Quiz 3 Week 3

A patient has a history of falls, syncope, dizziness, and blurred vision. The patient's symptomology is most likely related to deep vein thrombosis. hypertension. angina. hypotension.

hypotension. Hypotension is low blood pressure characterized by dizziness, blurred vision, syncope, and injury from falls. Hypertension is high blood pressure characterized by headache, confusion, chest pain, and difficulty breathing. Deep vein thrombosis is evidenced by calf pain or tenderness. Angina is characterized by chest, shoulder, or jaw pain.

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

Tachycardia 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.

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

β-hemolytic streptococcal infection. 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 β-hemolytic streptococci. Rheumatic heart disease is not associated with chronic IV drug abuse. Rheumatic fever is an acute inflammatory infectious disease. Cardiomyopathy does not cause rheumatic heart disease.

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? High-pressure workload leads to left ventricular atrophy. This is an expected blood pressure in the elderly and has little effect on left ventricular function. Left ventricular workload is increased with high afterload. High blood pressure enhances left ventricular perfusion during systole.

Left ventricular workload is increased with high afterload. 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.

Overproduction of nitric oxide is an important aspect of the pathophysiologic process of what type of shock? Septic Hypovolemic Cardiogenic Anaphylactic

Septic The overproduction of nitric oxide is seen in septic shock as a result of the release of immune cytokines. Nitric oxide is not seen in cardiogenic shock. Hypovolemic shock is not associated with the overproduction of nitric acid. The pathophysiologic process of anaphylactic shock is not associated with the overproduction of nitric oxide.

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

antiplatelet drugs. 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.

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

pulmonary congestion with dyspnea. 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.

The most commonly recognized outcome of hypertension is pulmonary disease. False True

False The most commonly recognized outcome of hypertension is cardiovascular disease.

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

a pressure gradient across the mitral valve. 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.

The majority of cardiac cells that die after myocardial infarction do so because of thrombus. insufficient glucose. apoptosis. cell rupture.

apoptosis. MI results when prolonged or total disruption of blood flow to the myocardium causes cellular death by necrosis or apoptosis. Cardiac cells do not die as a result of cellular rupture. Insufficient glucose is not associated with myocardial death. The initiating event of MI is believed to be related to thrombus, but the resulting disruption of flow to the myocardium is because of necrosis or apoptosis.

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

lengthening PR intervals and dropped P wave. 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.

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

mean arterial 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.

The effect of nitric oxide on systemic arterioles is not significant. opposed by nitrate drugs. vasoconstriction. vasodilation.

vasodilation. Nitric oxide causes vasodilation in the systemic arterioles. Vasoconstriction is not associated with nitric oxide. There is a significant effect on the systemic arterioles related to nitric oxide. The effects of nitric oxide are not known to be opposed by nitrate drugs.

An example of an acyanotic heart defect is transposition of the great arteries. tetralogy of Fallot. ventricular septal defect. all right-to-left shunt defects.

ventricular septal defect. An example of an acyanotic heart defect is a ventricular septal defect. In this condition, blood from the left ventricle leaks into the right ventricle because of a defect in the ventricular wall. This leakage causes extra pressure in the right ventricle resulting in pulmonary hypertension. Tetralogy of Fallot is a cyanotic congenital defect. Transposition of the great vessels is a cyanotic congenital defect. The category of cyanotic congenital defects refers to those that are right-to-left shunts.

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? Junctional tachycardia Ventricular escape rhythm Sinus bradycardia Third-degree heart block

Ventricular escape rhythm 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.

Tachycardia is an early sign of low cardiac output that occurs because of baroreceptor activity. acidosis. tissue hypoxia. anxiety.

baroreceptor activity. A number of compensatory responses are set in motion to restore tissue perfusion and oxygenation in the early stage of shock. Baroreceptors located in the aorta and carotid arteries quickly sense the decrease in pressure and transmit signals to the vasomotor center in the brainstem medulla. The sympathetic nervous system stimulates β1 receptors, which respond by increasing the heart rate in an attempt to increase cardiac output. Tachycardia is not caused initially by tissue hypoxia. An early sign of low cardiac output is not anxiety. Tachycardia does not occur because of acidosis.

