Chapter 4
Understanding the cardiovascular system
The cardiovascular system (CVS) begins its activity when the fetus is barely 1 month old (21st day), and
it’s the last system to cease activity at the end of life. The heart, arteries, veins, and lymphatic vessels make
up the CVS. These structures:
 transport life-supporting oxygen and nutrients to cells,
 remove metabolic waste products, and
 carry hormones from one part of the body to another.
Circulation requires normal heart function, which propels blood through the system by continuous
rhythmic contractions.
Despite advances in disease detection and treatment, cardiovascular disease remains the leading cause of
death. Heart attack, or myocardial infarction (MI), is the primary cause of cardiovascular-related deaths.
MI typically occurs with little or no warning.
Oxygen balancing act
A critical balance exists between myocardial oxygen supply and demand. A decrease in oxygen supply
or an increase in oxygen demand can disturb this balance and threaten myocardial function. The four major
determinants of myocardial oxygen demand
are: heart rate, contractile force, muscle mass, and ventricular wall tension. Cardiac workload and
oxygen demand increase if the heart rate speeds up or if the force of contractions becomes stronger. This
can occur in hypertension, ventricular dilation, or heart muscle hypertrophy.
The heart’s law of supply and demand
If myocardial oxygen demand increases, so must oxygen supply. To effectively increase oxygen supply,
coronary perfusion
must also increase. Tissue hypoxia causes coronary arteries to dilate and increases coronary blood flow.
Normal coronary vessels can dilate and increase blood flow five to six times above resting levels.
However, stenotic, diseased vessels can’t dilate, so oxygen deficit may result.
One-way ticket
Normally, blood flows unimpeded across the valves in one direction. The valves open and close in
response to a pressure gradient. When the pressure in the chamber proximal to the valve exceeds the
pressure in the chamber beyond the valve, the valves open. When the opposite occurs, the valves close. The
valve leaflets, or cusps, are so responsive that even a pressure difference of less than 1 mm Hg between
chambers will open and close them.
How low can you flow?
Valvular disease is the major cause of low blood flow. A diseased valve allows blood to flow backward
across leaflets that haven’t closed securely. This phenomenon is called regurgitation. The backflow of
blood through the valves forces the heart to pump more blood, increasing cardiac workload. The valve
opening may also become restricted and impede the forward flow of blood. This is referred to as stenosis.
The heart may fail to meet the tissues’ metabolic requirements for blood and fail to function as a pump.
Eventually, the circulatory system may fail to perfuse body tissues, and blood volume and vascular tone
may be altered.
Inner awareness and how the heart responds
The body closely monitors both blood volume and vascular tone. Blood flow to each tissue is monitored
by micro-vessels, which
measure how much blood each tissue needs and control the local blood flow. The nerves that control
circulation also help direct
blood flow to tissues. The heart pays attention to the tissues’ demands. It responds to the return of blood
through the veins and to nerve signals that make it pump the required amounts of blood.
Under pressure
Arterial pressure is carefully regulated by the body: If it falls below or rises above its normal mean
level, immediate circulatory
changes occur. If arterial pressure falls below normal, then an increase occurs in:
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• heart rate
• force of contraction
• constriction of arterioles.
If arterial pressure rises above normal, these changes occur:
• reflex slowing of heart rate
• decreased force of contraction
• vasodilation.
Risk factors
Risk factors for CVD fall into two categories: modifiable and non-modifiable.
Modifiable risk factors These factors include:
• elevated serum lipid levels
• hypertension(HTN)
• cigarette smoking
• diabetes mellitus (DM)
• sedentary lifestyle
• stress
• obesity—especially abdominal
• excessive intake of saturated fats, carbohydrates, and salt.
Non-modifiable risk factors

age
male gender
family history
race.
Better to be young at heart; Susceptibility to CVD increases with age; disease before age 40 is
unusual. However, the age-disease correlation may simply reflect the longer duration of exposure to other
risk factors.
An estrogen effect? Women are less susceptible than men to heart disease until after menopause; then
they become as susceptible as men. One theory proposes that estrogen has a protective effect.
Nature vs. nurture A positive family history also increases a person’s chances of developing premature
CVD. For example, genetic factors can cause some pronounced, accelerated forms of atherosclerosis such
as lipid disease. However, family history of CVD may reflect a strong environmental component. Risk
factors—such as obesity or a lifestyle that causes tension—
may recur in families.
