HF/Cardiogenic Shock Flashcards
S3
-Signifies vent failure from over stretching
“Sloshing-in” S1-S2-S3
-systolic HF
S4
“A-stiff-wall” S4-S1-S2
- sound of forced blood from atria into non compliant ventricular
- diastolic HF
Common causes of HF
CAD-long term dec O2 supply
HTN - increase vent work long term, hypertrophy
Valve deformities - valve stenosis - fixed afterload increases workload of heart
Cardiomyopathies - dec contractility, remodelling
Kidney dx - over stretched overworked heart from preload and chronic raas
All cause chronic activation of SNS AND RAAS in compensating for resultant dec CO
Types of HF
1.
-chronic - oupt, stable symptoms, meds to manage o2s/d beta blockers, ACEi etc
-acute decompensated - sudden onset, o2s/d imbalance, ie. MI, myocarditis, deterioration of chronic HF
2.
-Systolic - baggy distended L ventricle, dec CO from ineffective contractility, inc preload/afterload exacerbating, dec EF, low BP. S3 audible.
-Diastolic - vent hypertrophy, stiff non complaint vent, EF preserved but dec CO from dec preload present in smaller ventricular interior. Inc afterload from SNS/RAAS will exacerbate and cause HTN, prone to flash pulm edema, as no space in LV to inc preload. S4 audible.
e.g. “Acute decompensated Diastolic HF”
Pathophysiological Causes of Chronic HF symptoms
- Ventricular Remodeling - myocytic remodeling in response to injury/scarring/compensatory neurohormones
- Apoptosis - cell death from ischemia, causes scar tissue, decreased contractility, ectopic rhythms
- abnormal hypertrophy of myocytes - from chronic activation of SNS and RAAS
Neurohormonal action in SNS and RAAS cause damage to heart from ongoing demand and ischemia together
Natriuretic peptides
Atrial and Ventricular (Brain) NP
Released when cardiac myofibrils are overstretched - effects to dec preload and after load by dec na and water retention and dec production of vasoconstricting peptides, inhibits sympathetic tone
Broad effects: Vasodilation, diuretic, antiproliferative properties
Levels of BNP
<100 no HF
100-300 little indicator
300-600 mild HF
>600 mod HF
Management of acute decompensated HF
Diuretics - dec preload, lasix
Vasodilation - dec preload and after load - nitro
Treat afib HR and contract with dig
Morphine to dec cardiac o2 demand and coronary vasodilation
What do in acute HF when diuretics aren’t doing it
Inotropes
Milrinone - inotrope effects plus vasodilation dec preload and afterload
Dobutamine B1 for inotrope, min chronotropic effects, central vasodilation with B2 effects
Symptoms of HF
Fluid overload SS Dyspnea Hemodynamic instability dec CO Dysrhythmias Embolisms
Diagnostic tests for HF
Labs BNP, CK, Trop specific to HF CBC, lyres, ur cr, ex lytes Echo - EF Coronary angiogram ECG CXR
NYHA Classification for HF
Class I mild EF<40% - Structural Heart disease, but Asymptomatic. treated with ACEi and BB to limit progress of disease with remodelling of myocardium
Class II mild EF ~35% - Symptomatic with moderate exertion - add dig, nitro, hydralazine, diuretics, spironolactone
Class III mod EF 35-25%- Symptomatic with min exertion - Above but considering ICD, CRT devices
Class IV severe EF <20- Symptomatic at rest - Goals of care?, transplant, IVAD
Why ACEi and BB in asymptomatic HF
slows remodelling of myocardium by limiting action of compensatory mechanisms which strain the heart, exacerbating HF. They decrease HR, contractility, dec afterload
Example of ARB
Angiotensin receptor blocker - Candesartan
Same effects as ACEi, just hits different part of pathway
Vasodilation - dec afterlaod, dec myocardial work and o2 demand
Example of aldosterone receptor blocker
Spironolocatone
Hits the other part of RAAS, stopping aldosterone from reabsorbing Na and H2O, thus diuretic effects. decreasing preload, leading to improved contractility, thus inc CO and o2 supply.
