Heart Failure Kruse

Question 1

MOA of inotropes

Answer 1

1. b1 receptors (Gs)–> cAMP –> PKA –> activates Ca Channel–> Ca influx into myocyte –> Calcium activates SPR –> SPR releases its own Ca –> Ca binds troponin –> troponin moves tropomyosin moves off actin –> actin can bind myosin. Contraction occurs.

Question 2

MOA of Digoxin

Answer 2

blocks Na/K ATPase –> increases sodium in cell –> inhibits Calcium efflux (via Ca/Na exchanger) –> Ca builds up in myocyte

Question 3

4 Kaplan notes about Digoxin (drugs that enhance it, remove it, etc)

Answer 3

Question 4

Toxicities of Digoxin from Kaplan

Answer 4

Question 5

Digoxin uses Kaplan

Answer 5

Question 6

Digoxin ECG findings kaplan

Answer 6

1. ST depressions “scooping”
2. PR interval increase
3. QT interval decrease
4. T wave inversion
5. strange arrhythmias

Digoxcin is usually caused by

1. renal failure: digoxin is excreted by the kidneys
2. hypokalemia: worsens digoxin because its trying to bidn Na/K Exchanger, so the K and Dig fight to bind the receptor
3. Quinidine: decreases ability of kidneys to clear digoxin.

Question 7

Digoxin Toxicity Tx Kaplan

Answer 7

anti digitalist Fab fragments

Question 8

Congestive HF Kaplan

What are the MOAs of drugs known to have survival benefit in patients with congestive heart failure

Answer 8

1.

Question 9

Shortness of breath with minimal exertion, swelling of lower extremities, HTN, venous distention, pertibial edema

Answer 9

congestive heart failure with RHF.

Question 10

Diagnosis of CHF

Answer 10

1. CXR:
   
   1. enlarged cardiac silhouette
   2. pulmonary edema
   3. plural effusions
2. echocardiogram
   
   1. VHyper/Dil, wall motion abnormalities, reduced EF
3. Plasma B type natriuetic peptide is elevated in CHF

Question 11

Tx and Commonly used drugs in CHF

Answer 11

Tx: inhibit RAAS

Dxs: BB (carvediolol, metoproplol)

ACEI: captopril

ARBs: losartan

ARAs: spironolactone

Loop Diuretics: furosemide

Inotropes: digoxin

Question 12

CHF Drug Tx: BB

Answer 12

improved cardiac output

block sympathetic action of beta 1Rs on juxtaglomerular cells

decreases renin release

Question 13

CHF: Drug tx

ACEIs

Answer 13

decreased cardiac remodeling

decreases Angiotensin II creation

Question 14

CHF drugs: arbs

Answer 14

decrease cardiac modeling

decreases angiotensin II interaction with AT1 receptor on zona glomerulosa (decreases aldosterone secretion) and AT1Rs on blood vessels (decreases vasoconstriction of renal arterioles that would increase BP and activate baroreceptors in the juxtaglomerular cells)

Question 15

Aldosterone blockers

Answer 15

blocks myocardial fibrosis

Question 16

spironolactone

Answer 16

increases urinary output of Na and H2O but without causing hypokalemia: side effect is decreasing blood vol which decreases the preload which causes CO increase which causes arteriole BP increase, which activates baroreceptors

Question 17

what are the MOAs of drugs known to decrease mortality in patietns with CHF?

Answer 17

ACEI/ARBs, BBs, Spironolactone,

Question 18

signs, symptoms of CHF and relevant lab results

Answer 18

Question 19

Systolic failure

Answer 19

reduced cardiac output /contractility

reduced EF (<45%)