How Well Do You Know About Heart Failure? Trivia Quiz
How well do you know about heart failure? Most people are of the notion that heart failure involves the heart-stopping to beat for no reason, but in a real sense, heart failure occurs as a result of the heart not getting enough blood to pump to the other organs or lacking the force required to pump out the blood. Take this trivia quiz and test your understanding of this condition.
- 1._________ = volume ejected during contraction (systole).
- A.
Stroke Volume (SV)
- B.
Cardiac Output (CO)
- C.
Cardiac Index (CI)
- D.
Systemic Vascular Resistance (SVR)
- E.
Mean Arterial Pressure
- 2._________ = SV x HR (in L/min).
- A.
Stroke Volume (SV)
- B.
Cardiac Output (CO)
- C.
Cardiac Index (CI)
- D.
Systemic Vascular Resistance (SVR)
- E.
Mean Arterial Pressure
- 3._________ = CO + BSA.
- A.
Stroke Volume (SV)
- B.
Cardiac Output (CO)
- C.
Cardiac Index (CI)
- D.
Systemic Vascular Resistance (SVR)
- E.
Mean Arterial Pressure
- 4._________ = pressure LV is pumping against
- A.
Stroke Volume (SV)
- B.
Cardiac Output (CO)
- C.
Cardiac Index (CI)
- D.
Systemic Vascular Resistance (SVR)
- E.
Mean Arterial Pressure
- 5._________ = CO x SVR
- A.
Stroke Volume (SV)
- B.
Cardiac Output (CO)
- C.
Cardiac Index (CI)
- D.
Systemic Vascular Resistance (SVR)
- E.
Mean Arterial Pressure
- 6.____________ is amount of blood returning to heart prior to contraction (stroke volume dependant).
- A.
Preload
- B.
Afterload
- C.
Contractility
- D.
Ejection Fraction
- 7.____________ is amount of resistance that ventricle must overcome (stroke volume dependant).
- A.
Preload
- B.
Afterload
- C.
Contractility
- D.
Ejection Fraction
- 8.____________ is physical capability to pump volume (stroke volume dependant).
- A.
Preload
- B.
Afterload
- C.
Contractility
- D.
Ejection Fraction
- 9.____________ fraction of LVEDV ejected during systole (30% blood stays behind) (normal EF 60-70%); ________ = SV ÷ LVEDV (PCWP)
- A.
Preload
- B.
Afterload
- C.
Contractility
- D.
Ejection Fraction
- 10.What is the normal PCWP (This number gives us the pressure and thus the volume of blood entering the LV during systole)?
- A.
6-12 mmHg
- B.
5-10 mmHg
- C.
6-15 mmHg
- D.
5-15 mmHg
- 11.____________: Dilation of left ventricle = loss of muscle strength = inability to forcefully expel all blood from LV; “congestive” heart failure - fluid typically backs up to pulmonary system.
- A.
Systolic Heart Failure
- B.
Diastolic Heart Failure
- 12.____________: Thickening of LV tissue = smaller volume for blood to fill = less blood is pumped out; Edema is more likely to accumulate in peripheral areas.
- A.
Systolic Heart Failure
- B.
Diastolic Heart Failure
- 13.Systolic HF
- A.
Loss of muscle mass- ischemia, infarction
- B.
Volume overload- CKD, pregnancy (higher blood volume)
- C.
Pressure overload- HTN, pulmonary HTN
- D.
Dilated Cardiomyopathies- idiopathic, toxic, infx
- E.
Restrictive- HTN, hypertrophic CM, infiltrative disease (amyloid, sarcoid, SLE)
- F.
Constrictive- pericarditis (inflammation of pericard), tamponade (less space)
- 14.Diastolic HF
- A.
Loss of muscle mass- ischemia, infarction
- B.
Volume overload- CKD, pregnancy (higher blood volume)
- C.
Pressure overload- HTN, pulmonary HTN
- D.
Dilated Cardiomyopathies- idiopathic, toxic, infx
- E.
Restrictive- HTN, hypertrophic CM, infiltrative disease (amyloid, sarcoid, SLE)
- F.
Constrictive- pericarditis (inflammation of pericard), tamponade (less space)
- 15.What is the correct compensatory mechanism starting with Decrease Cardiac Output--> Increase in SNS activity-->
- A.
Increase in hr, contractility--> vasoconstriction--> inc SVR (afterload)--> inc in CO
- B.
Increase in hr, contractility--> inc in CO--> vasoconstriction--> inc SVR (afterload)
- C.
Vasoconstriction--> inc SVR (afterload)-->Increase in hr, contractility--> inc in CO
- D.
Inc SVR (afterload)--> vasoconstriction--> Increase in hr, contractility--> inc in CO
- 16.What is the correct compensatory mechanism starting with Decrease Cardiac Output--> decrease renal perfusion-->
- A.
