acute heart failure
TRANSCRIPT
MEDICINEPROJECT
BARAD AJAYRAJ BATCH
CONTENTS1. INTRODUCTION2. CLASSIFICATION3. CAUSES AND PRECIPITATING FACTORS4. PATHOPHYSIOLOGY5. SYMPTOMS6. SIGNS7. DIAGNOSIS8. TREATMENT
INTRODUCTION Heart failure is a global term for the physiological state in which cardiac output is
insufficient for the body’s needs. This occurs when
1. Cardiac output 2. Body’s O2 & nutrition requirement ,
Termed high output cardiac failure. Fluid overload is a common problem. Acute HF: rapid onset
Chronic HF: of longer duration
CLASSIFICATIONThere are different ways to classify the heart failure
1. According to side of heartRt. vs Lt. heart failure
2. According to abnormality in the contraction or relaxationSystolic vs. diastolic dysfunction
3. ed venous back pressure: backward failureFailure to supply adequate arterial perfusion: forward failure
4. c.o. & systemic vascular resistance: low output failure c.o. & systemic vascular resistance: high output failure
5. NYHA(NEW YORK HEART ASSOSSIATION) functional classification Class I: no limitation is experienced in any activities; there are no
symptoms from ordinary activities. Class II: slight, mild limitation of activity; the patient is comfortable at
rest or with mild exertion. Class III: marked limitation of any activity; the patient is comfortable
only at rest. Class IV: any physical activity brings on discomfort and symptoms occur
at rest.6. AMERICAN COLLEGE OF CARDIOLOGY/AMERICAN HEART ASSOCIATION
classification Stage A: Patients at high risk for developing HF in the future but no
functional or structural heart disorder; Stage B: a structural heart disorder but no symptoms at any stage; Stage C: previous or current symptoms of heart failure in the context of
an underlying structural heart problem, but managed with medical treatment;
Stage D: advanced disease requiring hospital-based support, a heart transplant or palliative care.
The ACC staging system is useful in that Stage A encompasses "pre-heart failure" - a stage where intervention with treatment can presumably prevent progression to overt symptoms. ACC stage A does not have a corresponding NYHA class. ACC Stage B would correspond to NYHA Class I. ACC Stage C corresponds to NYHA Class II and III, while ACC Stage D overlaps with NYHA Class IV.
ACUTE DECOMPENSATED HEART FAILURE
CAUSES AND PRECIPITATINNG FACTORS:
1. Decompensation of pre-existing chronic heart failure (e.g. cardiomyopathy)
2. Acute coronary syndromes
a. myocardial infarction/unstable angina with large extent of ischaemia and ischaemic dysfunction
b. mechanical complication of acute myocardial infarction
c. right ventricular infarction
3. Hypertensive crisis
4. Acute arrhythmia (ventricular tachycardia, ventricular fibrillation, atrial fibrillation or flutter, other supraventricular tachycardia)
5. Valvular regurgitation (endocarditis, rupture of chordae tendinae, worsening of pre-existing valvular regurgitation)
6. Severe aortic valve stenosis
7. Acute severe myocarditis
8. Cardiac tamponade
9. Aortic dissection
10. Post-partum cardiomyopathy
11. Non-cardiovascular precipitating factors
a. lack of compliance with medical treatment
b. volume overload
c. infections, particularly pneumonia or septicaemia
d. severe brain insult
e. after major surgery
f. reduction in renal function
g. asthma
h. drug abuse
i. alcohol abuse
j. phaeochromocytoma
12. High output syndromes
a. septicaemia
b. thyrotoxicosis crisis
c. anaemia
d. shunt syndromes
PATHOPHYSIOLOGY:
Heart failure is caused by any condition which reduces the efficiency of the myocardium, or heart muscle, through damage or overloading. As such, it can be caused by as diverse an array of conditions as myocardial infarction (in which the heart muscle is starved of oxygen and dies), hypertension (which increases the force of contraction needed to pump blood) and amyloidosis (in which protein is deposited in the heart muscle, causing it to stiffen). Over time these increases in workload will produce changes to the heart itself:
Reduced contractility, or force of contraction, due to overloading of the ventricle. In health, increased filling of the ventricle results in increased contractility (by the Frank-Starling law of the heart) and thus a rise in cardiac output. In heart failure this mechanism fails, as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient. This is due to reduced ability to cross-link actin and myosin filaments in over-stretched heart muscle.[23]
A reduced stroke volume, as a result of a failure of systole, diastole or both. Increased end systolic volume is usually caused by reduced contractility. Decreased end diastolic volume results from impaired ventricular filling – as occurs when the compliance of the ventricle falls (i.e. when the walls stiffen).
Reduced spare capacity. As the heart works harder to meet normal metabolic demands, the amount cardiac output can increase in times of increased oxygen demand (e.g. exercise) is reduced. This contributes to the exercise intolerance commonly seen in heart failure. This translates to the loss of one's cardiac reserve. The cardiac reserve refers to the ability of the heart to work harder during exercise or strenuous activity. Since the heart has to work harder to meet the normal metabolic demands, it is incapable of meeting the metabolic demands of the body during exercise.
Increased heart rate, stimulated by increased sympathetic activity in order to maintain cardiac output. Initially, this helps compensate for heart failure by maintaining blood pressure and perfusion, but places further strain on the myocardium, increasing coronary perfusion requirements, which can lead to worsening of ischemic heart disease. Sympathetic activity may also cause potentially fatal arrhythmias.
Hypertrophy (an increase in physical size) of the myocardium, caused by the terminally differentiated heart muscle fibres increasing in size in an attempt to improve contractility. This may contribute to the increased stiffness and decreased ability to relax during diastole.
