DIT review - Cardiology 2 Flashcards
1
Q
What is the source and function of ANP and BNP?
A
- Atrial natriuretic peptide (ANP)
- Released from atrial myocytes in response to increased blood volume
- Acts via cGMP
- Causes vasodilation and decreased Na+ reabsorption at the renal collecting tubule
- Dilates afferent arteriole and constricts efferent arterial, promoting diuresis
- B-type (brain) natriuretic peptide (BNP)
- Released from ventricular myocytes in response to ventricular stretch
- Similar action to ANP, with longer half-life
- Causes vasodilation and decreased Na+ reabsorption at the renal collecting tubule
- Dilates afferent arteriole and constricts efferent arterial, promoting diuresis
- BNP blood test used to diagnose heart failure
2
Q
Findings in L heart failure
A
- Dyspnea on exertion
- Cardiac dilation
- Pulmonary edema
- Paroxysmal nocturnal dyspnea – breathless awakening from sleep
- Orthopnea – SOB when lying flat which is alleviated by sitting up
3
Q
Findings in R heart failure
A
- Peripheral edema
- Jugular venous distension
- Hepatomegaly – “nutmeg liver”
4
Q
MOA of digoxin
A
- Inhibits Na+/K+ ATPase at the cell membrane (usually responsible for pumping K+ into the myocyte)
- Inhibition of this pump prevents K+ from being pumped into the cell and Na+ from being pumped out
- Increase in intracellular sodium concentration
- Increase in intracellular sodium promotes activation of Na+/Ca2+ exchanger
- This promotes calcium influx
- Increased cytoplasmic Ca2+ will lead to a rise in sarcoplasmic reticulum Ca2+ stores, resulting in improved myocyte contractility and LV function
Also exerts parasympathetic effects on SA and AV node via vagal stimulation
5
Q
Uses of Digoxin
A
- Symptomatic treatment of chronic systolic heart failure
- Used only for symptoms; does NOT reduce mortality
- Anti-arrhythmias
6
Q
Adverse effects of Digoxin
A
- Hyperkalemia (recall that dysfunctional Na+/K+ ATPase blocks K+ from entering the cell, so it builds up in the serum instead)
- = pile of bananas
- Premature ventricular contractions and other arrhythmias
- = various dances on the heart-shaped dancefloor
- Digitalis effect = T-wave changes, QT interval shortening, ST depression
- = taSTy scoop of ice cream = “scooped”/concave ST depression of EKG
- Associated with long-term use, NOT toxicity
- Bradycardia due to parasympathetic activity at SA node
- = SA music “note” (node) on top L of dancefloor
- = dangling heart watch = bradycardia
- Heart block due to excess parasympathetic activity of AV node in digoxin toxicity
- = AV music note
- = heart shield pendant on girl = heart block
- Contraindicated in heart block (or other drugs that depress SA or AV nodes e.g. beta-blockers)
- GI symptoms (nausea, vomiting, abd pain)
- Neuro sx (confusion and weakness)
- Alteration in color vision
- Xanthopsia (objects appear yellow)
7
Q
Factors that exacerbate Digitalis toxicity
A
- Hypokalemia (hypokalemia increases Digoxin binding to Na+/K+ ATPase)
- Can be caused by loop diuretics or diarrhea
- Renal insufficiency
- Increased the serum half life of digoxin, increasing susceptibility to toxicity
- Many antiarrhythmics inhibit renal clearance of digoxin, increasing susceptibility to toxicity
8
Q
Treatment of digoxin toxicity
A
- Digoxin-specific antibody fragment (Digoxin immune Fab)
9
Q
MOA of Milrinone
A
- Sketchy = “One in a million” sign
- Phosphodiesterase inhibitor, leading to decreased breakdown of cAMP, leading to a positive inotropic effect
- = “Don’t phoster disinterest” sign
- = CAMPaign
- = big muscles of donkey = positive inotropic effect
- Also causes arteriolar dilation and decreased afterload
10
Q
Uses of Milrinone
A
- Acute heart failure
11
Q
Adverse effects of Milrinon
A
Hypotension
12
Q
MOA of Nesiritide
A
- Sketchy = “Turn the tide” elephant
- Synthetic form of BNP, which increased cGMP in smooth muscles, leading to venous and arteriolar dilation (reducing afterload and preload)
- = BuMP
- = dilated red ears and blue legs
- Also causes natriuresis
13
Q
Uses of Nesiritide
A
Acute heart failure
14
Q
Effects of angiotensin II
A
- Vasoconstriction
- Increases GFR of the kidney
- This is caused because ATII constricts the efferent arteriole
- Acts directly on the proximal convoluted tubule to increase sodium bicarb resorption
- Also works at the collecting duct:
- Increases aldosterone (mineralocorticoid) release from the adrenal cortex
- Aldosterone will act on the collecting duct to increase Na+ retention at the expense of potassium
15
Q
Effects of ACEi
A
- Reverse all the effects of ATII:
- Dilate efferent arteriole
- Decrease GFR
- Decrease sodium-bicarb reabsorption at the PCT
- Decrease aldosterone release
31
Q
On a pressure-volume loop of the LV, describe where on the graph the mitral valve and aortic valve close and open
A
32
Q
Describe what happens to the pressure-volume loop with increased preload
A
- Increased Preload:
- THINK of drawing a “P” = curve moves out to the right
- Will cause and increased stroke volume with no change in end-systolic volume
33
Q
Describe what happens to the pressure-volume curve with increased afterload
A
- THINK of drawing an “A” = curve becomes taller and skinnier
- Increased aortic pressure means the LV must increase pressure more in order for aortic valve to open
- By the time the LV has used so much contraction to open the aortic valve, there is less contraction left to eject blood, plus higher aortic pressure causes the valve to close more rapidly
- This means there will be a decreased stroke volume and an increased end-systolic volume
34
Q
Describe what happens to the pressure-volume loop with increased contractility
A
- Increased Contractility:
- THINK of drawing a “C” = curve becomes bigger on the left
- Increasing contractility means you push more blood out of the LV, so stroke volume increases, end-systolic volume decreases, and ejection fraction increases
