AACN PCCN QUESTIONS AND ANSWERS
WITH LATEST2025-2026
Cardiac output equation - ANSWER CO = HR x SV
Stroke volume equation - ANSWER end diastolic volume - end systolic volume
also = preload + afterload + contractility
Mechanism of failure: initial adaptation to low CO - ANSWER drop in CO-->drop in EF-->increased EDV
(end-diastolic volume)-->fiber stretch-->increased contractility-->activation of neurohormonal system
activation of neurohormonal system in HF - ANSWER adrenergic system
renin-angiotensin-aldosterone system (RAAS)
hypothalamic-neurohypophyseal system
endothelium activated mediators
influence of activation of neurohormonal system in HF - ANSWER Goal: increased CO and BP
increased HR and contractility-->vasoconstriction--?Na and H2o retention
progressive HF mechanism of failure - ANSWER 1. continued activation of sympathetic nervous system
(SNS) and RAAS-->increased afterload
2. release of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP)
3. release of cytokines
4. cardiac hypertrophy and remodeling
5. reflex response of baroreceptors and stretch receptors
6. increased demand and decreased function-->increased progressive failure
hepatojugular reflux (HJR) - ANSWER used to test fluid retention: (JVD >3cm) when pressing liver
S4 - ANSWER the resistance of filling
paroxysmal nocturnal dyspnea (PND) - ANSWER pulmonary s/s of HF
classifications of HF - ANSWER 1. systolic vs. diastolic
2. R vs. L
3. high-output vs. low-output
4. compensated vs. decompensated
the primary cause of RHF: - ANSWER LHF
HFrEF - ANSWER EF<=40%
HFpEF - ANSWER ef>=50%
the only class of meds to treat cause of coronary artery disease: - ANSWER statins
Diuretics for HF management - ANSWER -Aldosterone antagonist (AKA potassium-sparing)
, -thiazide
-loop
vasodilators for HF management - ANSWER -ACE inhibitors (angiotensin-converting enzyme)-->reducing
vasoconstriction-->helps to dilate the vessels
-ARBs (angiotensin-receptor blockers)-->reducing vasoconstriction-->helps to dilate the vessels
-hydralazine: often recommended for African American patients
-nitroglycerin (NTG): sometimes for decompensated HF
-CCB: for dysthymias, but not recommended as standard therapies for HF patients, because they further
decrease contractility. normally used for HR although it can decrease BP as well
-ARNI: new; promotes increased levels of BNP, which promotes diuresis and dilation.
positive inotropes: reserved for decompensated HF - ANSWER they don't improve heart functions, or
length of life
-digoxin:
-dobutamine:
-milrinone: not specifically listed under PCCN test guideline, but dobutamine is
negative inotropes: - ANSWER -beta-blockers: works best to stop the compensatory negative spiral, and
reduce the activation of the SNS
maintaining BP is important as long as patient can tolerate beta- blockers dose (as high as possible)
decrease demands for HF management: three ways - ANSWER 1. intraaortic balloon pump (IABP)
2. impella
3. ventricular assist device (VAD)
decrease ectopy or maintain electrical stability for HF patients - ANSWER -approximately half of HF
deaths that occur outside the hospital are from dysrhythmia
-oral antidysrhythmic agents
-pacemakers
-implantable cardioverter defibrillator (ICD): for dilated cardiac myopathy if EF <35% after 3 months on
optimal medical therapy
goal of HF therapy - ANSWER 1. cardiac transplantation: only cure for HF
2. focus on quality of life
cardiomyopathy - ANSWER 1. dilated: most common type; causes in/c ischemia such as MI, alcohol,
postpartum myopathy, viruses, myocarditis, stress induced dilated cardiomyopathy (takotsubo
cardiomyopathy--the only one that can heel in time)
2. hypertrophic: only thick inside the heart; familiar with genetic issues
3. septal hypertrophy: septum can become a large part of the heart--?obstruct the outflow of the
ventricles, especially if the patient becomes dehydrated (e.g. young athletes)
4. restrictive: the heart becomes tight; it can't relax to fill well; can be caused by connective tissue
diseases (e.g. amyloid)
dilated cardiomyopathy can go into what dysrhythmia? - ANSWER atrial fibrillation;
need to prevent thromboembolic events