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

cardiac tamponade. The three classic symptoms of cardiac tamponade are hypotension, distended neck veins, and muffled heart sounds. There are many other manifestations as well. Myocardial infarction is not exhibited by the symptoms described. Classic symptoms of cardiac tamponade are hypotension, distended neck veins, and muffled heart sounds. Symptoms of CHF may include jugular venous distention. Cardiomyopathy is not exhibited by the symptoms described.

Low cardiac output in association with high preload is characteristic of ________ shock. anaphylactic hypovolemic cardiogenic septic

cardiogenic In cardiogenic shock, preload is high and cardiac output is low. In hypovolemic shock, preload and cardiac outputs are both low. In anaphylactic shock, blood volume may be normal. Septic shock is associated with infections.

Pulse pressure is defined as two thirds of systolic pressure + diastolic pressure. systolic pressure + diastolic pressure. systolic pressure - diastolic pressure. systolic pressure × systemic resistance.

systolic pressure - diastolic pressure. Pulse pressure is defined as the difference between systolic and diastolic blood pressure. Pulse pressure is the difference between systolic and diastolic pressure. Pulse pressure is not the sum of the systolic and diastolic pressures. Systemic resistance is not involved in determining the pulse pressure.

Massive release of histamine with consequent vasodilation and hypotension occurs with what type of shock? Anaphylactic Neurogenic Hypovolemic Cardiogenic

Anaphylactic Exposure to a specific antigen causes receptors on mast cells and basophils to cross-link and activate histamine. The release of histamine along with other vasoactive chemicals produces bronchoconstriction. Cardiogenic shock is not associated with histamine release. Hypovolemic shock is not associated with histamine release. Histamine release does not occur with neurogenic shock.

A middle-aged patient has a follow up visit for a recorded blood pressure of 162/96 mm Hg taken 3 weeks ago. The patient has no significant past medical history and takes no medications, but smokes 1 1/2 packs of cigarettes per day, drinks alcohol regularly, and exercises infrequently. The patient is about 40 lbs. overweight and admits to a high-fat, high-calorie diet. At the office visit today, the patient's blood pressure is 150/92 mm Hg. What is the least appropriate intervention for this patient at this time? Begin antihypertensive drug therapy. Recheck blood pressure in 4 to 6 weeks. Begin lifestyle modifications. Encourage smoking cessation.

Begin antihypertensive drug therapy. Antihypertensive drug therapy is not the first intervention in a person with modifiable risk factors. Therefore, lifestyle alterations are attempted first. Lifestyle alterations include exercise, smoking cessation, and weight loss. Blood pressure should be rechecked in 4 to 6 weeks. Smoking cessation counseling is an appropriate lifestyle alteration.

Patients with structural evidence of heart failure who exhibit no signs or symptoms are classified into which New York Heart Association heart failure class? Class I Class II Class III Class IV

Class I Patients who have structural heart disease but no signs or symptoms of heart failure are placed in Class I of the NYHA Classes. Class II patients have current or previous symptoms of heart failure. Class III patients have current or previous symptoms of heart failure, such as dyspnea or fatigue. Class IV patients have advanced structural heart disease and marked symptoms at rest.

In which stage of shock is a patient who has lost 1200 mL of blood, who has normal blood pressure when supine, but who experiences orthostatic hypotension upon standing? Class IV, Refractory Stage Class II, Compensated Stage Class III, Progressive Stage Class I, Initial Stage

Class II, Compensated Stage In compensated stage hemorrhage (Class II), the blood loss is between 750 and 1500 mL. Blood pressure remains normal when the patient is supine but decreases upon standing. In initial stage hemorrhage (Class I) blood loss is up to 750 mL, and the patient's vital signs remain normal. Class III hemorrhage (progressive stage) is blood loss of 1500 and 2000 mL. Vital signs are changing. Severe Class IV hemorrhage (refractory stage) occurs when more than 2000 mL is lost. The patient is lethargic, with severe hypotension.

After being diagnosed with hypertension, a patient returns to the clinic 6 weeks later. The patient reports "moderate" adherence to the recommended lifestyle changes and has experienced a decreased from 165/96 to 148/90 mm Hg in blood pressure. What is the most appropriate intervention for this patient at this time? Continue lifestyle modifications only. Continue lifestyle modifications plus b-blocker therapy. Continue lifestyle modifications plus diuretic therapy. Continue lifestyle modifications plus ACE inhibitor therapy.

