Patho test 2 practice questions

What results when systemic blood pressure is increased? a. Hypovolemia b. Decreased cardiac output c. Vasoconstriction d. Decreased vascular resistance

C At the smooth muscle of the arterial system, neurotransmitters bind to receptors to initiate vasoconstriction and increase systemic vascular resistance. An increase in vascular resistance causes the heart to work harder and thus increases blood pressure.

An erroneously low blood pressure measurement may be caused by a. positioning the arm above the heart level. b. using a cuff that is too small. c. positioning the arm at heart level. d. measuring blood pressure after exercise.

ANS: A An erroneous blood pressure result could occur with the arm above the level of the heart.

Aortic regurgitation is associated with a. diastolic murmur. b. elevated left ventricular/aortic systolic pressure gradient. c. elevated systemic diastolic blood pressure. d. shortened ventricular ejection phase.

ANS: A Aortic regurgitation results from an incompetent aortic valve that allows blood to leak back from the aorta into the left ventricle during diastole. In aortic regurgitation, there is not an elevated left ventricular/aortic pressure gradient. Diastolic blood pressure is generally lower because of rapid runoff of blood into the ventricle. Aortic regurgitation is associated with a longer ventricular ejection phase.

Constrictive pericarditis is associated with a. impaired cardiac filling. b. cardiac hypertrophy. c. increased cardiac preload. d. elevated myocardial oxygen consumption.

ANS: A Constrictive pericarditis results in a fibrous scarred pericardium that restricts cardiac filling. Chronic pericarditis may be the result of a previous cardiac surgery. Pericarditis is associated with increased workload of the heart because contraction is opposed by the surrounding structures. The constrictive process includes symptoms of exercise intolerance, weakness, and fatigue.

Which serum biomarker(s) are indicative of irreversible damage to myocardial cells? a. Elevated CK-MB, troponin I, and troponin T b. Markedly decreased CK-MB and troponin I c. Elevated LDL d. Prolonged coagulation time

ANS: A Elevated cardiac biomarkers are one indication of myocardial necrosis. Cardiac biomarkers may not be utilized if a patient presents with chest pain and evidence of acute ischemia on the electrocardiogram. Cardiac biomarkers are elevated in the presence of MI. Elevated LDL is a risk factor for coronary atherosclerosis. Coagulation times are not used to assess myocardial damage.

First-degree heart block is characterized by a. prolonged PR interval. b. absent P waves. c. widened QRS complex. d. variable PR interval.

ANS: A First-degree block is generally identified by a prolonged PR interval (more than 0.20 second) on ECG. P waves are not absent in first-degree heart block. A widened QRS complex is associated with a particular dysrhythmia, but not first-degree heart block. A variable PR interval is found in type I second-degree block.

While hospitalized, an elderly patient with a history of myocardial infarction was noted to have high levels of low-density lipoproteins (LDLs). What is the significance of this finding? a. Increased LDL levels are associated with increased risk of coronary artery disease. b. Measures to decrease LDL levels in the elderly would be unlikely to affect the progression of this disease. c. Increased LDL levels are indicative of moderate alcohol intake, and patients should be advised to abstain. d. Elevated LDL levels are an expected finding in the elderly and therefore are not particularly significant.

ANS: A High levels of low-density lipoproteins (LDLs), which are high in cholesterol, have been associated with the highest risk of coronary atherosclerosis.

patient with significant aortic stenosis is likely to experience a. syncope. b. hypertension. c. increased pulse pressure. d. peripheral edema

ANS: A In the patient with aortic stenosis, syncope and "greying out" episodes may occur when cerebral perfusion is inadequate. Low systolic blood pressure is a common sign of aortic stenosis. Faint pulses are a common sign of aortic stenosis. Peripheral edema is not associated with aortic stenosis.

Left-sided heart failure is characterized by a. pulmonary congestion. b. decreased systemic vascular resistance. c. jugular vein distention. d. peripheral edema.

ANS: A Left-sided heart failure is characterized by pulmonary congestion and edema. Right-sided heart failure is characterized by congestion in the systemic venous system that increases systemic vascular resistance. Jugular vein distention is a classic sign of right-sided heart failure. Peripheral edema is seen in right-sided failure.

