Heart Failure Pathophysiology

Question 1

heart failure

Answer 1

clinical syndrome

happens when the heart cannot produce enough cardiac output to meet the metabolic demands of the body

or

can only produce enough cardiac output at the expense of high cardiac filling pressures

or

both 1 and 2

Question 2

Stage A HF

Answer 2

no symptoms

+ risk factors for developing HF

Question 3

Stage B HF

Answer 3

no symptoms

+ structural disease that is strongly associated with the development of HF

Question 4

Stage C HF

Answer 4

symptomatic heart failure associated with underlying structural heart disease

Question 5

Stage D HF

Answer 5

advanced structural heart disease and marked symptoms of HF at rest despite maximal medical therapy

Question 6

equation for wall stress

Answer 6

wall stress (sigma) = (P x r)/2h

Question 7

What causes increased filling pressures?

Answer 7

impaired LV or RV relaxation

reduced LV or RV compliance (increased stiffness)

fluid overload (ex. renal failure)

Question 8

systolic HF vs systolic dysfunction

Answer 8

systolic dysfunction:

implies contractile dysfunction

clinically usually manifests as decreased EF

may or may not have signs or symptoms of HF

does not equal systolic HF

systolic HF:

systolic dysfunction along with signs/symptoms of HF

most patients will have decreased CO and increased filling pressures

Question 9

diastolic dysfunction vs. diastolic HF

Answer 9

diastolic dysfunction:

implies slowed relaxation, noncompliant ventricle, or both

clincially manifests as increased filling pressures

may or mat not hav signs of HF

diastolic HF:

diastolic dysfunction + signs/symptoms of HF

EF is normal

Question 10

ejection fraction cutoffs

Answer 10

reduced means EF < 40-45%

preserved means EF > 45-50%

Question 11

What is the main difference between SHF and DHF?

Answer 11

the anatomical structure and function of the myocardium and myocytes

Question 12

clinical features of DHF vs SHF

Answer 12

both have symptoms

both have a congestive state (edema)

both have neurohomonal activation (increased BNP, SNS, RAAS)

Question 13

LV structure and function of DHF vs SHF (LV ejection fraction, LV mass, relative wall thickness, LV EDV, LV EDP and LA size)

Answer 13

DHF

normal LV ejection fraction

increased LV mass

increased relative wall thickness

normal LV EDV

increased LV EDP and left atrial size

SHF

decreased LV EF

increased LV mass

decreased relative wall thickness

increased LV EDV

increased LV EDP and left atrial size

Question 14

exercise of DHF vs. SHF

Answer 14

DHF

decreased exercise capacity

decreased CO augmentation

increased EDP

SHF

decreased exercise capacity

decreased CO augmentation

increased EDP

Question 15

hemodynamic hypothesis of SHF

Answer 15

the sympathetic tone is maxed out so the only way to increase CO is by increasing LV filling pressures

Question 16

arginine vasopression (AVP)

Answer 16

aka antidiuretic hormone (ADH)

arterial baroreceptors and angiotensin II stimulate the posterior pituitary to secrete AVP which results in vasoconstriction (V1A), LV hypertrophy (V1A) and remodeling, and water retention (V2) depending on the receptor

V1B receptors lead to ACTH and beta-endorphin release

Question 17

natriuretic peptides

Answer 17

released into the circulation when the myocardium is under stress

beneficial homones that counterace the effects of the SNS, RAAS, and AVP

Question 18

B-type natriuretic peptide (BNP)

Answer 18

developed into a blood test to diagnose HF

increased levels increase the likelihood of a cardiac cause of dyspnea and elevated levels indicate a poor prognosis

can be elevated in cases of pulmonary embolism and acute coronary syndrome

Question 19

Why is neurohormonal activation bad?

Answer 19

except for antriuretic peptide,s activation of other neurohormones, though initially helpful, quickly cause worsening HF due to increased congestion, worsening CO

angiotensin II and aldosterone trigger fibrosis int he myocardium

Question 20

eccentric hypertrophy

Answer 20

caused by volume overload

LV dilation, globular shape, systolic dysfunction predominates

mitral regurgitation

sacromeres grow in series, making myocytes longer

Question 21

concentric hypertrophy

Answer 21

due to chronic pressure overload

normal cavity size, concentric LVH, diastolic dysfunction predominates

increased, wall thickness, decreased chamber compliance, increased filling pressures

more at risk for ischemia

parallel growth of sarcomeres

Question 22

three common types of electrical problems in HF

Answer 22

scar formation = focal re-entry = ventricular tachycardia

atrial enlargement/overload = atrial fibrosis = atrial fibrillation/atrial flutter

electric remodeling = intra- and interventricular dyssynchrony -> further determioration in cardiac output