Clinical Treatment of Heart Failure Flashcards
Goals of patients in stage A & B is all about prevention. What about patients in stage C?
Control symptoms, prevent hospitalization/ mortality!
HFpEF: identify comorbitities, diuresis, quality of life
HFrEF: patient education, diuretics, beta blockers, etc
What are the specific HF goals of Rx?
- Correction of underlying cause (if possible)
- Elimination of precipitating factors
- Reduction of congestion (ie. diuretics)
- Improve blood flow
Again (from last lecture) what tests/ procedures are done?
- Vitals
- ECG
- CBC
- Chest X ray (CXR)
- BNP
- Echo
- Coronary angiogram
What is the most common therapy for all HF patients?
Diuretics: reverses fluid retention
- Loop diuretics preferred because more potent
- Can be used chronically (oral) and acutely (IV in hospital)
Okay so diuretics decrease venous congestion, but describe with a SV (y axis) end-diastolic pressure (x axis) the FUNDAMENTAL treatment of heart failure…
The graph is logarithmic (increases fast then slows down)
-So large increases in diastolic pressure don’t increase SV very much and screw over your heart. But this is how your body compensates to increase SV (Na retention)
-Decreasing end-diastolic pressure to a degree saves the heart with only minimal decrease in stroke volume
Diuretics half short half lives and are pretty cheap, but what’s the big difference between furosemide vs bumetanide or torsemide
Furosemide doesn’t absorb as well in intestines
-bumetanide/ torsemide have better oral bioavailability
Grandpa eats at the brazilian steakhouse again and can’t breath (HFrEF) and vomits all night because of food poisoning. What do you give him?
Don’t use diuretics because he’s dehydrated
- Use IV Fluids (has lower stroke volume because low fluid)
Review: How does your body respond to low CO?
RAAS activation = vasoconstriction + Na retention > increased fluid volume/ pressure
Adrenergic = vasoconstriction + increase HR
What medications block the RAAS pathway? How?
ACE inhibitors (“-pril”)
- Blocks conversion of ATI => ATII (Angiotensin Converting Enzyme)
- Effects: direct vasodilation, decreased aldosterone release
What are the side effects of ACE inhibitors?
Hypotension Worse renal function Hyperkalemia COUGH Angioedema
What other medications block the RAAS pathway by blocking the receptor of angiotensin II?
ARBS (“-sartan”)
ARBS are essentially equivalent to ACE inhibitors. When would you decide to use these instead?
To avoid cough (not a side effect)
He talked a lot about LCZ696 as a new hot medicine. What is it?
ARB + sacubutril (neprolysin inhibitor)
Supposedly had better effects in ACEI
Mineralocorticoid Receptor Antagonists (MRA) are also pretty dope diuretics. What do they do?
The name just told you…
- block mineralocorticoids in kidney
- Also have some antifibrotic effects
=spironolactone and eplerene
What medications do you use to block the adrenergic pathway? How do they work?
Beta blockers (“-olols”)
-antagonize sympathetic system
Beta 1 block:
-negative chronotrope (slow HR)
-negative inotrope (decrease metabolic demand)
[sometimes block alpha 1, beta 2]
T/F: You should put someone on all three drugs (ACE/ARB, Beta blockers, aldosterone inhibitors) to reduce morbidity and death?
True
- Together they decrease remodeling best
- hypertrophy
- fibrosis
- apoptosis
If you have an african american patient that is using all three of these drugs and still has hypertension, what could you give him?
Hydralazine/ isosorbide dinitrate (arterial vasodilator)
There are other venous dilators and pulmonary arterial vasodilators too
Again, what are the 2010 guidelines for treating someone with stage 3 (NYHA Class I-IV) HfrEF?
Loop diuretics +
ACEI or ARB or ARB-neprolysin inhibitor +
aldosterone antagonist +
hydral-nitrates (African Americans)
Who should get an Implanted Cardioverter Defribillator (ICD)?
Patients with LVEF (left ventr. ejection fraction)
What other electrical therapy can you use to restore ventricular synchrony? Who should get it?
Cardiac Resynchronization Therapy (CRT) aka Bi-ventricular pacemaker (BiV)
-Shocks ventrical/ septal wall to contract together
> Patients with left bundle branch block, QRS > 120 msec
For an acute patient that comes in and is warm and wet (congested), you give IV diuretics. What about an acute patient that is cold and wet (ie. in shock)?
You need to give them a positive inotrope!
-also, address their precipitants to bring up their CO before using diuretics
Alright ER doc, summarize your plan of action for an acute hospitalized HF patient?
1) IV diuretics
2) IV vasodilators (if BP allows)
3) Ventilation (for hypoxia)
4) cut back beta blockers (severe cases)
5) IV inotropes (shock only)
So what’s the big difference between chronic vs. acute treatment
Chronic: trying to slow heart down (ie. beta blocker)
Acute: trying to stabilize (opposite effect of beta blocker)
-increase inotropy to bring SV back up
What are some good positive inotropes to use in an acute setting?
Epinephrine Norepinephrine Dopamine Dubutamine Digoxin (milrinone)
What happens if the patient moves into stage D?
Transplantation mechanical support (LVAD) Supportive care (shorter life - better quality) Inotrope infusion (shorter life - better quality)
That was all HFrEF. But with HFpEF the problem is lusitropy. What do you do to treat them?
-ACEI and ARBs don’t work!
=volume control (diuretic/ vasodilators) and treat underlying disease (hypertension, diabetes, kidney dysfxn)
**Not much you can do with HFpEF
