heart failure Flashcards

1
Q

Heart failure general info

A

when CO is inadequate to provide the oxygen needed by the body

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2
Q

Heart failure classifications

A
  1. Ejection fraction
  2. Symptoms
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3
Q

Ejection fraction

heart failure classifications

A
  1. Systolic heart failure
    * reduced EF (less than 40)
    * HFrEF- Heart failure reduce ejection fraction
    * impaired cardiac contractility
  2. Diastolic heart failure
    * normal EF
    * HFpEF- heart failure preserved ejection fraction
    * increased myocardial stiffness or an inability of the heart to relax in the absence of reduced contractility
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4
Q

Symptoms

heart failure classifications

A

Acute Heart failure- not stable
Chronic heart failure- stable

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4
Q

Symptoms

heart failure classifications

A

Acute Heart failure- not stable
Chronic heart failure- stable

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5
Q

Goals of tx for heart failure

A
  1. improve patient’s quality of life
  2. reduce symptoms–> (SOB, Nocturia, Fluid retention, Nausea due to edema of the gut)
  3. slow progression during stable periods
  4. prevent or minimize hospitalizaitons
  5. manage acute episodes of decompensated failure
  6. Prolong survival
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6
Q

Goals of tx for heart failure

A
  1. improve patient’s quality of life
  2. reduce symptoms–> (SOB, Nocturia, Fluid retention, Nausea due to edema of the gut)
  3. slow progression during stable periods
  4. prevent or minimize hospitalizaitons
  5. manage acute episodes of decompensated failure
  6. Prolong survival
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7
Q

General therapeutic approach to chronic heart failure

A
  1. determine cause and correct causative factors (tx htn or comorbitities, exercise, weight loss)
  2. sodium and fluid restriction
  3. drugs
  4. devices
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8
Q

pathophys of heart failure factors affecting cardiac function

A
  • cardiac contractility
  • cytokines
  • heart rate and rhythm
  • myocardial relaxation
  • renin-angiotensin sys
  • sympathetic nervous sys
  • ventricular preload and afterload

affect targets

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8
Q

pathophys of heart failure factors affecting cardiac function

A
  • cardiac contractility
  • cytokines
  • heart rate and rhythm
  • myocardial relaxation
  • renin-angiotensin sys
  • sympathetic nervous sys
  • ventricular preload and afterload

affect targets

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9
Q

Chronic systolic heart failure

general therapies BAD CAVA

A
  • diuretics
  • vasodilators, neprilysin inhibitor
  • beta blocker
  • aldosterone receptor antagonists
  • Angiotensin-converting enzyme inhibitors (ACE INHIBITORS)
  • angiotensin receptor blockers (ARBs)
  • Cardiac glycosides (Digoxin)
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10
Q

Acute heart failure

A
  • VID

temporary and trying to stabilize

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11
Q

heart failure stages

A

A: Risk factors- at risk without current or previous symptoms= HTN, CVD, diabetes, obesity, exposure to cardiotoxic agents
B: Structural (Pre heart failure)- evidence of increased filling pressures, RF + high NP or High cardiac troponin
C: Symptoms (symptomatic heart failure)
D: Not responding to drugs- symptoms that interfere with daily life and recurrent hospitalizations (advanced heart failure)

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12
Q

Stage A

at risk

what pts and meds?

A

at high risk for heart failure without structrual heart disease or symptoms

PT w/: HTN, atherosclerotic disease, diabetes, obesity, cardiotoxins, fam hist

TX:
1. Sodium glucose co transporter= TYPE 2 DIABETES AND EITHER CVD OR HIGH RISK CARDIOVASCULAR RISK

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13
Q

Sodium-glucose Cotransporter 2 inhibitor

Stage A

indications, Common SE

A

Dapaglifozin (Faxiga) and Empagliflozin (Jardiance)
Indications:
* pt with heart failure with Reduced ejection fraction
* pt with Type 2 DM with estabilshed cardiovascular disease
* Pt with Type 2 DM to improve glycemic control

SE:
Hypoglycemia, dehydration, vaginal and penile yeast infection (bc pee out glucose)

