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PCCN EXAM 2024/2025 WITH
VERIFIED QUESTIONS AND
ANSWERS
Coronary artery perfusion is dependent upon: A. diastolic pressure B. systolic pressure C. afterload D. systemic vascular resistance (SVR) A. diastolic pressure Diastolic pressure in the aortic root is higher than left ventricular end-diastolic pressure (LVEDP), the pressure exerted on the ventricular muscle at the end of diastole when the ventricle is full. This enables blood to flow from a higher pressure through open arteries to a lower pressure, a pressure gradient known as coronary artery prefusion pressure. As diastolic pressure drops, there is a decrease in coronary artery blood flow. Coronary artery perfusion is not affected by systolic pressure, afterload or SVR, but they all increase the demand of oxygen in the heart. A post-STEMI (ST elevation myocardial infarction) patient is started on an angiotensin-converting enzyme (ACE) inhibitor during his hospital stay. Which of the following is the most common serious side effect that may occur? A. a nonproductive cough B. pedal edema C. swelling of the tongue and face D. rhinorrhea C. swelling of the tongue and face Although all of the answers may occur, swelling og the tongue and face is the most serious and may require intervention. Patients should be instructed to seek medical attention immediately for any signs of swelling in the tongue or throat.
Which of the following best describes the fourth heart sound (S4): A. It occurs after ventricular contraction B. It is best heard with the diaphragm of the stethoscope C. It is a normal finding in children D. It occurs during late diastole when the atria contracts D. It occurs during late diastole when the atria contracts The presence of the extra heart sound S4 signifies a poorly compliant (stiff) left ventricle. An S4 is also called an atrial heart sound since it occurs at the end of diastolic filling when the atria contracts and fully fills the left ventricle. Known as "atrial kick", this filling is important to cardiac output. The increased end-diastolic volume in the ventricle improves cardiac output. When the left ventricle is stiff (decreased compliance with long term hypertension, aortic stenosis or with acute STEMI), the atrium has to pump harder to move blood from the atrium to the ventricle, causing a turbulent blood flow and extra heart sound. This heart sound is always pathologic. It occurs before ventricular contraction, is best heard with the bell of the stethoscope and is never a normal heart sound, even in children. Which pathologic changes found on the 12 - lead ECG indicate myocardial ischemia? A. ST-segment elevation B. ST-segment depression and T-wave elevation C. Q-wave formation D. ST-segment depression and T-wave inversion D. ST segment depression and T wave inversion Myocardial ischemia changes the repolarization of the ventricular muscle. That change is seen on the 12 lead ECG as ST-segment depression and T wave inversion, which demonstrate subendocardial ischemia -- the innermost layer of muscle in the myocardium. ST-segment elevation indicates acute injury or infarction, ST segment depression and T wave elevation may indicate an electrolyte abnormality, while Q wave formation indicates total infarction. Positive inotropic agents are used to: A. improve cardiac output and tissue perfusion
maintain BP. If the SVR (afterload) is low (as in early septic shock), the cardiac output is very high, thereby trying to support BP. The layer of the arterial vessel wall responsible for changes in the diameter of the artery is the: A. media B. intima C. externa D. adventitia A. media The media layer of the arterial wall contains vascular smooth muscle cells and is responsible for arterial tone. Vasoactive substances released in response to the sympathetic nervous system and/or the renin-angiotensin system determine arterial tone. Intima, externa and adventitia are incorrect. A patient presents in acute distress with rales halfway up bilaterally; cool and clammy extremities; elevated jugular venous distention (JVD); oxygen saturations at 95%, down from 99%; and complaints of shortness of breath. Which of the following findings correspond to the patient's cardiac status? A. no pulmonary congestion, normal perfusion B. no pulmonary congestion, low perfusion C. pulmonary congestion, normal perfusion D. pulmonary congestion, low perfusion D. pulmonary congestion, low perfusion Rales indicate fluid in the alveolar sacs, possibly secondary to pulmonary edema, causing pulmonary congestion. Pneumonia can also cause fluid in the alveolar sacs. The patient is complaining of shortness of breath, and the oxygen saturations are lowering, also indicating that the patient has pulmonary congestion. The patient's skin is cool and clammy, indicating that the skin is poorly perfused. Skin does not require oxygen and shunts blood away in decreased cardiac function; therefore, this
