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Study cards 2 > Heart failure > Flashcards

Heart failure Flashcards

1
Q

Heart Failure: What is it?

A

“HF is a pathological condition in which the heart is unable to pump blood in sufficient amounts from ventricles to meet body’s metabolic needs.”

Not a specific disease

Complex clinical syndrome resulting from any functional or structural impairment to the heart, specifically ejection of blood or ventricular filling

The heart is unable to pump blood in sufficient amounts from the ventricles to meet the body’s metabolic needs.

One of the most common causes for hospitalization in Canada

5 000 annual deaths from heart failure

5-year survival rate in those with heart failure is 50%.

Prevention is key.

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2
Q

Four Causes of HF

A

Failure of ventricle to eject blood
Fluid volume overload
Chamber dilation
Elevated intracardiac pressure

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3
Q

Left sided (Left = Lung) HF Symptoms

Systolic VS Diastolic

A

Pulmonary edema
Coughing
Shortness of breath
Dyspnea

Systolic: decreased contractility, decreased blood ejected

Diastolic: elevated filling pressures, muscle unable to relax

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4
Q

Right sided Symptoms

A

Systemic venous congestion
Pedal edema
Jugular venous distension
Ascites
Hepatic congestion

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5
Q

Three Consequences of HF

A

Blood supply to organs is reduced (kidney before heart and brains)

Impaired kidney filtration can lead to acute kidney injury or chronic kidney failure

Pulmonary edema can lead to shortness of breath and peripheral edema

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6
Q

Heart Failure: Causes

A

Myocardial deficiency
-Inadequate contractility
-Inadequate filling

Increased workload
-Pressure overload
-Volume overload

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7
Q

Inadequate contractility

A

Myocardial infarction
Coronary artery disease
Cardiomyopathy (harder for heart to pump blood)
Valvular insufficiency (heart valves fails to close; blood flows in the opposite direction)

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8
Q

Inadequate filling

A

Atrial fibrillation
Infection
Tamponade
Ischemia

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9
Q

Pressure overload

A

Pulmonary hypertension
Systemic hypertension
Outflow obstruction

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10
Q

Volume overload

A

Hypervolemia
Congenital abnormalities
Anemia
Thyroid disease
Infection
Diabetes

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11
Q

The New York Association’s Classification of Heart Failure

A

Class I
No physical activity limitations
Class II
Ordinary physical activity results in fatigue, dyspnea, or other symptoms.
Class III
Marked limitation in physical activity
Class IV
Symptoms at rest or with no physical activity at all

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12
Q

Class I

A

No physical activity limitations

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13
Q

Class II

A

Ordinary physical activity results in fatigue, dyspnea, or other symptoms.

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14
Q

Class III

A

Marked limitation in physical activity

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15
Q

Class IV

A

Symptoms at rest or with no physical activity at all

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16
Q

Drug Therapy for Heart Failure

A

Positive inotropic drugs
Positive chronotropic drugs
Positive dromotropic drugs

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17
Q

Positive inotropic drugs:

A

Positive inotropic drugs: increase the force of myocardial contraction

Positive inotropic drugs
-Phosphodiesterase inhibitors
-Cardiac glycosides
-B-type natriuretic peptides

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18
Q

Positive chronotropic drugs:

A

Positive chronotropic drugs: increase heart rate

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19
Q

Positive dromotropic drugs:

A

Positive dromotropic drugs: accelerate cardiac conduction

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20
Q

Other drugs used in heart failure

A

Angiotensin-converting enzyme inhibitors
Angiotensin receptor blockers
ß-Blockers
Diuretics (furosemide and spironolactone)

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21
Q

Drugs of Choice for Early Treatment of Heart Failure

A

Angiotensin-converting enzyme inhibitors (lisinopril, enalapril maleate, captopril, and others)

Angiotensin II receptor blockers (valsartan and others)

Certain ß-blockers (bisoprolol, extended-release metoprolol tartrate, and carvedilol)

Loop diuretics (furosemide) are used to reduce the symptoms of heart failure secondary to fluid overload.

Aldosterone inhibitors (spironolactone, eplerenone) are added as the heart failure progresses.