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14
Q

Farxiga MOA

Dapaglifozin, Sodium glucose cotransporter 2 inhibitor

A

Sodium glucose cotransporter 2= in proximalrenal tubules= responsible for reabsorp of glucose and sodium

excrete glucose= yeast infections

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15
Q

Stage B Pre- Heart failure

structural heart disease without S&S of failure

indications and therapy

A

Indications:
* Pt with previous myocardial infarction
* left ventricular remodeling (including LV hypertrophy and low EF)
* Asymptomatic valvular disease

Tx:
1. Sodium glucose Co-transporter 2 inhibitor (Diab only)
2. Angiotensin converting enzyme inhibitors (ACE inhibitors) or Angiotensin receptor blockers (ARBs)
3. beta blockers
4. statins

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16
Q

Stage B: Pre- heart failure tx

INDICATIONS BASS

A

KNOW THIS

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17
Q

Angiotensin converting enzyme inhibitors

ACE inhibitors

-pril

A
  1. Lisinopril (Zestril)
  2. Enalapril (Vasotec)
  3. Quinapril (Accupril)
  4. Ramipril (Altace)
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18
Q

Indications for ACE inhibitors PPHHD

A
  1. HTN- adult and pediatric
  2. Heart failure- 1st line for pt with Low Ejection Fractions as it has proven to reduce mortality
  3. Post myocardial infarction- 1st line for all pts as proven to reduce mortality
  4. Diabetes mellitus and those at risk for vascular disease- 1st line
  5. Proteinuria- 1st line
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19
Q

ACE benefits in Heart failure SAVVE BAP

A
  1. Improve survival benefit in pt with heart failure and systolic dysfunction= due to inhibit aldosterone and angiotensin 2
  2. improve exercise tolerance
  3. Provide balanced vasodilation (arteries and veins)
  4. Reduce Blood pressure
  5. prevents left ventricular remodeling
  6. reduce aldosterone secretions-> less retention-> reduction of preload
  7. reduced periph res-> reduction in afterload
  8. reduc angiotensin levels-> less symp activity-> by decreasing angiotensin presynaptic effects on norepinephrine release
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20
Q

ACE inhibitors MOA

A

MOA: Inhibit the angiotensin-converting enzymein the vascular endothelium of the lungs

Target: RAAS

MOA starred

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21
Q

ACE inhibitors MOA

A

MOA: Inhibit the angiotensin-converting enzymein the vascular endothelium of the lungs

Target: RAAS

MOA starred

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22
Q

ACE inhibitors AE HACH

A

1. COUGH- secondary to increased bradykinin
2. Angioedema- 2ndary to increased bradykinin
3. Hyperkalemia
4. Hypotension-> dizziness

5. headaches, rash, drug fever

Contraindications: Pregnancy (teratogenic) and bilateral renal artery stenosis

23
Q

ACE inhibitors- drug interactions

A
  1. Potassium sparing diuretics and potassium supplements= increased risk of hyperkalemia= MONITOR POTASSIUM
  2. bactrim + ACE= increased hyperkalemia= MONITOR POTASSIUM
  3. Nsaids= antagonism
  4. lithium= increases levels
  5. additive effects with other antihypertensives
24
Q

Angiotensin Receptor Blockers (ARBs)

-artan

indications, names

A

use of an ARB is recommended if a pt cannot tolerate one of the SE of the ACE inhibitor= cough

Indications:
* heart failur
* Hypertension
* Diabetic Nephrothy

Medication:
* Candesartan (atacand)
* Irbesartan (Avapro)
* Losartan (Cozaar)
* Valsartan (Diovan)

25
Q

ARBs MOA

A

MOA: Block the binding of angiotensin 2 to the angiotensin-1 (AT1) receptor (type 1)

Target: RAAS

26
Q

ARBs inhibitors AE and drug interactions

A

Effects similar to ACE inhibitors except no bradykinin effects
* hypotension
* hyperkalemia

MONITOR CREATININE AND POTASSIUM LEVELS

Drug interactions:
* antagonized by NSAIDS
* potentiate Calcium channel blockers, Digoxin, Lidocaine
* Lithium increase levels

