CH 35: Review Heart Structure/Function Flashcards

Question

Which vessel is responsible for draining most of the venous blood from the heart? A. Coronary sinus B. Superior vena cava C. Inferior vena cava D. Right atrium

Answer 1

A. Coronary sinus Rationale: The coronary sinus collects deoxygenated blood from the coronary veins and drains it into the right atrium. It plays a crucial role in venous return from the myocardium.

Answer 2

C. Left anterior descending and left circumflex arteries Rationale: The left main coronary artery divides into the left anterior descending (LAD) and left circumflex (LCX) arteries. A severe blockage in the left main artery is dangerous because it affects both major branches, leading to extensive myocardial ischemia.

Answer 3

B. SA node Rationale: The SA node is the heart’s natural pacemaker, typically generating 60-100 impulses per minute. Sinus bradycardia suggests that the SA node is firing at a slower rate than normal. If the SA node fails, the AV node (40-60 bpm) or Purkinje fibers (20-40 bpm) may take over.

Answer 4

C. Purkinje fibers Rationale: In third-degree (complete) AV block, the atrial impulses fail to reach the ventricles, causing the Purkinje fibers to become the dominant pacemaker. Since the Purkinje fibers fire at 20-40 bpm, this results in severe bradycardia, often requiring pacemaker placement.

Answer 5

B. AV node Rationale: This describes second-degree AV block Type I (Wenckebach), which results from a conduction delay at the AV node. The PR interval progressively lengthens until a ventricular beat is dropped.

Answer 6

A. The heart muscle cannot respond to any new stimulus. C. It prevents tetany and allows for proper cardiac filling. Rationale: The absolute refractory period is when the heart muscle is completely unresponsive to new electrical stimuli, ensuring that the heart does not enter tetany and can function as an effective pump. This period prevents premature ventricular contractions (PVCs) from causing life-threatening arrhythmias.

Answer 7

D. Purkinje fibers Rationale: A heart rate of 30 bpm suggests the Purkinje fibers are acting as the pacemaker. This often occurs in third-degree heart block, where the AV node fails to transmit impulses to the ventricles. The wide QRS complex is a hallmark of ventricular-origin beats.

Answer 8

C. AV node Rationale: Beta-blockers (e.g., metoprolol) slow conduction through the AV node, reducing ventricular response rate in conditions like atrial fibrillation. This helps prevent rapid and irregular ventricular contractions.

Answer 9

A. Impaired ventricular conduction and heart failure Rationale: The left bundle branch is responsible for conducting impulses to the left ventricle. Anterior wall MIs can damage this conduction pathway, leading to left bundle branch block (LBBB), causing ventricular dyssynchrony and decreased cardiac output, which can contribute to heart failure.

Answer 10

D. Purkinje fibers Rationale: The Purkinje fibers have the fastest conduction velocity, delivering impulses quickly to the ventricular myocardium. This ensures simultaneous right and left ventricular contraction, which is critical for effective cardiac output.

Answer 11

C. Torsades de Pointes Rationale: Torsades de Pointes is a life-threatening polymorphic ventricular tachycardia associated with prolonged QT intervals. This can result from electrolyte imbalances (low magnesium, low potassium), certain medications (antipsychotics, antiarrhythmics), or congenital long QT syndrome.

Answer 12

B. First-degree AV block Rationale: A normal PR interval is 0.12–0.20 seconds. A PR interval > 0.20 seconds suggests a first-degree AV block, which indicates delayed conduction through the AV node. This can be caused by beta-blockers, calcium channel blockers, aging, or structural heart disease.

Answer 13

B. Hyperkalemia D. Acute kidney injury Rationale: Tall, peaked T waves are a hallmark of hyperkalemia, which commonly occurs in acute kidney injury due to reduced potassium excretion. In contrast, hypokalemia is associated with a U wave rather than a peaked T wave.

Answer 14

D. U waves and flattened T waves Rationale: Hypokalemia is associated with flattened T waves and prominent U waves, which represent delayed repolarization of the Purkinje fibers. Severe hypokalemia can lead to ventricular dysrhythmias and cardiac instability.

