Pathophysiology Exam#2

Objectives
Quiz 4 week 5

Peripheral veins Superior +inferior vena cava right atrium tricuspid valve
right ventricle pulmonary valve pulmonary trunk left and right pulmonary
artery lungs pulmonary veins left atrium mitral valve left ventricle
aortic valve ascending aorta aortic arch descending aorta peripheral
arteries

1. List the valves of heart.

The human heart has four chambers: the two smaller chambers are called atria, and
they are located superiorly; the two larger chambers are called ventricles, and they
are located inferiorly. The valves of the heart are located within the chambers of the
heart
The four valves are known as:
The tricuspid valve (right atrioventricular valve)
The pulmonic or pulmonary valve (right semilunar valve)
The mitral valve (left atrioventricular valve)
The aortic valve (left semilunar valve)

2. Describe the function of heart valves.

Blood from the right atrium is pumped into the right ventricle through the
tricuspid valve. When the right ventricle contracts, the tricuspid valve
closes.
From the right ventricle, blood is pumped through the pulmonary valve
into the pulmonary trunk, which branches into left and right pulmonary
arteries that travel separately to each lung.
Pulmonary veins lead from the lungs to the left atrium, which pumps
blood through the mitral valve into the left ventricle.

Pathophysiology Exam#2

From the left ventricle blood is pumped through the aortic valve into the
ascending aorta, the aortic arch, and the descending aorta.

3. Describe great vessels of heart and its function.

The five great vessels enter and leave the heart: the superior and inferior vena
cava, the pulmonary artery, the pulmonary vein, and the aorta:
The superior vena cava and inferior vena cava are veins that return
deoxygenated blood from circulation in the body and empty into the
right atrium.
The pulmonary artery carries deoxygenated blood from the
right ventricle into the lungs for oxygenation.
The pulmonary veins carry oxygenated blood from the lungs into the left
atrium to be returned to systemic circulation.
The aorta is the largest artery in the body. It carries oxygenated blood from
the left ventricle of the heart into systemic circulation.

4. Compare closing of valves with heart sounds in the cardiac cycle.

A, During diastole, blood flows into atria, atrioventricular valves are pushed open, and blood begins to fill
ventricles. Atrial systole squeezes any blood remaining in atria out into ventricles. B, During ventricular
systole, ventricles contract, pushing blood out through semilunar valves into pulmonary artery (right
ventricle) and aorta (left ventricle)

The first heart sound (S1) is produced by vibrations generated by closure

of the mitral (M1) and tricuspid valves (T1) begin of diastole
The second heart sound (S2) is produced by the closure of the aortic (A2)
and the pulmonary valves (P2) at the end of systole

Pathophysiology Exam#2
1. Atrial systole. The ventricles have already been filling with blood passively
while the heart was relaxed. At the point when the ventricles are about 70% full and
pressure has begun to build in the ventricles, the atria contract. Contraction of the
atria is called atrial systole, and it lasts about 100 ms.
This pumps additional blood into the ventricles as pressure generated in the atria
exceeds pressure in the ventricles. The quantity of blood in each ventricle is
maximal after atrial systole, and the volume of blood in the ventricles at this time is
referred to as the end-diastolic volume (EDV).
The atria do not do much in the way of filling the ventricles, they are
already mostly full by the time the atria contract!
2. Early ventricular systole. As the atria relax after atrial systole, the ventricles
begin to contract in a process called ventricular systole. As pressure in the
ventricles rises, the AV valves shut and for a time all valves of the heart are closed.
This phase is referred to as isovolumetric contraction.
3. Late ventricular systole. Eventually, the pressure inside the ventricles rises
sufficiently to open the semilunar valves, and blood is ejected into the pulmonary
trunk and the aorta. The ventricles eject a quantity of blood referred to as the
stroke volume (SV).
SV is usually equal to about 60% of the EDV, and this percentage is
referred to as the ejection fraction.
The volume of blood in the heart at the end of ventricular systole is the
end-systolic volume (ESV).
4. Early ventricular diastole. Contraction of the ventricles is followed by
ventricular diastole.
As the ventricles begin to relax, pressure in the ventricles drops rapidly. At this
point, pressure in the aorta exceeds that in the ventricles, and the semilunar valves
close. For a brief period, all four valves are again closed at the same time. This
phase is referred to as isovolumetric relaxation. The ventricles relax, but the
volume does not change.
5. Late ventricular diastole. As pressure in the ventricles drops further, the AV
valves open and blood flows passively from the atria into the ventricles. This will
bring us back to step 1.

