Ch 13: Heart Failure & Anticoagulants Flashcards
Inadequate Cardiac Output causes:
fatiguability
decreased exercise tolerance
dyspnea
peripheral &/ or pulmonary edema
What is Congestion?
- 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)
Left or Right Heart failure
Left:
cough, dyspnea, orthopnea, nocturia (pulmonary congestion)
Right:
peripheral edema, abdominal pain, bloating, GI issues (systemic congestion)
Why congestion?
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
In abnormal situations Edema could occur from:
- increased hydrostatic pressure
- decreased oncotic pressure (less plasma proteins)
- increased venous pressure
Abnormal situations in CHF:
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
SV is impacted by:
- 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)
HR impacted by:
SNS through B-1 receptors at nodal tissue
Some causes of CHF
- 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
Systolic failure
reduced contractility (pumping action) and reduced ejection fraction
(More common in younger population)
Diastolic failure
stiffening of walls and reduced ability to relax (reduced filling and CO)
(more likely in elderly)
Mechanisms of CHF onset
Reduced CO leads to compensation
a. Increased Sympathetic tome
- Increase heart workload (from afterload/vasoconstriction)
- Venoconstriction increase edema
- Increased aldo»_space; Na+ and fluid retention
Heart Compensation
- Frank-Starling Law of the Heart (first improves CO)
- Tachycardia (first improves CO)
- Increased afterload (reduces CO)
- Cardiac Hypertrophy/ remodeling (first improves)
CHF strategies:
Increase myocardial contraction
(+ inotropes)
Digitalis glycosides
Amrinone/ mileinone
B-1 agonists
CHF strategies:
Decrease myocardial workload
ACE and AngII blockers
B blockers
diuretics
CHF treatment:
1) Diuretics
2) Vasodilators
3) Beta Agonists
4) Positive Inotropes
5) ACE inhibitors (and AT1 receptor blockers)
Diuretics
Hydrochlorothiazide and Loops (furosemide)
- reduce plasma volume (per-load)
- relieve edema
Vasodilators
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)
Beta agonists (Dopamine, Dobutamine)
- increase CO and contractility (not rate)
- do also cause B receptor down regulation
- used only short term or intermittently
Positive Inotropes
Milrinone
- block phosphodiesterase (incr. cAMP)
- increase contractility w/ vasodilation
used only in severe cases, as can cause arrhythmia and hypertension
ACE inhibitors (and AT1 receptor blockers)
- 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”)
Cardiac Glycosides
Digoxin (digitoxin, digitalis, etc. only outside USA)
Mechanism: inhibit Na-K-ATPase
a. increased intracellular Na+
b. increased intracellular Ca++ (Na+/Ca++ exchanger)
Digoxin
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.
Glycosides effects:
- reduce pre-load and after-load
- reduce HR
- reduce RAS and Aldo
- reduce heart size
Glycosides side effects:
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)
Beta Blockers
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)
