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Acute Heart Failure (Boards and Beyond) (Digoxin (not used as much for…
Acute Heart Failure (Boards and Beyond)
HF is acute or chronic
Acute
congested
Pulmonary edema
pitting edema
increased JVP
Chronic
received diuretics
Euvolemic
normal volume status\
Clear lungs
no pitting edema
JVP is flat
Continue to be at risk and need treatment
Acute Exacerbations (why they get worse)
1, Dietary indiscretion
hi Na diet
increased Na
increased plasma osm
Osmosensors sense: increase ADH,
Increase Free water
Normal Plasma [Na
Consequence: more body volume
RAAS falls
ADH falls
increases excretion of water
exacerbation of symptoms: pulmonary edema, LE edema
2, poor medication compliance
Other reasons
infection
ramps up SNS
NaCl and H20 retention
Ischemia (rarely)
worsens HF
NSAIDS
inhibits COX, lowers prostaglandins
can't maintain renal perfusion
more NaCl water retention
Goal of Acute heart failure therapy
symptom relief
same for diastolic or systolic HF
Mainstay
loop diuretics
delivers more Na to CD, result of more salt water loss
Furosemide, bumetanide, torsemide, ethacrinic acid
sulfa drugs
inhibid NaK2Cl pump
use IV drugs to bypass a swollen gut in acute HF
Side effects:
hypokalemia
dehydration
Add Metalozone
thiazide like diuretic acting on DCT
blocks resorption of Na in DCT
5mg Metolazone, 80mg iv furosemide
causes vigorous diuresis
Side effects: additional fluid loss, K wasting
Other treatments
Nitrates
decrease preload
pool blood in veins, away from lungs
less pulmonary edema
Side effects:
HA (meningeal vasodilation)
Flushing
Hypotension
Inotropes
increase contractility of the heart (systolic disfunction HF only)
Milrinone, dobutamine, dopamine, epinephrine
milrinone: PDE 3 inhibitor
PDE3: lowers cAMP in myocytes
inhibition increases cAMP for more contraction
increases cAMP increases vasodilation in sm. muscle
possible hypotension
Dobutamine
ß1 agonist
increases HR and contractility
weak ß2 agonist
vasodilator
hypotension similar to milrinone
Dopamine
dose dependent
low dose: dopamine receptor agonist
Medium dose: ß1 agonist
increased HR and contractility (good!)
Hi dose: alpha agonist
vasoconstriction
Epinephrine
mostly a vasoconstrictor
some inotropic properties
Dose dependent
low dose: ß agonist effects
1 more item...
high dose: alpha agonist (clinical), vasoconstriction
Inotropes can be bad
increased mortality w/ routine use
dangerous: last resort for a very sick patient
done in ICU w/ Swan Ganz
Increase O2 demand in a weak heart
dangerous
Typical A HF patient
Presentation
Dyspnea
Edema
sleeping in chair
Treatment in hospital
nitro drip to relieve dyspnea
furosemide BID to remove fluid
Day 3
weight down from diuresis
nitro drip stopped
oral furosemide til discharge'
Complex HF pt: sicker pt w/ poor EF needing inotropes
Presentation
Dyspnea
edema
sleeping in chair
known low EF
Treatment
nitro drip
furosemide
Day 2
Poor urine output
Cool extremities from low CO
increasing Cr: poor kidney perfusion
start dobutamine drip
Day 3-5: Good urine output
Day 6: stop dobutamine/furosemide
Day 7:: oral furosemide
Day 8 discharge
weight loss
improved breathing
Not necessarily a medical emergency
managed in outpatient setting
Recurrence of HF after discharge is very common
Chronic patients require daily furosemide
w/o they will retain fluid
some chronics requires daily long acting nitrates
isosorbide mononitrate
keeps them symptom free
Rare patients requiring treatment for low output
Chronic IV inotrope: dobutamine drip
Left ventricular assist devices
Heart transplants
Digoxin (not used as much for this)
no mortality benefit, despite being an oral inotrope
not effective for diastolic heart failure
creates serious side effects
Benefits
:
increased CO
Lower left end diastolic pressure
less pulmonary edema
improved symptoms and QoL
Downsides
:
Renal clearance: contraindicated in kidney disease
Hypokalemia (in conjunction w/ K wasting diuretic) promotes toxicity
monitor levels of Dig
Dig toxicity
GI symptoms
Neurologic
confusion
Fatigue
Lethargy
Visual changes
Scotomas
spots in visual field
color vision changes
blindness
Bradycardia from heart block
Arrhythmias
raises resting potential of atrial/vent cells
also raises phase 4 of AP: increased automaticity
Both changes predispose dig patient to spontaneous depolarization
atrial contractions
ventricular contractions
arrhythmias
in conjunction w/ AV node block
PVCs and PACs
2 classic rhythms:
regularized Afib
regular intervals: weird for Afib
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scooped ST: just anyone taking the drug
Bidirectional VT
Alternating QRS complexes: very rare, Dig toxic
Classic presentation
elderly woman
mild dementia
confuses her pills
Nausea
sees spots and color changes
Bradycardia
treatment: Dig antibody
Why use?
Only oral inotrope
symptom treatment in conjunction w/ maximal therapies