Enlargement of the ventricles, contributing to the enlargement and spherical shape of the failing heart. The increase in ventricular volume also causes a reduction in stroke volume due to mechanical and contractile inefficiency.[24]
The general effect is one of reduced cardiac output and increased strain on the heart. This increases the risk of cardiac arrest (specifically due to ventricular dysrhythmias), and reduces blood supply to the rest of the body. In chronic disease the reduced cardiac output causes a number of changes in the rest of the body, some of which are physiological compensations, some of which are part of the disease process:
Arterial blood pressure falls. This destimulates baroreceptors in the carotid sinus and aortic arch which link to the nucleus tractus solitarius. This center in the brain increases sympathetic activity, releasing catecholamines into the blood stream. Binding to alpha-1 receptors results in systemic arterial vasoconstriction. This helps restore blood pressure but also increases the total peripheral resistance, increasing the workload of the heart. Binding to beta-1 receptors in the myocardium increases the heart rate and make contractions more forceful, in an attempt to increase cardiac output. This also, however, increases the amount of work the heart has to perform.
Increased sympathetic stimulation also causes the hypothalamus to secrete vasopressin (also known as antidiuretic hormone or ADH), which causes fluid retention at the kidneys. This increases the blood volume and blood pressure.
Reduced perfusion (blood flow) to the kidneys stimulates the release of renin – an enzyme which catalyses the production of the potent vasopressor angiotensin. Angiotensin and its metabolites cause further vasocontriction, and stimulate increased secretion of the steroid aldosterone from the adrenal glands. This promotes salt and fluid retention at the kidneys, also increasing the blood volume.
The chronically high levels of circulating neuroendocrine hormones such as catecholamines, renin, angiotensin, and aldosterone affects the myocardium directly, causing structural remodelling of the heart over the long term. Many of these remodelling effects seem to be mediated by transforming growth factor beta (TGF-beta), which is a common downstream target of the signal transduction cascade initiated by catecholamines[25] and angiotensin II[26], and also by epidermal growth factor (EGF), which is a target of the signaling pathway activated by aldosterone[27]
Reduced perfusion of skeletal muscle causes atrophy of the muscle fibres. This can result in weakness, increased fatigueability and decreased peak strength - all contributing to exercise intolerance.[28]
The increased peripheral resistance and greater blood volume place further strain on the heart and accelerates the process of damage to the myocardium. Vasoconstriction and fluid retention produce an increased hydrostatic pressure in the capillaries. This shifts of the balance of forces in favour of interstitial fluid formation as the increased pressure forces additional fluid out of the blood, into the tissue. This results in edema (fluid build-up) in the tissues. In right-sided heart failure this commonly starts in the ankles where venous pressure is high due to the effects of gravity (although if the patient is bed-ridden, fluid accumulation may begin in the sacral region.) It may also occur in the abdominal cavity, where the fluid build-up is called ascites. In left-sided heart failure edema can occur in the lungs - this is called cardiogenic pulmonary oedema. This reduces spare capacity for ventilation, causes stiffening of the lungs and reduces the efficiency of gas exchange by increasing the distance between the air and the blood. The consequences of this are shortness of breath, orthopnoea and paroxysmal nocturnal dyspnea.
The symptoms of heart failure are largely determined by which side of the heart fails. The left side pumps blood into the systemic circulation, whilst the right side pumps blood into the pulmonary circulation. Whilst left-sided heart failure will reduce cardiac output to the systemic circulation, the initial symptoms often manifest due to effects on the pulmonary circulation. In systolic dysfunction, the
ejection fraction is decreased, leaving an abnormally elevated volume of blood in the left ventricle. In diastolic dysfunction, end-diastolic ventricular pressure will be high. This increase in volume or pressure backs up to the left atrium and then to the pulmonary veins. Increased volume or pressure in the pulmonary veins impairs the normal drainage of the alveoli and favors the flow of fluid from the capillaries to the lung parenchyma, causing pulmonary edema. This impairs gas exchange. Thus, left-sided heart failure often presents with respiratory symptoms: shortness of breath, orthopnea and paroxysmal nocturnal dyspnea.
In severe cardiomyopathy, the effects of decreased cardiac output and poor perfusion become more apparent, and patients will manifest with cold and clammy extremities, cyanosis, claudication, generalized weakness, dizziness, and syncope
The resultant hypoxia caused by pulmonary edema causes vasoconstriction in the pulmonary circulation, which results in pulmonary hypertension. Since the right ventricle generates far lower pressures than the left ventricle (approximately 20 mmHg versus around 120 mmHg, respectively, in the healthy individual) but nonetheless generates cardiac output exactly equal to the left ventricle, this means that a small increase in pulmonary vascular resistance causes a large increase in amount of work the right ventricle must perform. However, the main mechanism by which left-sided heart failure causes right-sided heart failure is actually not well understood. Some theories invoke mechanisms that are mediated by neurohormonal activation. Mechanical effects may also contribute. As the left ventricle distends, the intraventricular septum bows into the right ventricle, decreasing the capacity of the right ventricle.
Systolic dysfunction
Heart failure caused by systolic dysfunction is more readily recognized. It can be simplistically described as failure of the pump function of the heart. It is characterized by a decreased ejection fraction (less than 45%). The strength of ventricular contraction is attenuated and inadequate for creating an adequate stroke volume, resulting in inadequate cardiac output. In general, this is caused by dysfunction or destruction of cardiac myocytes or their molecular components. In congenital diseases such as Duchenne muscular dystrophy, the molecular structure of individual myocytes is affected. Myocytes and their components can be damaged by inflammation (such as in myocarditis) or by infiltration (such as in amyloidosis). Toxins and pharmacological agents (such as ethanol, cocaine, and amphetamines) cause intracellular damage and oxidative stress. The most common mechanism of damage is ischemia causing infarction and scar formation. After myocardial infarction, dead myocytes are replaced by scar tissue, deleteriously affecting the function of the myocardium. On echocardiogram, this is manifest by abnormal or absent wall motion.