Answer 15

C. Torsades de Pointes Rationale: A prolonged QT interval (> 0.44 seconds in men, > 0.46 seconds in women) increases the risk of Torsades de Pointes, a type of polymorphic ventricular tachycardia. This arrhythmia is associated with electrolyte imbalances (hypokalemia, hypomagnesemia) and certain medications (antiarrhythmics, antipsychotics, antibiotics).

Answer 16

B. Inferior wall myocardial infarction Rationale: ST segment elevation in leads II, III, and aVF indicates an inferior wall myocardial infarction (MI), which is typically caused by an occlusion of the right coronary artery. Anterior wall MIs show changes in leads V1-V4, and pericarditis typically causes diffuse ST elevation in multiple leads.

Answer 17

A. Stroke Rationale: Atrial fibrillation leads to blood stasis in the atria, increasing the risk of thrombus formation. If a clot dislodges, it can travel to the brain, causing a stroke. Patients with atrial fibrillation are often prescribed anticoagulants (e.g., warfarin, apixaban) to reduce this risk.

Answer 18

C. Atrial fibrillation Rationale: Atrial fibrillation is characterized by absent P waves and an irregularly irregular rhythm, indicating chaotic electrical activity in the atria. Unlike atrial flutter, which has sawtooth P waves, atrial fibrillation results in a completely disorganized atrial rhythm.

Answer 19

A. 3.2 L/min, which is low The normal CO range is 4–8 L/min. However, this patient has a high heart rate and low stroke volume, which may indicate compensatory tachycardia due to decreased stroke volume, possibly from hypovolemia, heart failure, or shock.

Answer 20

C. Myocardial infarction (MI) Rationale: A myocardial infarction (MI) damages the myocardium, reducing its ability to contract effectively, leading to decreased stroke volume (SV) and cardiac output (CO).

Answer 21

B. Decreased cardiac output Rationale: In cardiogenic shock, the damaged myocardium leads to severely decreased stroke volume and cardiac output, impairing perfusion. * Systemic vascular resistance (SVR) increases as a compensatory mechanism. * CO does not increase because the heart is too weak to pump effectively.

Answer 22

A. Increased heart rate (HR) B. Activation of the sympathetic nervous system (SNS) Rationale: When stroke volume (SV) decreases, the body compensates by: * Increasing heart rate (HR) to maintain cardiac output (CO = HR × SV). * Activating the sympathetic nervous system (SNS), which releases epinephrine and norepinephrine, increasing HR and contractility. Decreased preload and contractility would further reduce CO rather than compensate for it.

Answer 23

A. Cardiac output decreases because there are fewer cardiac cycles per minute Rationale: Bradycardia reduces CO because there are fewer contractions per minute, leading to less blood ejected per minute. While stroke volume may slightly increase, it typically does not compensate enough to maintain a normal CO.

Answer 24

D. Ventricular hypertrophy Rationale: In hypertension, increased arterial blood pressure increases afterload, making it harder for the left ventricle to pump blood. Over time, this causes ventricular hypertrophy—thickening of the ventricular wall without an increase in chamber size or cardiac output.

Answer 25

A. Afterload Rationale: Aortic stenosis increases afterload by creating obstruction at the aortic valve, making it harder for the left ventricle to eject blood. This increases myocardial workload, reduces cardiac output, and leads to myocardial ischemia (chest pain).

Answer 26

B. Decreased preload Rationale: Preload is the volume of blood in the ventricles at the end of diastole. Hypovolemia from blood loss reduces venous return, causing decreased preload, which lowers stroke volume and cardiac output.

Answer 27

A. Hypervolemia B. Aortic valve disease C. Hypertension Rationale: * Hypervolemia (excess fluid) increases venous return, raising preload. * Aortic valve disease (regurgitation or stenosis) increases volume retention in the ventricles. * Hypertension increases systemic vascular resistance, causing ventricular stretching over time.

Answer 28

C. Increased stroke volume Rationale: Sympathetic nervous system activation releases epinephrine and norepinephrine, which increase contractility, causing greater ventricular emptying and increased stroke volume.

Answer 29

D. Decreases heart rate, reducing cardiac output Rationale: Beta-blockers decrease sympathetic stimulation, leading to reduced heart rate and contractility, which lowers cardiac output.

