heart failure Flashcards

1
Q

HF

A

A mismatch between right and left heart volume

outputs”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

left side failure

A

becomes cecexic. backs up in lungs and coughs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

right heart failure

A

builds up fluid in abdomen (ascites)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

systolic hf

A

decrease contractility. decrease EF. patients tend to be younger. dialated hearts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

diastolic HF

A

decrease ventricular filling decrease CO. cannot fill because its stiff. older patients. hypertrophied heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

main hf causes

A

ischemia, idiopathic, viral, immune mediated, htn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ischemic HF

A

Can contribute to both systolic and diastolic
dysfunction
• Most common (~70%?) type of HF in
America.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

2) Idiopathic HF

A
Familial? (~ 1/3?)
• Toxins?
• Parasitic?
• Undiagnosed viral?
• Pregnancy-related?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

3) Viral HF

A
Viral” (another term for “idiopathic)
• Many, many viruses implicated. Viruses “errantly” take up residence in
myocardial cells…
• Moderate/severe cardiomyopathy (what’s
this?) develops…
• …and may or may not fully or completely
resolve (eventually)
• Might require valvular Sx due to new
cardiac “geometry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Immune-Mediated HF

A

Specific cardiac antibodies attack
cardiomyocytes
• Possible link to other immune-mediated
diseases (like what?) LUPUS RHEUMATOID ARTHRITIS
• Acute myocardial infarctions (AMIs) may
expose novel cardiac antigens affecting
long-term prognosis. inside of heart is supposed to be inside and body will develop immune response to heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

why does the heart remodel

A
Heart cells die…
…they’re replaced with
fibrotic tissues…
…and remaining cells
hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What forces contribute to the chronic

downhill HF slide?

A

chronic sympathetic stim. and renin angiotensin aldosterone system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

goals of therapy for HF

A
1) Improve/alleviate critter’s symptoms
• 2) Slow that “downhill slide” towards
transplant/VAD/death
• 3) Improve survival
***Increase critter’s QALYs*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

six classes of QALY improving drugs

A

1) Positive Inotropes
2) Diuretics
3) Renin/Angiotensin Blockers
4) Primary Vasodilators
5) β-Blockers
6) Aldosterone Antagonists
7) Neprilysin Inhibitor (the future?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

positive inotropes

A

Cardiac Glycosides

  • Catecholamines
  • Bipyridines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

digitalis

A
digoxin. cardiac glycoside. Positive Inotrope
• Negative Chronotrope
• Increased Baroreceptor
sensitivity. *Narrow therapeutic window
-Arrhythmias, GI symptoms
*No evidence these
drugs prolong life!
17
Q

how doe digitalis work

A

Blocks Na⁺/K⁺-ATPase “The Sodium Pump”

…and you know what THAT causes! increase NA INCREASE CA increase contraction

18
Q

PREFERRED DRUG FOR CARDIAC

ARREST!!

A

Epinephrine (Adrenaline). Also handy for anaphylactic (what’s this?)
reactions
-Predictable side effects.

19
Q

Dopamine

A

A relatively non-specific catecholamine; acts
on dopaminergic receptors
• Improves cardiac function in heart failure.
• Also used for renal failure
and shock
• Given by IV drip infusion

20
Q

DOBUTAMINE

A

Also acts on dopaminergic receptors but

more cardioselective

21
Q

Bipyridines what they do to the body

A

increase intracelular levels of cAMP =
increase intracellular levels of Ca⁺⁺ =
increase myocardial contractility

22
Q

bipyridines long term use results in

A

significantly higher mortality than that seen in untreated
patients!
*ONLY used in short-term (acute) HF patients…

23
Q

Frequently the D.O.C. at all stages of HF,
particularly in patients with low EF (what’s
this? what’s normal?)

A

Renin-Angiotensin Converting
Enzyme Blockers. Initiation of ACE-Inhibitor Rx after AMIs
is widely considered a standard of care
**
-Often used as part of a progressive multimodal
Rx (huh?..we’ll discuss in a minute

24
Q

losartan

A

cozaar. arb s. used as a replacement for ACE inhibitor in intolerant patientsmay also be used with ace inhibitors in decompensating patients

25
Q

D.O.C. venous dilators

for acute CHF episodes

A

nitrates

26
Q

patients intolerant of ace inhibitors and arbs or beta blockers. give

A

hydralazine or isosorbide

27
Q

Why would you be giving negative

inotropes to patients in HF?

A

block chronic sympathetic stimulation and prevent apoptosis of myocyte. not for acute HF

28
Q

aldosterone antagonist

A

prevent salt fluid retention myocardial hypertrophy and decrease K excretion. improve long term mortality

29
Q

lcz 696

A

A 50/50 mix of Valsartan (about which you
have a perfect & complete understanding)
and Sacubitril
• Sacubitril is metabolized into a neprilysin
inhibitor

30
Q

Neprilisyn

A

an enzyme which breaks down
atrial (ANP) & brain (BNP) natriuretic
peptides
• ANP is mostly released in response to
excessive blood volume (mostly in response
to excessive atrial “stretch”) and causes an
increase GFR, increase sodium loss, and decrease renin secretion

31
Q

morphine. acute HF

A
Classically used in
acute heart failure to
reduce preload, heart
rate, and (maybe?)
afterload.
• NO evidence it helps;
substantial evidence it
produces worse longterm
outcomes
32
Q

morphine chronic HF

A
– Lowers respiratory
rate which decreases
cardiac workload
– Decreases preload and
afterload (some…a
good reason to say why
you’re giving
morphine…)
– EASES ANXIETY! Do
you understand where
we’re going with thiS?
33
Q

RHF SYMPTOMS

A

FATIGUE, INCREASE PERIPHERAL RESISTANCE,ENLARGED LIVER SPLEEN,DISTENDED JUGULAR VEIN, ANOREXIA,GI DIDTRESS, SWELLING IN HANDS DEPENDENT EDEMA

34
Q

LEFT SIDED FAILURE

A

PAROXYSMAL NOCTURNAL DYSPNEA PULMONARY CONGESTION,CONFUSION,FATIGUE, RESTLESSNESS, CYANOSIS,ORTHOPNEA, Tachycardia