Color blind ; Although it affects all races, blacks are most susceptible to cardiovascular disease.
Cardiovascular disorders
The disorders discussed in this section include:
• abdominal aortic aneurysm
• cardiac tamponade
• cardiogenic shock
• coronary artery disease (CAD)
• dilated cardiomyopathy
• heart failure
• hypertension
hypertrophic cardiomyopathy
• MI
• pericarditis
• rheumatic fever and rheumatic heart disease.
Abdominal aortic aneurysm
It is, an abnormal dilation in the arterial wall occurs in the aorta between the renal arteries and the iliac
branches. In a false aneurysm, the out pouching occurs when the entire vessel wall is injured and leads to a
sac formation affecting the artery or heart. It is more common in men and most prevalent in ages 50 to 80.
Arteriosclerosis is responsible for 95% of cases.
It begins locally
First, a local weakness in the muscular layer of the aorta (tunica media), due to degenerative changes,
allows the inner layer (tunica intima) and outer layer (tunica adventitia) to stretch outward. Blood pressure
within the aorta progressively weakens the vessel walls and enlarges the aneurysm. Aneurysms can dissect
or rip when bleeding into the weakened artery causes the artery wall to split.
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What to look for
It is usually asymptomatic, but larger aneurysms may be evident (unless the patient is obese) as a
pulsating mass in the periumbilical area, accompanied by a systolic bruit over the aorta.
Reaching the breaking point A large aneurysm may continue to enlarge and eventually rupture.
Lumbar pain that radiates to the flank and groin may signify enlargement and impending rupture.
Other signs and symptoms of enlargement and rupture include:
• weakness
• sweating
• tachycardia
• hypotension
What tests tell you
Because it is usually asymptomatic, in many cases it’s detected accidentally as the result of an X-ray or
a routine physical examination. Several tests can confirm suspected abdominal aortic aneurysm:
Serial ultrasonography allows accurate determination of aneurysm size, shape, and location.
Anteroposterior and lateral X-rays of the abdomen
Computed tomography can visualize the aneurysm’s effect on nearby organs,
Aortography shows the condition of vessels proximal and distal to the aneurysm and the extent
of the aneurysm.
Treatments: may include:
Invasive interventions: Usually, an abdominal aortic aneurysm requires resection of the
aneurysm and replacement of the damaged aortic section OR endoluminal stent grafting.
Drug options: If the patient’s aneurysm is small and produces no symptoms, surgery may be
delayed. Beta-adrenergic blockers may be administered to decrease the rate of growth of the aneurysm.
Cardiac tamponade; is a rapid rise in intra-pericardial pressure impairs diastolic filling of the heart.
The rise in pressure usually results from blood or fluid
accumulation in the pericardial sac. As little as 200 ml of
fluid can create an emergency if it accumulates rapidly. If the
condition is left untreated, cardiogenic shock and death can
occur. If it occurs slowly such as in cancer, it may be
asymptomatic.
Too much fluid, not enough blood
In cardiac tamponade, the progressive
accumulation of fluid in the pericardium causes
compression of the heart chambers. This obstructs
blood flow into the ventricles and reduces the
amount of blood that can be pumped out of the
heart with each contraction. Reduced cardiac
output may be fatal without prompt treatment.
What to look for
• hypotension
with narrowing pulse pressure
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• elevated central venous pressure (CVP) with neck vein distention
• muffled heart sounds. • orthopnea • diaphoresis • anxiety • restlessness
• cyanosis • weak, rapid peripheral pulse.
What tests tell you • Chest X • ECG rules out other cardiac disorders.
• Pulmonary artery
pressure monitoring
• Echocardiography
Cardiogenic shock ( pump failure)
It is a condition of diminished cardiac output that severely impairs tissue perfusion as well as oxygen
delivery to the tissues. It reflects severe left-sided heart failure and occurs as a serious complication in
some patients hospitalized with acute MI. In these patients, mortality may exceed 85%.
How it happens
Regardless of the underlying cause, left ventricular dysfunction triggers a series of compensatory
mechanisms that attempt to increase cardiac output and, in turn, maintain vital organ function.