Because the ventricle is inadequately emptied, ventricular end-diastolic pressure and volumes increase. This is transmitted to the atrium. On the left side of the heart, the increased pressure is transmitted to the pulmonary vasculature, and the resultant hydrostatic pressure favors extravassation of fluid into the lung parenchyma, causing pulmonary edema. On the right side of the heart, the increased pressure is transmitted to the systemic venous circulation and systemic capillary beds, favoring extravassation of fluid into the tissues of target organs and extremities, resulting in dependent peripheral edema.
Diastolic dysfunction
Heart failure caused by diastolic dysfunction is generally described as the failure of the ventricle to adequately relax and typically denotes a stiffer ventricular wall. This causes inadequate filling of the ventricle, and therefore results in an inadequate stroke volume. The failure of ventricular relaxation also results in elevated end-diastolic pressures, and the end result is identical to the case of systolic dysfunction (pulmonary edema in left heart failure, peripheral edema in right heart failure.)
Diastolic dysfunction can be caused by processes similar to those that cause systolic dysfunction, particularly causes that affect cardiac remodeling.
Diastolic dysfunction may not manifest itself except in physiologic extremes if systolic function is preserved. The patient may be completely asymptomatic at rest. However, they are exquisitely sensitive to increases in heart rate, and sudden bouts of tachycardia (which can be caused simply by physiological responses to exertion, fever, or dehydration, or by pathological tachyarrhythmias such as atrial fibrillation with rapid ventricular response) may result in flash pulmonary edema. Adequate rate control (usually with a pharmacological agent that slows down AV conduction such as a calcium channel blocker or a beta-blocker) is therefore key to preventing decompensation.
Left ventricular diastolic function can be determined through echocardiography by measurement of various parameters such as the E/A ratio (early-to-atrial left ventricular filling ratio), the E (early left ventricular filling) deceleration time, and the isovolumic relaxation time.
SYMPTOMS Left sided failure
Figure 2 Pathophysiology of the syndrome of acute heart failure.
Nieminen M S et al. Eur Heart J 2005;26:384-416
© The European Society of Cardiology 2005. All rights reserved. For Permissions, please e-mail: [email protected]
Backward failure1. Dyspnea on exertion2. Dyspnea at rest (severe)3. Orthopnea4. Paroxysmal nocturnal dyspnea(cardiac asthma)5. Easy fatigueability6. Exercise intolerance
Forward failure1. Dizziness2. Confusion3. Syncope4. Cool extremities at rest
Right sided failure1. Peripheral edema(may be anasarca)
a. Foot and ankle edema (pedal edema):in standing positionb. Sacral edema: in lying down positon
2. Nocturia 3. Ascitis4. Hepatomegaly5. Jaundice6. Coagulopathy
SIGN: Left sided failure
1. Tachypnea2. Rales or crackles3. Cyanosis4. Laterally displaced apex beat5. Gallop rhythm6. Murmur(vhd: AS or MI)
Right sided failure1. Pitting peripheral edema2. Ascitis3. Hepatomegaly4. JVP es (hepatojugular reflux)5. Parasternal heave
BIVENTRICULAR FAILURE:1. Pulmonary edema2. Dullness of note on percussion
DIAGNOSIS:
Diagnosis of AHF.
Nieminen M S et al. Eur Heart J 2005;26:384-416
© The European Society of Cardiology 2005. All rights reserved. For Permissions, please e-mail: [email protected]
Laboratory tests in patients hospitalized with AHF
Blood count AlwaysPlatelet count AlwaysINR If patient anticoagulated or in severe heart failureCRP Always
D-dimerAlways (may be falsely positive if CRP elevated or patient has been hospitalized for prolonged period)
Urea and Electrolytes (Na+, K+, Urea, Creatinine) AlwaysBlood glucose AlwaysCKMB, cardiac TnI/TnT AlwaysArterial blood gases In severe heart failure, or in diabetic patientsTransaminases To be consideredUrinanalysis To be consideredPlasma BNP or NTproBNP To be consideredOther specific laboratory tests should be taken for differential diagnostic purposes or in order to identify end-organ dysfunction.
INR=international normalized ratio of thromboplastin time; TnI=troponin I; TnT=troponin T.
Terminology and common clinical and haemodynamic characteristics
Clinical status Heart rate
SBP mmHg
CI L/min/m2
PCWP mmHg
Congestion Killip/Forrester
Diuresis
Hypoperfusion
End organ hypoperfusion
Acute I decompensated congestive heart failure +/−
Low normal/High
Low normal/High
Mild elevation K II/F II + +/− −
Acute II heart failure with hypertension/hypertensive crisis
Usually increased High +/− >18 K II-IV/FII-III +/− +/−
+, with CNS symptoms
Acute III heart failure with pulmonary oedema +
Low normal Low
Elevated KIII/FII + +/− −
Cardiogenic shock*/low output syndrome IVa +
Low normal Low, <2.2 >16 K III-IV/F I-III low + +
Severe IVb cardiogenic shock >90 <90 <1.8 >18 K IV/F IV
Very low ++ +
High output V failure + +/− + +/− KII/FI-II + − −
Clinical status Heart rate
SBP mmHg
CI L/min/m2
PCWP mmHg
Congestion Killip/Forrester
Diuresis
Hypoperfusion
End organ hypoperfusion
Right VI sided acute heart failure
Usually low Low Low Low F I +/−
+/−, acute onset +/−
There are exceptions; the above values in table II are general rules.
*The differentation from low cardiac output syndrome is subjective and the clinical presentation may overlap these classifications.