Answer 30

D. Increased due to sympathetic nervous system activation Rationale: In early septic shock, vasodilation decreases systemic vascular resistance (SVR) and afterload, while sympathetic activation increases heart rate and contractility, leading to increased cardiac output.

Answer 31

A. Pulmonary hypertension B. Aortic stenosis Rationale: * Pulmonary hypertension increases right ventricular afterload. * Aortic stenosis increases left ventricular afterload due to narrowing of the aortic valve.

Answer 32

D. IV fluid bolus Rationale: An IV fluid bolus increases blood volume, which raises preload, potentially worsening fluid overload in heart failure.

Answer 33

B. Decreases afterload, reducing myocardial workload Rationale: Vasodilators reduce afterload, making it easier for the left ventricle to pump blood forward, thereby improving cardiac output and reducing myocardial oxygen demand.

Answer 34

A. Stroke volume decreases, cardiac output may decrease Rationale: At high heart rates (>150 bpm), diastolic filling time is reduced, leading to decreased stroke volume. If HR is too fast, cardiac output may decrease due to inadequate ventricular filling.

Answer 35

D. Increased afterload, leading to right ventricular hypertrophy Rationale: In pulmonary hypertension, the right ventricle must pump against increased pulmonary arterial pressure, leading to right ventricular hypertrophy and possible right-sided heart failure over time.

Answer 36

B. The difference between maximum and resting cardiac output Rationale: Cardiac reserve is the heart’s ability to increase cardiac output (CO) in response to demands such as exercise, stress, or hypovolemia. It is measured as the difference between resting CO and maximum CO.

Answer 37

D. Cardiac reserve Rationale: Patients with heart failure have a reduced cardiac reserve, meaning their heart cannot effectively increase cardiac output during exertion. This leads to fatigue, dyspnea, and exercise intolerance.

Answer 38

B. Increasing heart rate and contractility via the sympathetic nervous system Rationale: In hypovolemia, the body activates the sympathetic nervous system, which increases heart rate and contractility to temporarily sustain cardiac output. However, if volume loss continues, cardiac reserve becomes depleted, leading to decompensation.

Answer 39

B. Blood flows from the left side of the heart into arteries, arterioles, capillaries, venules, and veins. Rationale: Blood flows from the left side of the heart into arteries, arterioles, capillaries, venules, and veins, eventually returning to the right side of the heart. This is the basic pattern of systemic circulation.

Answer 40

A. Pulmonary arteries and veins Rationale: Pulmonary hypertension primarily involves the pulmonary arteries, where increased pressure can lead to right ventricular strain. The condition is characterized by elevated pressure in the pulmonary arteries that carry blood to the lungs.

Answer 41

C. Facilitate nutrient and gas exchange between blood and tissues Rationale: Capillaries are the smallest blood vessels where nutrient, gas, and waste exchange occurs between blood and tissues. Their thin walls allow for efficient diffusion.

Answer 42

D. Constriction of venules and veins Rationale: In hypovolemic shock, the body responds by constricting venules and veins to attempt to preserve circulating blood volume and increase venous return to the heart, maintaining perfusion to vital organs.

Answer 43

B. Arteries carry oxygenated blood away from the heart, except the pulmonary artery. Rationale: Arteries carry oxygenated blood away from the heart, with the exception of the pulmonary artery. The pulmonary artery carries deoxygenated blood to the lungs. Arteries also have thicker walls than veins due to higher pressure.

Answer 44

C. Incompetent valves in the veins causing blood pooling Rationale: Chronic venous insufficiency occurs when valves in the veins become incompetent, leading to blood pooling in the veins, causing venous dilation and skin pigmentation due to fluid leakage and stasis.

Answer 45

C. It provides structural integrity and allows for recoil after ventricular contraction. Rationale: Elastic tissue in large arteries like the aorta helps to cushion the impact of ventricular contraction and provides recoil, which propels blood forward into the circulation. This elasticity ensures smooth blood flow during systole and diastole.

Answer 46

A. To control arterial blood pressure and blood flow distribution Rationale: Arterioles play a key role in controlling arterial blood pressure and the distribution of blood flow to various tissues. They are more muscular than large arteries and can dilate or constrict based on local conditions.

Answer 47

C. Arterioles dilate to increase blood flow and improve oxygen delivery. Rationale: In response to low O2 levels and high CO2 levels, arterioles dilate to increase blood flow and improve the delivery of oxygen to tissues that need it most.