Continue lifestyle modifications only. The patient should be encouraged to continue compliance with lifestyle changes since the patient has exhibited some positive response to his changes. Diuretics are not needed at this time. ACE inhibitors should not be added to the therapy yet. β-blockers are not required at this time.

Administration of which therapy is most appropriate for hypovolemic shock? Inotropic agents Vasoconstrictor agents Crystalloids 5% dextrose in water

Crystalloids Crystalloids are solutions that contain electrolytes. Isotonic solutions, such as lactated Ringers, are commonly used crystalloid solutions. These solutions are preferred for volume resuscitation, because they remain in the extracellular space and are more effective in increasing blood volume. Vasoconstrictor agents are contraindicated in hypovolemic shock. Isotonic crystalloids are the most appropriate fluid for volume resuscitation. Isotonic fluids are preferred over glucose or hypotonic electrolyte solutions.

Increased preload of the cardiac chambers may lead to which patient symptom? Decreased respiratory rate Excitability Decreased heart rate Edema

Edema Preload reduces glomerular filtration resulting in fluid conservation, or edema. Increased preload may lead to an increased, not decreased, heart rate. Increased preload may lead to shortness of breath and an increased respiratory rate. Increased preload may lead to fatigue, not excitability, as the heart works harder to circulate blood.

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

Elevated CK-MB, troponin I, and troponin T 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.

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? High-pressure workload leads to left ventricular atrophy. High blood pressure enhances left ventricular perfusion during systole. This is an expected blood pressure in the elderly and has little effect on left ventricular function. Left ventricular workload is increased with high afterload.

Left ventricular workload is increased with high afterload. 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.

A patient presenting with fever, hypotension, and lactic acidosis is most likely to be experiencing what type of shock? Cardiogenic Neurogenic Anaphylactic Septic

Septic Patients presenting with septic shock may have fever and hypotension. In addition, lactic acidosis may be present because of tissue hypoxemia. Presentation of cardiogenic shock is not inclusive of fever or lactic acidosis. Patients in anaphylactic shock do not have fever or lactic acidosis, and may have normal vital signs initially. Neurogenic shock may result from depression of the vasomotor center in the medulla.

Restriction of which electrolytes is recommended in the management of high blood pressure? Calcium Magnesium Potassium Sodium

Sodium 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. It is not necessary to restrict the intake of calcium when managing high blood pressure. Potassium does not need to be restricted in the management of high blood pressure. Magnesium does not play a role in the management of high blood pressure.

Lactated Ringer solution and normal saline are commonly used crystalloid solutions that contain electrolytes. False True

True Lactated Ringer solution and normal saline are commonly used crystalloid solutions that contain electrolytes.

What results when systemic blood pressure is increased? Decreased vascular resistance Hypovolemia Vasoconstriction Decreased cardiac output

Vasoconstriction 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. Hypovolemia does not result in an increase in blood pressure. Cardiac output is not decreased when systemic blood pressure is increased. Vascular resistance is actually increased when the systemic blood pressure is increased.

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 right-sided heart failure. cardiomyopathy. a medication reaction. acute cardiogenic pulmonary edema.

acute cardiogenic pulmonary edema. 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.

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

afterload. 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.

The majority of cases of anaphylactic shock occur when a sensitized individual comes in contact with incompatible blood products. perfumes. antibiotics. animal proteins or dander.

antibiotics. Anaphylactic shock is most frequently associated with antibiotic therapy. Contact with perfumes is not the most frequent cause of anaphylactic shock. Incompatible blood products do not lead to anaphylactic shock. Animal dander may lead to an anaphylactic reaction, but does so less commonly than antibiotics.

Patent ductus arteriosus is accurately described as a(n) cyanotic heart defect associated with right-to-left shunt. stricture of the aorta that impedes blood flow. opening between the atria. communication between the aorta and the pulmonary artery.

communication between the aorta and the pulmonary artery. A patent ductus arteriosus is a normal channel between the pulmonary artery and the aorta that remains open during intrauterine life. A patent ductus arteriosus is not an opening or a stricture in the atria. Patent ductus arteriosus is an acyanotic congenital defect.