patient has pulmonary congestion and low perfusion state. The other answers are incorrect. When listening to heart sounds, S1 signifies which of the following? A. the beginning of ventricular systole B. the beginning of ventricular diastole C. the propulsion of blood into a non-compliant ventricle D. the blood going in the wrong direction A. the beginning of ventricular systole The heart sound of S1 indicates the opening of the aortic and pulmonic valves and marks the beginning of ventricular systole or ejection. The beginning of diastole is after S2, propulsion of blood into a noncompliant chamber is S4, and blood going in the wrong direction will cause a murmur. A patient with pulmonary edema has impaired diffusion due to: A. increased thickness of the alveolar capillary membrane B. retaining CO C. an elevated body temperature associated with pulmonary edema D. low barometric pressure A. increased thickness of the alveolar capillary membrane With increasing left ventricular pressures, blood moves back into the left atrium, then to the pulmonary veins. When the pressure in the pulmonary veins increases, capillary function decreases, and fluid then shifts to the interstitial space, causing interstitial edema, thereby, increasing the thickness of the space oxygen must travel. When left ventricular pressures increase, the fluid then shifts to the alveolar space, causing pulmonary edema. This fluid acts as a deterrent to oxygen diffusion. Retention of CO2 does not impair diffusion. An elevated body temperature associated with pulmonary edema is not causing a diffusion abnormality; increased temperature shifts the oxyhemoglobin curve to the right, more quickly releasing
patients may benefit from nutrition counseling; however, this is not a primary concern for this patient. A medication that dilates both the venous and arterial beds will cause which of the following results? A. increased preload, decreased afterload B. increased preload, increased afterload C. decreased preload, decreased afterload D. decreased preload, increased afterload C. decreased preload, decreased afterload When both the venous and arterial beds are dilated, there will be less venous return, causing a decreased preload (ex. nitroglycerin). With arterial vasodilation, the afterload will decrease (ex nitroprusside, ACE-I). Afterload in this case is resistant to LV pumping. Stable angina is best defined as: A. pain that increases in severity B. pain that is new C. pain that occurs at rest D. pain that has a predictable pattern over time D. pain that has a predictable pattern over time Stable angina is predictable -- the patient can describe the pain and how it is initiated accurately each time -- and occurs with exertion. Ex: The patient knows every time he or she climbs stairs, it will be accompanied by chest pain. The pain is relieved with rest and nitroglycerin (Nitrolingual). Pain that is new or occurs at rest is not stable angina. If the pain increases in severity, it is no longer stable.
The gold standard diagnostic tool for the identification, location of disease and severity of coronary artery disease is: A. a stress test B. an echocardiography C. cardiac catheterization D. a spiral computer tomography (CT scan) C. cardiac catheterization The gold standard, or best diagnostic tool, for the diagnosis, location and severity of coronary artery disease is the cardiac catheterization performed in the cath laboratory. Echocardiography is excellent in revealing structure changes, but not coronary artery disease. A stress test may be a good screening tool, but again, is not the gold standard, nor is CT scanning The most common complication after a STEMI is: A. heart failure B. dysrhythmia C. ventricular septal rupture D. ventricular wall rupture B. dysrhythmia The most common complication after a STEMI is dysrhthmia due to irritability of the ischemic myocardium and the dead myocardium that does not transmit electrical stimuli. With interior-wall STEMI, the most common dysrhythmia is bradycardia and heart block. With anterior-wall STEMI, tachydysrhythmias such as ventricular tachycardia and/or ventricular fibrillation are most common. Heart failure, ventricular septal wall rupture and ventricular rupture are infrequent complications after STEMI and carry a very poor prognosis. The most common cause of heart failure in the US is: A. valvular disease
B. increased activation of the sympathetic nervous system and the renin-angiotensin system C. increased production of hemoglobin D. increased production of cholesterol to make hormones B. increased activation of the sympathetic nervous system and the renin-angiotensin system With continued heart failure, the body compensates for the low cardiac output by stimulating the sympathetic nervous system and the renin-angiotensin system. This increases preload and afterload in an already poorly functioning heart. Neurohormonal blockers are the treatment. Activation of increased liver release of glycogen stores increases blood sugar, but not heart failure. Increased production of hemoglobin is a response to hypoxia, and increased production of cholesterol does not have a relation to the neurohormonal response to heart failure. Medications commonly used in the treatment of heart failure