SBP=systolic blood pressure; CI=cardiac index; PCWP=pulmonary capillary wedge pressure
Goals of treatment of the patient with AHF
Clinical↓ symptoms (dyspnoea and/or fatigue)↓ clinical signs↓ body weight↑ diuresis↑ oxygenationLaboratorySerum electrolyte normalization↓ BUN and/or creatinine↓ S-bilirubin↓ plasma BNPBlood glucose normalizationHaemodynamic↓ pulmonary capillary wedge pressure to <18 mmHg↑ cardiac output and/or stroke volumeOutcome↓ length of stay in the intensive care unit↓ duration of hospitalization↑ time to hospital re-admission↓ mortalityTolerabilityLow rate of withdrawal from therapeutic measuresLow incidence of adverse effectsBUN=blood urea nitrogen.
Immediate goals in treatment of the patients with AHF.
Nieminen M S et al. Eur Heart J 2005;26:384-416
© The European Society of Cardiology 2005. All rights reserved. For Permissions, please e-mail: [email protected]
Medication
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
1. Human B-type natriuretic peptides (hBNPs)
Dilate veins and arteries. Used in the treatment of acute severe CHF.
Nesiritide (Natrecor)
Recombinant DNA form of hBNP, which dilates veins and arteries. hBNP binds to particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells. Binding to receptor causes increase in cGMP, which serves as second messenger to dilate veins and arteries. Reduces PCWP and improves dyspnea in patients with acutely decompensated CHF.
Adult
2 mcg/kg IV bolus over 60 sec; follow by 0.01 mcg/kg/min continuous infusion; bolus volume (mL) = 0.33 X patient weight (kg); infusion flow rate of bolus (mL/h) = 0.1 X patient weight (kg)
Pediatric
Not established
Assessment of LV function in AHF.
Nieminen M S et al. Eur Heart J 2005;26:384-416
© The European Society of Cardiology 2005. All rights reserved. For Permissions, please e-mail: [email protected]
Diuretics
May improve symptoms of venous congestion through elimination of retained fluid and preload reduction. Used in CHF. Help counteract the sodium and water retention caused by activation of the RAAS.
Torsemide (Demadex)
Acts from within the lumen of the thick ascending portion of the loop of Henle, where inhibits the Na/K/2Cl carrier system. Increases urinary excretion of sodium, chloride, and water, but does not significantly alter glomerular filtration rate, renal plasma flow, or acid-base balance.
Adult
10-20 mg PO/IV qd; not to exceed 200 mg/d; titrate dose upward by approximately doubling the dose until desired diuretic effect reached; doses >200 mg/d not adequately studied
Pediatric
Not established
Furosemide (Lasix)
Increase excretion of water by interfering with chloride-binding cotransport system, which in turn inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Bumetanide does not appear to act in the distal renal tubule. Dose must be individualized to patient. Depending on response, administer at small dose increments until desired diuresis occurs.
Adult
20-80 mg/d PO/IV/IM; titrate up to 600 mg/d for severe edematous states; depending on response, administer at increments of 20-40 mg no sooner than 6-8 h after previous dose
Pediatric
1-2 mg/kg/dose PO; not to exceed 6 mg/kg/dose; not to administer more frequently than q6h
Spironolactone (Aldactone)
For management of edema resulting from excessive aldosterone excretion. Competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions.
Adult
25-200 mg/d PO qd or divided bid
Pediatric
1.5-3.5 mg/kg/d PO qd or divided qid
Bumetanide (Bumex)
Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium, potassium, and chloride reabsorption in ascending loop of Henle. These effects
increase urinary excretion of sodium, chloride, and water, resulting in profound diuresis. Renal vasodilation occurs following administration, renal vascular resistance decreases, and renal blood flow is enhanced.
Individualize dose to patient. Start at 1-2 mg IV; titrate to as high as 10 mg/d. Rarely, doses as high as 24 mg/d are used for edema but generally are not required for treatment of hyperkalemia.
One mg of bumetanide is equivalent to approximately 40 mg of furosemide.
Adult
0.5-2 mg/dose PO 1-2 times/d; titrate dose upward until desired diuretic effect is reached; not to exceed 10 mg/d; alternatively, 0.5-1 mg/dose IV/IM; not to exceed 10 mg/d
Pediatric
Not established
Angiotensin receptor blockers
Interfere with the binding of formed Ang II to its endogenous receptor. Used primarily when patients are intolerant of ACE inhibitors because of adverse effects but are gaining wider use as first-line vasodilator agents. Equally effective as ACE inhibitors.
Valsartan (Diovan)
Prodrug that produces direct antagonism of angiotensin II receptors. Displaces angiotensin II from AT1 receptor and may lower blood pressure by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. For use in patients unable to tolerate ACE inhibitors.
Adult
80 mg/d PO; may increase to 160 mg/d if needed
Pediatric
Not established
Losartan (Cozaar)
Block the vasoconstrictor and aldosterone-secreting effects of Ang II. May induce more complete inhibition of RAAS than ACE inhibitors, do not affect response to BK, and are less likely to be associated with cough and angioedema. For patients unable to tolerate ACE inhibitors.
Adult
25-100 mg PO qd/bid
Pediatric
Not established
Candesartan (Atacand)
Blocks vasoconstriction and aldosterone-secreting effects of angiotensin II. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. Use in patients unable to tolerate ACE inhibitors.
Angiotensin II receptor blockers reduce blood pressure and proteinuria, protecting renal function, and delaying onset of end-stage renal disease.
Adult
8-16 mg/d PO initially; not to exceed 32 mg/d
Pediatric
Not established
Vasodilators
The use of a vasodilators reduces SVR, thus allowing more forward flow and improving cardiac output. Indicated for CHF.