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

conversion of angiotensin I to angiotensin II. 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.

A patient presents to the emergency department with a diastolic blood pressure of 132 mm Hg, retinopathy, and symptoms of an ischemic stroke. This symptomology is likely the result of arthrosclerosis. angina. myocardial infarction. hypertensive crisis.

hypertensive crisis. Hypertensive crisis is characterized by a diastolic blood pressure of greater than 120 mm Hg, and symptoms of end-organ damage such as retinopathy and ischemic stroke. Blood pressure is not an indication of arthrosclerosis. Angina may accompany hypertensive crisis, but the question stem relates directly to hypertensive crisis. The patient may be having a myocardial infarction, but the addition of end-organ damage symptoms points to hypertensive crisis.

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

impaired cardiac filling. 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.

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

impaired diastolic relaxation. 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.

Tumor necrosis factor α and interleukin-1 contribute to shock states because they induce production of catecholamines. clotting factors. vasopressin. nitric oxide.

nitric oxide. In septic shock, tumor necrosis factor-α, interleukin-1, and other inflammatory mediators induce vascular cells to produce excessive amounts of the vasodilator nitric oxide. Catecholamines are not produced by TNF-α and IL-1. The production of clotting factors is not induced by tumor necrosis factor-α and interleukin-1. Vasopressin production is not induced by TNF-α and IL-1.

Hypertension is closely linked to spinal stenosis. obstructive sleep apnea. de Quervain syndrome. urinary tract infection.

obstructive sleep apnea. Hypertension is present in 45% to 60% of those diagnosed with obstructive sleep apnea. Urinary tract infection is not directly linked to hypertension. de Quervain syndrome is a type of tendonitis and is not linked to hypertension. Spinal stenosis is not closely associated with hypertension.

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

paroxysmal nocturnal dyspnea. 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.

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

positioning the arm above the heart level. An erroneous blood pressure result could occur with the arm above the level of the heart. It is important to measure blood pressure with the appropriate size cuff. The arm should be positioned at the level of the heart for a more accurate reading. Measuring pressure after exercise yields a higher measurement.

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

reduce cardiac output. 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.

Cardiogenic shock is characterized by reduced cardiac output. reduced systemic vascular resistance. elevated SvO2. hypovolemia.

reduced cardiac output. Cardiogenic shock occurs primarily as a result of severe dysfunction of the left or right ventricles, or both, that results in inadequate cardiac pumping. The low cardiac output state is associated with a high left ventricular diastolic filling pressure. Cardiogenic shock is not manifested by hypovolemia. Sympathetic activation leads to increases in heart rate, vasoconstriction, and a narrow pulse pressure. Low cardiac output leads to reduced SvO2.

Atherosclerotic plaques with large lipid cores are prone to attachment. rupture. binding. dislodgement.

rupture. 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.

Improvement in a patient with septic shock is indicated by an increase in SvO2. systemic vascular resistance. serum lactate level. cardiac output.

systemic vascular resistance. Systemic vascular resistance results in intravascular pooling in the venous system. Some portions of tissue are overperfused, and some are underperfused. Improvement in systemic vascular resistance is an indication of improvement in septic shock. In septic shock, the heart rate and stroke volume increase, and cardiac output is higher than normal. In septic shock, SvO2 levels may already be higher than normal. An increase in serum lactate levels may increase levels of acidosis and tissue hypoxia.

The progressive stage of hypovolemic shock is characterized by cardiac failure. hypertension. tachycardia. lactic acidosis.

tachycardia. In the progressive stage of hypovolemic shock, the patient is anxious and confused, with decreased blood pressure and heart rate greater than 120 beats/minute. In this stage of shock, the blood pressure is decreased. Lactic acidosis does not occur in the progressive stage of hypovolemic shock. Cardiac failure is not likely to occur in the earlier stages of hemorrhagic shock.

A patient is diagnosed with cardiogenic shock. The patient is hyperventilating and is therefore at risk for the respiratory complication of respiratory acidosis. False True

False A patient diagnosed with cardiogenic shock who is hyperventilating is at risk for respiratory alkalosis.

