cardiac failure Flashcards

1
Q

Explain the Renin angiotensin cascade

A

a decrease in blood pressure or in renal perfusion is detected by the cells in the kidney and they trigger the release of renin
Renin converts angiotensinogen released by the liver into angiotensin 1, which is converted by ACE to angiotensin 2
angiotensin 2 acts on the adrenal glands and stimulates the release of aldosterone which stimulates salt and water retention
it also causes the constriction of the efferent arterioles of the glomerulus and causing an increase in GFR and blood pressure
lastly it acts on the Pituitary gland and stimulates the release of ADH which stimulates water retention

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2
Q

side effects of ACE inhibitors

A

chronic dry cough
hypotension
hyperkalemia

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3
Q

why should the combination of spironolactone and ACE be used cautiously

A

Main mechanisms contributing to hyperkalemia with ACEi/ARB include decreased aldosterone concentrations, decreased delivery of sodium to the distal nephron
Spironolactone is a K+ sparing diueretic this will lead to hyperkalemia if they were to be combined without caution

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4
Q

clinical features of ACE induced ACE-I induced angioedema

A

tongue, lips and face swelling

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5
Q

why don’t we just use ARB instead of ACE inhibitors

A

lower risk of death

lower risk of arrhythmias

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6
Q

mechanisms of ACE inhibitors

A

they inhibit ACE, thus inhibiting the conversion of AG1 to AG2 in order to decrease blood pressure

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7
Q

how do ACE inhibitors cause angioedema and coughing

A

ACE- inhibitors inhibit the breakdown of bradykinin leading to its increased effects
rising levels of bradykinin, a vasodilator that triggers blood vessels to widen and become more permeable, leading to swelling.

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8
Q

which beta blockers are recommended and why

A

carvedilol

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9
Q

which heart failure patients should be treated with beta blockers

A

stable grade 2 or 3 patients or their condition may deteriorate further

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10
Q

contraindications of beta blockers

A
Asthma 
2nd or 3rd AV block
Peripheral arterial disease
symptomatic hypotension
heart rate less than 60
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11
Q

mechanism of action of beta blockers

A

the block the effects of epinephrine causing the heart to beat more slowly and with less force

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12
Q

which beta blockers are recommended and why

A

carvedilol, because it has vasodilating properties also

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13
Q

major safety concerns with spironolactone

A

hyperkalemia

affinity for steroid receptors- gynecomastia, hirsutism, sexual dysfunction

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14
Q

why should we not stop beta blockers abruptly

A

that can lead to ischemia and infarction

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15
Q

why are beta blockers used rather than calcium channel blockers

A

beta blockers can prevent heart attacks and death

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16
Q

mechanism of action of furosemide

A

inhibits the Na-k-cl co transporter in the loop
side effects:
hypovolemia
hyperglycemia, sensitivity and uricaemia
hearing loss (reversible)

17
Q

explain low and high ceiling diuretics’

A

high ceiling diuretics when you increase the dose the effect of the drug increases

18
Q

major cardiac and general adverse effects of digoxin

A

cardiac- palpitations, arrhythmia, syncope
GIT- nausea, anorexia, vomiting, diarrhea
insomnia, fatigue, confusion

19
Q

mechanism of action of thiazides

A

thiazides inhibit the Nacl transporter in the proximal convoluted tubule
side effected
hypercalcemia
use with caution in gout patients

20
Q

morphine use in acute severe heart failure

A

venodilatory

21
Q

what should you look out for in a morphine patient

A

respiratory depression

22
Q

why is preload reduction important in heart failure

A

it provides symptomatic relief

23
Q

role of digoxin in heart failure

A

strengthens force of contraction
improves blood circulation
restores heart rhythm

24
Q

why should furosemide be given intravenously for acute severe CF

A

it is a high ceiling diuretics’

25
Q

why should furosemide be increased in renal failure

A

increase in dosage leads to an increased response, water loss because there would be pulmonary congestion

26
Q

pulmonary oedema treatment

A

fowlers position

administer oxygen

27
Q

morphine use in acute severe heart failure

A

venodilatory

28
Q

pulmonary edema treatment

A

fowlers position

administer oxygen

29
Q

emergency management of morphine induced resp depression

A

administer naloxane

30
Q

why should furosemide be given intravenously for acute severe CF

A

it is a high ceiling diuretic and rapid onset of diuresis is required in acute severe CF since there is pulmonary edema

31
Q

Explain why the ability of furosemide to venodilate is important in acute severe heart failure.

A

because it helps reduce systemic vascular resistance and help decrease preload and relieve symptoms