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Pharmacology > Heart Failure With Reduced EF > Flashcards

Heart Failure With Reduced EF Flashcards

(67 cards)

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1
Q

HF

A

Not able to pump enough blood to supply metabolic needs of the body

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2
Q

Classification according to duration

A

Acute
Chronic

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3
Q

According to side of the heart

A

Left sided
Right sided
Combined left and right side

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4
Q

According to CO

A

Low
High

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5
Q

According to severity

A

Class 1- no limitation of physical activity
Class 2 - slight limitation so symptoms with ordinary activity but non at rest
Class 3 - marked limitation so symptoms with less than ordinary activity
Class 4 - symptoms occur even at rest

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6
Q

Compensatory heart

A

Hypertrophy and dilation - preload
Sympathetic stimulation - afterload

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7
Q

Decreased renal blood flow

A

Decreased GFR
Increased renin(sympathetic stimulation) for angiotensin and aldosterone for VC and edema

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8
Q

Increased residual blood in heart

A

Left - systemic congestion, liver congestion and neck veins
and right sided heart failure - pulmonary congestion plus dyspnea

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9
Q

Remodelling

A

Sympathetic
AT1
Aldosterone

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10
Q

Chronic heart failure with reduces ejection fraction

A

ACEIs
AT1 receptor agonists
Aldosterone receptor agonists
Beta blockers
Diuretics
Neprilysin Inhibitor
Hyperpolarisation activated cyclic nucleotide gated channel blockers - Ivabradin
SGLT 2 inhibitors
Cardiac Glycosides - digitalis

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11
Q

ACEIs - mixed vaso d
Used in:

A

Left ventricular failure
Asymptomatic and symptomatic HF
**start low and increase gradually

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12
Q

AT1 Receptor agonists

A

No dry irritant cough otherwise the same

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13
Q

Aldosterone antagonists - spironolactone and eplerenone

A

For sever HF or those with recent MI

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14
Q

Beta blockers - selective on the heart: Nebivolol, bidoprolol, metoprolol plus carvedilol for some reason

A

No cardiotoxic effect of sympathetic so decr3ased mortality in HF peeps
No mitogenic effect (remodelling and the rest)
**low doses them increase gradually

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15
Q

Diuretics

A

Thiazide - arterio d so take in HF plus hypertension
Loop - veno d
Decreasing blood volume- Decreasing VR and EDV and preload plus pulmonary congestion

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16
Q

Active form sacubatril

A

Sacubatrilat

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17
Q

Sacubatrilat

A

Prevents ANP and BNP so yes VD plus naturesis and diuresis lower BP reduces sympathetic tone plus aldosterone and BV
Prevents bradykinin break down
Prevents ang2 break down

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18
Q

Combination with neprilysin to get rid of the ang 2

A

Take ARBs not ACEIs as this will add to the already present bradykinin from inhibiting neprilysin

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19
Q

Adverse Angiotensin Receptor Neprilysin Inhibitor

A

Hypotension
Hyperkalemia
Renal Failure
Cough
Angioedema

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20
Q

Ivab.

A

The thing for sinus rhythm and funny current

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21
Q

SGLT2 Inhibitors - gliflozin
Dapagliflozin empagliflozin canaglifozin
Even without diabetes

A

Normal reduced glucose and sodium diuretic effect
Additional resetting tubuloglomerular feedback without touching sympathetic

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22
Q

Digitalis - HF with AF
Otherwise don’t take it 😑

A

Orally from DUODENUM
Distribution passes bbb
Specific for the heart 15 -30 times plasma
And 25%bound to plasma protein
1.5 days half life