27
Q

Adrenoceptors

A
  1. Adrenal glands synth Catecholamines: Dopamine, Norepinephrine, Epinephrine
  2. Catecholamines act as neurotransmitters and hormones-> maintain homeostasis in multiple different ways within the body
  3. Receptors that respond to catecholamines are names ADRENOCEPTORS
  4. Types of adrenoceptors: alpha 1 type, alpha 2 type, Beta type, Dopamine type
  5. Receptors- drugs act as agonists and antagonists
28
Q

Adrenoceptors types and what they cause

A
29
Q

Catecholamines

A

Norepinephrine and epinephrine
* via Beta 1 receptors: increase the force and rate of contraction of the heart
* Myocardial excitability-> extrasystoles-> serious cardiac arrhythmias

Norepinephrine
* Alpha 1 receptor: Vasoconstriction
* Systolic and diastolic bp rise when infused slowly

Epinephrine
* Beta 2 receptor: dilates the BV in skeletal muscle and liver
* widening pulse pressure-> increase of cardiac rate and output

30
Q

Beta type Adrenoceptors

types, what they do, then what Beta blocker does

A

types of Beta receptors:
1. Beta 1= heart, lipocytes, brian juxtaglomerular apparatus of renal tubules
2. B2= bronchial smooth musc and some cardiac muscle
3. B3= muscle of bladder and induces relaxation

Effects:
1. Activation
2. Stim adenylyl cyclase
3. Increased intracellular levels of cAMP
4. cAMP causes cascade
* liver: activation of glycogen phosphorylase
* heart: increases influx of calcium across the cell membrane
* smooth musc: promotes relaxation

Beta blocker= binds to receptor that inhibits Adenylyl cyclase that would increase cAMP which would activate the pump for CAlcium to enter the body and contract muscle

Beta blocker= decreases Calcium that slows heart to relax and fill effectively to pump to body

31
Q

Beta blockers overview

objective

A
32
Q

Beta blockers

common clinical uses, AE, Interactions

A

Clinical uses:
* HTN
* Heart failure
* Arrythmias
* Angina
* Post MI

AE:
* Hypotension
* Heart block
* bradycardia
* Fatigue- sedation
* SEXUAL DYSFUNCTION
* depression
* exercise impairment
DEPRESSED COCK BLOCK O BRADY

Interactions:
* with other cardiac drugs-> hypotension, and iatrogenic heart failure

33
Q

Beta Blockers and Heart failure

meds and why we use them, relative contraindications

A

Meds:
* Carvedilol
* Metoprolol (sustained release)
* Bisoprolol

Why we use?
* Excessive tachy and ae of high catecholamine levels
* B1 antagonist in kidney= decreases renin release
* Prevent myocardial remodeling
* Mortality benefit in pts with chronic heart failure
TRRM

Relative contraindications: risk vs reward
* asthma/COPD
* AV Block
* Bradycardia
* Labile diabetes
CAL

34
Q

Advantage of Beta blockers in compensated heart failure

A
  1. improve ventricular function
  2. improve exercise tolerance
  3. decrease oxidative damage
  4. slow progression of heart failure

not used in decomp bc of acute negative inotropic effects= weaken the heart’s contractions and slow the heart rate

35
Q

Stage C symptomatic heart failure

Structural heart disease with prior or current Symptoms of Heart failure

Goals, Drugs, drugs for selected pts

A

Goals:
* control symptoms
* pt education
* prevent hospitalization
* prevent mortality

Drugs:
* Sodium glucose co-transporter 2 inhibitor
* Renin angiotensin system blocker
* beta blockers
* Diuretics for fluid retention
* MIneralocorticoid antagonists (MRAs/Aldosterone antagonists)

Drugs for selected pts:
Hydralazine/Isosorbide dinitrate

Edema, SOB, wheelchair

36
Q

Chronic Systolic Heart failure= reduced Ejection Fraction

1st line agents

A
  1. Diuretic
  2. Sodium glucose cotransporter 2 inhibitor
  3. Renin angiotensin system blocker
    * ARNI
    * ACE inhibitor
    * ARB
  4. Beta blocker
    DR BS
    | MOST DATA FOR PHARM AGENTS
37
Q