5. State the structures involved in conduction system of heart.

The rate at which the heat beats is determined by both intrinsic and extrinsic
control mechanisms.
Intrinsic control is related to the property of automaticity. Basically, the heart
tends to beat at its own rhythm. However, the rate at which the heart beats
can be affected by extrinsic (external) factors (remember the effects of the
autonomic nervous system).
Cells of the conducting system cannot maintain stable resting potentials.
After repolarization, the membrane potential inevitably drifts toward
threshold and depolarization. The rate of spontaneous depolarization varies in
different regions of the conducting system, but it is fastest in the sinoatrial
(SA) node. Therefore, depolarization of the SA node sets the pace for the
heart, and the SA node is referred to as the pacemaker of the heart. When
fibers of the sinoatrial node contract, the electrical impulse spreads across
both atria and causes the atria to contract.

Pathophysiology Exam#2

The layer of connective tissue between the atria and ventricles prevents the
direct spread of this impulse from the atria to the ventricles.
A structure called the atrioventricular (AV) node carries the impulse to the
ventricles, but at a slower speed. This creates a delay between excitation of
the atria and excitation of the ventricles. The atrioventricular bundle (or
bundle of His) and Purkinje fibers then rapidly spread the impulse through
the ventricles and cause the ventricles to contract.
o The bundle of his gives rise to the right and left bundle branches
The right bundle branch (RBB) travels without much branching
to the right ventricular apex
The left bundle branch (LBB) arises perpendicularly from the
bundle of his and divides into two branches
The Purkinje fibers are terminal branches of RBB and LBB. They
extend
from the ventricular apexes to the fibrous rings
and penetrate he heart wall to the outer myocardium

6. Describe the neural control of heart.

Although the heart has its own intrinsic rhythm, the heart rate can be adjusted
extrinsically by control centers in the medulla.
The cardioacceleratory center of the medulla sends signals to the heart
via sympathetic pathways in spinal nerves T1-T5; these signals accelerate
the heart rate, and they also increase contractility (the force with which the
heart contracts).
o Basically, it increases cardiac output and peripheral resistance, which
leads to an increase of heart rate, increase stroke volume, and
increase Mean Arterial Pressure
o What neurotransmitter is released onto the heart when the
cardioacceleratory center is active? Norepinephrine
The cardioinhibitory center of the medulla sends signals to the heart via
parasympathetic pathways in the vagus nerves; these signals slow the
heart rate.
o It basically stimulates increased vessel diameter and decreases heart
rate, cardiac output, peripheral resistance, and blood pressure
o What neurotransmitter is released onto the heart when the
cardioinhibitory center is active? Acetylcholine

Pathophysiology Exam#2

7. Define S1, S2, and S3.

The "lub" is the first heart sound, commonly termed S1, and is caused by
turbulence caused by the closure of mitral and tricuspid valves at the start of
systole.
The second heart sound, "dub" or S2, is caused by the closure of the aortic
and pulmonic valves, marking the end of systole.
A third heart sound or S3 occurs early in diastole. In young people and
athletes it is a normal phenomenon. In older individuals it indicates the
presence of congestive heart failure. The third heart sound is caused by a
sudden deceleration of blood flow into the left ventricle from the left atrium.

Exam 2 week 8
1. Explain the role of preload, afterload and contractility in cardiac
output.

