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• Sodium nitroprusside (Nipride) is a potent IV vasodilator
that reduces both preload and afterload.
• Morphine. Morphine sulfate reduces preload and
afterload.
• Positive Inotropes. Inotropic therapy increases myocardial
contractility. Drugs include β-adrenergic agonists (e.g.,
dopamine [Intropin], dobutamine [Dobutrex], epinephrine,
norepinephrine [Levophed]), the phosphodiesterase
inhibitor milrinone (Primacor), and digitalis.](https://image.slidesharecdn.com/heartfailure-200411152423/85/Heart-failure-44-320.jpg)
![• Vasodilators:
• hydralazine
(Apresoline)*
• isosorbide dinitrate/
hydralazine (BiDil)*
• nitrates (e.g.,
nitroglycerin [Nitro-Bid],
isosorbide dinitrate
[Isordil])
• nesiritide (Natrecor)†
• nitroprusside (Nipride)†
• Reduce cardiac afterload,
leading to increased CO
• Dilate the arterioles of
the kidneys, leading to
increased renal perfusion
and fluid loss
• Decrease BP
• Decrease preload
• Relieve symptoms of
heart failure (e.g., dyspnea)](https://image.slidesharecdn.com/heartfailure-200411152423/85/Heart-failure-48-320.jpg)
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Heart failure
- 1. Heart Failure/ CCF/CHF Prepared by: Kopila Mugrati MSN.
- 2. Definition • Heart failureis a physiologic state in which the heart cannot pump enough blood to meet the metabolic needs of the body. (oxygen consumption) resulting in hypoperfusion of the tissue, followed by pulmonary and systemic venous congestion.
- 3. • It isclinical syndrome manifested by volume overload, inadequate tissue perfusion, poor exercise tolerance. • Due to vascular congestion during heart failure, it often called as congestive heart failure.
- 4. • Is alsoknown as chronic heart failure, cardiac decompensation, cardiac insufficiency, and ventricular failure
- 5. Incidence : • Affectsat least 26 million people worldwide and is increasing • Affects about 5 million people every year in US • Affects both males and females, mortality is higher among females. • Leading cause of hospitalization in older patients.
- 6. Etiology & Riskfactors Extrinsic factors Intrinsic factors Due to Caused by conditions that weaken or damage the myocardium.
- 7. Intrinsic factors • Cardiomyopathies •MI • Myocarditis • Ischemic heart diseases • Pericarditis • Cardiac tamponade
- 8. Extrinsic factors • Drugtoxicity • Arrythmias • Metabolic/ respiratory acidosis • AV shunts • Pulmonary embolism • anaemia
- 9. Causes: 1. Abnormal musclefunction MI Myocarditis Cardiomyopathy Ventricular aneurysm Long term alcohol consumption Coronary heart disease Metabolic heart disease Endocrine heart disease
- 10. 2. Increase inpreload: Regurgitatio n of mitral or tricuspid valve Hypervolemi a Congenital defects Ventricular septal defects (VSD) Atrial septal defect Patent ductus arteriosus
- 11. 3.Limited ventricular filling: Mitralor tricuspid stenosis Cardiac tamponade Constrictive pericarditis Hypertrophic obstructive cardiomyopathies
- 12. 4.Increase in afterload: Hypertension Pulmonary oraortic stenosis Peripheral vascular resistance
- 13. Functional classification ofheart failure
- 14. Pathophysiology • Due toetiological factors • Decrease in pumping action of the heart • Stimulates the compensatory mechanism a. Ventricular dilation b. Increased sympathetic nervous system stimulation c. Renin angiotensin system activation d. Remodeling e. Sustained neurohormonal activities
- 15. Continue.. • Increase inHR • Increase in myocardial oxygen use • Increase in cardiac output • Increase preload increase afterload • Congestive heart failure
- 16. 1.Increased sympathetic nervoussystem stimulation Further contraction of ventricles Epinephrine and norepinephrine release Vasoconstriction of arterioles Causes increase in rate and force of contraction of ventricles Stimulation of SNS Decrease in BP Due to decreased cardiac output
- 17. 2. Renin angiotensinsystem activation Leads to increase in BP Further causes vasoconstriction Stimulates secretion of aldosterone by adrenal gland Stimulate thirst center in brain Angiotensin II causes vasoconstriction and constricts renal arterioles Converts Angiotensin I to AngiotensinII Acts on angiotensinogen ( which is released by liver) Renal juxtaglomerular cells release Rennin Decrease in BP
- 18. 3. Ventricular dilation Leadingto hypoxia of heart, decrease in contraction. If stretched beyond certain point, becomes ineffective ( Starling's law) Dilation causes increase in preload Ventricular dilation refers to lengthening of muscle fibers of heart chambers.