As cardiac output falls, baroreceptors in the aorta and carotid arteries initiate responses in the
sympathetic nervous system. These responses, in turn, increase heart rate, left ventricular filling
pressure, and peripheral resistance to flow to enhance venous return to the heart.
These compensatory responses initially stabilize the patient but later cause the patient to deteriorate as
the oxygen demands of the already compromised heart rise. These events comprise a vicous cycle of
low cardiac output, sympathetic compensation, myocardial ischemia, and even lower cardiac output.
What to look for
• cold, pale, clammy skin
• drop in systolic blood pressure
• weak peripheral pulses
• tachycardia • rapid, shallow respirations
• oliguria (urine output less than 20 ml/hour)
• restlessness
• confusion
• narrowing pulse pressure • cyanosis
Coronary artery disease
CAD causes the loss of oxygen and nutrients to myocardial tissue because of poor coronary blood flow.
More than 50% of men age 60 or older showing signs of CAD on autopsy.
How it happens
Atherosclerosis is the most common cause of CAD. In this condition, fatty, fibrous plaques, possibly
including calcium deposits, progressively narrow the coronary artery lumens, which reduces the volume
of blood that can flow through them. This can lead to myocardial ischemia (a temporary deficiency of
blood flow to the heart) and eventually necrosis (heart tissue death).
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What you can and can’t control
Many risk factors are associated with atherosclerosis and CAD. Some are modifiable and some are nonmodifiable. Non-modifiable risk factors include being older than age 40,
being male, being white, and having a family history of CAD. Researchers
have identified more than 250 genes that may play a role in CAD. CAD
commonly results
from combined effects of multiple genes. Modifiable risk factors include:
• systolic blood pressure greater than 140 mm Hg or diastolic blood
pressure greater than 95 mm Hg
• increased low-density and decreased high-density lipoprotein levels
• smoking (risk dramatically drops within 1 year of quitting)
• stress
•obesity, which increases the risk of diabetes mellitus,
hypertension, and high cholesterol
• inactivity
• diabetes mellitus, especially in women.
From aerobic to anaerobic
Transient ischemia causes reversible changes at the cellular and tissue levels, depressing myocardial
function. Untreated, it can lead to tissue injury or necrosis. Oxygen deprivation forces the myocardium
to shift from aerobic to anaerobic metabolism. As a result, lactic acid (the end product of anaerobic
metabolism) accumulates. This reduces cellular pH.
With each contraction, less blood
The combination of hypoxia, reduced energy availability, and acidosis rapidly impairs left ventricular
function. The strength of contractions in the affected myocardial region is reduced as the fibers shorten
inadequately with less force and velocity. In addition, the ischemic section’s wall motion is abnormal.
This generally results in less blood being ejected from the heart with each contraction..
Compliance counts
These increases in left-sided heart pressures is magnified by changes in wall compliance induced by
ischemia. Compliance is reduced, magnifying the elevation in pressure. During ischemia, sympathetic
nervous system response leads to slight elevations in blood pressure and heart rate before the onset
of pain. With the onset of pain, further sympathetic activation occurs.
What to look for
Angina is the classic sign of CAD. The patient may describe a burning, squeezing, or crushing tightness
in the sub-sternal or precordial area that radiates to the left arm, neck, jaw, or shoulder blade. He may
clench his fist over his chest or rub his left arm when describing it. Pain is commonly accompanied by
nausea, vomiting, fainting, sweating, and cool extremities. Angina commonly occurs after physical
exertion but may also follow emotional excitement, exposure to cold, or the consumption of a large
meal.
When to label it stable or unstable If the pain is predictable and relieved by rest or nitrates,
it’s called stable angina. If it increases in frequency and duration and is more easily induced, it’s called
unstable or unpredictable angina.
What tests tell you
• ECG during an episode of angina shows ischemia, as demonstrated by T-wave inversion, STsegment depression and, possibly, arrhythmias
• Treadmill or bicycle exercise stress test may provoke chest pain
• Coronary angiography reveals the location and extent of coronary artery stenosis or obstruction.
• Myocardial perfusion imaging
Treating CAD:
Controlling risk
Noninvasive measures : Drug therapy also consists of nitrates, such as nitroglycerin, isosorbide dinitrate
Invasive measures; coronary artery bypass graft (CABG) surgery, percutaneous transluminal coronary
angioplasty (PTCA), and laser angioplasty.
