmonary artery carries oxygenated blood back to the lungs, rather than to the left side of the heart. The transposed aorta returns unoxygenated blood to the systemic circulation rather than to the lungs. Communication between the pulmonary and systemic circulations is necessary for survival. In infants with isolated transposition, blood mixes only at the patent foramen ovale and at the PDA, resulting in slight mixing of unoxygenated systemic blood and oxygenated pulmonary blood. In infants with concurrent cardiac defects, greater mixing of blood occurs.
COMPLICATIONS
Heart failure
Arrhythmias
Signs and Symptoms
Hypoxemia, cyanosis, tachypnea, and dyspnea
Gallop rhythm, tachycardia, hepatomegaly, and cardiomegaly
Murmurs of ASD, VSD, or PDA; loud S2
Diminished exercise tolerance, fatigue, and clubbing
VENTRICULAR SEPTAL DEFECT
VSD is an opening in the septum between the ventricles that allows blood to shunt between the left and right ventricles. However, the defect is usually small and will close spontaneously. VSD is associated with Down syndrome and other autosomal trisomies, renal anomalies, prematurity, fetal alcohol syndrome, PDA, and coarctation of the aorta.
Pathophysiology
In neonates with a VSD, the ventricular septum fails to close completely by 8 weeks’ gestation. VSDs are located in the membranous or muscular portion of the ventricular septum and vary in size. Some defects close spontaneously; in other defects, the septum is entirely absent, creating a single ventricle.
A VSD isn’t readily apparent at birth because right and left pressures are approximately equal and pulmonary artery resistance is elevated. Alveoli aren’t yet completely opened, so blood doesn’t shunt through the defect. As the pulmonary vasculature gradually relaxes, between 4 and 8 weeks after birth, right ventricular pressure decreases, allowing blood to shunt from the left to the right ventricle. Initially, large VSD shunts cause left atrial and left ventricular hypertrophy.
COMPLICATIONS
Right ventricular hypertrophy
Heart failure
Endocarditis
Signs and Symptoms
Failure to thrive
Loud, harsh systolic murmur (along the left sternal border at the third or fourth intercostal space) and palpable thrill
Loud, widely split pulmonic component of S2
Displacement of point of maximal impulse to left or down
Prominent anterior chest, cyanosis, and clubbing
Liver, heart, and spleen enlargement
Diaphoresis, tachycardia, and rapid, grunting respirations
Diagnostic Test Results
Chest X-ray reveals cardiomegaly and ventricular and aortic enlargement.
ECG may be normal or may reveal ventricular hypertrophy or axis deviation.
Echocardiography detects the presence and size of a defect.
Fetal echocardiogram can reveal a defect before birth.
Cardiac catheterization confirms the diagnosis and damage.
Arterial blood gas analysis reveals hypoxemia and acid-base disturbances.
Atrial balloon septostomy (for transposition of the great arteries).
Treatment
Surgery
Medications, such as diuretics, angiotensin-converting enzyme inhibitors, indomethacin (for PDA), and prostaglandin
Oxygen therapy
Antibiotic prophylaxis
Atrial balloon septostomy (for transposition of the great arteries)
Treatment of complications
 CONGENITAL HEART DEFECTS (continued) |
CORONARY ARTERY DISEASE
Coronary artery disease (CAD) results from the narrowing of the coronary arteries over time because of atherosclerosis. The primary effect of CAD is a diminished supply of oxygen and nutrients to myocardial tissue because of decreased blood flow.
AGE ALERT
The lifetime risk of CAD after age 40 is 49% for men and 32% for women. As women age, their risk increases.Causes
Atherosclerosis (most common)
Dissecting aneurysm
Infectious vasculitis
Syphilis
Congenital abnormalities
Radiation to the chest
Pathophysiology
Fatty, fibrous plaques progressively occlude the coronary arteries, reducing the volume of blood that can flow through them and leading to myocardial ischemia.
As atherosclerosis progresses, luminal narrowing is accompanied by vascular changes that impair the ability of the diseased vessel to dilate. The consequent precarious balance between myocardial oxygen supply and demand threatens the myocardium distal to the lesion. When oxygen demand exceeds what the diseased vessel can supply, the result is localized myocardial ischemia.
Myocardial cells become ischemic within 10 seconds after coronary artery occlusion. Transient ischemia causes reversible changes at the cellular and tissue levels, depressing myocardial function. Within several minutes, oxygen deprivation forces the myocardium to shift from aerobic to anaerobic metabolism, leading to accumulation of lactic acid and reduction of cellular pH. Without intervention, this sequence of events can lead to tissue injury or necrosis.
The combination of hypoxia, reduced energy availability, and acidosis rapidly impairs left ventricular function. As the fibers become unable to shorten normally, the force of contractions and velocity of blood flow in the affected myocardial region become inadequate. Moreover, wall motion in the ischemic area becomes abnormal and each contraction ejects less blood from the heart. Restoring blood flow through the coronary arteries restores aerobic metabolism and contractility.
COMPLICATIONS
Angina pectoris
Myocardial infarction
Cardiac arrest
Signs and Symptoms
Angina (pain may be described as burning, squeezing, or tightness that radiates to the left arm, neck, jaw, or shoulder blade)
Nausea and vomiting
Cool extremities and pallor
Diaphoresis caused by sympathetic stimulation
Fatigue and dyspnea
Xanthelasma (fat deposits on the eyelids)
AGE ALERT
The older adult with CAD may be asymptomatic because the sympathetic response to ischemia is impaired. In an active older adult, dyspnea and fatigue are two key signals of ischemia.Diagnostic Test Results
ECG shows ischemic changes during anginal episode.
Stress testing detects ST-segment changes during exercise or pharmacologic stress.
Coronary angiography reveals the location and degree of coronary artery stenosis or obstruction, collateral circulation, and the condition of the artery beyond the narrowing.
Myocardial perfusion imaging with thallium 201 or technetium 99m (Cardiolite) may be performed during treadmill exercise to detect ischemic areas of the myocardium.
Stress echocardiography shows abnormal wall motion in ischemic areas.
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