Heart Failure

Question 1

Clopedigrel blocks ________ and tirofiban blocks _________.

Answer 1

Clopedigrel: P2Y12
Tirofiban: GP IIb/IIIa

Tirofiban stops fibrin from TYing platelets together.

Question 2

What three measures by the heart in response to decreased arterial pressure (i.e. in heart failure) are like drinking salt water when you’re thirsty?

Answer 2

1. increased sympathetic drive (baroreceptor reflex)
2. cardiac dilation
3. anti-diuresis (RAAS)

Question 3

How does the Frank-Starling Law apply to heart failure drugs?

Answer 3

It’s aimed at getting the ranges capable stroke volume to a better level with respect to ranges of venous blood pressure.

Question 4

What bottle of diuretics gets opened when the HF is severe?

Answer 4

Spirolactone, K-sparing

Question 5

What are the first line two groups for HF for addressing fluid retention?

Answer 5

Loops, thiazides.

Question 6

You’ve given diuretics for the fluid retention and how they’re arrhythmic. What’s happened?

Answer 6

Diuretics have lead to an electrolyte imbalance.

Question 7

3 symptoms of thiazides that aren’t hypokalaemia, hyponatraemia or metabolic alkalosis.

Answer 7

gout, impotence, glucose intolerance

Question 8

Think about it - why thiazides instead of loops for HF?

Answer 8

Loops are really more for serious fluid retention or oedema, they’re much stronger.

Question 9

Thiazides and loops. Which one causes impotence and which one hypovolaemia?
(Otherwise the same side effects).

Answer 9

Loops (stronger): hypovolaemia

Thiazides: impotence.

Question 10

What 2 side effects of ACEIs aren’t dry cough, hyperkalaemia or first-dose hypertension?

Answer 10

Rashes

RARE angiooedema

Question 11

T or F: ACEIs are a cornerstone of HF therapy?

Answer 11

TRUE.

Question 12

What are the only two side effects listed for ARBs? (wha..)

Answer 12

hyperkalaemia

RARE angioedema

Question 13

Why are ACEIs loved more than ARBs?

Answer 13

Bradykinins are thought to reduce cardiac remodelling.

Question 14

What’s the significance of bradykinin in HF?

Answer 14

More kinins helps reduce cardiac remodelling. Hence ACEI>ARBs.

Question 15

Why is B2 blockage BAD in HF and normal B2 stimulation GOOD?

Answer 15

B2 - lungs and arteriolar SMCs (among other places).

B2 - stimulation

Question 16

What Bblockers are appropriate for HF because they show (dose dependent) B1 selectivity?
I met a guy who ate too many biscuits which prolly attentuated his health.

Answer 16

Bisoprolol, atenolol and metaprolol

Question 17

Which Bblockers are preferred in HF?

prolly not atenolol

Answer 17

bisoprolol and metaprolol.

Question 18

What are the only real indications for B-blockers in HF

Answer 18

HF with A-fib to improve ventricular filling.

Diastolic HF to improve ventricular filling.

Question 19

What CV does the slow titration of dose MAJORLY apply to?

Answer 19

Beta-blockers.

Question 20

If you hear carvedilol, just know:

Answer 20

new Bblocker with good vasodilation and a1 block (to balance out the negative ionotropy…)

Question 21

In systolic HF, the what is a short term risk other than bradyarrhythmia, hypotension or worse HF?

Answer 21

Worsened renal failure.

Question 22

What’s an example of a sympathomimetic?

Like someone who pretends to be sympathetic but then just dobs you in?

Answer 22

Dobutamine

Question 23

What’s dobutamine?

Answer 23

B1 agonsit (sympathomimetic)

Question 24

What’s the rational for spironolactone added to ACEI therapy?

Answer 24

undermines “aldesterone escape”, where aldesterone will return to pre-treatment levels.

Question 25

What does digoxin ideally do?

Answer 25

Increases cardiac output but slows it down. Thus reduces the baroreceptor reflex and sympathetic drive AND improves renal blood flow, settling RAAS.

Question 26

Why doesn’t digoxin prolong life?

Answer 26

No effect on cardiac remodelling.

Question 27

Why does inhibiting the Na/K ATPase increase contractility? (digoxin)

Answer 27

More Na+ in the cell for the preferable Na/Ca2+ pump, so more calcium gets pumps into the cells. Better calcium accumulation.

Question 28

Digoxin: renal or hepatic excretion?

Answer 28

RENAL. Renal function important.

Question 29

Digoxin in a PK nightmare.
Absorption?
Half life?
Distribution time?

Answer 29

Variable absorption
Half life 1-1.5 days
6 hour distribution time

Bonus: maintenance dose requires testing and renal function analysis.

Question 30

What are 3 cons of digoxin?

Answer 30

Highly sensitive to electrolyte imbalances
Very narrow therapeutic index
High risk of arrhythmia
No food syndrome - nausea, anorexia, vomiting, diahhorea

Question 31

What’s the major digoxin risk?

Answer 31

Arrhythmia

Question 32

In case you see milrinone, that’s:

Answer 32

Milrinone: HF drug: positive ionotrope (calcium)

Question 33

You’ve got a patient on ACEI + BB + Diuretic. You’re starting low and going slow. You hit a bump in the road wrt dosin - which stays the same while the others’ doses are reduced?

Answer 33

The beta blocker. The beta blockers stays the same.

Fine tuning can take months of monitoring.

Question 34

Do I add digoxin yet doctor? I know it’s not severe yet but…

Answer 34

Only in A-fib or when ACEI+diuretics isn’t working.

Question 35

OMG there’s a-fib with rapid ventricular fibulation?

Which drug bursts into the room and asks really confidently “Did someone say…….

Answer 35

….. DIGOXIN?”

Question 36

Acute cardiogenic pulmonary oedema. What comes between frusemide and positive ionotropes?

If I got pulmonary oedema I’d feel MOC’D by nature.

Answer 36

morphine then organic nitrates then constant positive oxygen then dopamine.

Question 37

Acute cardiogenic pulmonary oedema. What comes between frusemide and positive ionotropes?

Answer 37

morphine, organic nitrates, CPAP then dopamine.