Heart failure Flashcards
What is Heart failure?
CO is inadequate to provide oxygen requirements of the body
What is systolic HF?
Ventricles cannot pump hard enough during systole
What is diastolic HF?
Not enough blood fills into ventricles during diastole. Ejection fraction may be normal.
What are the symptoms of R-sided HF (SWELLING)
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)
What are the symptoms of L-sided HF? (DROWNING)
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
What does Calcium ATPase do with regards to heart contraction?
It returns the calcium to the SR
What happens when there is reduced Calcium ATPase activity?
Less calcium stored in SR which causes a weaker contraction, contributing to reduced CO in HF
One approach is to increase cardiac contractility with inotropics. Which drug is used for this?
Digoxin
What are the indications for Digoxin?
HF (with reduced ejection fraction) & atrial fibrillation
What are the side effects of Digoxin?
Nausea, vomiting, anorexia, visual disturbances, bradycardia & arrythmias
How long does Digoxin take to work (IV and oral)
Oral: 2 hours
IV: 30 minutes
What is the dosage of Digoxin during maintenance?
0.125-0.25mg/day
What are interactions with Digoxin?
- Hypokalemia increases toxicity risk (caution with diuretics)
- Interacts with verapamil, amiodarone & quinidine
- Reduced clearance with kidney dysfunction (adjust dose)
How does Inotropics work?
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
What inotropics due at low doses?
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
What do inotropics do at high doses (toxic levels)?
Sympathetic outflow is increased.
This can sensitize the myocardium & result in any type of arrythmia.
What is the MOA of dobutamine in HF?
Beta 1 agonist (inotropic agent). Stimulates Beta 1 receptors, increasing myocardial contractility & CO.
How is dobutamine administered?
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.
What are indications for dobutamine?
Acute HF, cardiogenic shock
Key notes for dobutamine?
Minimal effects on HR/BP at low doses; risk of tachyarrhythmias at higher doses
What is the MOA of dopamine?
Dose dependent effects: low = renal perfusion
Medium = inotropic support
High = vasopressor effect
How is dopamine administered?
IV infusion
What are the effects of dopamine at low, medium & high dosages?
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)
What are indications for dopamine?
Shock, HF & hypotension
Key notes of dopamine?
Can cause tachycardia, arrythmias/excessive vasoconstriction at high doses
Another way to deal with HF is to reduce cardiac workload; through which 4 methods can this be achieved?
ACE-inhibitors; beta blockers; diuretics & vasodilators
During HF, there is increased secretion of renin which causes water retention & increases cardiac preload. How can this problem be solved?
Diuretics are used to decrease ECF volume which decreases cardiac preload
Venous dilators: organic nitrates can also be used at low concentrations
Which diuretics are used for HF?
- Hydrochlorothiazide: mild side effects on diuresis
- Furosemide: suitable in acute HF/ with massive congestion of chronic HF
- Spironolactone: milder diuresis & no deleterious effects on potassium
Choices of diuretics?
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)
During HF, peripheral resistance is increased which leads to an increase in afterload. How can this problem by solved?
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.
Another way to reduce cardiac workload is to decrease cardiac remodeling & decreased sympathetic action. How can this be accomplished?
- 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.)
- Blockade of beta receptors: counteracts SNS activity. Eg of drugs: bisoprolol & carvedilol
What types of drugs are used as a first-line for LV dysfunction?
ACE-1 which reduce preload & afterload. Slows ventricular dilation which delays HF progression
What are the effects of ACE-inhibitors?
- Increase bradykinin (only ACE-1) which causes vasodilation
- Decreases angiotensin 2 which leads to vasodilation, decreasing LV hypertrophy
- Decreases aldosterone secretion which restores salt & H2O balance
- effective in all patient subsets
ARBs (angiotensin receptor blockers) are also used to decrease cardiac remodeling & decrease sympathetic action. How does it do this?
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.
Thirdly, beta-blockers can also be used to reduce cardiac remodeling & sympathetic action. How is this done?
-Decreasing beta-adrenergic effects (dysrhythmias)
-Increased ventricular function (longer filling time)
-Increased exercise tolerance
-Decreased risk of secondary myocardial infarctions