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Heart failure
When the myocardium can’t pump effectively enough to meet the body’s metabolic needs, heart failure
occurs. Pump failure usually occurs in a damaged left ventricle, but it may also happen in the right
ventricle. Usually, left-sided heart failure develops first. Heart failure is classified as:
• high-output or low-output
• acute or chronic
• left-sided or right
• forward or backward.
Symptoms of heart failure may restrict a person’s ability to perform activities of
daily living and severely affect quality of life.
But the good news is…
Advances in diagnostic and therapeutic techniques have greatly improved the
outlook for these patients. However, the prognosis still depends on the underlying
cause and its response to treatment.
How it happens
Heart failure may result from a primary abnormality of the heart muscle—for
example, an infarction—that impairs ventricular function and prevents the heart
from pumping enough blood.
Heart failure may also be caused by problems unrelated to MI:
• Mechanical disturbances in ventricular filling during diastole, occur in mitral
stenosis secondary to rheumatic heart disease or constrictive pericarditis and in
atrial fibrillation.
• Systolic hemodynamic disturbances—such as excessive cardiac workload caused by volume overload
or pressure overload, as in mitral or aortic insufficiency, which leads to volume overload.
Factors favorable to failure
Certain conditions can predispose a patient to heart failure include:
• arrhythmias, such as tachyarrhythmias, which can reduce ventricular filling time; and bradycardia,
which can reduce cardiac output
• pregnancy and thyrotoxicosis, which increase cardiac output
• pulmonary embolism, which elevates PAP, causing right-sided heart failure
• infections, which increase metabolic demands and further burden the heart
• anemia, which leads to increased cardiac output to meet the oxygen needs of the tissues
• increased physical activity, increased salt or water intake, emotional stress, or failure to comply with
the prescribed treatment regimen for the underlying heart disease.
Getting complicated
Eventually, sodium and water may enter the lungs, causing pulmonary edema, a life-threatening
condition. Decreased perfusion to the brain, kidneys, and other major organs can cause them to
fail. MI can occur because the oxygen demands of the overworked heart can’t be
met.
Acute or insidious
The patient’s underlying condition determines whether heart failure is acute or
insidious. Heart failure is commonly associated with systolic or diastolic
overloading and myocardial weakness. As stress on the heart muscle reaches a
critical level, the muscle’s contractility is reduced and cardiac output declines.
Venous input to the ventricle remains the same, however.
The long and short of it
When blood in the ventricles increases, the heart compensates, or adapts.
Adaptations may be short term or long term:
• Short-term adaptations—As the end-diastolic fiber length increases, the ventricular muscle responds
by dilating and increasing the force of contraction.
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• Long-term adaptations—Ventricular hypertrophy increases the heart muscle’s ability to contract and
push its volume of blood into the circulation.
Compensation may occur for long periods before signs and symptoms develop.
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What to look for; The early signs and symptoms of heart failure include:
• fatigue • exertional, paroxysmal, and nocturnal dyspnea
• neck vein engorgement
• hepatomegaly.
Later signs and symptoms include:
• tachypnea
• palpitations
• dependent edema
• unexplained, steady weight gain
• nausea
• chest tightness • slowed mental response
• anorexia
• hypotension
• diaphoresis
• narrow pulse pressure
• pallor
• oliguria
• hemoptysis
• cyanosis
• marked hepatomegaly
• pitting ankle enema
• sacral edema in bedridden
What tests tell you
These tests help diagnose heart failure:
• ECG reveals ischemia, tachycardia, and extrasystole.
• Echocardiogram identifies the underlying cause as well as
the type and severity of the heart failure.
• Laboratory studies, such as B-type natriuretic peptide, confirm the presence of heart failure.
• Chest X-ray shows increased pulmonary vascular markings, interstitial edema, or pleural effusion and
cardiomegaly.
Hypertension
Hypertension is an intermittent or sustained elevation of diastolic or systolic blood pressure. Generally,
a sustained systolic blood pressure of 139 mm Hg or higher or a diastolic blood pressure of 89 mm Hg
or higher indicates hypertension.
Listen up—this is essential
The two major types of hypertension are essential (also called primary or idiopathic) and secondary. The
etiology of essential hypertension, the most common type, is complex. It involves several interacting
homeostatic mechanisms.
