Heart failure

Question 1

What is Heart failure?

Answer 1

CO is inadequate to provide oxygen requirements of the body

Question 2

What is systolic HF?

Answer 2

Ventricles cannot pump hard enough during systole

Question 3

What is diastolic HF?

Answer 3

Not enough blood fills into ventricles during diastole. Ejection fraction may be normal.

Question 4

What are the symptoms of R-sided HF (SWELLING)

Answer 4

S- swelling of legs & hands
W- weight gain
E- edema (pitting)
L- large neck veins
L- lethargy/fatigue
I- irregular heart beat
N- nocturia
G- girth (ascites)

Question 5

What are the symptoms of L-sided HF? (DROWNING)

Answer 5

D- dyspnea
R- rales (crackles)
O- orthopnea
W- weakness/fatigue
N- nocturnal paroxysmal dyspnea
I- increased HR
N- nagging cough (frothy, blood -tinged sputum)
G- gain weight

Question 6

What does Calcium ATPase do with regards to heart contraction?

Answer 6

It returns the calcium to the SR

Question 7

What happens when there is reduced Calcium ATPase activity?

Answer 7

Less calcium stored in SR which causes a weaker contraction, contributing to reduced CO in HF

Question 8

One approach is to increase cardiac contractility with inotropics. Which drug is used for this?

Answer 8

Digoxin

Question 9

What are the indications for Digoxin?

Answer 9

HF (with reduced ejection fraction) & atrial fibrillation

Question 10

What are the side effects of Digoxin?

Answer 10

Nausea, vomiting, anorexia, visual disturbances, bradycardia & arrythmias

Question 11

How long does Digoxin take to work (IV and oral)

Answer 11

Oral: 2 hours
IV: 30 minutes

Question 12

What is the dosage of Digoxin during maintenance?

Answer 12

0.125-0.25mg/day

Question 13

What are interactions with Digoxin?

Answer 13

1. Hypokalemia increases toxicity risk (caution with diuretics)
2. Interacts with verapamil, amiodarone & quinidine
3. Reduced clearance with kidney dysfunction (adjust dose)

Question 14

How does Inotropics work?

Answer 14

Bind to & inhibit the Na-K ATPase pump in cardiac myocytes which causes:
- Initial increased intracellular Na which drives an increase in the activity of sodium-calcium exchange pump to extradite Na in favour of importing calcium into the cell.
Increased intracellular calcium levels with increase the amount of Calcium taken up into the SR, leading to greater Ca release during depolarisation & thereby improved contractility of the cardiac muscle

Question 15

What inotropics due at low doses?

Answer 15

Have a parasympathetic effects: increases vagal nerve activity leading to:
- decreased SA node automaticity
-Decreased AV node conduction velocity by increasing the refractory period (dromotropy)
-Bradycardia

Question 16

What do inotropics do at high doses (toxic levels)?

Answer 16

Sympathetic outflow is increased.
This can sensitize the myocardium & result in any type of arrythmia.

Question 17

What is the MOA of dobutamine in HF?

Answer 17

Beta 1 agonist (inotropic agent). Stimulates Beta 1 receptors, increasing myocardial contractility & CO.

Question 18

How is dobutamine administered?

Answer 18

As an IV infusion in refractory cardiac failure. Short term IV treatment: down regulation of beta-adrenoreceptors is observed over longer periods
Not suitable in CAD due to tachycardia & increased myocardial O2 consumption.

Question 19

What are indications for dobutamine?

Answer 19

Acute HF, cardiogenic shock

Question 20

Key notes for dobutamine?

Answer 20

Minimal effects on HR/BP at low doses; risk of tachyarrhythmias at higher doses

Question 21

What is the MOA of dopamine?

Answer 21

Dose dependent effects: low = renal perfusion
Medium = inotropic support
High = vasopressor effect

Question 22

How is dopamine administered?

Answer 22

IV infusion

Question 23

What are the effects of dopamine at low, medium & high dosages?

Answer 23

Low dose (1-5mcg/kg/min): dopaminergic effects = renal dilation
Medium dose (5-10mcg/kg/min): Beta 1 effects = increased contractility
High dose (more than 10mcg/kg/min): alpha 1 effects (vasoconstriction)

Question 24

What are indications for dopamine?

Answer 24

Shock, HF & hypotension

Question 25

Key notes of dopamine?

Answer 25

Can cause tachycardia, arrythmias/excessive vasoconstriction at high doses

Question 26

Another way to deal with HF is to reduce cardiac workload; through which 4 methods can this be achieved?

Answer 26

ACE-inhibitors; beta blockers; diuretics & vasodilators

Question 27

During HF, there is increased secretion of renin which causes water retention & increases cardiac preload. How can this problem be solved?

Answer 27

Diuretics are used to decrease ECF volume which decreases cardiac preload Venous dilators: organic nitrates can also be used at low concentrations

Question 28

Which diuretics are used for HF?

Answer 28

1. Hydrochlorothiazide: mild side effects on diuresis 2. Furosemide: suitable in acute HF/ with massive congestion of chronic HF 3. Spironolactone: milder diuresis & no deleterious effects on potassium

Question 29

Choices of diuretics?

Answer 29

Acute/serious: loop diuretics Moderate: thiazide diuretics K loss: K sparing- careful with ACE-1, beta agonists/NSAIDS Diuretic resistance: loop diuretic + thiazide diuretic (synergistic)

Question 30

During HF, peripheral resistance is increased which leads to an increase in afterload. How can this problem by solved?

Answer 30

Hydralazine is used as a direct-acting arteriolar vasodilator. Elicits reflex tachycardia which makes it unsuited for treated of HF unless its combined with a nitrate such as isosorbide dinitrate/ a beta-blocker.

Question 31

Another way to reduce cardiac workload is to decrease cardiac remodeling & decreased sympathetic action. How can this be accomplished?

Answer 31

1. Inhibition of RAAS with ACE-inhibitors & ARBs (eliminates vasopressor effects of angiotensin 2 & dilates venous & arterial vascular beds, no reflex tachycardia) (reduces Na & H2O retention caused by aldosterone.) 2. Blockade of beta receptors: counteracts SNS activity. Eg of drugs: bisoprolol & carvedilol

Question 32

What types of drugs are used as a first-line for LV dysfunction?

Answer 32

ACE-1 which reduce preload & afterload. Slows ventricular dilation which delays HF progression

Question 33

What are the effects of ACE-inhibitors?

Answer 33

1. Increase bradykinin (only ACE-1) which causes vasodilation 2. Decreases angiotensin 2 which leads to vasodilation, decreasing LV hypertrophy 3. Decreases aldosterone secretion which restores salt & H2O balance 4. effective in all patient subsets

Question 34

ARBs (angiotensin receptor blockers) are also used to decrease cardiac remodeling & decrease sympathetic action. How does it do this?

Answer 34

Similar effects to ACE-1: vasodilation, decreased aldosterone, less salt & water retention. Alternative for ACE-1 intolerance ACE-1 are generally superior but ARBs can be used when ACE-1 aren't tolerated.

Question 35

Thirdly, beta-blockers can also be used to reduce cardiac remodeling & sympathetic action. How is this done?

Answer 35

-Decreasing beta-adrenergic effects (dysrhythmias) -Increased ventricular function (longer filling time) -Increased exercise tolerance -Decreased risk of secondary myocardial infarctions