Answer 48

B. Constriction of arterioles increasing vascular resistance Rationale: Constriction of arterioles increases vascular resistance, contributing to higher blood pressure. This is a key factor in the pathophysiology of hypertension.

Answer 49

D. It promotes blood flow and inhibits coagulation under normal conditions. Rationale: The endothelium plays an important role in maintaining hemostasis, promoting blood flow, and inhibiting blood coagulation under normal conditions. When disrupted, such as in atherosclerotic plaque rupture, the coagulation cascade is triggered.

Answer 50

A. Formation of a fibrin clot due to activation of the coagulation cascade Rationale: When the endothelium is disrupted (e.g., due to a ruptured atherosclerotic plaque), the coagulation cascade is activated, resulting in the formation of a fibrin clot.

Answer 51

B. Thick walls composed mainly of elastic tissue with some smooth muscle Rationale: Large arteries like the aorta have thick walls composed mainly of elastic tissue. This helps to cushion the pressure from ventricular contraction and aids in the propulsion of blood forward.

Answer 52

D. Arterioles Rationale: Arterioles have the most smooth muscle relative to their size and play a crucial role in regulating arterial blood pressure and blood flow distribution.

Answer 53

C. Have thin walls due to low pressure Rationale: Large arteries such as the aorta have thick walls made mainly of elastic tissue, not thin walls. These thick walls help cushion the pressure from ventricular contraction and provide recoil to propel blood forward.

Answer 54

B. To facilitate the exchange of cellular nutrients and metabolic waste products Rationale: Capillaries are specialized for the exchange of nutrients, gases, and metabolic waste between the blood and tissues due to their thin endothelial walls.

Answer 55

A. Thin endothelial walls with no elastic or muscle tissue Rationale: Capillaries have thin endothelial walls without elastic or muscle tissue, which allows for efficient exchange of nutrients and metabolic waste products.

Answer 56

C. Arterioles and venules Rationale: Capillaries serve as the connecting vessels between arterioles and venules, facilitating the exchange of substances between the blood and tissues.

Answer 57

A. They are low-pressure, high-volume vessels that return blood to the heart. Rationale: Veins are part of the low-pressure, high-volume system that returns blood to the heart, unlike arteries, which operate under high pressure.

Answer 58

B. To prevent the backward flow of blood and maintain unidirectional flow Rationale: Semilunar valves in veins prevent backward blood flow and ensure that blood continues toward the heart, despite the low-pressure environment in veins.

Answer 59

C. Skeletal muscle compression and changes in thoracic and abdominal pressures Rationale: Skeletal muscle compression and changes in thoracic and abdominal pressures (e.g., during breathing or physical activity) are crucial in helping the venous system move blood toward the heart.

Answer 60

A. Inferior vena cava Rationale: The inferior vena cava returns blood from the lower part of the body to the right atrium of the heart.

Answer 61

A. It can cause distended neck veins or liver engorgement. Rationale: Elevated right atrial pressure increases resistance to blood flow, which can lead to distended neck veins or liver engorgement, as blood is unable to flow properly back to the heart.

Answer 62

C. Collect blood from capillary beds and channel it to larger veins Rationale: Venules collect blood from the capillary beds and channel it into larger veins for return to the heart.

Answer 63

C. It compresses veins and assists in moving blood toward the heart Rationale: Skeletal muscle contraction helps compress veins, which propels blood toward the heart, increasing venous return.

Answer 64

B. The head, neck, and arms Rationale: The superior vena cava returns deoxygenated blood from the head, neck, and arms to the right atrium of the heart.

Answer 65

D. Prevent the backward flow of blood in veins Rationale: Semilunar valves in veins are responsible for maintaining unidirectional blood flow, preventing backflow and ensuring blood moves toward the heart.

Answer 66

B. Sympathetic nervous system Rationale: The sympathetic nervous system is responsible for the “fight or flight” response. It increases heart rate, cardiac output, and blood pressure in response to stress or physical activity by releasing norepinephrine and stimulating the heart’s beta receptors.