Only after these drugs are used is digoxin added.

dobutamine: positive inotropic drug

hydralazine/isosorbide dinitrate recommended specifically for use in Black patients

22
Q

dobutamine

A

positive inotropic drug; increase froce of contraction

adrenergic; sympathomimetic

23
Q

Angiotensin-Converting Enzyme Inhibitors

A

Prevent sodium and water resorption by inhibiting aldosterone secretion

Diuresis results, which decreases preload, or the left ventricular end volume, and the work of the heart

Examples: lisinopril, enalapril maleate, fosinopril sodium, quinapril hydrochloride, captopril, ramipril, trandolapril, and perindopril erbumine.

24
Q

lisinopril (Prinivil®, Zestril®)

Uses
AEs

A

Uses: hypertension, heart failure, and acute myocardial infarction

Hyperkalemia (due to aldosterone inhibition; increased NA+ excretion; more K+ retained)

Dry cough

Decreased renal function

25
Q

Angiotensin II Receptor Blockers function

A

Potent vasodilators; decrease systemic vascular resistance (afterload)

Used alone or in combination with other drugs such as diuretics in the treatment of hypertension or heart failure

Examples: valsartan (Diovan®), candesartan cilexetil, eprosartan mesylate, irbesartan, telmisartan, olmesartan medoximil, and losartan potassium

26
Q

valsartan (Diovan®)

similarities and difference with ACE inhibitors

A

Valsartan shares many of the same adverse effects as lisinopril.

Angiotensin II receptor blockers are not as likely to cause the cough associated with the angiotensin-converting enzyme inhibitors.

Angiotensin II receptor blockers are not as likely to cause hyperkalemia.

27
Q

β-Blockers

A

Cardioprotective quality of ß-blockers: prevent catecholamine-mediated actions on the heart by reducing or blocking sympathetic nervous system stimulation to the heart and the heart’s conduction system

NE normally stimulate SNS

metoprolol
carvedilol

28
Q

Aldosterone Antagonists

A

spironolactone and eplerenone

Useful in severe stages of heart failure

Action: activation of the renin-angiotensin-aldosterone system causes increased levels of aldosterone, which causes retention of sodium and water, leading to edema that can worsen heart failure.

29
Q

spironolactone

A

potassium-sparing diuretic and aldosterone antagonist shown to reduce the symptoms of heart failure

eplerenone (Inspra®): selective aldosterone blocker, blocking aldosterone at its receptors in the kidney, heart, blood vessels, and brain

30
Q

ACE cause

ARBs are

ACE and ARBs also effective in slowing ____ & _____

Β Blockers stop

A

ACE cause diuresis which decreases blood volume and blood return to heart (preload)
* ACE inhibitors decrease BV and preload (workload)

ARBs are potent vasodilators, decrease systemic vascular resistance (afterload)
* Vasodilator; decrease afterload

ACE and ARBs also effective in slowing ventricular remodeling and hypertrophy

Β Blockers stop catecholamine mediated actions on the heart

31
Q

dobutamine hydrochloride drug class

structurally similar to?

A

β1-selective vasoactive adrenergic drug; increae HR, FOC, and renin release

Structurally similar to dopamine

32
Q

hydralazine/isosorbide dinitrate

A

Drug approved specifically for individuals who are Black.

33
Q

Phosphodiesterase Inhibitors action and 1 drug

A

One drug in this category available in Canada: milrinone.

Work by inhibiting the enzyme phosphodiesterase

Result in:
-Intracellular increase in cyclic adenosine monophosphate
-Positive inotropic response (increased contractility)
-Vasodilation
-Increase in calcium for myocardial muscle contraction.

Inodilators (inotropics and dilators)

34
Q

Phosphodiesterase Inhibitors:Indication

A

Short-term management of heart failure for patients in the Critical Care Unit.

The 2012 Canadian Cardiovascular Society Heart Failure Management Guidelines advise against long-term infusions of milrinone.

35
Q

Milrinone

AEs

Interactions

What must not be given IV with this?

A

Only available phosphodiesterase inhibitor
Available only in injectable form
Adverse effects: cardiac dysrhythmias, hypotension, angina, hypokalemia, tremor, and thrombocytopenia
Interactions: diuretics (additive hypotensive effects) and digoxin (additive inotropic effects)
Furosemide must not be injected into intravenous lines with milrinone.

36
Q

Cardiac Glycosides is used in?

A

No longer used as first-line treatment

Digoxin is the prototype.