Cardiac output is the volume of blood flowing through either the systemic or
the pulmonary circuit per minute and is expressed in liters per minute
(L/min).
Cardiac output = heart rate (beats per minute) x stroke volume (liters per
beat).
The factors that determine cardiac output are (1) preload, (2) afterload, (3)
myocardial contractility, and (4) heart rate.
Preload, afterload, and contractility affect stroke volume, which directly
affects cardiac output

Preload is the volume and associated pressure generated in the ventricle at the
end of diastole
o Increased blood flow from the veins into the heart distends the ventricle
by increasing preload, which increases the stroke volume and,
subsequently, cardiac output, up to a certain point. However, an excessive
increase in preload leads to decreased stroke volume Increases in preload

Pathophysiology Exam#2

(VEDV) not only cause a decline in stroke volume, but also result in
increases in VEDP
Left ventricular afterload is the resistance to ejection of blood from the left
ventricle.
o Low aortic pressures (decreased afterload) enable the heart to contract
more effectively, whereas high aortic pressures (increased afterload) slow
contraction and cause higher workloads against which the heart must
function so it can eject less blood
Stroke volume, or the volume of blood ejected per beat during systole, also
depends on the force of contraction, which depends on myocardial contractility
or the degree of myocardial fiber shortening.
o Three major factors determine the force of contraction:
Changes in the stretching of the ventricular myocardium
caused by changes in VEDV (preload).
Alterations in the inotropic stimuli of the ventricles. Chemicals
affecting contractility are called inotropic agents. The most
important positive inotropic agents are epinephrine and norepinephrine
released from the sympathetic nervous system.
The most important negative inotropic agent is acetylcholine
released from the vagus nerve.
Many drugs have positive or negative inotropic properties that can
have profound effects on cardiac function.
Adequacy of myocardial oxygen supply.
With severe hypoxemia (arterial oxygen saturation less than 50%),
contractility is decreased.
With less severe hypoxemia (saturation more than 50%),
contractility is stimulated.
Moderate degrees of hypoxemia may increase contractility by
enhancing the myocardial response to circulating catecholamines

2. Describe factors affecting heart rate.

The control of heart rate includes activity of the central nervous system,
autonomic nervous system, neural reflexes, atrial receptors, and hormones
Cardiovascular control center is in the brain
Cardiovascular control center is in the brain stem in the medulla, with secondary
areas in the hypothalamus, cerebral cortex, and thalamus along with complex
networks of excitatory or inhibitory interneurons (connecting neurons) throughout
the brain

The nerve fibers from the cardiovascular control center synapse with autonomic
neurons that influence the rate of firing of the SA node
Increased heart rate occurs with sympathetic (adrenergic) stimulation. Thus the
interneurons that cause sympathetic neuronal excitation are collectively called
the cardioexcitatory center
When the parasympathetic nerves to the heart are stimulated (primarily via the
vagus nerve), heart rate slows and the sympathetic nerves to the heart,
arterioles, and veins are inhibited
Neural reflexes

Pathophysiology Exam#2
The baroreceptor reflex facilitates both blood pressure changes and heart rate
changes

If blood pressure is decreased, the baroreceptor reflex accelerates heart rate and
causes vessels to constrict which increases blood pressure
When blood pressure is increased, the pressoreceptors increase their rate of
discharge, sending neural impulses over the glossopharyngeal nerve (ninth
cranial nerve) and through the vagus nerve to the cardiovascular control centers
in the medulla to increase parasympathetic activity and decrease sympathetic
activity, causing blood vessels to dilate and heart rate to decrease
Atrial receptors
Receptors that influence heart rate exist in both atria
Distention of the atria causes stimulation of these atrial receptors (for example,
when intravascular volume is increased by intravenous infusions). This causes
activation of the Bainbridge reflex, which increases heart rate
Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are released
from atrial tissue in response to the increases in blood volume. ANP and BNP
have powerful diuretic and natriuretic (salt excretion) properties, resulting in
decreased blood volume and pressure
Hormones and biochemical
Hormones and biochemicals affect the arteries, arterioles, venules, capillaries,
and contractility of the myocardium.
Norepinephrine increases heart rate, enhances myocardial contractility, and
constricts blood vessels.
Epinephrine dilates vessels of the liver and skeletal muscle and also causes an
increase in myocardial contractility