A patient with a history of myocardial infarction continues to complain of intermittent chest pain brought on by exertion and relieved by rest. The likely cause of this pain is a. stable angina. b. myocardial infarction. c. coronary vasospasm. d. unstable angina.

ANS: A Stable angina is the most common form of chest pain and is characterized by pain that is caused under conditions of increased myocardial workload, such as physical exertion or emotional strain. Pain related to myocardial infarction is not relieved by rest. Coronary vasospasm is characterized by unpredictable attacks of angina pain. A patient with unstable angina presents with symptoms similar to myocardial infarction.

Which is a true statement about the affect of the Frank-Starling law on the heart? a. Increased diastolic stretching of myocardial fibers produces increased stroke volume. b. Sympathetic activation leads to increased myocardial contractility and heart rate. c. An increase in heart chamber diameter increases myocardial wall tension. d. An increase in coronary artery diameter results in less rapid coronary blood flow.

ANS: A The Frank-Starling law states that an increase in resting muscle fiber length results in a greater development of muscle tension that produces increased stroke volume. An increase in preload result in a greater force of contraction according to the Frank-Starling law.

During which phase of the cardiac cycle is the mitral valve normally open? a. Atrial systole b. Isovolumic contraction c. Isovolumic relaxation d. Ventricular ejection

ANS: A The mitral valve is open during the period of ventricular contraction, which is the period of systole. Isovolumic contraction is a period immediately following atrial systole. The isovolumic relaxation phase begins with semilunar valve closure in response to falling ventricular pressures and ends when the AV valves open to allow ventricular filling. Ventricular contraction results in a rapid rise in ventricular pressure. As ventricular pressure exceeds aortic pressure (or pulmonic), the valve is forced open and a period of rapid ejection of blood from the ventricle follows.

An elderly patient's blood pressure is measured at 160/98. How would the patient's left ventricular function be affected by this level of blood pressure? a. This is an expected blood pressure in the elderly and has little effect on left ventricular function. b. Left ventricular workload is increased with high afterload. c. High blood pressure enhances left ventricular perfusion during systole. d. High-pressure workload leads to left ventricular atrophy.

ANS: B Activation of the sympathetic nervous system increases the heart rate, contractility, blood pressure, and fluid retention by the kidney. Unfortunately, these compensatory efforts impose a greater workload on the heart. A blood pressure of 160/90 mm Hg is a higher than expected blood pressure in an elderly patient. High blood pressure does not enhance ventricular perfusion. Greater workload on the heart may contribute to further ischemic damage.

Angiotensin-converting enzyme (ACE) inhibitors block the a. release of rennin. b. conversion of angiotensin I to angiotensin II. c. conversion of angiotensinogen to angiotensin I. d. effect of aldosterone on the kidney.

ANS: B Angiotensin I is converted into angiotensin II while it is circulating through the pulmonary vessels, by the angiotensin-converting enzyme. ACE inhibitors block the conversion of angiotension I to angiotension II. Renin plays a role in the regulation of arterial blood pressure. ACE inhibitors do not block the conversion of angiotensinogen to angiotensin or the effect of aldosterone on the kidney.

Beta-blockers are advocated in the management of heart failure because they a. increase cardiac output. b. reduce cardiac output. c. enhance sodium absorption. d. reduce blood flow to the kidneys.

ANS: B Beta-blockers are advocated in the management of heart failure to inhibit the cardiac effects of sympathetic activation. These drugs are negative inotropes and have the potential to reduce cardiac output. The goal with the use of beta-blockers in heart failure is to reduce cardiac output. Beta-blockers do not affect sodium reabsorption. Angiotensin II and aldosterone enhance sodium and water reabsorption by the kidney, contributing to an elevated blood volume.

The most reliable indicator that a person is experiencing an acute myocardial infarction (MI) is a. severe, crushing chest pain. b. ST-segment elevation. c. dysrhythmias. d. pain radiating to the lower legs.

