Week 6 - Cardio Part 1 Flashcards
Cardiac output calculation
Heart Rate (HR) x Stroke volume (SV)
Normal Cardiac output
4-8 L/min
Normal Stroke Volume
~ 70 mL per heart beat
Define preload and afterload
Preload is the amount of blood in the ventricle at the end of diastole (filling pressure in the ventricle at end-diastole).
Afterload is the pressure at which the ventricle must generate to pump blood through the aortic valve into the aorta.
Also known as SVR (Systemic Vascular Resistance).
HTN causes increased afterload or SVR
Hypotension is indicative of decreased afterload
Frank Starling Law states that
As left ventricular filling pressures increase (also known as the pulmonary capillary wedge pressure – PCWP), SV and CO increase.
Etiologies of most cases of HF due to what 4 causes
Ischemic (CAD)
Rheumatic valvular disease
Hypertensive heart disease
COPD
ANP and BNP come from where? and do what?
Atrial natriuretic peptides - from atria in response to stretch
-Leads to vasodilation
Brain (B-type) natriuretic peptides - from ventricles in response to pressure or volume overload
- protective effect by antagonizing RAAS and decreasing preload (but not enough to compensate for the effects of HF)
Three categories of HF and their Left Ventricular Ejection fractions
HFpEF (Heart Failure with preserved Ejection Fraction): LVEF ≥50%
HFmEF (HF with mid-range Ejection Fraction): LVEF 41-49%
HFrEF (HF with reduced Ejection Fraction)
LVEF ≤40%
What are Kerley B lines ?
fine horizontal opacified lines that represent fluid in interstitial space
Normal BNP levels and BNP levels indicating HF
BNP < 100pq/ml → HF unlikely
BNP > 400pq/ml → HF highly likely
MOA of furosemide
Inhibits Na/K/Cl co-transporter at thick portion of ascending loop of Henle (where ⅓ Na is reabsorbed) → inhibits Na & water reabsorption
A/E of furosemide
Electrolyte abnormalities (hypokalemia, hyponatremia, hypomagnesaemia)
Hypotension
Renal dysfxn
Ototoxicity (at high doses or rapid IV administration)
Hyperuricemia/ May precipitate gout
Quadruple Therapy Treatment for HFrEF (LVEF ≤40%) includes:
Beta blocker
ARNI or ACEi/ARB
MRA
& SGLT2 inhibitor
MOA of ARNI
(ie. valsartan/sacubitril )
ARB: - Angiotensin receptor antagonist
- Blocking Angiotensin II binding/effects → v.d., decreases aldosterone release → decreases Na & H2O absorption → decrease BP
neprilysin Inhibitor → increases natriuretic peptides → induces vasodilation & natriuresis (Na excretion in urine)
MOA of ACE inhibitors
Inhibit production of angiotensin II → vasodilation.
- Decrease aldosterone release → increases excretion of Na & H2O while retaining K+
- Suppress degradation of bradykinin (vasodilator) → increase bradykinin → increase v.d. → decrease BP
- Decrease afterload & preload
- Increase SV
- Decrease activation of SNS