Answer 67

B. It decreases heart rate and promotes relaxation. Rationale: The parasympathetic nervous system, mainly through the vagus nerve, decreases heart rate and promotes relaxation by releasing acetylcholine, which acts to slow down the heart rate and reduce the force of contraction. This helps in maintaining a resting or “rest and digest” state.

Answer 68

D. Sympathetic nervous system Rationale: The sympathetic nervous system is responsible for the “fight or flight” response. It increases heart rate, cardiac output, and blood pressure in response to stress or physical activity by releasing norepinephrine and stimulating the heart’s beta receptors.

Answer 69

A. It decreases heart rate and promotes relaxation. Rationale: The parasympathetic nervous system, mainly through the vagus nerve, decreases heart rate and promotes relaxation by releasing acetylcholine, which acts to slow down the heart rate and reduce the force of contraction. This helps in maintaining a resting or “rest and digest” state.

Answer 70

C. It increases heart rate, speed of impulse conduction, and force of contraction. Rationale: Stimulation of the sympathetic nervous system increases heart rate, speed of impulse conduction through the AV node, and force of atrial and ventricular contractions. This effect is mediated through beta-adrenergic receptors that respond to norepinephrine and epinephrine.

Answer 71

B. Beta-adrenergic receptors Rationale: The effects of the sympathetic nervous system on the heart, such as increased heart rate and force of contraction, are mediated through beta-adrenergic receptors, which respond to the neurotransmitters norepinephrine and epinephrine.

Answer 72

D. Decreased heart rate and slowed impulse conduction through the AV node Rationale: The parasympathetic nervous system, mediated by the vagus nerve, slows the heart rate and decreases impulse conduction through the AV node, promoting a resting state for the heart.

Answer 73

B. Norepinephrine Rationale: Norepinephrine is the primary neurotransmitter released during sympathetic stimulation of the heart, which binds to beta-adrenergic receptors, resulting in increased heart rate, impulse conduction, and force of contraction.

Answer 74

D. It has no effect on heart rate. Rationale: Parasympathetic stimulation primarily decreases heart rate by inhibiting the SA node and decreasing the conduction of impulses through the AV node. This is mediated by the vagus nerve and acetylcholine.

Answer 75

B. Vasoconstriction Rationale: Stimulation of alpha-1 (α1)-adrenergic receptors in vascular smooth muscle results in vasoconstriction, which increases vascular resistance and blood pressure.

Answer 76

C. Vasodilation Rationale: Decreased stimulation of alpha-1 (α1)-adrenergic receptors causes vasodilation, which lowers vascular resistance and facilitates blood flow.

Answer 77

C. The sympathetic nervous system controls blood vessel tone through alpha-1 adrenergic receptors. Rationale: The sympathetic nervous system regulates blood vessel tone through the alpha-1 (α1)-adrenergic receptors, leading to vasoconstriction when stimulated.

Answer 78

D. Increased systemic vascular resistance Rationale: Vasoconstriction mediated by alpha-1 (α1)-adrenergic receptors leads to increased systemic vascular resistance, which raises blood pressure.

Answer 79

C. In the aortic arch and carotid sinus Rationale: Baroreceptors are located in the aortic arch and carotid sinus, where they detect stretch or pressure changes in the arterial system.

Answer 80

C. Inhibition of sympathetic nervous system and enhancement of parasympathetic influence Rationale: Baroreceptor stimulation from volume overload leads to the inhibition of the sympathetic nervous system and the enhancement of parasympathetic influence, which decreases heart rate and causes peripheral vasodilation.

Answer 81

A. Increased sympathetic nervous system activity Rationale: Decreased arterial pressure results in increased sympathetic nervous system activity to increase heart rate and vascular tone, in contrast to the response to volume overload.

Answer 82

B. They regulate blood pressure by detecting stretch or pressure changes and adjusting autonomic nervous system activity. Rationale: Baroreceptors monitor blood pressure by detecting stretch or pressure changes, sending signals to the vasomotor center to adjust autonomic nervous system activity accordingly.

Answer 83

C. Decreased heart rate and vasodilation Rationale: Baroreceptor stimulation due to high blood volume causes decreased heart rate and peripheral vasodilation to lower blood pressure.

Answer 84

B. Decreased arterial pressure causing reduced stretch on baroreceptors Rationale: Decreased arterial pressure, which reduces stretch on the baroreceptors, results in an increased heart rate and vasoconstriction as the body attempts to raise blood pressure.