ANS: B Injuries to cardiac tissue caused by myocardial ischemia and infarction are indicated on the ECG by ST-segment changes. ST-segment elevation on the ECG indicates that ischemic injury is ongoing and that efforts to improve perfusion or reduce oxygen demand may be effective in preserving myocardial muscle

A patient with pure left-sided heart failure is likely to exhibit a. jugular vein distention. b. pulmonary congestion with dyspnea. c. peripheral edema. d. hepatomegaly.

ANS: B Left-sided heart failure is most often associated with left ventricular infarction and systemic hypertension. The ineffective pumping of the left ventricle results in an accumulation of blood within the pulmonary circulation. As a result, pulmonary congestion with dyspnea is an expected finding. Jugular vein distention is more often associated with right-sided failure. Peripheral edema is associated with right-sided failure. Hepatomegaly is not seen in pure left-sided edema.

Lusitropic impairment refers to a. poor contractile force. b. impaired diastolic relaxation. c. altered action potential conduction rate. d. altered automaticity.

ANS: B Lusitropic impairment refers to an energy-requiring process that removes free calcium ions from the cytoplasm by pumping them back into the sarcoplasmic reticulum and across the cell membrane into the extracellular fluid. Ischemia interferes with this process in the active phase of diastolic relaxation. Poor contractile force is not associated with lusitropic impairment. The conduction rate is not associated with the energy-requiring process known as lusitropy. Automaticity is not a factor in lusitropy.

Mitral stenosis is associated with a. a prominent S4 heart sound. b. a pressure gradient across the mitral valve. c. left ventricular hypertrophy. d. a muffled second heart sound (S2).

ANS: B Mitral stenosis is characterized by an abnormal left atrial-left ventricular pressure gradient during ventricular diastole. Mitral stenosis is not associated with an S4 heart sound. Mitral stenosis is associated with left atrial hypertrophy, not left ventricular hypertrophy. Mitral stenosis does not have a symptom of a muffled second heart sound.

Patients presenting with symptoms of unstable angina and no ST segment elevation are treated with a. cardiac catheterization. b. antiplatelet drugs. c. acute reperfusion therapy. d. cardiac biomarkers only.

ANS: B Patients presenting with symptoms of unstable angina and no ST elevation on the ECG would be treated with antiplatelet drugs as a cornerstone of therapy. Coronary angiography may be used as an additional method of diagnosis but would not be the primary option. The patient with symptoms of unstable angina would not benefit from reperfusion strategies. Cardiac biomarkers may be assessed in the unstable angina patient, but are not the primary indicator.

Primary treatment for myocardial infarction (MI) is directed at a. protecting the heart from further ischemia. b. decreasing myocardial oxygen demands. c. reducing heart rate and blood pressure.

ANS: B Reducing oxygen demand may be effective in preserving myocardial muscle. Decreasing demand increases myocardial oxygen supply. Once the cardiac muscle has been damaged, it is more important to preserve remaining muscle and prevent further loss of the myocardium. Reduction in the heart rate and blood pressure is not the primary treatment goal in MI care.

The common denominator in all forms of heart failure is a. poor diastolic filling. b. reduced cardiac output. c. pulmonary edema. d. tissue ischemia.

ANS: B The common manifestation of all forms of heart failure is the failure of the heart to pump blood adequately. The clinical presentation may differ depending on which ventricle fails (left or right, or both). Poor diastolic filling is not seen in all forms of heart failure. Pulmonary edema is seen in left-sided failure. Tissue ischemia is directly related to myocardial infarction, which may induce heart failure.

Critically ill patients may have parenterally administered vasoactive drugs that are adjusted according to their _____ pressure. a. systolic b. mean arterial c. diastolic d. pulse

ANS: B The mean arterial pressure is used to make incremental adjustments to vasoactive drugs. The MAP is the calculated average pressure within the circulatory system throughout the cardiac cycle. The systolic pressure is a part of the calculation but is not the data element used in adjustment of vasoactive medications. The diastolic reading is involved in calculating the MAP, but is not the number used in titration of vasoactive medications. The pulse pressure is the difference between the systolic and diastolic pressure.

Hypotension, distended neck veins, and muffled heart sounds are classic manifestations of a. myocardial infarction. b. cardiac tamponade. c. congestive heart failure (CHF). d. cardiomyopathy.