Thyroid hormones enhance sympathetic activity, promoting increased cardiac

output

3. Compare and contrast pressure and resistance in blood flow.

Blood flow is the amount of fluid moved per unit of time and is usually expressed
as liters per minute (L/min) or milliliters per minute (ml/min), or as cubic
centimeters per second (cm3/sec
Pressure in a liquid system is the force exerted on the liquid per unit area and is
expressed as millimeters of mercury (mm Hg)
o Fluid moves from the arterial side of the capillaries, a region of greater
pressure, to the venous side, a region of lesser pressure.
Resistance is the opposition to force.
o Most opposition to blood flow is provided by the diameter and length of
the blood vessels themselves.
o Resistance in a vessel is inversely related to blood flow
o Resistance to blood flow in a single vessel is determined by the radius and
length of the blood vessel and by the blood viscosity.
Resistance to flow is generally greater in longer tubes because
resistance increases with length.
Blood flow varies inversely with the viscosity of the fluid
o Vessels arranged in series will generally provide less resistance than
vessels arranged in parallel

Pathophysiology Exam#2

The greater number of arterioles arranged in parallel leads to great

resistance to flow in the arteriolar system

4. Compare and contrast velocity and flow.

Blood velocity is the distance blood travels in a unit of time, usually centimeters
per second (cm/sec).
It is directly related to blood flow and inversely related to the cross-sectional
area of the vessel in which the blood is flowing.
As blood moves from the aorta to the capillaries, the total cross-sectional area of
the vessels increases and the velocity of flow decreases.

5. Describe factors affecting blood pressure: arterial pressure, cardiac

output, peripheral resistance and hormones.

Arterial blood pressure is determined by the cardiac output times the peripheral
resistance
The mean arterial pressure (MAP), which is the average pressure in the arteries
throughout the cardiac cycle, depends on the elastic properties of the arterial walls
and the mean volume of blood in the arterial system
Effects of Cardiac Output
o An increase in cardiac output without a decrease in peripheral resistance
will cause both arterial volume and arterial pressure to increase
o The higher arterial pressure increases blood flow through the arterioles
o A decrease in the cardiac output causes an immediate drop in the mean
arterial blood pressure and arteriolar flow.
Effects of Total Peripheral Resistance

Pathophysiology Exam#2
Arteriolar constriction increases mean arterial pressure by preventing the
free flow of blood into the capillaries.
o Dilation has the opposite effect
o Information about pressure and resistance is sensed by neural receptors
(baroreceptors, chemoreceptors) in arterial walls and delivered to the
medullary centers.
o Baroreceptors.
o They respond to changes in smooth muscle fiber length by altering their
rate of discharge and supply sensory information to the cardioinhibitory
center in the brain stem
o When activated, these baroreceptors decrease cardiac output (heart rate
and stroke volume) and peripheral resistance, and thus lower blood
pressure.
o Arterial chemoreceptors.
o Specialized areas within the aortic and carotid arteries are sensitive to
concentrations of oxygen, carbon dioxide, and hydrogen ions (pH) in the
blood
o If arterial oxygen concentration or pH falls, a reflexive increase in blood
pressure occurs, whereas an increase in carbon dioxide concentration
causes a slight increase in blood pressure.
Effect of Hormones
o Antidiuretic hormone
o Antidiuretic hormone (ADH) is released by the posterior pituitary and
causes reabsorption of water by the kidney.
o It increases the blood plasma volume, increasing blood pressure
o Renin-angiotensin system
o Renin is an essential factor that interacts with many other systems to
control vascular tone and renal sodium excretion
The primary factor that stimulates renin release is a drop in renal
perfusion. Other factors include a decrease in the amount of sodium
chloride delivered to the kidney, B-adrenergic stimuli, and low
potassium concentrations in plasma.
o Angiotensin I (Ang I). This is converted by an enzyme, angiotensinconverting enzyme (ACE), to angiotensin II (Ang II).
Ang II causes vasoconstriction and aldosterone secretion.
The renin-angiotensin system is activated after volume depletion or
hypotension, and is suppressed after volume repletion.
o Natriuretic peptides
o The natriuretic peptides (NPs) include atrial natriuretic peptide (ANP),
brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP), and
urodilatin.
These peptides help regulate sodium excretion (natriuresis),
diuresis, vasodilation, and antagonism of the renin-angiotensin
system
o Atrial natriuretic peptide (ANP) is a hormone secreted from cells in
the right atrium when right atrial blood pressure increases.
o