Chronic elevation of myocardial wall tension results in atrophy. False True

False Chronic elevation of myocardial wall tension results in hypertrophy.

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

Prinzmetal variant 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.

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

prolonged PR interval. 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.

A patient with significant aortic stenosis is likely to experience syncope. peripheral edema. increased pulse pressure. hypertension.

syncope. 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.

A patient with cold and edematous extremities, low cardiac output, and profound hypotension is likely to be experiencing a progressive stage of ________ shock. obstructive septic cardiogenic hypovolemic

septic In the progressive stage of septic shock, some patients deteriorate to a hypodynamic state. This is characterized by decreased cardiac output and cold, clammy skin as a result of narrowed pulse pressure. Profound hypotension generally occurs which is unresponsive to treatment. Cardiogenic shock is evidenced by decreased cardiac output, elevated left ventricular end-diastolic pressure, S3 heart sounds, and pulmonary edema. Hypotension occurs with hypovolemic shock, but extremities are not likely to be cold and edematous. Cold edematous extremities along with low cardiac output and profound hypotension are not manifestations of obstructive shock.

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

Atrial fibrillation with a ventricular rate of 220 beats/minute 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. Fever-induced tachycardia will correct itself once the fever is lowered. Dysrhythmias are treated if they produce significant symptoms or are expected to progress to a more serious level.

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? Increased LDL levels are associated with increased risk of coronary artery disease. Measures to decrease LDL levels in the elderly would be unlikely to affect the progression of this disease. Elevated LDL levels are an expected finding in the elderly and therefore are not particularly significant. Increased LDL levels are indicative of moderate alcohol intake, and patients should be advised to abstain.

Increased LDL levels are associated with increased risk of coronary artery disease. High levels of low-density lipoproteins (LDLs), which are high in cholesterol, have been associated with the highest risk of coronary atherosclerosis. Even when lipid metabolism is normal, a high-fat diet can overwhelm the liver's ability to clear LDL cholesterol from the circulation and result in hyperlipidemia. Dietary fat restriction may be beneficial in reducing cholesterol in this case. Increased LDL levels are not indicative of alcohol intake. Elevated LDL levels are not an expected finding in the elderly and should be treated.

Which dysrhythmia is thought to be associated with reentrant mechanisms? Sinus bradycardia Junctional escape Preexcitation syndrome tachycardia (Wolf-Parkinson-White syndrome) Second-degree AV block

Preexcitation syndrome tachycardia (Wolf-Parkinson-White syndrome) Reentry is a complex process in which a cardiac impulse continues to depolarize in a part of the heart after the main impulse has finished its path and the majority of the fibers have repolarized. Wolff-Parkinson-White syndrome is caused by accessory pathways that originate in the atria, bypass the AV node, and enter a site in the ventricular myocardium. This causes the ventricles to contract prematurely, resulting in a reentrant tachycardia. Second-degree block is a conduction failure between the sinus impulse and its ventricular response. Sinus bradycardia is a slowed impulse generation by the sinus node. A junctional escape rhythm originates in the AV node.

Sepsis has been recently redefined as a systemic inflammatory response to infection. severe hypotension in an infected patient. a systemic infection with viable organisms in the bloodstream. a systemic inflammatory response to ischemia.

a systemic inflammatory response to infection. Systemic inflammatory response syndrome is the body's response to infection or other insults, which result in systemic signs and symptoms of widespread inflammation. Sepsis results from the presence of microorganisms in the bloodstream (bacteremia). Sepsis occurs as a result of bacteremia and is defined as a systemic inflammatory response to infection. Severe hypotension may be the result of sepsis, but it is not the definition.

Administration of a vasodilator to a patient in shock would be expected to increase contractility. decrease vascular resistance. decrease left ventricular afterload. increase tissue perfusion.

decrease left ventricular afterload. Vasodilators are used to decrease the workload of the heart by decreasing left ventricular afterload. Nitroprusside and nitroglycerin are examples of vasodilators. Dobutamine is used to decrease vascular resistance. Positive inotropic drugs are used to increase contractility. Positive inotropes include β-adrenergic agonists, which have the ability to increase tissue perfusion.