WITH LATEST2025-2026
Cardiac output equation - ANSWER CO = HR x SV
Stroke volume equation - ANSWER end diastolic volume - end systolic volume
also = preload + afterload + contractility
Mechanism of failure: initial adaptation to low CO - ANSWER drop in CO-->drop in EF-->increased EDV
(end-diastolic volume)-->fiber stretch-->increased contractility-->activation of neurohormonal system
activation of neurohormonal system in HF - ANSWER adrenergic system
renin-angiotensin-aldosterone system (RAAS)
hypothalamic-neurohypophyseal system
endothelium activated mediators
influence of activation of neurohormonal system in HF - ANSWER Goal: increased CO and BP
increased HR and contractility-->vasoconstriction--?Na and H2o retention
progressive HF mechanism of failure - ANSWER 1. continued activation of sympathetic nervous system
(SNS) and RAAS-->increased afterload
2. release of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP)
3. release of cytokines
4. cardiac hypertrophy and remodeling
5. reflex response of baroreceptors and stretch receptors
6. increased demand and decreased function-->increased progressive failure
hepatojugular reflux (HJR) - ANSWER used to test fluid retention: (JVD >3cm) when pressing liver
S4 - ANSWER the resistance of filling
paroxysmal nocturnal dyspnea (PND) - ANSWER pulmonary s/s of HF
classifications of HF - ANSWER 1. systolic vs. diastolic
2. R vs. L
3. high-output vs. low-output
4. compensated vs. decompensated
the primary cause of RHF: - ANSWER LHF
HFrEF - ANSWER EF<=40%
HFpEF - ANSWER ef>=50%
the only class of meds to treat cause of coronary artery disease: - ANSWER statins
Diuretics for HF management - ANSWER -Aldosterone antagonist (AKA potassium-sparing)
, -thiazide
-loop
vasodilators for HF management - ANSWER -ACE inhibitors (angiotensin-converting enzyme)-->reducing
vasoconstriction-->helps to dilate the vessels
-ARBs (angiotensin-receptor blockers)-->reducing vasoconstriction-->helps to dilate the vessels
-hydralazine: often recommended for African American patients
-nitroglycerin (NTG): sometimes for decompensated HF
-CCB: for dysthymias, but not recommended as standard therapies for HF patients, because they further
decrease contractility. normally used for HR although it can decrease BP as well
-ARNI: new; promotes increased levels of BNP, which promotes diuresis and dilation.
positive inotropes: reserved for decompensated HF - ANSWER they don't improve heart functions, or
length of life
-digoxin:
-dobutamine:
-milrinone: not specifically listed under PCCN test guideline, but dobutamine is
negative inotropes: - ANSWER -beta-blockers: works best to stop the compensatory negative spiral, and
reduce the activation of the SNS
maintaining BP is important as long as patient can tolerate beta- blockers dose (as high as possible)
decrease demands for HF management: three ways - ANSWER 1. intraaortic balloon pump (IABP)
2. impella
3. ventricular assist device (VAD)
decrease ectopy or maintain electrical stability for HF patients - ANSWER -approximately half of HF
deaths that occur outside the hospital are from dysrhythmia
-oral antidysrhythmic agents
-pacemakers
-implantable cardioverter defibrillator (ICD): for dilated cardiac myopathy if EF <35% after 3 months on
optimal medical therapy
goal of HF therapy - ANSWER 1. cardiac transplantation: only cure for HF
2. focus on quality of life
cardiomyopathy - ANSWER 1. dilated: most common type; causes in/c ischemia such as MI, alcohol,
postpartum myopathy, viruses, myocarditis, stress induced dilated cardiomyopathy (takotsubo
cardiomyopathy--the only one that can heel in time)
2. hypertrophic: only thick inside the heart; familiar with genetic issues
3. septal hypertrophy: septum can become a large part of the heart--?obstruct the outflow of the
ventricles, especially if the patient becomes dehydrated (e.g. young athletes)
4. restrictive: the heart becomes tight; it can't relax to fill well; can be caused by connective tissue
diseases (e.g. amyloid)
dilated cardiomyopathy can go into what dysrhythmia? - ANSWER atrial fibrillation;
need to prevent thromboembolic events