Hypertension is classified as secondary if it’s related to a systemic disease that raises peripheral
vascular resistance or cardiac output. Malignant hypertension is a severe, fulminant form of the disorder
that may arise from either type.
How it happens
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Hypertension may be caused by increases in cardiac output, total peripheral resistance, or both. Cardiac
output is increased by conditions that increase heart rate or stroke volume. Peripheral resistance is
increased by factors that increase blood viscosity or reduce the lumen size of vessels, especially the
arterioles. Family history, race, stress, obesity, a diet high in fat or sodium, use of tobacco or hormonal
contraceptives, a sedentary lifestyle, and aging may all play a role. Their effects continue to be studied.
Sly as a fox
Essential hypertension usually begins insidiously as a benign disease. If left untreated, even mild cases
can cause major complications and death. Carefully managed treatment, which may include lifestyle
modifications and drug therapy, improves prognosis.
Why? Why? Why?
Several theories help to explain the development of hypertension. Such as:
• changes in the arteriolar bed, causing increased resistance
• abnormally increased tone in the sensory nervous system , causing increased peripheral vascular
resistance
• increased blood volume resulting from renal or hormonal dysfunction
• an increase in arteriolar thickening caused by genetic factors, leading to increased peripheral vascular
resistance
• abnormal renin release resulting in the formation of angiotensin II, which constricts the arterioles and
increases blood volume
Secondary hypertension; Secondary hypertension may be caused by:
• renovascular disease
• renal parenchymal disease
• pheochromocytoma
• primary hyperaldosteronism
• Cushing’s syndrome
• diabetes mellitus
• dysfunction of the thyroid, pituitary, or parathyroid gland
• coarctation of the aorta
• pregnancy
Underneath it all
The pathophysiology of secondary hypertension is related to the underlying disease. For example,
consider these points:
• The most common cause of secondary hypertension is chronic renal disease. Insult to the kidney from
chronic glomerulonephritis or renal artery stenosis interferes with sodium excretion, the reninangiotensin-aldosterone system, or renal perfusion. This causes blood pressure to rise.
• In Cushing’s syndrome, increased cortisol levels raise blood pressure by increasing renal sodium
retention, angiotensin II levels, and vascular response to norepinephrine.
• In primary aldosteronism, increased intravascular volume, altered sodium concentrations in vessel
walls, or very high aldosterone levels cause vasoconstriction (increased resistance).
• Pheochromocytom is a secreting tumor of chromaffin cells, usually of the adrenal medulla. It causes
hypertension due to increased secretion of epinephrine and norepinephrine. Epinephrine functions
mainly to increase cardiac contractility and rate. Norepinephrine functions mainly to increase peripheral
vascular resistance.
Late complications
Complications occur late in the disease and can attack any organ system. Cardiac complications include
CAD, angina, MI, heart failure, arrhythmias, and sudden death. Neurologic complications include
stroke and hypertensive encephalopathy. Hypertensive retinopathy can cause blindness. Renovascular
hypertension can lead to renal failure.
What to look for
Hypertension usually doesn’t produce signs and symptoms until vascular changes in the heart, brain, or
kidneys occur. Severely elevated blood pressure damages the intima of small vessels, resulting
in fibrin accumulation in the vessels, local edema and, possibly, intravascular clotting.
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Location, location, location
Symptoms depend on the location of the damaged vessels, for example:
• brain—stroke, transient ischemic attacks
• retina—blindness
• heart—MI
• kidneys—proteinuria, edema and, eventually, renal failure.
A heavy heart workload
Hypertension increases the heart’s workload. This causes left ventricular
hypertrophy and, later, left-sided heart failure, pulmonary edema, and
right-sided heart failure.
What tests tell you
• Urinalysis may show protein, red blood cells, or white blood cells (WBCs), suggesting renal disease;
or glucose, suggesting diabetes mellitus.
• Excretory urography may reveal renal atrophy, indicating chronic renal disease.
• Serum potassium levels less than 3.5 mEq/L may indicate adrenal dysfunction (primary
hyperaldosteronism).
• Blood urea nitrogen (BUN) levels that are elevated to more than 20 mg/dl and serum creatinine levels
that are elevated to more than 1.5 mg/dl suggest renal disease.
These tests may help detect cardiovascular damage and other complications:
• ECG may show left ventricular hypertrophy or ischemia.
