Ch 13: Heart Failure & Anticoagulants

Question 1

Inadequate Cardiac Output causes:

Answer 1

fatiguability
decreased exercise tolerance
dyspnea
peripheral &/ or pulmonary edema

Question 2

What is Congestion?

Answer 2

• increased fluid

why?
B/c inadequate blood flow (reduced CO) leads to reduced kidney blood flow and retention of water, leading to increased fluids in lungs & body (edema)

Question 3

Left or Right Heart failure

Answer 3

Left:
cough, dyspnea, orthopnea, nocturia (pulmonary congestion)

Right:
peripheral edema, abdominal pain, bloating, GI issues (systemic congestion)

Question 4

Why congestion?

Answer 4

At capillaries, we have both hydrostatic pressure (from heart pumping and arteries constricting) and oncotic pressures (from proteins in vascular vs interstitial fluid) at work

Usually at the arterial end, there’s more hydrostatic pressure forcing fluid OUT than oncotic forcing fluid in.
Once fluid exits, the hydrostatic pressure drops in vessel, and now oncotic pressure forcing fluid in is greater, so fluid enters back into capillary at the venous end

Question 5

In abnormal situations Edema could occur from:

Answer 5

• increased hydrostatic pressure
• decreased oncotic pressure (less plasma proteins)
• increased venous pressure

Question 6

Abnormal situations in CHF:

Answer 6

Reduced CO leads to increased SNS activity, which increases the BP/ preload

This causes the heart to work against more BP, and causes an increase in SNS activity

As the hydrostatic pressure goes up, SNS leads to increased vasoconstriction thus increasing the hydrostatic pressure in veins, and reduces the fluid back to vessels

Question 7

SV is impacted by:

Answer 7

• preload amount of blood returning to heart (affects ED volume)
• after load amount of resistance to blood flow (TPR)
• contractility- strength of each beat (impacted by SNS)

Question 8

HR impacted by:

Answer 8

SNS through B-1 receptors at nodal tissue

Question 9

Some causes of CHF

Answer 9

• hypertension (Lt ventricular hypertrophy)
• MI (better treatment following MI means more HF patients)
• Ischemic Heart Disease (inadequate coronary perfusion)
• Valvular Disease (inadequate CO from prolapse)
• Thyroid disease, alcohol, viral infection, etc

Question 10

Systolic failure

Answer 10

reduced contractility (pumping action) and reduced ejection fraction

(More common in younger population)

Question 11

Diastolic failure

Answer 11

stiffening of walls and reduced ability to relax (reduced filling and CO)

(more likely in elderly)

Question 12

Mechanisms of CHF onset

Answer 12

Reduced CO leads to compensation

a. Increased Sympathetic tome
- Increase heart workload (from afterload/vasoconstriction)
- Venoconstriction increase edema
- Increased aldo&raquo_space; Na+ and fluid retention

Question 13

Heart Compensation

Answer 13

• Frank-Starling Law of the Heart (first improves CO)
• Tachycardia (first improves CO)
• Increased afterload (reduces CO)
• Cardiac Hypertrophy/ remodeling (first improves)

Question 14

CHF strategies:

Increase myocardial contraction

Answer 14

(+ inotropes)
Digitalis glycosides
Amrinone/ mileinone
B-1 agonists

Question 15

CHF strategies:

Decrease myocardial workload

Answer 15

ACE and AngII blockers
B blockers
diuretics

Question 16

CHF treatment:

Answer 16

1) Diuretics
2) Vasodilators
3) Beta Agonists
4) Positive Inotropes
5) ACE inhibitors (and AT1 receptor blockers)

Question 17

Diuretics

Answer 17

Hydrochlorothiazide and Loops (furosemide)

• reduce plasma volume (per-load)
• relieve edema

Question 18

Vasodilators

Answer 18

a. morphine sulfate (IV, IM)
- reduces pain and anxiety
- causes vasodilation (reduce afterload)

usually initially, then switch to others

b. nitrates (nitropursside, etc)
- dilate venous and arterial vessels (including pulmonaries)
- reduce pulmonary congestion**

c. Hydralazine
d. prazosin (alpha-1 blocker)

Question 19

Beta agonists (Dopamine, Dobutamine)

Answer 19

• increase CO and contractility (not rate)
• do also cause B receptor down regulation
• used only short term or intermittently

Question 20

Positive Inotropes

Answer 20

Milrinone

• block phosphodiesterase (incr. cAMP)
• increase contractility w/ vasodilation

used only in severe cases, as can cause arrhythmia and hypertension

Question 21

ACE inhibitors (and AT1 receptor blockers)

Answer 21

• reduce pre- and after-load
• reduce fluid volume
• reduce caridad remodeling (humoral affect on remodeling is blocked)
• shown to improve various symptoms and mortality
• commonly used in CHF** (“cornerstone of treatment for HF”)

Question 22

Cardiac Glycosides

Answer 22

Digoxin (digitoxin, digitalis, etc. only outside USA)

Mechanism: inhibit Na-K-ATPase

a. increased intracellular Na+
b. increased intracellular Ca++ (Na+/Ca++ exchanger)

Question 23

Digoxin

Answer 23

used to treat heart failure, usually along with other medications. It is also used to treat certain types of irregular heartbeat (such as chronic atrial fibrillation). Treating heart failure may help maintain your ability to walk and exercise and may improve the strength of your heart.

Question 24

Glycosides effects:

Answer 24

• reduce pre-load and after-load
• reduce HR
• reduce RAS and Aldo
• reduce heart size

Question 25

Glycosides side effects:

Answer 25

a. vomiting, diarrhea, nausea, fatigue
b. blurred vision, confusion, depression
c. unconsciousness, coma, death

** watch with hypokalemia, hypomagnesemia, hypercalcemia (tend to reduce sodium pump action already…… so with glycoside, can enhance the effect)

Question 26

Beta Blockers

Answer 26

Carvedilol
seem anti-intuitive, but work…. by:

• reducing ventricular mass
• improving ventricular shape
• reducing and-systolic and diastolic volumes
• anti-arrythmic
• reversing remodeling
• decreasing mortality (all cause with systolic HF)