Indications and dosing of vasodilators in AHF
Vasodilator Indication Dosing Main side effects
Other
Glyceryl trinitrate, 5-mononitrate
Acute heart failure, when blood pressure is adequate
Start 20 µg/min, increase to 200 µg/min
Hypotension, headache
Tolerance on continuous use
Isosorbide dinitrate
Acute heart failure, when blood pressure is adequate
Start with 1 mg/h, increase to 10 mg/h
Hypotension, headache
Tolerance on continuous use
Nitroprusside
Hypertensive crisis, cardiogenic shock combined with intoropes
0.3–5µg/kg/min
Hypotension, isocyanate toxicity
Drug is light sensitive
Nesiritidea
Acute decompensated heart failure
Bolus 2 µg/kg + infusion 0.015–0.03 µg/kg/min Hypotension
aLimited sales approval in ESC countries.
Nitroglycerin (Nitrostat, Deponit, Transderm-Nitro Patch)
Isosorbide dinitrate (Isordil), Isosorbide mononitrate (Imdur)--First-line therapy for patients who are not hypotensive. Provides excellent and reliable preload reduction. Higher doses provide mild afterload reduction. Has rapid onset and offset (both within minutes), allowing rapid clinical effects and rapid discontinuation of effects in adverse clinical situations.
Adult
NitroglycerinTopical: Apply topically 1/2-2" q6hTransdermal: 0.3-0.6 mg/h qdIntravenous: 0.2-10 mcg/kg/min IV infusion; titrate by 10 mcg/min increments until desired hemodynamic effect achieved or until maximally tolerated dose reachedSpray: Single spray (0.4 mg), which is equivalent to single 1/150 sublingual; dose may be repeated q3-5min as hemodynamics permit, up to maximum of 1.2 mgIsosorbide dinitrate: 10-80 mg PO bid/qidIsosorbide mononitrate: 30-90 PO mg qd
Pediatric
Not established
Hydralazine (Apresoline)
Decreases systemic resistance through direct vasodilation of arterioles.
Adult
10-25 mg PO tid/qid initially; adjust dose based on individual response; typical dose range is 200-600 mg PO qd in 2-4 divided doses
Pediatric
Not established
Isosorbide dinitrate and hydralazine (BiDil)
Fixed-dose combination of isosorbide dinitrate (20 mg/tab), a vasodilator with effects on both arteries and veins, and hydralazine (37.5 mg/tab), a predominantly arterial vasodilator. Indicated for heart failure in black patients, based in part on results from the African American Heart Failure Trial. Two previous trials in the general population of patients with severe heart failure found no benefit but suggested a benefit in black patients. Compared with placebo, black patients showed a 43% reduction in mortality rate, a 39% decrease in hospitalization rate, and a decrease in symptoms from heart failure.
Adult
1 tab PO tid; may titrate upward, not to exceed 2 tab tid
Pediatric
Not established
Nitroprusside (Nitropress)
Produces vasodilation and increases inotropic activity of the heart. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate.
Adult
Begin infusion at 0.3-0.5 mcg/kg/min IV and use increments of 0.5 mcg/kg/min; titrate to desired effect; average dose is 1-6 mcg/kg/minInfusion rates >10 mcg/kg/min IV may lead to cyanide toxicity
Pediatric
Administer as in adults
Inotropic agents
Augment both coronary and cerebral blood flow present during the low flow states. Used in severe acute CHF with low cardiac output.
Digoxin (Lanoxin, Lanoxicaps)
Cardiac glycoside with direct inotropic effects in addition to indirect effects on cardiovascular system. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.
Adult
0.125-0.375 mg PO qd
Pediatric
Rationale for inotropic drugs in AHF.
Nieminen M S et al. Eur Heart J 2005;26:384-416
© The European Society of Cardiology 2005. All rights reserved. For Permissions, please e-mail: [email protected]
Not established
Dobutamine (Dobutrex)
Produces vasodilation and increases inotropic state. At higher dosages may cause increased heart rate, exacerbating myocardial ischemia.
Adult
0.5 mcg/kg/min IV initially; titrate until desired therapeutic effect attained
Pediatric
Administer as in adults
Dopamine (Intropin)
Naturally occurring catecholamine that acts as a precursor to norepinephrine. Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dose-dependent. Low-dose use is associated with dilation within renal and splanchnic vasculature, resulting in enhanced diuresis. Moderate doses enhance cardiac contractility and heart rate. Higher doses cause increased afterload through peripheral vasoconstriction.Administer by continuous IV infusion. Usually used in severe heart failure. Reserved for patients with moderate hypotension (eg, systolic blood pressure 70-90 mm Hg). Typically, moderate or higher doses used.
Adult
5 mcg/kg/min IV continuous infusion initially; titrate to blood pressure stabilization; not to exceed 20 mcg/kg/min
Pediatric
Not established
Norepinephrine (Levophed)
Naturally occurring catecholamine with potent alpha-receptor and mild beta-receptor activity. Stimulates beta1- and alpha-adrenergic receptors, resulting in increased cardiac muscle contractility, heart rate, and vasoconstriction. Increases blood pressure and afterload. Increased afterload may result in decreased cardiac output, increased myocardial oxygen demand, and cardiac ischemia. Generally reserved for use in patients with severe hypotension (eg, systolic blood pressure <70 mm Hg) or hypotension unresponsive to other medication.
Adult
0.5-1 mcg/min IV infusion initially, titrated to effect; not to exceed 30 mcg/min
Pediatric
Not established
Phosphodiesterase enzyme inhibitors
Inhibition of type III cAMP phosphodiesterase(s) and other mechanisms. Bipyridine-positive inotropic agents and vasodilators with little chronotropic activity. Different from both digitalis glycosides and catecholamines in mode of action. These agents are balanced vasodilators, having equal reduction in both afterload and preload, to same degree as ACE inhibitors.