Answer 85

B. In the aortic and carotid bodies and the medulla Rationale: Chemoreceptors are located in the aortic and carotid bodies and the medulla, where they play a role in monitoring respiratory and cardiovascular changes.

Answer 86

C. Increased arterial CO2 pressure (hypercapnia) Rationale: Chemoreceptors respond to increased arterial CO2 pressure (hypercapnia) and, to a lesser degree, decreased plasma pH (acidosis) and decreased arterial O2 pressure (hypoxia), affecting both respiratory rate and blood pressure.

Answer 87

C. Increased blood pressure Rationale: When chemoreceptors in the medulla are stimulated, they activate the vasomotor center, resulting in increased blood pressure.

Answer 88

B. Hypercapnia (increased CO2) Rationale: Hypercapnia (increased CO2) is the most common stimulus for chemoreceptors to trigger changes in both blood pressure and respiratory rate. Although hypoxia and acidosis can also have effects, hypercapnia is a primary trigger.

Answer 89

A. In the left atrium Rationale: Chemoreceptors in the aortic bodies, carotid bodies, and medulla have direct effects on blood pressure regulation, whereas chemoreceptors in the left atrium are not primarily involved in regulating blood pressure through changes in respiratory rate.

Answer 90

B. The residual pressure in the arteries during ventricular relaxation Rationale: Diastolic blood pressure (DBP) represents the residual pressure in the arteries during ventricular relaxation (or filling), whereas systolic blood pressure (SBP) is the pressure during ventricular contraction.

Answer 91

B. Small arteries and arterioles Rationale: Systemic vascular resistance (SVR) is primarily created in small arteries and arterioles. These vessels regulate the resistance to blood flow, impacting blood pressure.

Answer 92

B. SBP less than 120 mm Hg and DBP less than 80 mm Hg Rationale: Normal blood pressure is defined as a systolic blood pressure (SBP) of less than 120 mm Hg and a diastolic blood pressure (DBP) of less than 80 mm Hg.

Answer 93

A. Cardiac output (CO) Rationale: Cardiac output (CO), which is the amount of blood pumped by the heart per minute, and systemic vascular resistance (SVR) are the main factors influencing blood pressure (BP).

Answer 94

C. The peak pressure exerted against the arteries during ventricular contraction Rationale: Systolic blood pressure (SBP) is the peak pressure exerted on the arterial walls during ventricular contraction.

Answer 95

D. Blood pressure increases Rationale: An increase in systemic vascular resistance (SVR) increases the resistance to blood flow, which in turn increases blood pressure.

Answer 96

A. 180/120 mm Hg Rationale: The first Korotkoff sound represents the systolic BP (SBP) and the fifth Korotkoff sound represents the diastolic BP (DBP).

Answer 97

A. It requires catheter insertion into an artery and a transducer to measure pressure directly. Rationale: Invasive arterial BP monitoring involves catheter insertion and a transducer to measure pressure directly.

Answer 98

A. Assessing the patient’s pulse in the radial artery. Rationale: Before invasive BP monitoring, the nurse should assess the pulse to ensure the artery is patent for catheter insertion.

Answer 99

B. Palpate the brachial pulse and inflate the cuff until the pulse ceases. Rationale: If the SBP is unknown, palpating the brachial pulse and inflating the cuff until the pulse ceases provides an estimate for SBP.

Answer 100

A. Using the correct size cuff. B. Positioning the arm at heart level. E. Ensuring the patient is seated quietly for at least 5 minutes before measurement. Rationale: Correct cuff size, arm positioning at heart level, and a quiet rest period are essential for accurate BP readings.

Answer 101

D. A loss of sound between the systolic and diastolic pressures. Rationale: An auscultatory gap occurs when the Korotkoff sounds disappear between the SBP and DBP, which can lead to inaccurate readings.

Answer 102

A. Inflate the cuff 20 to 30 mm Hg above the expected SBP. Rationale: The Doppler ultrasonic flowmeter requires cuff inflation to 20 to 30 mm Hg above the expected SBP to ensure the return of the pulse sounds.

