Please enable JavaScript.
Coggle requires JavaScript to display documents.
Heart Failure (ACE Inhibitors
Angiotensin Converting Enzyme inhibitors
…
Heart Failure
ACE Inhibitors
- Angiotensin Converting Enzyme inhibitors
- Prevent action of Angiotensin II decreasing peripheral vascular resistance
- Prevent action of Aldosterone thereby reducing preload
- Decrease sympathetic NS activity
- Potentiate effects of diuretics
- SE (ACE COUGH, RENAL DYSFUNCTION, HYPERKALEMIA)
-
-
-
Nitrates
- Acute treatment of HF when both preload + afterload are elevated
- Dilates both arterial + venous smooth muscle
- Smooth muscle relaxation by increasing cGMP levels
- IV/Oral/Transdermal/Sublingual
- SE (HEADACHE HYPOTENSION)
-
-
-
Beta Blockers
- Antagonise the effect of chronic sympathetic stimulation
- May reduce down-regulation of B-receptors in response to chronically elevated sympathetic tone (occurs in HF)
- Reduce mortality in HF
- Low doses + titrate upwards
-
-
-
Beta-1 Adrenoreceptor Agonist
Digoxin
- Also useful in treatement of A-fib (slows SA)
PDE inhibitor
- Short term
- Increase CO
- Milrinone
Diuretics
- Enhance Na+ excretion in kidney as a result reduce preload
- Major concern is loss of electrolytes (e.g. Na+, K+)
- Hypokalemia
Loop Diuretics
- Stronger
- Act on thick ascending limb of loop of Henle
- Inhibit Na/K/Cl transporter
- Prevent excretion of Na+
- Increases water excretion
- Oral/IV
Furosemide
- Can also increase venous capacitance thereby decreasing preload
Thiazide Diuretics
- Weaker
- Acts on distal tubule
- Binds to Na/Cl co-transport
- Oral/IV
- Hyper-everything except electrolytes
Spironolactone
- Antagonist of aldosterone receptor
- Hyperkalemia
- Gynaecomastia
Hydralazine
- Relax smooth muscle in precapillary vessels
- Combo w/ nitrates (reduces mortality in HF)
- Ineffective alone in treatment of HF