ANS: B The three classic symptoms of cardiac tamponade are hypotension, distended neck veins, and muffled heart sounds. There are many other manifestations as well.

Second-degree heart block type I (Wenckebach) is characterized by a. absent P waves. b. lengthening PR intervals and dropped P wave. c. constant PR interval and dropped QRS complexes. d. no correlation between P waves and QRS complexes.

ANS: B Type I second-degree block is associated with progressively lengthening PR intervals until one P wave is not conducted and becomes a dropped beat. Second-degree block is not characterized by an absence of P waves. Type II second-degree block is associated with a consistent PR interval and dropped beats. The ECG of third-degree block shows regularly occurring P waves that are independent of the ventricular rhythm.

Creatine phosphate is a. a waste product of cellular metabolism. b. synthesized when ATP levels are high. c. enzymatically degraded to form creatine kinase. d. an indicator of myocardial cell damage.

ANS: B Under conditions of ATP excess, myocardial cells are able to transfer energy to a storage form called creatine phosphate. Creatine phosphate provides an immediate source of energy when ATP levels drop. Creatine kinase is an enzyme that enhances transfer from ATP to creatine phosphate. Elevated levels of blood CK (creatine kinase) are indicative of myocardial damage.

A patient who reports dizziness and who has absent P waves, wide QRS complexes, and a heart rate of 38 beats/minute on an ECG is most likely in which rhythm? a. Third-degree heart block b. Junctional tachycardia c. Ventricular escape rhythm d. Sinus bradycardia

ANS: C A ventricular escape rhythm originates in the Purkinje fibers, has a rate of 15 to 40 beats/minute, and is characterized by a wide QRS complex. An important clue to identifying escape rhythms is the absence of normal P waves and PR intervals. The rhythm involved in third-degree heart block includes regularly occurring P waves. Junctional tachycardia has a heart rate between 70 and 140 beats/minute. P waves are preceding, following, or buried in the QRS complex. Sinus bradycardia has a normal pattern on the ECG, but with a rate of less than 60 beats/minute.

Cor pulmonale refers to a. biventricular failure. b. left ventricular hypertrophy secondary to lung disease. c. right ventricular hypertrophy secondary to pulmonary hypertension. d. right ventricular failure secondary to right ventricular infarction.

ANS: C Pulmonary disorders that result in increased pulmonary vascular resistance impose a high afterload on the right ventricle. The resultant right ventricular hypertrophy known as cor pulmonale may progress to right ventricular failure as the lung disease worsens. Biventricular failure is most often the result of primary left ventricular failure that progresses to the right. Cor pulmonale is not associated with left ventricular hypertrophy. Only 3% of MIs occur in the right ventricle.

Pulse pressure is defined as a. two thirds of systolic pressure + diastolic pressure. b. systolic pressure + diastolic pressure. c. systolic pressure - diastolic pressure. d. systolic pressure systemic resistance.

ANS: C Pulse pressure is defined as the difference between systolic and diastolic blood pressure.

Rheumatic heart disease is most often a consequence of a. chronic intravenous drug abuse. b. viral infection with herpesvirus. c. -hemolytic streptococcal infection. d. cardiomyopathy.

ANS: C Rheumatic heart disease is an uncommon but serious consequence of rheumatic fever. Rheumatic fever is an acute inflammatory disease that follows infection with group A -hemolytic streptococci.

Atherosclerotic plaques with large lipid cores are prone to a. dislodgement. b. binding. c. rupture. d. attachment

ANS: C Rupture of atherosclerotic plaques with large lipid cores initiates platelet aggregation and thrombus formation. Dislodgement is not an occurrence of atherosclerotic plaques with large lipid cores. Atherosclerotic plaques with large lipid cores are not prone to binding. Large lipid cores of atherosclerotic plaques are not prone to attachment.

Hypertension with a specific, identifiable cause is known as _____ hypertension. a. primary b. orthostatic c. secondary d. malignant

ANS: C Secondary hypertension has a specific identifiable cause such as a specific pathology or a condition that results in hypertension. Primary hypertension does not have a clearly identifiable etiology and is therefore an idiopathic disorder. Positional changes do not generally result in hypertension. Malignant hypertension is a hypertensive crisis.