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

decreasing myocardial oxygen demands. 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. Parasympathetic activation is not the primary treatment for myocardial infarction.

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

diastolic murmur. 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.

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

digitalis. 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 is diagnosed with heart failure with normal ejection fraction. This patient is most likely characterized by a(n) young sedentary male with a high-stress job. middle-aged man with a previous history of MI. young female athlete with cardiomegaly. elderly woman without a previous history of MI.

elderly woman without a previous history of MI. Heart failure with normal ejection fraction is particularly likely to develop in the elderly, in women, and in those without a history of MI. A middle-aged man with a previous history of MI may have heart failure, but the older woman fits the criteria of heart failure with normal ejection fraction. A young female athlete with cardiomegaly may experience heart failure, but is not the normal patient profile for this condition. A young sedentary male with a high-stress job may experience heart failure, but this patient does not fit the normal profile for this condition.

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

mitral regurgitation. 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. Blood rushing through the narrowed mitral valve during ventricular diastole can sometimes be heard as a low-pitched, rumbling diastolic murmur at the heart's apex.

The prevalence of high blood pressure is higher in non-Hispanic black adults. non-Hispanic white adults. Mexican-American adults. Asian children.

non-Hispanic black adults. The prevalence of high blood pressure remains higher among non-Hispanic black adults. Non-Hispanic white adults have a lower prevalence of high blood pressure. Mexican-American adults have a lower prevalence than black adults. Asian children do not display a high prevalence for high blood pressure.

A patient who was involved in a fall from a tree becomes short of breath. The lung sounds are absent on one side. This patient is experiencing ________ shock. hypovolemic cardiogenic distributive obstructive

obstructive This type of obstructive shock is the result of a tension pneumothorax and is caused by shifting and compression of mediastinal structures including the heart, which compromise left ventricular filling. Accumulation of air in the pleural space may occur because of trauma. Prompt relief of the obstructive event is necessary to restore cardiac output and prevent cardiovascular collapse. Cardiogenic shock is not related to a traumatic event. Hypovolemic shock results when circulating blood volume is inadequate to perfuse tissues. Distributive shock is characterized by an abnormally expanded vascular space caused by excessive vasodilation.

Hypotension associated with neurogenic and anaphylactic shock is because of hypovolemia. high afterload. poor cardiac contractility. peripheral pooling of blood.

peripheral pooling of blood. Profound peripheral vasodilation of both arterioles and veins leads to peripheral pooling of blood and hypotension. Decreased venous return to the heart results in decreased cardiac output and hypotension. Hypovolemia is not the source of the hypotension involved in neurogenic and anaphylactic shock. Cardiac output is generally adequate in neurogenic and anaphylactic shock. Hypotension in neurogenic and anaphylactic shock is not related to high afterload.

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

premature ventricular complexes. 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.

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

pulmonary stenosis. 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.

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

reduced cardiac output. 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.

The majority of tachydysrhythmias are believed to occur because of defective gap junctions. enhanced automaticity. triggered activity. reentry mechanisms.

reentry mechanisms. Reentry is thought to be the culprit in most tachydysrhythmias. Reentry is a complex process in which a cardiac impulse continues to depolarize in a part of the heart after the main impulse has finished its path. Triggered activity occurs when an impulse is generated during or just after repolarization. Alterations in automaticity create electrolyte imbalances. Defective gap junctions are not related to tachydysrhythmias.

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

renin 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.

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

right ventricular hypertrophy secondary to pulmonary hypertension. 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.

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

right-sided heart failure. 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.

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

secondary 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.

A laboratory test that should be routinely monitored in patients receiving digitalis therapy is serum calcium. albumin level. serum potassium. serum sodium.

serum potassium. Digitalis slows the heart rate through parasympathetic system activation and promotes sodium and water excretion through improved cardiac output to the kidney. Depletion of serum potassium (hypokalemia) may potentiate digitalis toxicity. Sodium and water excretion is activated through the parasympathetic system because of improved cardiac output to the kidneys. Albumin level is not affected by digitalis. Digitalis allows more calcium to remain in the cell through a slowing of the sodium-dependent calcium pump.

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 unstable angina. stable angina. coronary vasospasm. myocardial infarction.

stable angina. 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.