Milrinone (Primacor)
Milrinone: Positive inotropic agent and vasodilator. Results in reduced afterload, reduced preload, and increased cardiac output. Several studies comparing milrinone to dobutamine have demonstrated that milrinone showed greater improvements in preload and afterload and improvements in cardiac output, without significant increases in myocardial oxygen consumption.
Adult
50 mcg/kg IV loading dose over 10 min, followed by continuous infusion at 0.25-1.0 mcg/kg/min; titrate to maintain adequate systolic blood pressure and cardiac output
Pediatric
Not established
Inamrinone (Inocor)
Produces vasodilation and increases inotropic state. More likely to cause tachycardia than dobutamine; may exacerbate myocardial ischemia.
Adult
0.75 mg/kg IV bolus slowly over 2-3 min; maintenance infusion is 5.0-10 mcg/kg/min; not to exceed 10 mg/kg; adjust dose according to patient response; not to exceed 10 mg/kg
Pediatric
Administer as in adults
2. Beta-adrenergic blockers
Inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation. Particularly useful in the patient with elevated blood pressure and relative tachycardia. Inhibits sympathetic nervous stimulation, particularly E and norepinephrine and blocks alpha1-adrenergic vasoconstrictor activity. Has moderate afterload reduction properties and results in slight preload reduction as well.
Carvedilol (Coreg)
Nonselective beta- and alpha1-adrenergic blocker. Does not appear to have intrinsic sympathomimetic activity. May reduce cardiac output and decrease peripheral vascular resistance.
Adult
3.125 mg PO bid; maintain for 1-2 wk if tolerated and double dose q1-4wk to maximally tolerated dose or to maximum of 50 mg bid
Pediatric
Not established
Metoprolol XL (Toprol)
Selective beta1-adrenergic blocker at lower doses; inhibits beta2-receptors at higher doses. Does not have intrinsic sympathomimetic activity. May reduce cardiac output, but does not appear to decrease peripheral vascular resistance to any significant degree.
Adult
100 mg PO qd; titrate to maximum dose of 400 mg/d PO in 1-2 divided doses.
Pediatric
Not established
Aldosterone Inhibitor
Decreases blood pressure and sodium reabsorption.
Eplerenone (Inspra)
Selectively blocks aldosterone at the mineralocorticoid receptors in epithelial (eg, kidney) and nonepithelial (eg, heart, blood vessels, and brain) tissues; thus, decreases blood pressure and sodium reabsorption. Indicated to improve survival for congestive heart failure or left ventricular dysfunction following acute MI. Compared to placebo, a significant risk reduction (15%) was observed.
Adult
25 mg PO qd initially, titrate as tolerated up to 50 mg/d within 4 wk
Pediatric
Not established
Angiotensin-converting Enzyme (ACE) Inhibitors
Inhibit renal systemic and tissue generation of Ang II by ACE; decrease metabolism of bradykinin (BK). Their blockade of Ang II and the delayed clearance of BK by ACE blocks the direct vasoconstriction of Ang II, as well as the activation of the sympathetic nervous system, and promotes arterial and venous dilation. In addition, ACE inhibitors reduce intracavitary pressures and diminish Wass stress, thereby decreasing myocardial oxygen demand. They inhibit the release of aldosterone, thereby reducing intravascular volume and preload. Among vasodilators, the ACE inhibitors are the most balanced vasodilators, having an equal effect on reducing both afterload and preload.
Ramipril (Altace)
Prevent conversion of Ang I to Ang II (a potent vasoconstrictor), resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
Adult
2.5 mg PO bid initially; titrate up to 5 mg bid, when possible
Pediatric
Not established
Enalapril (Vasotec)
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.Helps control blood pressure and proteinuria. Decreases pulmonary-to-systemic flow ratio in the catheterization laboratory and increases systemic blood flow in patients with relatively low pulmonary vascular resistance. Has favorable clinical effect when administered over a long period. Helps prevent potassium loss in distal tubules. Body conserves potassium; thus, less oral potassium supplementation needed.Patients who develop a cough, angioedema, bronchospasm, or other hypersensitivity reactions after starting ACEIs should receive an angiotensin-receptor blocker.
Adult
2.5-5 mg/d PO (increase as necessary); dosing range: 10-40 mg/d PO in 1-2 divided doses; alternatively, 1.25 mg/dose IV over 5 min q6h
Pediatric
Not established
Quinapril (Accupril)
Prevent conversion of Ang I to Ang II (a potent vasoconstrictor), resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
Adult
10 mg PO qd
Pediatric
Not established
Captopril (Capoten)
Lisinopril (Prinivil, Zestril); Ramipril (Altace); Fosinopril (Monopril)--Prevent conversion of Ang I to Ang II (a potent vasoconstrictor), resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
Adult
6.25-12.5 mg PO tid; not to exceed 150 mg tid
Pediatric
Not established
Lisinopril (Prinivil, Zestril)
Prevent conversion of Ang I to Ang II (a potent vasoconstrictor), resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
Adult
10 mg/d PO qd or divided bid; increase by 5-10 mg/d at 1- to 2-wk intervals; not to exceed 80 mg/d
Pediatric
Not established
SURGERY
Certain scenarios will require emergent consultation with cardiothoracic surgery. Heart failure due to acute aortic regurgitation is a surgical emergency associated with high mortality. Heart failure may occur after rupture of ventricular aneurysm. These can form after myocardial infarction. If it ruptures on the free wall, it will cause cardiac tamponade. If it ruptures on the intraventricular septum, it can create a ventricular septal defect. Other causes of cardiac tamponade may also require surgical intervention, although emergent treatment at bedside may be adequate. It should also be determined whether the patient had a history of a repaired congenital heart disease as they often have complex cardiac anatomy with artificial grafts and shunts that may sustain damage, leading to acute decompensated heart failure.