Pathophysiology Exam#2

o
o
o
o

ANP increases urine sodium loss, leading to the formation of a large

volume of dilute urine that decreases blood volume and blood
pressure
Brain natriuretic peptide (BNP) is secreted from cardiac cells and also
increases sodium loss from the kidney.
It is used both as a marker and as a treatment for acute heart
failure
Adrenomedullin (ADM) is present in cardiovascular, pulmonary, renal,
gastrointestinal, cerebral, and endocrine tissues. ADM is secreted by the
adrenal medulla and from endothelial and smooth muscle cells and
mediates vasodilation and sodium excretion
Insulin has direct vascular actions that contribute to both vascular
protection and vascular injury
Adipokines.
Adipocytes synthesize and release several hormones that influence blood
pressure, including adiponectin, leptin, and resistin.
Leptin and resistin levels are increased in obesity and are associated with
increased blood pressure and hypertension

6. Describe coronary circulation.

Coronary arteries
Branching off the aorta (just as it leaves the heart) are the coronary arteries,

which supply the heart itself with blood

The right coronary artery supplies blood to the right atrium, portions of both
ventricles, and portions of the hearts electrical conduction system. The left
coronary artery supplies blood to the left atrium, portions of both ventricles,
and the interventricular septum. Near the apex of the heart, branches of the
right and left coronary arteries merge at junctions called anastomoses.
Because the blood vessels merge, there is collateral circulation of the blood
flow. This means that blood can reach much of the heart via different pathways.
This collateral circulation may allow blood to flow to the entire heart even when
an artery is blocked.
A heart attack typically results from blockage of a coronary artery, which cuts off
the supply of oxygen to part of the heart.
Coronary veins
Cardiac veins bring deoxygenated blood from capillaries of the heart to the
coronary sinus, which dumps blood into the right atrium.

Pathophysiology Exam#2

7. State the classification of hypertension.

Hypertension
Hypertension is consistent elevation of systemic arterial blood pressure .
All stages of hypertension are associated with increased risk for target organ
disease events, such as myocardial infarction, kidney disease, and stroke; thus both
stage I and stage II hypertension need effective long-term therapy

8. Describe predisposing factors of hypertension.

Risk factors:
Family history
Gender (men > women before age
55, women > men after 55)
Advancing age
Black race
Cigarette smoking
High dietary sodium intake
Obesity
Low dietary intake of potassium,
Heavy alcohol consumption
calcium, magnesium
Glucose intolerance

9. Describe pathophysiologic, treatment and complication of

hypertension.

PATHOPHYSIOLOGY OF HYPERTENSION
Primary hypertension
Numerous genetic vulnerabilities have been linked to hypertension and these, in

