Heart Failure Flashcards

1
Q

Heart Failure

A

Complex clinical syndrome that can result from any cardiac disorder that impairs the ability of the ventricle to deliver adequate blood to tissues

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2
Q

Left sided failure

A

Blood not pumped adequately from left ventricle to the peripheral circulation and accumulates in the ventricle.

Portion of fluid backs up into the pulmonary alveoli, developing pulmonary edema, causing
Shortness of breath,
Dyspnea on exertion
A third heart sound

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3
Q

Right sided failure

A
Blood not pumped from right ventricle.
The fluid portion backs up throughout the body (veins liver legs bowel)
Systemic edema
Peripheral edema
Jugular vein distention
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4
Q

Diastolic dysfunction

A

Inability for ventricles to fill with blood during diastole (ventricular relaxation)
Stiffness in ventricular walls due to hypertension, aortic stenosis, diabetes, myocardial infarction and cardiac ischemia.

Normal or slight Reduced left ventricular ejection fraction LVEF> 50%
HF symptoms
Increased diastolic filling pressure

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5
Q

Systolic dysfunction

A

Impaired degree of ventricular contraction
Decrease inotropy
Decrease stroke volume
Lower than normal Ejection fraction < 40%

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6
Q

Drugs promoting Na retention

A
Androgens
Corticosteroids
Diazoxide
Estrogen
Licorice
Li Carbonate
NSAIDs
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7
Q

Drugs producing Osmotic Effect

A
Albumin
Glucose
Mannitol
Saline
Urea
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8
Q

Drugs reducing contractility

A
Anti arrhythmic
B Blockers
1st gen Ca channel blockers
Direct Cardiotoxins
(Doxorubicin, ethanol, cocaine, amphetamines)
TCAs
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9
Q

Drug Ranking system for HF

A

Size of Treatment effect:

Class I : Benefit&raquo_space;> Risk
Class IIa : Benefit&raquo_space; Risk
Class IIb : Benefit >= Risk
Class III : Benefit < Risk

Certainty of treatment effect:

Level A : multiple popular evaluated
Level B : Limited population evaluated
Level C : Very Limited Population

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10
Q
HF Patients class 
Stage A
A

Patient: risk of developing HF , No structural or functional abnormalities, no sign symptoms

Goals: treat Hypertension, stop smoking, treat lipid disorders
Encourage exercise, discourage alcohol, control metabolic syndrome

Drugs: ACEIs or ARBs in appropriate Patients

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11
Q
HF Patients class 
Stage B
A

Structural heart change
No symptom

Goals: same as A

Drugs: ACE , ARBs , B blockers

Inolant defibrillator in selective patients

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12
Q
HF Patients class 
Stage C
A

Structural change
Symptoms present

Treat htn
Stop smoking & alcohol
Exercise
Treat lipid disorder and metabolic syndrome
Dietry salt restrictions

Diuretics
ACEIs
B Blockers

In selective patients
Ald antagonist
Arbs
Digitalis
Hydralazine
Biventricular pacing
Implantable de fibrilator
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13
Q
HF Patients class 
Stage D
A

Patients with refractory HF who require special intervention

Goals Same as A B C
Decision concerning appropriate level of care

Palliative care
Heart transplant
Chronic inotropes
Permanent mechanical support
Experimental surgery or drugs
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14
Q

Compensation mechanism

A

Sympathetic stimulation (epinephrine)
Hormonal stimulation (renin angiotensin aldosterone system)
Cardiac hypertrophy
Frank starling mech

Over time these mechanism work harder and harder causing more harm to the heart and exhausting themselves

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15
Q

Afterload

A

Tension in ventricular muscles during contractions to overcome pressure in aorta or pulmonary artery

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16
Q

Preload

A

Force exerted on ventricular muscle at tye end of diastole determines the degree of muscle stretch

17
Q

Signs and symptoms of Heart Failure

A

Dyspnea
Dry wheezing cough
Exertional fatigue
Nocturia

Rales indicate movement of air through fluid filled passages
Tachycardia
S3 ventricular Gallop (rapid filling of ventricle early in diastole)
S4 aterial Gallop (increased resistance to sudden forceful ejection of atrial blood in late diastole

18
Q

Diagnostic test in HF

A

Cardiomegaly by chest radiography, ECG, echocardiography, radionuclide ventriculography

Arm to tongue circulation time

Transudative pleural effusion by radiography

LFT increase ALT
Checking Natriuretic peptides

19
Q

Moderate Na restriction

A

2 to 4g / day

20
Q

ACE inhibitor

A

Can cause angio-edema in Less than 1% patients

21
Q

B blockers

A

Metoprolol
Bisoprolol
Carvedilol
Life saving

22
Q

Nitroprusside

A

Nitropress
0.3 to 10mcg/kg/min

Long term use causes Thiocyanate toxicity

23
Q

Nesiritide

A

Binds to Natriuretic Peptide receptor results in increase production of cGMP in target tissues which causes vasodilation

24
Q

Digoxin lanoxin side effects

A

Hypokalemia causes digoxin increases effect
Hypercalcemia increase digoxin activity
Hypermagnesemia decreses digoxin activity

Digoxin normal serum level : 0.8 to 1.0ng/ml

Dose : 0.125 to 0.25 mg daily tablet

25
Q

Digoxin toxicity

A
Anorexia
Fatigue
Headache
Malaise
Nausea vomiting
Mental confusion
Altered visual perception (blurring, yellow halo)
Cardiac effect such as 
Premature vent cont
SA AV block
Atrial tachycardia
26
Q

Digoxin toxicity treatment

A

Discontinue digitalis
Discontinue any K sparring diuretic
If Hypokalemia — give K supplement unless patient has AV block
Treat arrhythmia with Lidocaine 100 mg bolus followed by infusion at 2 to 4 mg/min
Cholestyramine (Questran) bind to digitalis preventing Its re Absorption
Digoxin immune FAB digifab . 1 vial 40 mg will bind with 0.5mg of digitalis.

27
Q

Inamrinone

A

Non glycoside, non sympathomimetic inotrope
Positive inotropic effect
Vasodilating Effect
Inhibits phosphodiesterase located in cardiac cells, increases cAMP
Used for refractory patients
IV 0.75 mg/kg over 2 to 3 min followed by maintenance at 5 to 10 mg/kg/min

28
Q

Inamrinone precautions

A
Unstable in dextrose
Given in saline (careful in HF Patients)
Monitoring for hypotension
Thrombocytopenia
Ventricular tachy