• Chest X-ray may demonstrate cardiomegaly
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Myocardial infarction
MI, an acute coronary syndrome, results from reduced blood flow through one of the coronary arteries.
This causes myocardial ischemia, injury, and necrosis.
Leading the way
MI is one of the leading causes of death. Death usually results from cardiac damage or complications.
sudden deaths occur within 1 hour after the onset of symptoms. Men are more susceptible to MI than
premenopausal women, although the incidence is increasing in women who smoke and take hormonal
contraceptives. The incidence in postmenopausal women is similar to that in men.
How it happens
MI results from occlusion of one or more of the coronary arteries. Occlusion can stem from
atherosclerosis, thrombosis, platelet aggregation, or coronary artery stenosis or spasm.
Predisposing factors include:
• aging
• diabetes mellitus
• elevated serum triglyceride, low-density lipoprotein and cholesterol, and decreased serum
high-density lipoprotein levels
• excessive intake of saturated fats, carbohydrates, or salt
• hypertension
• obesity
• positive family history of CAD
• sedentary lifestyle • smoking
• stress
• use of amphetamines or cocaine.
Susceptibility increases with age
Elderly patients are more prone to complications and death. The most common complications after an
acute MI include:
• arrhythmias
• cardiogenic shock
• heart failure causing pulmonary edema • pericarditis.
Other complications include:
• rupture of the atrial or ventricular septum, ventricular wall, or valves
• ventricular aneurysms
• mural thrombi causing cerebral or pulmonary emboli
• extensions of the original infarction
• psychological problems caused by fear of another MI or organic brain disorder from tissue hypoxia
• personality changes.
Heavy reductions
MI results from prolonged ischemia to the myocardium with irreversible cell damage and muscle death.
Functionally, MI causes:
• reduced contractility with abnormal wall motion
• altered left ventricular compliance
• reduced stroke volume
• reduced ejection fraction
• elevated left ventricular end-diastolic pressure
Insult…that is…ischemia added to injury
All MIs have a central area of necrosis or infarction surrounded by an area of injury. The area of injury
is surrounded by a ring of ischemia. Tissue regeneration doesn’t occur after an MI because the affected
myocardial muscle is dead.
A compensatory kick
Scar tissue that forms on the necrotic area may inhibit contractility. When this occurs, the compensatory
mechanisms (vascular constriction, increased heart rate, and renal retention of sodium and water) kick in
to try to maintain cardiac output. Ventricular dilation also may occur. If a lot of scar tissue forms,
contractility may be greatly reduced. The patient may develop heart failure or
cardiogenic shock.
What to look for; The cardinal symptom of MI is persistent, crushing substernal pain that may
radiate to the left arm, jaw, neck, or shoulder blades. The pain is commonly described as heavy,
squeezing, or crushing and may persist for 12 hours or more. However, in some patients—particularly
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elderly or diabetic patients—pain may not occur at all. In others, it may be mild and confused with
indigestion.
An infarction on the horizon?
In patients with CAD, angina of increasing frequency, severity, or duration (especially if not provoked
by exertion, a heavy meal, or cold and wind) may signal an impending infarction.
Other clinical effects include:
• a feeling of impending doom
• fatigue
• nausea
• vomiting
• shortness of breath
• cool extremities
• diaphoresis
• anxiety
• restlessness.
Fever is unusual at the onset of an MI, but a low-grade temperature may develop during the next few
days. Blood pressure varies. Hypotension or hypertension may occur.
What tests tell you
These tests help diagnose MI:
• Serial 12-lead ECG may be normal or inconclusive during the first few hours after an MI.
Abnormalities include serial STsegment depression and ST-segment elevation and Q waves,
• Serum creatine kinase (CK) levels are elevated, especially the CK-MB isoenzyme, the cardiac muscle
fraction of CK.
• Troponin I, a structural protein found in cardiac muscle, is elevated. Troponin levels increase within 4
to 6 hours of myocardial injury.
• Myoglobin is released with cardiac muscle damage and elevated levels may be detected as soon as 2
hours after an MI.
• Echocardiography shows ventricular wall dyskinesia
• Nuclear ventriculography can show acutely damaged muscle by picking up accumulations of
radionuclide, which appear as a “hot spot’’ on the film.
