DIT review - Cardiology 2

Question 1

What is the source and function of ANP and BNP?

Answer 1

• 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

Question 2

Findings in L heart failure

Answer 2

• 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

Question 3

Findings in R heart failure

Answer 3

• Peripheral edema
• Jugular venous distension
• Hepatomegaly – “nutmeg liver”

Question 4

MOA of digoxin

Answer 4

• 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

Question 5

Uses of Digoxin

Answer 5

• Symptomatic treatment of chronic systolic heart failure
  
  • Used only for symptoms; does NOT reduce mortality
• Anti-arrhythmias

Question 6

Adverse effects of Digoxin

Answer 6

• 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)

Question 7

Factors that exacerbate Digitalis toxicity

Answer 7

• 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

Question 8

Treatment of digoxin toxicity

Answer 8

• Digoxin-specific antibody fragment (Digoxin immune Fab)

Question 9

MOA of Milrinone

Answer 9

• 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

Question 10

Uses of Milrinone

Answer 10

• Acute heart failure

Question 11

Adverse effects of Milrinon

Answer 11

Hypotension

Question 12

MOA of Nesiritide

Answer 12

• 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

Question 13

Uses of Nesiritide

Answer 13

Acute heart failure

Question 14

Effects of angiotensin II

Answer 14

• 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

Question 15

Effects of ACEi

Answer 15

• Reverse all the effects of ATII:
  
  • Dilate efferent arteriole
  • Decrease GFR
  • Decrease sodium-bicarb reabsorption at the PCT
  • Decrease aldosterone release

Question 16

Incidental effects of ACEI

Answer 16

• Due to decreased GFR, can cause an expected rise in creatinine levels
  
  • = credit card of guy with floppy suspenders
• Can cause hypotension and syncope in patients with high renin levels (e.g. heart failure)
  
  • Abrupt removal of vasoconstrictive effects leads to a rapid loss of BP
• Increase levels of ATI and renin due to negative feedback
• Natriuresis and Hyperkalemia due to decreased aldosterone levels

Question 17

Uses of ACEI

Answer 17

• First line agents in the treatment of heart failure
  
  • Reducing peripheral resistance causes reduce in afterload
  • Reduce of salt and water retention causes reduce in preload
  • Less ATII reduces sympathetic activity on the heart
• Reduce mortality in heart failure and MI
  
  • Due to decreased ATII mediated cardiac remodeling
• Acute myocardial infarction
• Primary HTN
• Slows the progression of diabetic nephropathy
  
  • Patients with albuminuria and BP greater than 130/80 are started on ACEI

Question 18

Adverse effects of ACEI

Answer 18

• Dry cough
  
  • This is because ACEI can increase bradykinins, causing lung irritation

Question 19

Contraindications of ACEI

Answer 19

• Hereditary angioedema (due to C1 esterase deficiency)
  
  • = “C” shaped ring on fat lip of woman getting escorted out
  • Increased complement will lead to excessive vasodilation
• Pregnancy
  
  • = pregnant woman with tarantula on back
• Co-administration of ACEI and NSAIDs can precipitate kidney injury
  
  • NSAIDs decrease prostaglandins, which are normally responsible for afferent dilation to preserve blood flow and GFR
    
    • So NSAIDs constrict afferent and thus decrease GFR
  • ACEI also decrease GFR by counteracting efferent constriction
• Bilateral renal artery stenosis
  
  • These patients are reliant on ATII efferent vasoconstriction to preserve GFR
  • Indicated as significant increase in serum creatinine (more than expected)

Question 20

What drugs are angiotensin receptor blockers (ARBs)

Answer 20

• Mechanism of action:
  
  • Directly block ATI receptors
• Drugs:
  
  • “-sartan” suffix
    
    • = “SoRry TAkeN” sign

Question 21

Uses of ARBs

Answer 21

• Uses:
  
  • Heart failure
  • HTN
  • Diabetic nephropathy
• Especially useful for patients that are intolerant to ACEI (e.g. persistant cough)
  
  • ARBs do not cause increase in Bradykinin

Question 22

Adverse effects of ARBs

Answer 22

• Hyperkalemia due to decreased aldosterone

Question 23

MOA of Aliskiren

Answer 23

• Sketchy = “High risk” slots
• Mechanism of action
  
  • Direct Renin inhibitor
  • Prevents conversion of angiotensinogen to ATI

Question 24

Uses of Aliskiren

Answer 24

HTN

Question 25

Adverse effects of Aliskiren

Answer 25

* Hypotension * Decreased renal function * Hyperkalemia

Question 26

What drugs improve mortality in chronic CHF patients vs. drugs that treat symptoms?

Answer 26

* Improved survival: * ACEI * ARBs * Aldosterone antagonists * B-blockers * Symptomatic relief: * Diuretics * Digoxin * Vasodilators

Question 27

Cause, CO, SVR, and Rx of hypovolemic shock

Answer 27

* Hypovolemic: * Decreased volume – hemorrhage, dehydration, burns * Skin will be cold and clammy (low output shock) * CO = Decreased * SVR = Increased (due to body trying to compensate) * Rx = IV fluids

Question 28

Cause, CO, SVR, and Rx of Cardiogenic shock

Answer 28

* Inability of heart to distribute blood – acute MI, HF, pulmonary embolism, valvular dysfunction, arrhythmia, cardiac tamponade, tension pneumothorax * Skin will be cold and clammy (low output shock) * CO = Decreased * SVR = Increased (due to compensation) * Rx = Inotropes (e.g. Dobutamine)

Question 29

Cause, CO, SVR, and Rx of Septic/Anaphylactic shock

Answer 29

* Sepsis/anaphylaxis * Sepsis and anaphylaxis cause vasodilation and leaky capillaries * Skin will be warm and flushed to do vasodilation * SVR = Decreased (this is part of the cause of septic shock) * CO = Increased (compensatory tachycardia) * Rx = Antibiotics, IV fluids, vasopressors (norepinephrine)

Question 30

Cause, CO, SVR, and Rx of Neurogenic shock

Answer 30

* Brain is not communicating properly with the heart – e.g. brain injury, spinal cord injury * CO = Decreased * SVR = Decreased * Rx = IV fluids

Question 31

On a pressure-volume loop of the LV, describe where on the graph the mitral valve and aortic valve close and open

Answer 31

Question 32

Describe what happens to the pressure-volume loop with increased preload

Answer 32

* 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

Question 33

Describe what happens to the pressure-volume curve with increased afterload

Answer 33

* 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

Question 34

Describe what happens to the pressure-volume loop with increased contractility

Answer 34

* 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