Chronic Systolic Heart failure= reduced Ejection Fraction

1st line agents

A
  1. Diuretic
  2. Sodium glucose cotransporter 2 inhibitor
  3. Renin angiotensin system blocker
    * ARNI
    * ACE inhibitor
    * ARB
  4. Beta blocker

MOST DATA FOR PHARM AGENTS

38
Q

Angiotensin Receptor Neprilysin inhibitor (ARNI)

meds, black box, Indications, SE

A

Meds: Valsartan/Sacubitril (Entresto)
Black box warning: fetal toxicity
Indications:
* Reduce risk of cardiovasc death and hospitalization for heart failure in pts with chronic heart failure and reduced ejection fraction STAGE C ONLY
* TX OF SYMPTOMATIC HEART FAILURE WITH SYSTEMIC LEFT VENTRICULAR SYSTOLIC DYSFUNCTION IN PEDS

SE:
* hypotension
* dizziness
* worsening kidney fxn
* hyperkalemia
SIMILAR TO ACE AND ARB

Allows BNP to work bc neprilysin breaks it down
1. sodium and fluid excretion
2. myocardial relaxation
3. inhibit hypertrophy and fibrosis
4. supress sympathetic outflow
5. stim vasodilation

DO NOT GIVE WITH ACE INHIBITORS OR ARBS SINCE VALSARTAN IS AN ARB

39
Q

Angiotensin Receptor Neprilysin inhibitor (ARNI)

meds, black box, Indications, SE

A

Meds: Valsartan/Sacubitril (Entresto)
Black box warning: fetal toxicity
Indications:
* Reduce risk of cardiovasc death and hospitalization for heart failure in pts with chronic heart failure and reduced ejection fraction STAGE C ONLY
* TX OF SYMPTOMATIC HEART FAILURE WITH SYSTEMIC LEFT VENTRICULAR SYSTOLIC DYSFUNCTION IN PEDS

SE:
* hypotension
* dizziness
* worsening kidney fxn
* hyperkalemia
SIMILAR TO ACE AND ARB

Allows BNP to work bc neprilysin breaks it down
1. sodium and fluid excretion
2. myocardial relaxation
3. inhibit hypertrophy and fibrosis
4. supress sympathetic outflow
5. stim vasodilation

DO NOT GIVE WITH ACE INHIBITORS OR ARBS SINCE VALSARTAN IS AN ARB

40
Q

Sodium removal

A

Maintstay of tx in symptomatic heart failure
1. Diuretics- lasix- 1st line to help feel good
2. Dietary salt restriction= reasonable to reduce congestive symptoms

removal of sodium leads to los of potassium
* potassium supplementation
* add ACE inhibitor bc hyperkalemia
* potassium sparing diuretics

41
Q

Diuretics for heart failure

general principles

A

agents/meds that increase urine volume
* reduce heart failure symptoms-> do not improve survival (star)
* reduce venous pressure and preload
* reduce cardiac size-> improved pump efficacy
* sodium excretion has slight vasodilating effect

42
Q

Aldosterone antagonists

Potassium sparing diuretics

MOA and meds

A

MOA: Antagonists of the effects of aldosterone in collecting tubules
1. direct antagonism of mineralcorticoid receptors= spironolactone and Eplerenone
2. inhibit sodium entrance via ion channels in luminal mem= Amiloride and triamterene

Meds:
* Spironolactone (aldactone)
* binds to androgen receptor= abnormal menstraul cycles, gynecomastia (male mammary enlargement), decreased libido

43
Q

Why target aldosterone?

