Cardiac Failure Flashcards
ACE inhibitors
Enalapril and captopril
ARB
Valsartan
Neprilysin inhibitors
Valsartan+sacubitril
SGLT2 inhibitor
Dapagliflozin
Vasopressors
NE
Inotropic agents are
Beta 1 adrenoreceptor agonist, cardiac glycoside, calcium channel sensitizers and PDE3 inhibitor
Calcium channel sensitizers
Levosimendane
Cardiac glycoside
Digoxin
PDE 3inhibitor
Milrinone
Beta 1 adrenoreceptor agonist
Dopamine and dobutamine
Treatment for heart failure mechanisms used
1.stimulation of cardiac performance 2.reductionmof heart load if necessary 3.delay in cardiac remodelling and fibrosis
Reduction of heart load can be done by
Negative chronotropy, reduce preload and afternoon,reduced circulating blood volume
Cardiac performance can be increased by
Increase in cardiac contractility, increase preload, increase ventricular filling time (diastole extension), increase amount of circulating blood volume
Vasodilators are
ACE inhibitors,ARB,ARNI,, 3rd gen BAB, calcium sensitizers, PDE3inhibitor, organic nitrate , Sodium nitroprusside
Dilation of arteries are done by
SGLT2 inhibitor
Reduction in circulatory blood volume is done by
ARNI,MRA, SGLT2 inhibitor, Diuretic
Negative chronotropy done by
2 Nd and 3rd gen BAB and SA node inhibitor, cardiac glycoside
Increase in contractility (inotropy) done by
Cardiac glycoside, calcium sensitizers, PDE3inhibitor,beta 1 adrenoreceptor agonist
Delay of remodeling is done by
ACE inhibitors,ARB,ARNI,MRA,2 Nd ge and 3rd gen , SGLT2 inhibitor
ACE-I fn
Vasodilation and delay of cardiac remodelling
ARB fn
Vasodilation and delay of cardiac remodelling
ARNI fn
Vasodilation,delay of remodeling and reduction in circulatory blood volume
MRA fn
Reduction in circulatory blood volume and delay in cardiac remodelling
Second gen BAB fn
Negative chronotropy and delay in cardiac remodelling
3rd gen BAB fn
Negative chronotropy,delay in cardiac remodelling and vasodilation
SGLT2 inhibitor fn
Arterial dilation, reduce circulating volume and delay in cardiac remodelling
Diuretic fn
Reduction in circulatory blood volume
Sinus node inhibitor fn
Negative chronotropy
Cardiac glycoside fn
Negative chronotropy and positive inotropy
Beta 1 adrenoreceptor agonist fn
Positive inotropy
Calcium sensitizers fn
Vasodilation and positive inotropy
PDE3INHIBITOR fn
Vasodilation and positive inotropy
Organic nitrate and sodium nitroprusside fn
Vasodilation
ACE I names
Captopril enalapril enalaprilat perindopril,ramipril
ARB names
Valsartan candesartan losartan
ACE I and ARB are
Antifibrotic and remodelling inhibitor
Natriuretic peptide function
Vasodilation, sodium excretion, diuresis,anti fibrotic
Neprilysin is
An enzyme that degrade Natriuretic peptide
Neprilysin inhibitors are
Sacubitril
ARB +neprilysin inhibitors are
ARNI
Sacubitril is combined with ARB group because
Of increase in AT2, because neprilysin was responsible for both NP and AT2
ARNI use
CHF
ACE I is not used with sacubitril because
They can increase bradykinin leading to angioedema
Spironolactone is
Non-selective MRA
SGLT2 inhibitor are
Dapagliflozin and empagliflozin
SGLT2 inhibitor acts on
SGLT2 receptor in proximal renal tubule causing glycosuria,in NHS exchanger in heart causing reduction in sodium and calcium ions intracellular and same happens when acts on SGLT2 1receptor in heart,but also reduces body weight
Use of SGLT2 inhibitor (Dapagliflozin and empagliflozin)are
CHF
Side effects of SGLT2 inhibitor are
Urinary tract infection due to glycosuria
Furosemide is
Short acting,so also used in Acute Heart failure
Loop diuretic cause SE
Hypokalemia, hypocalcemia and ototoxicity
Ivabradine use
CHF
Cardiac glycoside, Digoxin inhibits
Na K pump,which further affects na Cal pump and increase intracellular calcium ions
Potassium depleting diuretic with cardiac glycoside cause
Cardiotoxicity
Negative chronotropy of cardiac glycoside is due to
N vagus parasympathomimetic effect
Use of cardiac glycoside
AHF and CHF(They can accumulate: caution)
SE cardiac glycoside
Rhythm disorders, extrasystole, atrial tachycardia,AV block, nausea diarrhea visual disturbance
Digoxin T1/2
30 to 50 HR(depends on renal fn
Acute overdose of cardiac glycoside cause symptoms
Nausea, vomiting, hyperkalemia, cardiac arrythmia
ECG features of Digoxin
Increased PR I, decreased QT I,ST segment depression (hockey stick configuration)
Treatment of Digoxin toxicity
Digoxin specific antibody, calcium gluconate/calcium chloride, sodium bicarbonate and glucose IV with insulin -to treat hyperkalemia
Heart block or bradykardia can be treated by
Atropine
Ventricular tachyarrhythmia can also be treated by
Lidocaine and phenytoin in case of hypokalemia and hypomagnesemia
Dobutamine has
Positive inotropy effect by increasing calcium intracellular
Dopamine acts on
D1,alpha 1 and beta 1 receptor
Dopamine at low dose
Improves renal microcirculation
Dopamine at medium dose
Positive inotropic and cardiotonic effect
Dopamine at high dose
Vasopressor effect
Levosimendane has triple action
Positive inotropy without using extraoxygen, vasodilation,cardioprotection
Use of levosimendane (calcium sensitizers)
AHF
Milrinone use
AHF
GTN and sodium nitroprusside use
AHF
Opioid receptor agonists morphine use
Reduce tachypnoea
Vasopressor agents in hypotensive patients
NE