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23
Q

Narrow safety margin
0.5 - 1.4

A

Digoxin

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24
Q

Mechanisms of action digoxin

A

Vagal effect
Direct effect

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25
Vagal effects (in small doses of digitalis)
Inhibit: SAN Atrial conductivity AVN
26
Direct (extra vagal)
Therapeutic dose - +ve inotroy Large - inhibits SAN and AVN Toxic - increased automaticity and arrhythmia
27
+ve inotropy of digitalis
Inhibit Na/K atpase Increases intracellular Na blocking Na/Ca exchanger Retention of Ca Activation of Ca so more Ca Then tropinin tropomyosin and sliding All the Contraction -inhibits ATPase with Ca (K and Mg decrease it) - excess inhibition causes arrhythmia
28
-ve chronotropy (Less than. 60 beats means toxicity)
Small dose - vagal increase (antagonise with atropine) Large dose - vagal and direct inhibition of SAN
29
-ve dromotropy Heart block (long PR than 0.25 secs) in toxicity
Vagal and direct effect Protects ventricles Why you use it for AF
30
Increases
Excitability and automaticity
31
Arrhythmia- pulses bi and tri Geminus with digitalis toxicity
Ectopic foci
32
Other effects of digitalis
Circulation Kidney - increase CO so decrease renin, increased GFR GIT - Nausea and vomiting CNS Endocrine - gyneacomastia
33
Circulation
COP - increased emptying, filling and pumping ABP - normalisation
34
Full digitalisation
Stimulates CRTZ
35
CNS effect
Stimulates VMC, vagal and CTZ
36
Endocrine
Gynecomastia in male
37
Uses
HF as last resort at low conc.(0.5 to 0.8) AF - Delays AV conduction, which worsens the atrium and atrium flutter but protects the ventricles
38
Effects of digitalis on ventricles
Slower More regular More regular Eliminate pulse deficit
39
No digitalis in
Arrhythmia SAN Heart block (decreases AV conduction) Cardiac ischaemia (increases HR)
40
Digitalis drug interactions
Increase absorption Decrease absorption
41
Decrease absorption
Hyperkalemia Anti acids: Al and Mg
42
Increase digitalis
Hypokalemia and such drugs (them loop and thiazide) Hypercalcemia and such drugs Beta blocker because heart block
43
Toxic plasma digitalis conc.
>2ng
44
CVS effects
Early - bradycardia Late - heart block plus and arrhythmia
45
Chromatopsia
In digitalis toxicity
46
Hallucinations delusions delirium confusion convulsion
Digitalis toxicity CNS manifestations
47
Kidney diseases extremities of age and hypothyroidism
Jncrease digitalis toxicity
48
Ttt
Stop digitalis Use activated charcoal HB
49
Arrhythmia + HB
Phenytoin
50
Arrhythmia with no HB
Lidocaine
51
Sinus bradycardia
Atropine
52
VF
Electro cardio eversion
53
Acute decompensated HF
Either first occurrence(de novo) or worsening of chronic ad a result of a trigger like infection, arrhythmia, anemia, pulmonary embolism, acute coronary syndrome and nonadherence
54
Goal of AF treatment
Decongestants Adequate Perfusion with: Vaso Ds Inotropes Vassopressors
55
Diuretics for the pulmonary oedema - decongestion
Loop
56
Vaso Ds - hypertensive ADHF
Veno D - Nitrate Mixed - Sodium Nitro Prusside (especially in HF with hypetensive emergency)and Nesiritide : synthetic analogue of BNP from E.coli with recombinant DNA tech
57
Inotropes (in advanced HF and low O2) - increase Contractility and increased ionised calcium ** Improving CAMP
Beta 1 agonists PDEIs CCB
58
Beta 1 agonists
Dopamine, Dobutamine (increase CAMP) - IV for short term treatment Epinephrine- cardiac arrest and anaphylactic shock, alpha agonist at higher doses Isoproterenol - cardiogenic shock secondary to bradycardia or with excessive beta blockade
59
PDEIs (Bipyridines - Amrinone milrinone enoximone) **used IV for resistance JF to augment Digilis
Amrinone inhibits PDEI 3 so CAMP( ino dilator)
60
CAMP functions
Direct on heart (HR) increasing COP Mixed VD on bv Minimal change in HR and BP
61
Adverse amrinone effects
Allergy Increased Myocardial oxygen consumption
62
More powerful and less toxic than amrinone
Milrinone
63
Methyl xantgines like theophylline inhibit
PDE IV
64
Calcium sensitizers
Levosimendan
65
Levosimendan
Increases sensitivity of trooping C to calcium
66
Used in short term ADHF as well but
In the absence of severe hypotension
67
Active long acting metabolites leaving hemodynamic effects lasting up to at least a week after stoppage of infusion
Levosimendan

Pharmacology (27 decks)

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