Heart Failure With Reduced EF Flashcards
HF
Not able to pump enough blood to supply metabolic needs of the body
Classification according to duration
Acute
Chronic
According to side of the heart
Left sided
Right sided
Combined left and right side
According to CO
Low
High
According to severity
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
Compensatory heart
Hypertrophy and dilation - preload
Sympathetic stimulation - afterload
Decreased renal blood flow
Decreased GFR
Increased renin(sympathetic stimulation) for angiotensin and aldosterone for VC and edema
Increased residual blood in heart
Left - systemic congestion, liver congestion and neck veins
and right sided heart failure - pulmonary congestion plus dyspnea
Remodelling
Sympathetic
AT1
Aldosterone
Chronic heart failure with reduces ejection fraction
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
ACEIs - mixed vaso d
Used in:
Left ventricular failure
Asymptomatic and symptomatic HF
**start low and increase gradually
AT1 Receptor agonists
No dry irritant cough otherwise the same
Aldosterone antagonists - spironolactone and eplerenone
For sever HF or those with recent MI
Beta blockers - selective on the heart: Nebivolol, bidoprolol, metoprolol plus carvedilol for some reason
No cardiotoxic effect of sympathetic so decr3ased mortality in HF peeps
No mitogenic effect (remodelling and the rest)
**low doses them increase gradually
Diuretics
Thiazide - arterio d so take in HF plus hypertension
Loop - veno d
Decreasing blood volume- Decreasing VR and EDV and preload plus pulmonary congestion
Active form sacubatril
Sacubatrilat
Sacubatrilat
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
Combination with neprilysin to get rid of the ang 2
Take ARBs not ACEIs as this will add to the already present bradykinin from inhibiting neprilysin
Adverse Angiotensin Receptor Neprilysin Inhibitor
Hypotension
Hyperkalemia
Renal Failure
Cough
Angioedema
Ivab.
The thing for sinus rhythm and funny current
SGLT2 Inhibitors - gliflozin
Dapagliflozin empagliflozin canaglifozin
Even without diabetes
Normal reduced glucose and sodium diuretic effect
Additional resetting tubuloglomerular feedback without touching sympathetic
Digitalis - HF with AF
Otherwise don’t take it 😑
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
Narrow safety margin
0.5 - 1.4
Digoxin
Mechanisms of action digoxin
Vagal effect
Direct effect
Vagal effects (in small doses of digitalis)
Inhibit:
SAN
Atrial conductivity
AVN
Direct (extra vagal)
Therapeutic dose - +ve inotroy
Large - inhibits SAN and AVN
Toxic - increased automaticity and arrhythmia
+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
-ve chronotropy
(Less than. 60 beats means toxicity)
Small dose - vagal increase (antagonise with atropine)
Large dose - vagal and direct inhibition of SAN
-ve dromotropy
Heart block (long PR than 0.25 secs) in toxicity
Vagal and direct effect
Protects ventricles
Why you use it for AF
Increases
Excitability and automaticity
Arrhythmia- pulses bi and tri Geminus with digitalis toxicity
Ectopic foci
Other effects of digitalis
Circulation
Kidney - increase CO so decrease renin, increased GFR
GIT - Nausea and vomiting
CNS
Endocrine - gyneacomastia
Circulation
COP - increased emptying, filling and pumping
ABP - normalisation
Full digitalisation
Stimulates CRTZ
CNS effect
Stimulates VMC, vagal and CTZ
Endocrine
Gynecomastia in male
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
Effects of digitalis on ventricles
Slower
More regular
More regular
Eliminate pulse deficit
No digitalis in
Arrhythmia
SAN
Heart block (decreases AV conduction)
Cardiac ischaemia (increases HR)
Digitalis drug interactions
Increase absorption
Decrease absorption
Decrease absorption
Hyperkalemia
Anti acids: Al and Mg
Increase digitalis
Hypokalemia and such drugs (them loop and thiazide)
Hypercalcemia and such drugs
Beta blocker because heart block
Toxic plasma digitalis conc.
> 2ng
CVS effects
Early - bradycardia
Late - heart block plus and arrhythmia
Chromatopsia
In digitalis toxicity
Hallucinations delusions delirium confusion convulsion
Digitalis toxicity CNS manifestations
Kidney diseases extremities of age and hypothyroidism
Jncrease digitalis toxicity
Ttt
Stop digitalis
Use activated charcoal
HB
Arrhythmia + HB
Phenytoin
Arrhythmia with no HB
Lidocaine
Sinus bradycardia
Atropine
VF
Electro cardio eversion
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
Goal of AF treatment
Decongestants
Adequate Perfusion with:
Vaso Ds
Inotropes
Vassopressors
Diuretics for the pulmonary oedema - decongestion
Loop
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
Inotropes (in advanced HF and low O2) - increase Contractility and increased ionised calcium
** Improving CAMP
Beta 1 agonists
PDEIs
CCB
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
PDEIs
(Bipyridines - Amrinone milrinone enoximone)
**used IV for resistance JF to augment Digilis
Amrinone inhibits PDEI 3 so CAMP( ino dilator)
CAMP functions
Direct on heart (HR) increasing COP
Mixed VD on bv
Minimal change in HR and BP
Adverse amrinone effects
Allergy
Increased Myocardial oxygen consumption
More powerful and less toxic than amrinone
Milrinone
Methyl xantgines like theophylline inhibit
PDE IV
Calcium sensitizers
Levosimendan
Levosimendan
Increases sensitivity of trooping C to calcium
Used in short term ADHF as well but
In the absence of severe hypotension
Active long acting metabolites leaving hemodynamic effects lasting up to at least a week after stoppage of infusion
Levosimendan