Answer 103

D. To obtain noninvasive, indirect BP measurements. Rationale: The sphygmomanometer and stethoscope are used to measure BP noninvasively by detecting Korotkoff sounds in the brachial artery.

Answer 104

C. Inflate the cuff 20 to 30 mm Hg above the point where the sounds were first heard. Rationale: The auscultatory gap should be accounted for by inflating the cuff above the point where the sounds were first heard to ensure accurate BP measurement.

Answer 105

all of the choices are correct Rationale: Any of these factors can contribute to inaccuracies in BP measurement, leading to erroneous readings.

Answer 106

B. The positioning of the catheter and transducer. Rationale: For continuous invasive BP monitoring, the nurse must ensure that the catheter and transducer are positioned correctly to obtain accurate readings.

Answer 107

A. Avoid placing the cuff over clothing. Rationale: Placing the cuff over clothing can result in inaccurate readings, so the cuff should be placed directly on the skin.

Answer 108

A. 150/110 mm Hg Rationale: The tapping sound corresponds to the systolic pressure, and the muffled sound corresponds to the diastolic pressure.

Answer 109

B. Diastolic BP. Rationale: The fifth phase of Korotkoff sounds represents the disappearance of sounds, which indicates the diastolic BP.

Answer 110

A. The patient talking during the measurement. C. The cuff being too tight. D. The nurse listening for Korotkoff sounds accurately. E. The cuff size being appropriate for the patient’s arm. Rationale: Talking, a tight cuff, and incorrect sound interpretation can lead to inaccurate readings, while correct positioning and cuff size ensure accuracy.

Answer 111

D. Repeat the measurement at least twice for accuracy. Rationale: To ensure accuracy, the BP measurement should be repeated and averaged, especially when using a Doppler ultrasonic flowmeter.

Answer 112

A. 50 mm Hg Rationale: Pulse pressure is the difference between systolic and diastolic BP. In this case, 140 - 90 = 50 mm Hg.

Answer 113

C. Atherosclerosis of the larger arteries Rationale: Atherosclerosis can cause increased pulse pressure due to the stiffening of the large arteries, leading to higher systolic BP.

Answer 114

B. 65 mm Hg Rationale: MAP is calculated as DBP + (SBP - DBP)/3. In this case, MAP = 60 + (90 - 60)/3 = 60 + 30/3 = 65 mm Hg.

Answer 115

A. Heart failure B. Hypovolemia Rationale: Decreased pulse pressure may occur in conditions like heart failure or hypovolemia, as these conditions reduce the difference between SBP and DBP.

Answer 116

B. Diastole lasts longer than systole, so the MAP gives more weight to DBP. Rationale: MAP takes into account the fact that diastole is longer than systole, so it is not a simple average of SBP and DBP.

Answer 117

A. MAP is 65 mm Hg, and it is adequate for perfusion. Rationale: MAP = DBP + (SBP - DBP)/3, so MAP = 50 + (110 - 50)/3 = 50 + 60/3 = 65 mm Hg. A MAP greater than 60 mm Hg is usually adequate for organ perfusion.

Answer 118

B. Ischemia of vital organs Rationale: A MAP below 60 mm Hg for a prolonged period can lead to ischemia of vital organs due to inadequate perfusion.

Answer 119

B. Decreased sensitivity to β-adrenergic agonist drugs Rationale: As people age, the number and function of β-adrenergic receptors in the heart decrease, leading to a reduced cardiovascular response to physical and emotional stress and less sensitivity to β-adrenergic drugs.

Answer 120

A. Orthostatic hypotension Rationale: In older adults, the sympathetic nerve pathway’s blunted response to changes in position can lead to orthostatic hypotension, which causes a drop in blood pressure when standing, resulting in dizziness or lightheadedness.

Answer 121

C. Arterial thickening and loss of elasticity Rationale: As arteries thicken and lose elasticity with aging, systolic blood pressure (SBP) tends to rise while diastolic blood pressure (DBP) remains the same or decreases, leading to an increased pulse pressure.

Answer 122

A. Systolic murmur with a whooshing sound Rationale: Aortic stenosis causes narrowing of the aortic valve orifice, which leads to turbulent blood flow during systole, producing a systolic murmur that is often described as a whooshing sound.