Inc Angiotensin I,Angiotensin II, Aldosterone, Na and H2O retention --> Angiotensinogen release--> inc Renin--> inc LVEDV (Preload)--> inc Cardiac Output
- B.
Angiotensinogen release--> inc Renin--> inc LVEDV (Preload)--> inc Cardiac Output--> Inc Angiotensin I, Angiotensin II, Aldosterone, Na and H2O retention
- C.
Angiotensinogen release--> inc Renin--> Inc Angiotensin I, Angiotensin II, Aldosterone, Na and H2O retention--> inc LVEDV (Preload)--> inc Cardiac Output
- D.
Inc Renin--> inc LVEDV (Preload)--> inc Cardiac Output--> Inc Angiotensin I,Angiotensin II, Aldosterone, Na and H2O retention --> Angiotensinogen release
- 17.What is the correct compensatory mechanism starting with Decrease Cardiac Output--> Ventricular Dilation-->
- A.
Inc Angiotensin I,Angiotensin II, Aldosterone, Na and H2O retention --> Angiotensinogen release--> inc Renin--> inc LVEDV (Preload)--> inc Cardiac Output
- B.
Inc LVEDV (Preload)--> inc Cardiac Output
- C.
Angiotensinogen release--> inc Renin--> Inc Angiotensin I, Angiotensin II, Aldosterone, Na and H2O retention--> inc LVEDV (Preload)--> inc Cardiac Output
- D.
Inc Renin--> inc LVEDV (Preload)--> inc Cardiac Output--> Inc Angiotensin I,Angiotensin II, Aldosterone, Na and H2O retention --> Angiotensinogen release
- 18.Net effects in HF: Vasoconstriction SVR, stimulates NE release from adrenals, stimulates aldosterone release, constriction efferent arteriole to maintain perfusion pressure.
- A.
Angiotensin II
- B.
Norepinephrine
- C.
Aldosterone
- D.
Natriuretic Peptides
- E.
Arginine Vasopressin
- 19.Plays a central role in compensation: Increases SNS activity, tachycardia, vasoconstriction, increase contractility; Stimulates renin activity and production of angiotensin increases the risk for arrhythmias and stimulates apoptosis; Contributes to ventricular hypertrophy and remodeling.
- A.
Angiotensin II
- B.
Norepinephrine
- C.
Aldosterone
- D.
Natriuretic Peptides
- E.
Arginine Vasopressin
- 20.Plays a key role in Na and H2O retention, and CARDIAC REMODELING. Key roles: Production of interstitial cardiac fibrosis through collagen deposition (Decreased systolic function and/or increased stiffness), Increases target organ fibrosis and vascular remodeling, Induction of pro-inflammatory state, increased oxidative stress, wasting of soft-tissue and bone, secondary hyperparathyroidism, mineral/micronutrient hemostasis alterations, Increased risk of arrhythmias
- A.
Angiotensin II
- B.
Norepinephrine
- C.
Aldosterone
- D.
Natriuretic Peptides
- E.
Arginine Vasopressin
- 21.ANP and BNP (it’s good) released in HF: counteracts these problems--> Balance effects of RAAS stimulation by causing natriuresis, diuresis, vasodilation, decreased aldosterone release, decreased hypertrophy, inhibition of SNS and RAAS; Measurement of blood levels predicts mortality and severity of HF (Normal < 100 pg/mL)
- A.
Angiotensin II
- B.
Norepinephrine
- C.
Aldosterone
- D.
Natriuretic Peptides
- E.
Arginine Vasopressin
- 22.An important role in water/solute excretion. Release of AVP results in vasoconstriction and increased contractility through V1a, reabsorption of free water through V2. In HF, increased AVP results in Renal free water reabsorption - volume overload, Increased arterial vasoconstriction, Stimulation of cardiac hypertrophy
- A.
Angiotensin II
- B.
Norepinephrine
- C.
Aldosterone
- D.
Natriuretic Peptides
- E.
Arginine Vasopressin
- 23.Decrease Mortality: ACEIs
- A.
Afterload reduction, Ventricular remodeling
- B.
Afterload reduction, remodeling
- C.
Improve chronotropy, ↓ SNS
- D.
Prevention of remodeling
- E.
Preload/afterload reduction
- 24.Decrease Mortality: ARBs
- A.
Afterload reduction, Ventricular remodeling
- B.
Afterload reduction, remodeling
- C.
Improve chronotropy, ↓ SNS
- D.
Prevention of remodeling
- E.
Preload/afterload reduction
- 25.Decrease Mortality: β-blockers
- A.
Afterload reduction, Ventricular remodeling
- B.
Afterload reduction, remodeling
- C.
Improve chronotropy, ↓ SNS
- D.
Prevention of remodeling
- E.
Preload/afterload reduction
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