include: A. ACE inhibitors, beta blockers B. calcium channel blockers C. nitrates D. calcium channel blockers and digoxin (Lanoxicaps) A. ACE inhibitors, beta blockers The most effective and evidence-based practice treatment of heart failure is neurohormonal blockade. These medications include beta blockers and ACE inhibitors. They reduce preload and afterload as well as controlling heart rate and BP. Calcium channel blockers are not used in heart failure since they tend to increase the absorption of sodium and water. Nitrates are used for treatment in conjunction with other drugs. Beta blockers are ACE-I are the foundation of treatments. Digoxin is also used but only after the beta blockers and ACE-I are started. The heart's primary compensatory response to chronic aortic stenosis includes: A. left arterial hypertrophy
B. left ventricular hypertrophy C. left ventricular dilation D. right ventricular dysfunction B. left ventricular hypertrophy With chronic aortic stenosis, the left ventricle hypertrophies over time due to the increased workload of pumping blood through a narrowed opening. This leads to diastolic dysfunction as well as hypertrophy. The left atrium will enlarge over time, but the primary result is left ventricular hypertrophy, not dilation. The right ventricle remains normal for a period of time. Patients with pericardial effusions should be assessed for the development of which of the following complications: A. thrombocytopenia B. tamponade C. low hemoglobin and hematocrit D. endocarditis B. tamponade Any patient with a pericardial effusion should be assessed for cardiac tamponade physiology. Any accumulation of fluid in the pericardial sac can compress the myocardium, producing tamponade signs and symptoms. All patients are assessed for thrombocytopenia, low H+H and endocarditis; they are not the focus of complications with effusions but could be additional signs of tamponade (low H+H and thrombocytopenia). Nursing interventions in the patient with pericarditis include all the following except: A. providing comfort by administering pain medications and proper positioning B. auscultating heart sounds to assess for muffled heart sounds C. administering anticoagulants to prevent thrombus in the pericardium D. monitoring for jugular venous distention (JVD) and hypotension
stretch, facilitating electrophysiological abnormalities. Other complications include bleeding, stroke, and ventricular fibrillation, but they are not the most common. An NSTEMI is differentiated from an unstable angina by: A. location of chest pain B. cardiac biomarker elevation C. ECG changes D. extent of cardiac history B. cardiac biomarker elevation In the NSTEMI vs unstable angina patient, the location of pain may be the same. Regarding ECG changes, both may have ST-Twave depression in the associated leads. The history of a patient with myocardial ischemia may not be pertinent. In an unstable angina, the patient may have ECG changes, but no cardiac enzyme changes. In NSTEMI, the patient will have cardiac enzyme elevation. The nurse auscultates an S3 on a patient just admitted with NSTEMI. What does that indicate? A. normal heart sounds B. mitral valve stenosis C. fluid overload D. increased afterload C. fluid overload The auscultation of an S3 is always abnormal in the adult patient. It indicates an overfilled left ventricle at the beginning of ventricular diastole and is a marker of poor ventricular function as well as fluid overload. S3 does not reflect mitral valve stenosis (diastolic murmur) or increased afterload The primary function of beta blocker therapy in heart failure is to:
A. increase BP B. block compensatory vasoconstriction and increase heart rate C. increase urine output D. decrease preload B. block compensatory vasoconstriction and increase heart rate The treatment of heart failure is to reduce the actions of the sympathetic nervous system and the renin-angiotensin system. Beta blockers block the SNS and reduce afterload, slightly reduce contractility and improve heart rate regulation. These decrease the demands of oxygen for the patient with reduced ventricular function. Beta blockers do not increase heart rate, nor do they increase urine output or change preload in any way. Early symptoms of fluid overload and pulmonary edema are: A. rales and hypoxia B. S3 heart sound and tachycardia C. complaint of shortness of breath and orthopnea D. ST segment elevation in the chest leads C. complaint of shortness of breath and orthopnea Remember that symptoms are what the patient complains of, not signs that the nurse measures. Rales and hypoxia, S3 and tachycardia are signs that are measured at the bedside. ST segment elevation is a sign of cardiac injury/infarction. A complaint of shortness of breath and the inability to lie down are symptoms of early left-ventricular failure. An elderly patient is admitted and placed on warfarin (Coumadin) for arterial fibrillation. What is a therapeutic range for anticoagulation for this patient? A. international normalized ration (INR) less than 1. B. INR between 1.0 and 1. C. INR between 2.5 and 3.