Answer 123

A. Stiffening of the heart valves B. Decreased number of pacemaker cells E. Thickening and loss of elasticity in arteries Rationale: Age-related changes include stiffening of the heart valves, a decrease in pacemaker cells in the SA node, and thickening and loss of elasticity in arteries. These changes contribute to cardiovascular issues such as heart murmurs, dysrhythmias, and elevated blood pressure.

Answer 124

C. Postprandial hypotension Rationale: Postprandial hypotension is a condition common in older adults where a significant drop in blood pressure occurs within 75 minutes after eating. It can lead to symptoms like dizziness and increase the risk of falls.

Answer 125

D. Decreased cardiac output during exercise Rationale: In older adults, due to changes in heart muscle function, the cardiovascular response to exercise is blunted, and the increase in cardiac output (CO) is much smaller compared to younger adults.

Answer 126

B. Decreased collagen and decreased elastin in the heart Rationale: Aging results in increased collagen and decreased elastin in the heart muscle, which affects its ability to stretch and contract efficiently, leading to reduced cardiac output and symptoms like fatigue with less activity.

Answer 127

A. Age B. Physical inactivity D. Smoking Rationale: Age is a major risk factor for CVD, and physical inactivity and smoking are significant contributors to cardiovascular disease in older adults. A healthy diet and low cholesterol levels are protective factors.

Answer 128

B. Increased QT interval Rationale: The number of pacemaker cells in the SA node and conduction cells in the heart decreases with age, which often results in prolonged conduction times, such as an increased QT interval on the ECG.

Answer 129

A. Venous insufficiency due to weakened leg vein valves Rationale: In older adults, the valves in the large veins of the legs become less effective, leading to venous insufficiency and the accumulation of fluid in the lower extremities, causing edema.

Answer 130

B. Atherosclerosis Rationale: Atherosclerosis, the buildup of plaque in the arteries, is the most common cause of CAD, and it is a primary contributor to cardiovascular disease in older adults.

Answer 131

A. Orthostatic hypotension B. Postprandial hypotension D. Decreased heart rate variability E. Blunted heart rate response to positional changes Rationale: Orthostatic hypotension, postprandial hypotension, decreased heart rate variability, and blunted heart rate response to positional changes can all increase the risk of falls in older adults with cardiovascular issues.

Answer 132

c. Right atrium and right ventricle

Answer 133

a. AV node b. Left ventricle d. Right ventricle

Answer 134

b. Endothelial layer of the arteries

Answer 135

a. Baroreceptors that inhibit the sympathetic nervous system, causing vasodilation

Answer 136

b. Firing of the SA node and depolarizing the atria

Answer 137

a. Dysrhythmia

Answer 138

c. Difficulty isolating the apical pulse

Answer 139

c. Electrocardiographic monitoring Rationale: Pulse deficit is a difference between simultaneously obtained apical and radial pulses. It indicates that there may be a cardiac dysrhythmia that would best be detected with ECG monitoring. Frequent BP monitoring, cardiac catheterization, and emergent cardioversion are used for diagnosis and/or treatment of cardiovascular disorders but would not be as helpful in determining the immediate reason for the pulse deficit.

Answer 140

b. Bruit Rationale: A bruit is the sound created by turbulent blood flow in an artery. Auscultating a bruit in an artery is not normal and indicates pathology. Thrills are palpable vibrations felt when there is turbulent blood flow through the heart or in a blood vessel. A murmur is the sound caused by turbulent blood flow through the heart.

Answer 141

c. Pulmonary vascular resistance (PVR) Rationale: PVR is a measure of right ventricular afterload, which is elevated in conditions such as pulmonary hypertension The other parameters do not directly assess for right ventricular afterload.

Answer 142

b. Position the zero-reference stopcock line level with the phlebostatic axis. Rationale: For accurate measurement of pressures, the zero-reference level would be at the phlebostatic axis. There is no need to rebalance and recalibrate monitoring equipment every 2 hours. Accurate hemodynamic readings are possible with the patient‘s head raised to 45 degrees or in the prone position. Alarms should be activated; if the pressure in the line falls (e.g., when the line is disconnected), the low-pressure alarm sounds immediately and notifies staff to promptly correct the problem.

CH 35: Review Heart Structure/Function Flashcards

pages 768-773