cardiac failure Flashcards
Explain the Renin angiotensin cascade
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
side effects of ACE inhibitors
chronic dry cough
hypotension
hyperkalemia
why should the combination of spironolactone and ACE be used cautiously
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
clinical features of ACE induced ACE-I induced angioedema
tongue, lips and face swelling
why don’t we just use ARB instead of ACE inhibitors
lower risk of death
lower risk of arrhythmias
mechanisms of ACE inhibitors
they inhibit ACE, thus inhibiting the conversion of AG1 to AG2 in order to decrease blood pressure
how do ACE inhibitors cause angioedema and coughing
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.
which beta blockers are recommended and why
carvedilol
which heart failure patients should be treated with beta blockers
stable grade 2 or 3 patients or their condition may deteriorate further
contraindications of beta blockers
Asthma 2nd or 3rd AV block Peripheral arterial disease symptomatic hypotension heart rate less than 60
mechanism of action of beta blockers
the block the effects of epinephrine causing the heart to beat more slowly and with less force
which beta blockers are recommended and why
carvedilol, because it has vasodilating properties also
major safety concerns with spironolactone
hyperkalemia
affinity for steroid receptors- gynecomastia, hirsutism, sexual dysfunction
why should we not stop beta blockers abruptly
that can lead to ischemia and infarction
why are beta blockers used rather than calcium channel blockers
beta blockers can prevent heart attacks and death
mechanism of action of furosemide
inhibits the Na-k-cl co transporter in the loop
side effects:
hypovolemia
hyperglycemia, sensitivity and uricaemia
hearing loss (reversible)
explain low and high ceiling diuretics’
high ceiling diuretics when you increase the dose the effect of the drug increases
major cardiac and general adverse effects of digoxin
cardiac- palpitations, arrhythmia, syncope
GIT- nausea, anorexia, vomiting, diarrhea
insomnia, fatigue, confusion
mechanism of action of thiazides
thiazides inhibit the Nacl transporter in the proximal convoluted tubule
side effected
hypercalcemia
use with caution in gout patients
morphine use in acute severe heart failure
venodilatory
what should you look out for in a morphine patient
respiratory depression
why is preload reduction important in heart failure
it provides symptomatic relief
role of digoxin in heart failure
strengthens force of contraction
improves blood circulation
restores heart rhythm
why should furosemide be given intravenously for acute severe CF
it is a high ceiling diuretics’
why should furosemide be increased in renal failure
increase in dosage leads to an increased response, water loss because there would be pulmonary congestion
pulmonary oedema treatment
fowlers position
administer oxygen
morphine use in acute severe heart failure
venodilatory
pulmonary edema treatment
fowlers position
administer oxygen
emergency management of morphine induced resp depression
administer naloxane
why should furosemide be given intravenously for acute severe CF
it is a high ceiling diuretic and rapid onset of diuresis is required in acute severe CF since there is pulmonary edema
Explain why the ability of furosemide to venodilate is important in acute severe heart failure.
because it helps reduce systemic vascular resistance and help decrease preload and relieve symptoms