In some cases, doctors recommend surgery to treat the underlying problem that led to heart failure. [12] Different procedures are available depending on the level of necessity and include coronary artery bypass surgery, heart valve repair or replacement, or heart transplantation. During these procedures, devices such as heart pumps, pacemakers, or defibrillators might be implanted. The treatment of heart disease is rapidly changing and thus new therapies for acute heart failure treatment are being introduced to save more lives from these massive attacks. [13]
Bypass surgery is performed by removing a vein from the arm, leg, or chest and replacing the blocked vein in the heart. This allows the blood to flow more freely through the heart. Valve repair is where the valve that is causing heart failure is modified by removing excess valve tissues that cause them to close too tightly. In some cases, annuloplasty is required to replace the ring around the valves. If the repair of the valve isn't possible, it is replaced by an artificial heart valve. The final step is heart replacement. When severe heart failure is present and medicines or other heart procedures are not effective, the diseased heart needs to be replaced.
Another common procedure used to treat heart failure patients is an angioplasty. Is a procedure used to improve the symptoms of coronary artery disease (CAD), reduce the damage to the heart muscle after a heart attack, and reduce the risk of death in some patients. [14] This procedure is performed by placing a balloon in the heart to open an artery that is blocked by atherosclerosis or a build up of plaque on the artery walls. Patients whom are experiencing heart failure because of CAD or recent heart attack, can benefit from this procedure.
A pacemaker is a small device that's placed in the chest or abdomen to help control abnormal heart rhythms. [15] They work by sending electric pulses to the heart to prompt it to beat at a rate that is considered to be normal and are used to treat patients with arrhythmias. They can be used to treat hearts that are classified as either a tachycardia that beats to fast, or a bradycardia that beats too slow.
CIRCULATORY & VENTRICULAR ASSIST DEVICES:1. Abiomed AB5000™ Ventricular Assist Device (Abiomed, Inc., Danvers, MA)
The ABIOMED AB5000™ Circulatory Support System is a short-term mechanical system that can provide left, right, or biventricular support for patients whose hearts have failed but have the potential for recovery. The AB5000™ can be used to support the heart, giving it time to rest – and potentially recover native heart function. The device can also be used as a bridge to definitive therapy. The AB5000™, recently approved by the US Food and Drug Administration (FDA), builds upon more than 20 years of research and development for similar technologies, including the ABIOMED BVS 5000™.2. Abiomed BVS 5000™ Ventricular Assist Device (Abiomed, Inc., Danvers, MA)
The ABIOMED BVS 5000™ is used worldwide for temporary left, right, or biventricular (both ventricles) support in patients with potentially reversible heart failure. It was the first heart assist device approved by the US Food and Drug Administration for the support of post-cardiotomy patients (those who have developed heart failure as a result of heart surgery). Since that time, hundreds of patients have been sustained by the BVS 5000.
3. Abiomed™ Impella Percutaneous Ventricular Assist Device
The Abiomed™ Impella 2.5 is a minimally invasive, catheter-based cardiac assist device designed to assist the failing heart. The Impella 2.5 is the "world's smallest heart pump", designed to be inserted percutaneously in the catheterization laboratory (cath lab) via the femoral artery into the left ventricle. Up to 2.5 liters of blood per minute are delivered by the pump from the left ventricle into the ascending
aorta, providing the heart with active support in critical situations. The Impella 2.5 is FDA 510(k) for short-term circulatory support.
4. Berlin Heart® Ventricular Assist Device (Berlin, Germany)
The Berlin Heart® is a ventricular assist device which can be configured to support any size pediatric patient from newborn to full-grown teenager. The Berlin Heart has been used extensively in Europe as a bridge to transplant, and in some cases, a bridge to recovery. Although it is not currently FDA approved, special permission can be obtained for implantation in the United States. At the University of Michigan's C.S. Mott Children's Hospital, many children have undergone ventricular assist device implantation using a variety of devices, including the Berlin Heart®.
5. Cardiac Assist TandemHeart™ pVAD Ventricular Assist Device
The CardiacAssist TandemHeart™ Percutaneous Ventricular Assist Device (pVAD) differs from other assist devices in that it can be inserted either by cardiovascular surgeons in the operating room or by a cardiologist in the cardiac catheterization laboratory. The TandemHeart™ has been used in postcardiotomy cardiogenic shock patients (those who have developed heart failure as a result of heart surgery or a heart attack) and as a bridge to a more definitive therapy. The TandemHeart™ pVAD provides short-term support from a few hours up to 14 days, giving the heart time to recover and regain native function.6. Cardio West™ temporary Total Artificial Heart (TAH-t)
This medical device is the modern version of the Jarvik 7 artificial heart first implanted into Barney Clark in 1982. The CardioWest™ temporary Total Artificial Heart is the only FDA approved temporary total artificial heart in the world. The TAH-t is used as a bridge to heart transplant for eligible patients suffering from end-stage biventricular failure.