After sitting in a chair for an hour, an elderly patient develops moderate lower extremity edema. His edema is most likely a consequence of a. arterial obstruction. b. isolated left-sided heart failure. c. right-sided heart failure. d. peripheral vascular disease.

ANS: C The backward effects of right-sided heart failure are as a result of congestion in the systemic venous system and lead to lower extremity edema. Arterial obstruction is not associated with dependent edema of the lower extremities. Left-sided heart failure is associated with pulmonary symptoms. Edema may be associated with peripheral vascular disease, but dependent edema over a 1-hour period is related to right-sided heart failure.

Restriction of which electrolytes is recommended in the management of high blood pressure? a. Calcium b. Potassium c. Sodium d. Magnesium

ANS: C The balance of the intake of water and sodium with their excretion by the kidney remains the central feature of long-term blood pressure maintenance. Sodium is not rapidly eliminated by the kidney like water and adds to the body's fluid volume.

A loud pansystolic murmur that radiates to the axilla is most likely a result of a. aortic regurgitation. b. aortic stenosis. c. mitral regurgitation. d. mitral stenosis.

ANS: C The murmur of mitral regurgitation usually occurs throughout ventricular systole (pansystolic), radiates toward the left axilla, and has a high-pitched blowing character. Aortic insufficiency is characterized by a high-pitched blowing murmur during ventricular diastole. A characteristic murmur of aortic stenosis occurs during ventricular systole and varies in intensity, progressively getting louder and then diminishing (crescendo-decrescendo). The murmur of aortic stenosis generally radiates to the neck.

Which physiologic change increases cardiac work but does not enhance cardiac output? a. Increased preload b. Increased heart rate c. Increased contractility d. Increased afterload

ANS: D A major determinant of stroke volume is afterload, which refers to the impedance or resistance that must be overcome to eject blood from the chamber. The workload imposed on the heart chambers by preload is sometimes called the volume work of the heart. An increase in preload increases the volume work of the heart which must be met by increased oxygen uptake to maintain adequate ATP production. An increase in heart rate results in an increase in cardiac output. However, the increased heart rate is undermined by impaired pumping efficiency. Contractility is independent of fiber end-diastolic length and is therefore not affected by preload.

A patient is exhibiting severe dyspnea and anxiety. The patient also has bubbly crackles in all lung fields with pink, frothy sputum. This patient is most likely experiencing a. right-sided heart failure. b. cardiomyopathy. c. a medication reaction. d. acute cardiogenic pulmonary edema.

ANS: D Acute cardiogenic pulmonary edema is a life-threatening condition requiring immediate treatment. It is associated with left ventricular failure that severely impairs gas exchange, and produces dramatic signs and symptoms including anxiety, severe dyspnea, an upright posture to breathe effectively, and pink frothy sputum. Right-sided heart failure produces systemic venous congestion. Cardiomyopathy is not associated with bubbly crackles and pink frothy sputum. A medication reaction is not the reason for the patient to exhibit severe dyspnea, anxiety, bubbly crackles, and frothy sputum.

What compensatory sign would be expected during periods of physical exertion in a patient with limited ventricular stroke volume? a. Hypotension b. Bradycardia c. Aortic regurgitation d. Tachycardia

ANS: D An individual with reduced stroke volume would exhibit compensatory increases in heart rate. Hypertension is associated with decreased ventricular stroke volume. An individual with reduced stroke volume would exhibit compensatory increases in heart rate; therefore, bradycardia would not be expected. Aortic regurgitation would not be an expected compensatory sign of limited stroke volume.

In which dysrhythmias should treatment be instituted immediately? a. Asymptomatic sinus bradycardia at a heart rate of 50 beats/minute b. Fever-induced tachycardia at 122 beats/minute c. Premature atrial complexes occurring every 20 seconds d. Atrial fibrillation with a ventricular rate of 220 beats/minute

ANS: D Atrial fibrillation is a completely disorganized and irregular atrial rhythm accompanied by an irregular ventricular rhythm of variable rate. Atrial fibrillation causes the atria to quiver rather than to contract forcefully. This allows blood to become stagnant in the atria and may lead to formation of thrombi. This condition requires resuscitation because of the reduction in cardiac output. The cause of the bradycardia should be investigated, but is not treated emergently when an individual is not exhibiting any symptoms

The therapy that most directly improves cardiac contractility in a patient with systolic heart failure is a. afterload reduction. b. -antagonist agents. c. preload reduction. d. digitalis.