Used in heart failure and to control ventricular response to atrial fibrillation

37
Q

Cardiac Glycosides:Mechanism of Action

A

Increase myocardial contractility

Change electrical conduction properties of the heart

-Decrease rate of electrical conduction
-Prolong the refractory period
* Area between sinoatrial node and atrioventricular node

38
Q

Cardiac Glycosides

Positive inotropic effect

A

Increased force and velocity of myocardial contraction (without an increase in oxygen consumption)

39
Q

Cardiac Glycosides

Negative chronotropic effect

A

Reduced heart rate

40
Q

Cardiac Glycosides

Negative dromotropic effect

A

Decreased automaticity at sinoatrial node

Decreased atrioventricular node conduction

41
Q

Cardiac Glycosides:Drug Effects

A

Increased stroke volume (amount of blood pumped by ventricles)

Reduction in heart size during diastole

Decrease in venous blood pressure and vein engorgement

Increase in coronary circulation

Decrease in exertional and paroxysmal nocturnal dyspnea, cough, and cyanosis

Promotion of tissue perfusion and diuresis

Improved symptom control, quality of life, and exercise tolerance, with no apparent reduction in mortality

42
Q

digoxin (Lanoxin®)

Drug levels?
What increases its toxicity?
What must be monitored?

A

Very narrow therapeutic window
Drug levels must be monitored.
0.8 to 2 ng/mL
Low potassium levels increase its toxicity.
Electrolyte levels must be monitored.

43
Q

digoxin (Lanoxin) AE

A

Cardiovascular: dysrhythmias, including bradycardia or tachycardia

Central nervous system: headaches, fatigue, malaise, confusion, convulsions

Eyes: coloured vision (seeing green, yellow, purple), halo vision

Gastrointestinal: anorexia, nausea, vomiting, diarrhea

MOST ADVERSE EFFECTS SIGNS AND SYMPTOMS OF TOXICITY

44
Q

Digoxin Toxicity

treatment

A

digoxin immune Fab therapy
-Hyperkalemia (serum potassium greater than 5 mmol/L) in a digitalis-toxic patient
-Life-threatening cardiac dysrhythmias
-Life-threatening digoxin overdose

45
Q

Digoxin

Large amounts of ____ negatively affect absorption of oral digoxin

NHP that increase digoxin levels:

Serum digoxin, _____ levels important

Apical pulse between _____bpm

A

Large amounts of bran negatively affect absorption of oral digoxin
NHP that increase digoxin levels: ginseng, hawthorn, licorice; St John’s Wort may reduce digoxin level
Serum digoxin, potassium levels important
Apical pulse between 60-100 bpm

46
Q

Conditions That Predispose to Digoxin Toxicity

A

Hypokalemia
Use of cardiac pacemaker
Atrioventricular block
Hypercalcemia
Dysrhythmias
Hypothyroid, respiratory, or renal disease
Advanced age
Ventricular fibrillation

47
Q

Heart Failure Drugs:Nursing Implications

A

Assess history, drug allergies, and contraindications.

Assess clinical parameters, including
-blood pressure
-Both radial and apical pulse for 1 full minute
-Heart sounds, breath sounds

Assess clinical parameters
-Weight, input, and output measures
-Electrocardiogram
-Serum labs: potassium, sodium, magnesium, calcium, renal, and liver function studies

Before giving any dose, count apical pulse for 1 full minute.

For an apical pulse less than 60 or greater than 100 beats/min
-Hold dose.
-Notify prescriber.

48
Q

Hold dose and notify prescriber if the patient experiences signs or symptoms of toxicity.

A

Anorexia, nausea, vomiting, diarrhea
Visual disturbances (blurred vision, seeing green or yellow halos around objects)

49
Q

Heart Failure Drugs: Nursing Implications

A

Check dosage forms carefully and follow instructions for administering.

Avoid giving digoxin with high-fibre foods (fibre binds with digitalis).

Patients should immediately report a weight gain of 1 kg or more in 24 hours or 2 kg or more in 1 week.

50
Q

milrinone NC

A

Use an infusion pump.

Monitor input and output, heart rate and rhythm, blood pressure, daily weights, respirations, and so on

51
Q

Monitor for therapeutic effects.

A

Monitor for therapeutic effects.
Increased urinary output
Decreased edema, shortness of breath, dyspnea, crackles, fatigue
Resolution of paroxysmal nocturnal dyspnea
Improved peripheral pulses, skin colour, temperature
Monitor for adverse effects.

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