7. HeartWare™ Left Ventricular Assist Devices (LVAD)
The HeartWare™ Left Ventricular Assist System (LVAS) is a third-generation continuous flow blood pump for the treatment of advanced heart failure. It features a miniaturized centrifugal pump, which is small enough to be implanted above the diaphragm in all patients. The device is capable of generating up to 10 liters per minute of blood flow. The pump has only one moving part, the impeller, which spins at rates between 2,000 and 3,000 revolutions per minute. The impeller is suspended within the pump housing through a combination of passive magnets and a hydrodynamic thrust bearing. This hydrodynamic suspension is achieved by a gentle incline on the upper surfaces of the impeller blades. When the impeller spins, blood flows across these inclined surfaces, creating a "cushion" between the impeller and the pump housing. The HeartWare VAD, has been approved for sale in the European Union and is currently in clinical trial in the United States.8. Terumo Heart DuraHeart™ LVAD
The DuraHeart™ LVAD is a third-generation continuous flow blood pump designed for long-term patient support. It incorporates a centrifugal flow rotary pump with a magnetically levitated impeller to pump blood from the heart around the body. The DuraHeart™ LVAD is the first device to reach clinical trial that combines centrifugal pump and magnetic-levitation technologies. Weighing 19 ounces (about 540 grams) and measuring about 2.87 inches in diameter and 1.82 inches thick, it is a small device that provides support to a wider range of patient. The unique design of the DuraHeart™ LVAS incorporates, flow rates from two to eight liters per minute with motor speeds between twelve hundred and twenty-four
hundred revolutions per minute and flow rates that vary with physiological changes. The DuraHeart™ is an investigational device and is currently in clinical trial in the United States.9. Thoratec HeartMate II® Left Ventricular Assist Device
The HeartMate II® is a high-speed, axial flow, rotary blood pump. As an axial flow device, the HeartMate II® produces no pulsatile action. Weighing 12 ounces (about 375 grams) and measuring about 1.5 inches (4 cm) in diameter and 2.5 inches (6 cm) long, it is significantly smaller than other currently approved devices. As such, it may be suitable for a wider range of patients, including small adults and children. The University of Michigan Center for Circulatory Support participated in the first clinical testing of the HeartMate II® device in the United States.10. Thoratec HeartMate® XVE Left Ventricular Assist Device
The Thoratec HeartMate® XVE LVAD (vented electric) was developed and tested by Thermo Cardiosystems, Inc. This titanium blood pump consists of a blood chamber, motor chamber, drive-line, and inflow and outflow conduits. The pump weighs 1150 grams. Each conduit contains a 25-mm porcine (pig) valve within a woven Dacron™ fabric graft. A polyurethane diaphragm separates the blood chamber and the motor chamber. Textured surfaces within the blood chamber promote the development of a cellular lining, which helps prevent blood clots and infection. The XVE LVAS has a maximum stroke volume of 83 milliliters. It can be operated at up to 120 beats per minute, resulting in flow rates of up to 10 liters per minute.11. Thoratec CentriMag® Blood Pump
The Thoratec CentriMag® blood pump is an extracorporeal circulatory support device for patients with a failing heart. The CentriMag® is a magnetically-levitated pump impeller which provides a contact-free environment to help minimize blood-related complications such as hemolysis. It is capable of delivering high flows up to 9.9 LPM. FDA 510K approved, the CentriMag can be used as a short-term solution to support the circulation while longer-term options are considered. CentriMag is approved for use as an RVAD for periods of support up to 30 days for patients in cardiogenic shock due to acute right ventricular failure. CentriMag is also being evaluated in the United States for use in failure to wean patients as a bridge to recovery, transplant, or a long-term VAD in patients unable to be weaned from cardiopulmonary bypass.
12. Thoratec IVAD™ Ventricular Assist Device
The Thoratec IVAD™ is now FDA approved for use in bridge-to-transplantation and post-cardiotomy recovery patients who are unable to be weaned from cardiopulmonary bypass. The IVAD™ is the only currently approved, implantable cardiac assist device that can provide left, right or biventricular support. It was recently approved for use in Europe. The IVAD's compact size facilitates implants to assist both ventricles and enables it to accommodate a wide range of patients, including those who were previously unable to receive an implantable, pulsatile device.
13. Dialysis System Pump Motors & Drives
Hemodialysis (HD) therapy systems require reliable
peristaltic pumps to accurately control patient's
blood and the dialysis solution through the machine's
dialyzer.
HD system manufacturers rely on Allied Motion's
precision brushless motors with on-board drive
electronics to provide reliable, quiet, long-service life
solutions for their HD pump subsystems.
14. Powered Surgical Handpiece Motors
Small, light, efficient, high-powered, brushless,
autoclavable: These are the extremely important
requirements of powered surgical handpiece motors.
For the surgical instrument industry Allied Motion's engineers developed
miniature precision motors with twice the performance of same-size competitive units.
15. Cardiopulmonary Heart Bypass System Pump
Motor
Allied Motion designed a magnetically-coupled
brushless pump motor to drive a disposable integrated
oxygenator module, the "heart" of this innovative
heart bypass system.
The optimized low-voltage winding of the motor, a
version of Allied Motion's Megaflux brushless servo
torque motor series, is driven by a custom-designed two-quadrant brushless drive
module.
16. Angiographic CT Contrast Injector Syringe
Pump Motor
Contrast injectors are essential accessories for
modern CT scanners. They inject X-ray contrast fluid
intravenously, which provides dramatic improvement in the overall quality of CT images of
the circulatory system and many soft organs. The
enhanced images enable more accurate diagnoses to
be made.
Allied Motion brushless servo motors and drives are used to
precisely drive the injector piston to achieve smooth,
accurate fluid delivery.
17. Left Ventricular Heart Assist Device (LVAD)
Motor
Left ventricular heart assist devices (LVAD) were
developed to help heart transplant candidates while
they await the availability of a heart, and also for permanent support for end stage heart
failure patients.
Advanced LVAD pumps are implanted in the patient, and
use an axial flow pump powered by a compact, highly efficient brushless DC torque motor such as those designed
by Allied Motion for LVAD applications.
18. PAP Respiratory Ventilation Air Pump
Motor
Sleep apnea treatment often involves the assistance of
Positive Airway Pressure (PAP) respirators. All PAP systems (APAP, IPAP/EPAP) control a stream of compressed air (4 to 20 cm H2O) to keep the
patient's airway open in order to assist breathing.
Allied Motion's small, precision brushless DC motors like the BL 21 EE are an ideal choice for PAP systems owing
to their compactness, long life, and quiet operation.