A physiologic reason for sinus tachycardia is: A. elevated serum potassium B. elevated creatinine C. decreased urine output D. tissue hypoxia D. tissue hypoxia Sinus tachycardia is generally a compensatory mechanism for decreased tissue oxygenation. Fever, pain, anxiety, hypovolemia and decreased blood pressure all are reasons for tachycardia. The physiology in all is the lack of oxygen delivery at the tissue level. Elevated potassium does not increase heart rate, but if it is high enough, causes sinus bradycardia. Elevated creatinine is a marker of renal failure, and increased potassium would cause sinus bradycardia. Decreased urine output may or may not affect heart rate. A patient is admitted with decompensated heart failure. The patient is receiving furosemide (Lasix), digoxin (Lanoxin), metoprolol (Lopressor) and lisinopril (Zestril) at home. What drug can be added to reduce preload? A. spironolactone (Aldactone) b. verapamil (Calan) c. dabigatran etexilate (Pradaza) d. No other drugs are essential A. spironolactone (Aldactone) When the heart failure patient continues to have volume overload on appropriate medications, an aldosterone inhibitor such as spironolactone or eplerenone (Inspera) should be added. Aldosterone inhibition will decrease sodium reabsorption from the kidneys and therefore decrease intravascular volume. The nurse would carefully monitor potassium since aldosterone blockers are potassium-sparing diuretics. Remember not to use verapamil in heart failure; it will increase sodium and water
retention. Dabigatran etexilate is an anticoagulant used only for non-vascular atrial fibrillation. Which condition would stimulate renin production? A. increased blood supply to the renal tubules B. decreased blood pressure C. decreased sympathetic output D. increased sodium concentration B. decreased blood pressure Renin secretion is regulated by blood flow to the juxtaglomerular apparatus. Decreased blood pressure would be identified, and renin secretion would occur. This begins a compensatory mechanism that causes vasoconstriction with increased blood pressure as well as sodium and water reabsorption in the kidneys, thereby effectively increasing blood pressure. Increased blood flow would maintain normal renin production. Decreased sympathetic output would not affect renin secretion from the kidneys (it is stimulated by low renal blood flow). Low serum sodium concentrations would stimulate renin production due to decreased osmolality. Symptoms of acute endocarditis of the mitral valve cause: A. symptoms similar to heart failure B. severe chest pain mimicking STEMI C. Claudication-type pain D. pain that is relieved by sitting up A. symptoms similar to heart failure Symptoms of acute endocarditis are very similar to heart failure. The mitral valve with infection may become incompetent and cause increased pulmonary pressures just like left ventricular heart failure. The pateint will need heart failure treatment as well as antibiotics. Claudication-type pain is caused by ischemia to the lower extremities. Pain relieved by sitting up is usually pericarditis in nature.
An elderly patient with an abdominal aortic aneurysm decline surgery for the condition. What medication may be helpful in the prevention of rupture of this aneurysm? A. benazepril (Lotensin) B. captopril (Capoten) C. metoprolol (Lopressor) D. ramipril (Altace) C. metoprolol (Lopressor) Beta blockers are the best treatment for the prevention of an abdominal aortic aneurysm rupture. The other answers are all angiotensin-converting enzyme inhibitors and will decrease the patient's hypertension; it is the beta blocker that is suggested for this patient. Beta blockers, while decreasing blood pressure, also inhibit the force of ventricular contraction, which helps prevent tension on the aortic wall, thereby reducing stress and the possibility of rupture. During the treatment of supraventricular tachycardia, which medication is given rapidly intravenous (IV) push and may result in a brief sinus pause? A. lidocaine (Xylocaine) B. epinephrine (Adrenaclick) C. adenosine (Adenocard) D. procainamide C. adenosine (Adenocard) Adenosine is used for the treatment of supraventricular tachycardia. It is given as a rapid IV push with a large saline flush. It often results in a sinus pause, then the rhythm converts to sinus. None of the other medications are used for supraventricular tachycardia.
You are caring for a patient recently admitted with an inferior wall MI. Which of the following 12 - lead ECG findings would you anticipate? A. T wave inversion in leads I and aVL B. Q wave formation and ST segment elevation in leads II, III, and aVF C. QRS duration greater than 0.01 in all leads D. R wave taller in V B. Q wave formation and ST segment elevation in leads II, III, and aVF With STEMI, the patient will have ST segment elevation. The inferior leads are II, III, and aVF. T wave inversion in leads I and aVL indicate ischemia in the anterior leads. QRS duration that is prolonged may indicate an intraventricular conduction defect, and an R wave taller in V6 is a bundle branch block. A thoracic aortic aneurysm causes chest pain that: A. radiates to the left arm B. radiates through to the back C. is sharp and worse while reclining D. is associated with diminished breath sounds B. radiates through to the back Typically aortic aneurysms present with severe, acute onset of chest pain that radiates through to the back. Pain that radiates to the left arm may indicate myocardial ischemia. Sharp pain worsening with the reclined position may be pericarditis, and diminished breath sounds could be anything that is caused by decreased tidal volume. The most common ECG changes that occur during pulmonary embolus are: A. Q waves in AVR and Lead I B. tachycardia C. Bradycardia and ST segment depression