combination with environmental risks, cause neurohumoral dysfunction

(sympathetic nervous system [SNS], renin-angiotensin-aldosterone [RAA]
system, adducin (cytoskeleton protein involved with Na/K ATPase), and
natriuretic hormones) and promote inflammation and insulin resistance. Insulin
resistance and neurohumoral dysfunction contribute to sustained systemic
vasoconstriction and increased peripheral resistance. Inflammation contributes
to renal dysfunction, which, in combination with the neurohumoral alterations,
results in renal salt and water retention and increased blood volume. Increased
peripheral resistance and increased blood volume are two primary causes of
sustained hypertension.
Secondary hypertension
Secondary hypertension is caused by an underlying disease process or
medication that raises peripheral vascular resistance or cardiac output.
If the cause is identified and removed before permanent structural changes
occur, blood pressure returns to normal.
Complicated hypertension
As hypertension becomes more severe and chronic, tissue damage can occur in
the blood vessels and tissues leading to target organ damage in the heart,
kidney, brain, and eyes
Cardiovascular complications of sustained hypertension include:
o Left ventricular hypertrophy
o Angina pectoris
o Heart failure
o Coronary artery disease
o Myocardial infarction
o Sudden death.
Hypertrophy is characterized by changes in the myocyte proteins, apoptosis of
myocytes, and deposition of collagen in heart muscle, which causes it to become
thickened, scarred, and less able to relax during diastole

The increased size of the heart muscle increases demand for oxygen delivery
over time, the contractility of the heart is impaired, and the individual is at
increased risk for systolic heart failure.
Vascular complications include:
o The formation, dissection, and rupture of aneurysms (outpouchings in
vessel walls)
o and atherosclerosis leading to vessel occlusion

Malignant hypertension
Malignant hypertension is rapidly progressive hypertension in which diastolic
pressure is usually greater than 140 mm Hg.
High arterial pressure renders the cerebral arterioles incapable of regulating
blood flow to the cerebral capillary beds.
High hydrostatic pressures in the capillaries cause vascular fluid to exude into
the interstitial space
If blood pressure is not reduced, cerebral edema and cerebral dysfunction
(encephalopathy) increase until death occurs.
Malignant hypertension can cause:
o Papilledema
o Cardiac failure
o Uremia
o Retinopathy
o Cerebrovascular accident.
CLINICAL MANIFESTATIONS OF HYPERTENSION
The early stages of hypertension have no clinical manifestations other than
elevated blood pressure; for this reason, hypertension is called a silent disease
Some hypertensive individuals never have signs, symptoms, or complications,
whereas others become very ill
Most clinical manifestations of hypertensive disease are caused by complications
that damage organs and tissues outside the vascular system.
Besides elevated blood pressure, the signs and symptoms therefore tend to be
specific for the organs or tissues affected.
TREATMENT OF HYPERTENSION
Treatment of primary hypertension depends on its severity.

Important lifestyle modifications include:

o Following an exercise program
o Making dietary modifications
o Stopping smoking
o Losing weight
Pharmacologic treatment of hypertension reduces the risk of end-organ damage
and prevents major diseases:
o Diuretics have been shown to be the safest and most effective
medications for lowering blood pressure and preventing the cardiovascular
complications of hypertension.
o Some individuals require two drugs for blood pressure control, including
combinations of diuretics and other antihypertensives, such as betablockers, calcium channel blockers, and ACE inhibitors.

10.

Differentiate STEMI and non-STEMI acute coronary syndrome.

Pathophysiology of Acute Coronary Syndromes.
The atherosclerotic process can lead to stable plaque formation and stable
angina or can result in unstable plaques that are prone to rupture and thrombus.
Thrombus formation on a ruptured plaque that disperses in less than 20 minutes
leads to transient ischemia and unstable angina. If the vessel obstruction is
sustained, myocardial infarction with inflammation and necrosis of the
myocardium results. In addition, myocardial infarction is associated with other
structural and functional changes, including myocyte stunning and hibernation
and myocardial remodeling

Unstable angina is the result of reversible myocardial ischemia and is a

harbinger of impending infarction.