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Rheumatic fever and rheumatic heart disease
A systemic inflammatory disease of childhood, acute rheumatic fever develops after infection of the
upper respiratory tract with group A beta-hemolytic streptococci. It mainly involves the heart, joints,
central nervous system, skin, and subcutaneous tissues and commonly recurs. If rheumatic fever isn’t
treated, scarring deformity of the cardiac structures results in rheumatic heart disease.
The disease strikes most often during cool, damp weather in the winter and early spring.
All in the family?
Rheumatic fever tends to run in families, lending support to the existence of genetic predisposition.
Environmental factors also seem to be significant in development of the disorder. For example,
in lower socioeconomic groups, the incidence is highest in children between ages 5 and 15, probably
due to malnutrition and crowded living conditions.
How it happens
Rheumatic fever appears to be a hypersensitivity reaction. For some reason, antibodies produced to
combat streptococci react and produce characteristic lesions at specific tissue sites. Because only about
0.3% of people infected with Streptococcus bacteria contract rheumatic fever, altered immune response
probably is involved in its development or recurrence.
Getting complicated
The mitral and aortic valves are commonly destroyed by rheumatic fever’s long-term effects. Their
malfunction leads to severe heart inflammation (called carditis) and, occasionally, produces pericardial
effusion and fatal heart failure. Of the patients who survive this complication, about 20% die within 10
years. Carditis develops in up to 50% of patients with rheumatic fever and may affect the endocardium,
myocardium, or peri- cardium during the early acute phase. Later, the heart valves may be damaged,
causing chronic valvular disease.
Follow the infection
The extent of heart damage depends on where the infection strikes:
• Myocarditis produces characteristic lesions in the interstitial tissue of the heart as well as cellular
swelling and fragmentation of interstitial collagen. These lesions lead to formation of progressively
fibrotic nodules and interstitial scars.
• Endocarditis causes valve leaflet swelling, erosion along the lines of leaflet closure, and blood,
platelet, and fibrin deposits, which form beadlike vegetation. Endocarditis strikes the mitral
valve most commonly in females and the aortic valve in males. It affects the tricuspid valves in both
sexes and, rarely, affects the pulmonic valve.
What to look for
In 95% of patients, rheumatic fever follows a streptococcal infection that appeared a few days to 6
weeks earlier. A temperature of at least 100.4º F (38° C) occurs. Most patients complain of migratory
joint pain or polyarthritis. Swelling, redness, and signs of effusion usually accompany such pain, which
most commonly affects the knees, ankles, elbows, and hips.
Rash talk
About 5% of patients (usually those with carditis) develop a nonpruritic, macular, transient rash called
erythema marginatum. This rash gives rise to red lesions with blanched centers. These same patients
may also develop firm, movable, nontender subcutaneous nodules about 3 mm to 2 cm in diameter,
usually near tendons or bony prominences of joints. These nodules persist for a few days to several
weeks.
What tests tell you
No specific laboratory tests can determine the presence of rheumatic fever, but these test results support
the diagnosis:
• WBC count and ESR may be elevated during the acute phase; blood studies show slight anemia caused
by suppressed erythropoiesis during inflammation.
• C-reactive protein is positive, especially during the acute phase.
• Cardiac enzyme levels may be increased in severe myocarditis.
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• Throat
cultures may continue to show group A beta-hemolytic streptococci
• ECG reveals no diagnostic changes, but 20% of patients show a prolonged PR interval.
• Chest X-ray shows normal heart size, except with myocarditis, heart failure, and pericardial effusion.
• Echocardiography helps evaluate valvular damage, chamber size, ventricular function, and the
presence of a pericardial effusion.
• Cardiac catheterization evaluates valvular damage and left ventricular function in severe cardiac
dysfunction
• Antistreptolysin-O titer is elevated in 95% of patients within 2 months of onset.
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Quick Quiz:
1. Which factor is a major modifiable risk factor for CAD?
A. High cholesterol
B. Genetic predisposition C. Age
D. Family history
2. Which of the following is the major pathophysiologic effect of cardiac tamponade?
A. Atelectasis
B. Hypertension
C. Compressed heart
D. Distended pericardium
3. Which liver enzyme stimulates the adrenal cortex to secrete
aldosterone?
A. Angiotensin I
B. Angiotensin II
C. Renin
D. Antidiuretic hormone
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