Heart failure Flashcards
Heart Failure: What is it?
“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.
Four Causes of HF
Failure of ventricle to eject blood
Fluid volume overload
Chamber dilation
Elevated intracardiac pressure
Left sided (Left = Lung) HF Symptoms
Systolic VS Diastolic
Pulmonary edema
Coughing
Shortness of breath
Dyspnea
Systolic: decreased contractility, decreased blood ejected
Diastolic: elevated filling pressures, muscle unable to relax
Right sided Symptoms
Systemic venous congestion
Pedal edema
Jugular venous distension
Ascites
Hepatic congestion
Three Consequences of HF
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
Heart Failure: Causes
Myocardial deficiency
-Inadequate contractility
-Inadequate filling
Increased workload
-Pressure overload
-Volume overload
Inadequate contractility
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)
Inadequate filling
Atrial fibrillation
Infection
Tamponade
Ischemia
Pressure overload
Pulmonary hypertension
Systemic hypertension
Outflow obstruction
Volume overload
Hypervolemia
Congenital abnormalities
Anemia
Thyroid disease
Infection
Diabetes
The New York Association’s Classification of Heart Failure
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
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
Drug Therapy for Heart Failure
Positive inotropic drugs
Positive chronotropic drugs
Positive dromotropic drugs
Positive inotropic drugs:
Positive inotropic drugs: increase the force of myocardial contraction
Positive inotropic drugs
-Phosphodiesterase inhibitors
-Cardiac glycosides
-B-type natriuretic peptides
Positive chronotropic drugs:
Positive chronotropic drugs: increase heart rate
Positive dromotropic drugs:
Positive dromotropic drugs: accelerate cardiac conduction
Other drugs used in heart failure
Angiotensin-converting enzyme inhibitors
Angiotensin receptor blockers
ß-Blockers
Diuretics (furosemide and spironolactone)
Drugs of Choice for Early Treatment of Heart Failure
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
dobutamine
positive inotropic drug; increase froce of contraction
adrenergic; sympathomimetic
Angiotensin-Converting Enzyme Inhibitors
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.
lisinopril (Prinivil®, Zestril®)
Uses
AEs
Uses: hypertension, heart failure, and acute myocardial infarction
Hyperkalemia (due to aldosterone inhibition; increased NA+ excretion; more K+ retained)
Dry cough
Decreased renal function
Angiotensin II Receptor Blockers function
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
valsartan (Diovan®)
similarities and difference with ACE inhibitors
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.
β-Blockers
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
Aldosterone Antagonists
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.
spironolactone
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
ACE cause
ARBs are
ACE and ARBs also effective in slowing ____ & _____
Β Blockers stop
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
dobutamine hydrochloride drug class
structurally similar to?
β1-selective vasoactive adrenergic drug; increae HR, FOC, and renin release
Structurally similar to dopamine
hydralazine/isosorbide dinitrate
Drug approved specifically for individuals who are Black.
Phosphodiesterase Inhibitors action and 1 drug
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)
Phosphodiesterase Inhibitors:Indication
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.
Milrinone
AEs
Interactions
What must not be given IV with this?
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.
Cardiac Glycosides is used in?
No longer used as first-line treatment
Digoxin is the prototype.
Used in heart failure and to control ventricular response to atrial fibrillation
Cardiac Glycosides:Mechanism of Action
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
Cardiac Glycosides
Positive inotropic effect
Increased force and velocity of myocardial contraction (without an increase in oxygen consumption)
Cardiac Glycosides
Negative chronotropic effect
Reduced heart rate
Cardiac Glycosides
Negative dromotropic effect
Decreased automaticity at sinoatrial node
Decreased atrioventricular node conduction
Cardiac Glycosides:Drug Effects
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
digoxin (Lanoxin®)
Drug levels?
What increases its toxicity?
What must be monitored?
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.
digoxin (Lanoxin) AE
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
Digoxin Toxicity
treatment
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
Digoxin
Large amounts of ____ negatively affect absorption of oral digoxin
NHP that increase digoxin levels:
Serum digoxin, _____ levels important
Apical pulse between _____bpm
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
Conditions That Predispose to Digoxin Toxicity
Hypokalemia
Use of cardiac pacemaker
Atrioventricular block
Hypercalcemia
Dysrhythmias
Hypothyroid, respiratory, or renal disease
Advanced age
Ventricular fibrillation
Heart Failure Drugs:Nursing Implications
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.
Hold dose and notify prescriber if the patient experiences signs or symptoms of toxicity.
Anorexia, nausea, vomiting, diarrhea
Visual disturbances (blurred vision, seeing green or yellow halos around objects)
Heart Failure Drugs: Nursing Implications
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.
milrinone NC
Use an infusion pump.
Monitor input and output, heart rate and rhythm, blood pressure, daily weights, respirations, and so on
Monitor for therapeutic effects.
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.