Myocardial infarction (MI) occurs when coronary blood flow is interrupted for
an extended period of time, myocyte necrosis occurs.
o Pathologically, there are two major types of myocardial infarction:
subendocardial infarction and transmural infarction
o Clinically, however, myocardial infarction (MI) can be further subdivided
into non-ST elevation MI (non-STEMI) and ST elevation MI (STEMI).
Sudden cardiac death can occur as a result of any of the acute
coronary syndromes.
If the thrombus disintegrates before complete distal tissue necrosis has
occurred, the infarction will involve only the myocardium directly beneath the
endocardium (subendocardial MI). This infarction will usually present with ST
segment depression and T wave inversion without Q waves; therefore it is
termed non-STEMI.
o Recurrent clot formation on the disrupted atherosclerotic plaque is likely.
If the thrombus lodges permanently in the vessel, the infarction will extend
through the myocardium all the way from endocardium to epicardium, resulting
in severe cardiac dysfunction (transmural MI). Transmural myocardial
infarction will usually result in marked elevations in the ST segments on ECG
and these individuals are categorized as having ST segment elevation MI, or
STEMI

11.

State electrophysiological changes of myocardial ischemia and

infarction.

12.

Explain diagnosis and treatment of ACS (acute coronary

syndrome)
DIAGNOSIS

The diagnosis of acute myocardial infarction is made on the basis of history,

physical examination, ECG, and serial cardiac biomarker alterations
The cardiac troponins (troponin I and troponin T) are the most specific indicators
of MI
Blood is drawn for troponin and isoenzyme determinations as soon as possible
after the onset of symptoms, and serial serum levels of these markers are
assessed for several days. If serologic tests show abnormally high levels of
troponin and isoenzymes, acute myocardial infarction probably has occurred.
Elevation of troponin and isoenzymes (CK-MB, and LDH1) levels may not occur
immediately after infarction and laboratory confirmation that an infarction has
occurred may be delayed up to 12 hours.
Myocardial infarction can occur in various regions of the heart wall
Twelve-lead electrocardiograms (ECGs) help to localize the affected area through
identification of Q waves and changes in ST segments and T waves

Myocardial infarction documented by elevated levels of troponins and

isoenzymes but with no elevation of the ST segment on electrocardiogram (ECG)
is termed non-STEMI
Transmural infarction presents with significant ST segment elevation on ECG
(STEMI).

TREATMENT
Acute myocardial infarction requires admission to the hospital, often directly into
a coronary care unit
The individual should be placed on supplemental oxygen and given an aspirin
immediately (ticlopidine if allergic to aspirin).
Both non-STEMI and STEMI are managed with the urgent administration of
thrombolytics or by PCI along with antithrombotics. Further management may
include ACE inhibitors and beta-blockers
Individuals who are in shock require aggressive fluid resuscitation, ionotropic
drugs, and possible emergent invasive procedures.
Individuals not receiving thrombolytic or heparin infusion must receive deep
venous thrombosis prophylaxis as long as their activity is significantly limited
Stool softeners are given to eliminate the need for straining, which can
precipitate bradycardia and can be followed by increased venous return to the
heart, causing possible cardiac overload
Hyperglycemia is treated with insulin.
Treatment of dyslipidemia with hydroxymethylglutaryl coenzyme A (HMG Co-A)
reductase inhibitors (statins) can reduce the risk of future cardiovascular events
Education regarding appropriate diet and caffeine intake, smoking cessation,
exercise, and other aspects of risk factor reduction is crucial for secondary
prevention of recurrent myocardial ischemia.

13.

Describe the clinical manifestation and assessment of

pericardial effusion.
Acute pericarditis is acute inflammation of the pericardium. The etiology of
acute pericarditis is most often idiopathic or caused by viral infection by
coxsackie, influenza, hepatitis, measles, mumps, or varicella viruses.
o The pericardial membranes become inflamed and roughened, and a
pericardial effusion may develop that can be serous, purulent, or fibrinous
o Treatment for uncomplicated acute pericarditis consists of relieving
symptoms and includes administration of anti-inflammatory agents, such
as salicylates and nonsteroidal anti-inflammatory drugs
Tamponade: compression of the heart by an accumulation of fluid in the
pericardial sac
Pericardial effusion is the accumulation of fluid in the pericardial cavity and
can occur in all forms of pericarditis
o More often the fluid is an exudate, which reflects pericardial inflammation
like that seen with acute pericarditis, heart surgery, some
chemotherapeutic agents, infections, and autoimmune disorders such as
systemic lupus erythematosus
o Pericardial effusion indicates an underlying disorder
Clinical findings:
o Pulsus paradoxus, in which arterial blood pressure during expiration
exceeds arterial pressure during inspiration by more than 10 mm Hg.
Pulsus paradoxus accompanied by pericardial effusion indicates
tamponade and reflects impairment of diastolic filling of the left