ANS: D Digitalis may be used for symptom management of heart failure. Cardiac glycosides directly inhibit the sodium-potassium pump present in the cell membrane of all cells. The intracellular changes allow more calcium to remain in the cell, thus strengthening myocardial contraction. Contractility is not improved through afterload reduction. Beta-blockers inhibit the effects of sympathetic activation and have the potential to reduce cardiac output. Preload reduction is not the therapy of choice in improving cardiac contractility.

A patient with heart failure who reports intermittent shortness of breath during the night is experiencing a. orthopnea. b. paroxysmal atrial tachycardia. c. sleep apnea. d. paroxysmal nocturnal dyspnea.

ANS: D Dyspnea that occurs at night is known as paroxysmal nocturnal dyspnea. Orthopnea is known as dyspnea when lying down. Intermittent shortness of breath at night is not known as paroxysmal atrial tachycardia. Sleep apnea is an absence of breathing during sleep.

High blood pressure increases the workload of the left ventricle, because it increases a. stroke volume. b. blood volume. c. preload. d. afterload.

ANS: D Hypertension reflects an elevation in SVR; rising afterload increases myocardial oxygen demand and overall cardiac workload. The workload of the left ventricle does not increase the stroke volume, blood volume, or preload.

Hypertrophy of the right ventricle is a compensatory response to a. aortic stenosis. b. aortic regurgitation. c. tricuspid stenosis. d. pulmonary stenosis.

ANS: D Right ventricular hypertrophy is the direct result of pulmonary disorders that increase pulmonary vascular resistance and impose a high afterload on the right ventricle. Aortic stenosis does not lead to right ventricular hypertrophy. Aortic regurgitation is not associated with right ventricular hypertrophy. Hypertrophy of the right ventricle is not a compensatory response to tricuspid stenosis.

An abnormally wide (more than 0.10 second) QRS complex is characteristic of a. paroxysmal atrial tachycardia. b. supraventricular tachycardia. c. junctional escape rhythm. d. premature ventricular complexes.

ANS: D The QRS of the premature complex is prolonged (greater than 0.10 second) and bizarre in appearance. Paroxysmal atrial tachycardia does not display a QRS complex that is greater than 0.10 seconds. Supraventricular tachycardia does not display a wide QRS complex. Escape rhythms may have a P wave that is inverted and located before, during, or after the QRS.

Which is true about the mitral valve? a. Opens during ventricular systole b. Is located between the right atrium and right ventricle c. Has three valve leaflets d. Allows blood to flow from the left atrium to the left ventricle

ANS: D The mitral valve directs blood flow from the left atrium to the left ventricle. Papillary muscles prevent the valve leaflets from opening during ventricular contraction. The mitral valve is located between the left atrium and left ventricle.

Angina caused by coronary artery spasm is called _____ angina. a. stable b. classic c. unstable d. Prinzmetal variant

ANS: D Variant, or Prinzmetal, angina is the term applied to vasospasm-initiated anginal symptoms caused by significant atherosclerotic plaques. These spasms usually respond promptly to vasodilating agents. Coronary artery spasm does not produce stable angina. Classic or typical angina is often associated with physical exertion. Unstable angina presents a similar clinical picture as myocardial infarction.

Low cardiac output to the kidneys stimulates the release of _____ from juxtaglomerular cells. a. aldosterone b. norepinephrine c. angiotensinogen d. renin

ANS: D When cardiac output is reduced, juxtaglomerular cells in the kidney release renin and initiate the renin-angiotensin-aldosterone cascade leading to salt and water retention by the kidney. Aldosterone is not released from juxtaglomerular cells. Norepinephrine is not released by cells within the kidney. Angiotensin is not involved in the process of cellular release within the kidneys.