A
  1. increases resorption of sodium, water, renal excretion of potassium
  2. causes myocardial and vascular fibrosis
44
Q

Advantages of Spironolactone in heart failure

A

Proven improvement in mortality statistics
* blocks effects of aldosterone-> NA/Fluid secretion, Potassium reabsorption, prevents myocardial fibrosis (reduce likelihood of arrhythmia), reduce vascular fibrosis
* prevent myocardial remodeling which improves heart function

45
Q

Summary of diuretics in heart failure

A
46
Q

Vasodilators for heart failure: categories

A
  1. Selective arteriolar dilators-> reduces afterload= Hydralazine- pts with fatigue and low LV output
  2. Selective venous dilators-> reduces preload= Isosorbide dinitrate- angina
  3. Nonselective (mixed) vasodilators= Isosorbide dinitrate/Hydralazine (Bidil)- Indications= adjunct therapy in African Americans with heart failure= DIDNT RESPOND TO ARB, ARNI, ACE
47
Q

2ND LINE- positive inotropes

increase strength of contraction, SV, CO

A
  1. increased cytoplasmic calcium concentration
  2. increased cardiac contractility
  3. increased CO

Meds:
1. Cardiac glycosides
2. Beta agonists
3. phosphodiesterase inhibitors

48
Q

Cardiac glycoside (Digitalis): Digoxin

2nd line- positive inotropic

indication, MOA, benefits

A

Indications: Heart failure (when diuretics and ACE inhibitors have failed) and Atrial fibrillation
MOA: Inhibits Na+K+ATPase enzyme (sodium pump) in the myocyte-»> increases intracellular sodium leading to increased calcium-» increased cardiac contractility
* slows conduction velocity through AV node-> Atrial Fibrillation

Benefits of digoxin therapy:
1. increased cardiac-> increased stroke volume and CO
2. slows the rate and vasodilates
3. decreases preload with improved renal dynamics

49
Q

Digoxin toxicity

A

Toxicity:
Narrow therapeutic index: goal is 1 ng/ml, 2 is toxic
High variability
High plasma protein binding
70% renal excretion-> must monitor creatinine
MUST MONITOR ELECTROLYTES REGULARLY: POTASSIUM, CALCIUM, AND MAGNESIUM- Bc messing with Pump

Signs of toxicity:
1. GI symptoms first
2. Visual disturbance- yellow/green haloes, fuzzy

Managing:
Mild: reduce dose, discontinue potassium depleting drugs, give K+
Severe: administer Digibind- digoxin specific antibody, insert temp pacemaker

50
Q

Digoxin drug interacitons

A

increased levels:
* amiodarone
* spironolactone

Decreased levels:
* Rifampin
* Metoclopramide

highlighted

51
Q

Sinus node inhibitor

indications, MOA, SE

A

Ivabradine (Corlanor
Indications:
1. pt with heart failure w/ persistent heart rate of equal to or >70 bpm with a maximally tolerated beta blocker dose

MOA: slows heart rate by inhibitig cardiac pacemaker current

SE: transitory bright lights and bradycardia

52
Q

Diastolic heart failure- Heart failure preserved ejection fraction

goal, tx

A

Goal: prevent symptoms and decrease hospitalizations
TX:
1. Diuresis to relieve symptoms of congestion
2. Follow guideline driven indications for comorbidities
3. some therapies that may be useful in reducing risk of hospitalization (but not mortality): sodium glucose cotransporter 2 inhibitor and a Mineralocorticoid Receptor Antagonist (MRA)

53
Q

Acute Decompensated heart failure agents

A

ALL IV
IV diuretics
IV vasodilators
IV inotropes

54
Q

Acute decomp heart failure: Positive Inotropic drugs

A

Bipyridines-> Milrinone
* MOA: inhibits phophodiesterase-> increase in cAMP, increase in contractility and vasodilation
* indicated for acute heart failure

Beta-adrenoceptor agonists
* Dobutamine: increases contractility and decreases afterload
* Dopamine: activates beta and alpha receptors

55
Q

Acute decompensated heart failure: Vasodilators

A

Reduction in afterload-> improve ejection fraction
1. Nitroprusside = arteriolar and venodilator
2. Nitroglycerine= reduces preload
3. Nesiritide= only in acute heart failure

56
Q

Cardiogenic shock

Goal, agents used

A

Goal: manage hypoperfusion and hypotension

Agents:
1. manage fluid status= diuretics vs fluid administration
2. Vasopressors and inotropes= augment both coronary and cerebral blood flow
* Norepinephrine
* Dopamine
3. Irreversibly inhibit platelet aggregation (ASA) may improe morbidity

just a reference