ventricle plus reduction of blood volume within all four cardiac

chambers.
o Distant or muffled heart sounds, poorly palpable apical pulse, dyspnea on
exertion, and dull chest pain.
Treatment of pericardial effusion or tamponade generally consists of
pericardiocentesis (aspiration of excessive pericardial fluid) and treatment of the
underlying condition.
o Persistent pain may be treated with analgesics, anti-inflammatory
medications, or steroids.
o Surgery may be required if the underlying cause of tamponade is trauma
or aneurysm.

14.

Compare and contrast right and left heart failure.

Heart failure is when the heart is unable to generate an adequate cardiac
output, causing inadequate perfusion of tissues or increased diastolic filling
pressure of the left ventricle, or both, so that pulmonary capillary pressures are
increased
o Ischemic heart disease and hypertension are the most important
predisposing risk factors
LEFT HEART FAILURE
Left heart failure is commonly called congestive heart failure and can be
further categorized as systolic heart failure or diastolic heart failure.
o It is possible for these two types of heart failure to occur simultaneously in
one individual.
RIGHT HEART FAILURE
Right heart failure is defined as the inability of the right ventricle to provide
adequate blood flow into the pulmonary circulation at a normal central venous
pressure.
It can result from left heart failure when an increase in left ventricular filling
pressure is reflected back into the pulmonary circulation because as pressure in
the pulmonary circulation rises, the resistance to right ventricular emptying
increases
o The right ventricle will dilate and fail. When this happens, pressure will
rise in the systemic venous circulation, resulting in peripheral edema and
hepatosplenomegaly
When right heart failure occurs in the absence of left heart failure, it is typically
attributable to:
o Diffuse hypoxic pulmonary disease such as chronic obstructive pulmonary
disease (COPD), cystic fibrosis, and acute respiratory distress syndrome
(ARDS).
These disorders result in:
An increase in right ventricular afterload
Myocardial infarction
Cardiomyopathies
Pulmonic valvular disease interfere with right ventricular
contractility and can lead to right heart failure

15.

Compare and contrast systolic and diastolic failure.

Left ventricular (LV) failure can be divided into systolic and diastolic dysfunction.
Echocardiography is currently the most relevant technique for non-invasive
differentiation of the two forms
Systolic Heart Failure
It is characterized by a reduced ejection fraction and an enlarged LV chamber
Systolic dysfunction is clinically associated with left ventricular failure in the
presence of marked cardiomegaly
Systolic dysfunction is easily assessable by estimation of global ejection fraction
and regional wall motion
Systolic dysfunction treatment is well defined, consisting of ACE inhibitors,
followed by diuretics and digitalis. Calcium channel blockers are usually
contraindicated.
Diastolic Heart Failure
It is characterized by an increased resistance to filling with increased filling
pressures
Diastolic dysfunction is accompanied by pulmonary congestion together with a
normal or only slightly enlarged ventricle.
Diastolic dysfunction can be diagnosed indirectly by means of a normal or nearly
normal ejection fraction and changes of the mitral filling pattern in the context of
LV failure.

For an exact determination of diastolic dysfunction LV catheterization is

required.
Diastolic dysfunction therapy is more dependent on the underlying disease.
o Calcium channel blockers, ACE inhibitors or beta-blockers are first line
drugs in most instances: diuretics can be added with increasing
symptoms.
o Digitalis should be avoided, except in atrial fibrillation, to control heart
rate.
o