Cardiovascular Flashcards

1
Q

What period during the action potential is important for the prevention of constant state of contraction from recycling impulses in cardiac cells?

A

Refractory

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2
Q

Name 3 basic mechanisms that come into play when cardiac function is compromised

A
Autoregulation of muscle fibre length (hypertrophy)
Neural/autonomic control (heart rate and contractility)
Endocrine control (RAAS)
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3
Q

What are the major determinants of cardiac output?

A

Heart rate, contractility, venous return (preload), total peripheral resistance

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4
Q

Outline some of the major objectives of treating cardiac complications

A
Stop/reverse arrhythmias
Increase/maintain cardiac output
Maintain correct vascular tone
Relieve fluid retention or treat hypovolemia
Supportive therapy
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5
Q

What are potential causes of hypotension?

A
Trauma / severe haemorrhage
Cardiac disease 
Cardiogenic shock
Cardiac arrhythmias 
Addison's disease
Iatrogenic (anaesthetics / other drugs)
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6
Q

Outline the general approach that may be taken to alleviate acute hypotension

A

correct hypothermia, check and correct volume deficits / electrolyte imbalances, stop / withdraw hypotension inducing drugs, consider vasopressors and positive inotropes

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7
Q

Which drugs may potentiate / aggravate hypotension

A

Most general anaesthetics and premeds (alpha1-antagonists, beta-blockers, alpha2-agonists), antiarrhythmogenic drugs, furosemide

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8
Q

Cardiac glycoside, causes positive inotropy, has narrow therapeutic index

A

Digoxin

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9
Q

Membrane stabiliser, drug of choice for ventricular arrhythmias given IV

A

Lignocaine

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10
Q

Beta-blocker, useful against hypertrophic cardiomyopathy, and ventricular arrhythmia

A

Propranolol

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11
Q

Sympathomimetic, causes positive inotropy, only used for a short period

A

Dobutamine

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12
Q

A loop diuretic of choice against congestive heart failure

A

Furosemide

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13
Q

Non-catecholamine, positive inotropy and vasodilator (inodilator). May be useful against dilated cardiomyopathy.

A

Pimobendan

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14
Q

What is an inodilator?

A

Has both positive inotropic and vasodilatory effects

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15
Q

Causes vasodilation by inhibiting ACE

A

Enalapril

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16
Q

Used against vagal-mediated bradycardia, asystolic cardiac arrest

A

Atropine

17
Q

What is AV block?

A

Marked slowing or blocking of impulses going through the AV node to cause ventricular depolarisation

18
Q

What is the difference between first and second degree AV block?

A

First degree - the impulse is only slowed (characterised by prolonged PR intervals on the ECG)
Second degree - total blockade of the impulse transmission (characterised by the presence of P waves with no corresponding QRS complexes)

19
Q

What is the treatment of choice for AV block?

A

A cholinergic antagonist - Atropine

20
Q

How can propranolol cause AV block?

A

Blockade of sympathetic drive to the heart allows the parasympathetic system to dominate - slows impulses through the AV node

21
Q

What side affects are associated with arrhthmogenic drugs?

A

Hypotension, AV block, depressed cardiac contractility, CNS toxicity, hypersensitivity

22
Q

Describe the mechanism of action of cardiac glycosides

A

Blocks the Na-K-ATPase pump, increases intracellular Na, slowing the Na/Ca exchanger and increasing intracellular Ca2+

23
Q

What are the pharmalogical effects of cardiac glycosides?

A

Positive inotropy, decreased heart rate secondary to hemodynamic changes, slowed sinus and AV consuction, diuresis

24
Q

What are the effects of Quinidine on glycoside therapy?

A

Quinidine displaces cardiac glycosides from binding sites in muscle which may the elevate glycoside plasma levels and cause toxicity

25
Q

What are the signs of glycoside toxicity?

A

Anorexia, vomiting and lethargy
Hypothermia, AV conduction block and bradycardia
Ventricular tachyarrhythmias, renal toxicity

26
Q

How can you treat glycoside toxicity?

A

Withdraw the glycoside, symptomatic treatment, cholestyramine resin and activated charcoal

27
Q

Why can combining NSAIDs with furosemide lead to serious pharmacodynamic interactions?

A

NSAIDs inhibit the natriuretic effect of furosemide due to inhibition of renal blood flow. Some animals may develop furosemide/loop diuretic resistance.

28
Q

Depolarisation of cardiac cells is characterised by a rapid influx of ____ ions, a slow influx of ____ ions and an outflow of ____ ions. Fill in the blanks.

A

Rapid Na+ influx, Slow Ca2+ influx, Efflux of K+