- 19. 4. Remodeling Over timechanges in structure, function of myocardial cells takes place known as remodeling. Increased wall thickness reduces wall stress Occurs due to hypertrophy of myocardial cells and sustained neurohormonal activation Remodeling takes place during decompensated heart failure
- 20. 5. Sustained neurohormonalactivation • Remodeling occurs • Stimulates neurohormonal activity
- 21. Continue.. If the compensatorymechanism fails Blood in left ventricle increases Leads to more work load in heart Leads to hypertrophy of chambers Cannot receive blood from pulmonary veins Leads to increase in left atrial pressure And finally causes pulmonary edema
- 23. Clinical manifestations: • Shortnessof breath often with activities or while lying flat • Weakness and fatigue • Awakening short of breath at night • Need for increased pillows at night – helps lungs drain of excess fluid • Coughing or wheezing • Swelling of feet and legs or other “dependent” areas • Anorexia/loss of appetite • Weight gain • Fatigue Activity decrease Cough (especially supine) Edema Shortness of breath
- 24. Types of heartfailure Left ventricular failure Right ventricular failure Backward Vs Forward High output Vs low output
- 26. Left heart Failure •Left heart failure occurs when the output of the left ventricle is less than the total volume of blood received from the right side of the heart via pulmonary circulation. • Results in congested pulmonary circuit with blood that cannot be moved forward and the systemic blood pressure falls.
- 27. Causes of leftheart failure • Myocardial infarction • Systemic hypertension • Aortic stenosis • Cardiomyopathy
- 28. Pathophysiology of LVF Backwardeffect: Due to ventricular failure of inability to pump Decrease emptying of left ventricle Increase volume &end diastolic pressure Increase volume in pulmonary veins& pressure Increase volume in pulmonary capillary bed Transudation of fluid from capillaries to alveoli Filling of alveolar space Leading to pulmonary edema
- 29. Forward effect Increase bloodvolume and BP Increase extracellular fluid volume Increase secretion of sodium and water retention Increase reabsorption of Na+ and H2O, vasoconstriction Decrease blood flow to kidneys and glands Decrease body tissue perfusion Decrease in cardiac output
- 30. Clinical manifestations ofLHF • Dyspnea ( more in case of ventricular failure) • Exertional Dyspnea • Pulmonary congestion • Orthopnea (due to increase in amount of blood returning from lower extremities to heart and lungs)
- 31. Continue.. • Paroxysmal nocturnaldyspnea (PND: frightening sensation of suffocation) • Labored and wheezing respiration • Cheyne- Strokes respiration (due to prolonged circulation time between pul. Circulation and central nervous system)
- 32. Continue.. • Cough (verycommon in LVF: frothy, blood-tinged sputum) • Cerebral hypoxia (causing confusion, restlessness, impaired memory etc..) • Fatigue and muscular weakness • Slow removal of metabolic wastes • Disturbed sleep and rest • Nocturia • Later when cardiac output declines, leads to oliguria.
- 33. Complications of LVF •Acute pulmonary edema • Death due to suffocation
- 34. DIAGNOSTIC EVALUATION Physical Examination/History collection • Bilateral crackles on auscultation. • Inspection and palpation of precordium reveals enlarged or displaced apical pulse. • S3 or S4 may be heard as early finding. • Blood tests- Like LFT, KFT & TSH, A blood test to check for a chemical called N-terminal pro-B-type natriuretic peptide (NT-proBNP) may help in diagnosing heart failure. are peptide (small proteins) that are either hormones or part of the peptide. They are continually produced in small quantities in the heart and released in larger quantities when the heart senses that it needs to work harder.
- 35. • Chest X-ray-heart may appear enlarged and fluid buildup may be visible in your lungs. • Electrocardiogram (ECG) • Echocardiogram • Stress test- measure how heart and blood vessels respond to exertion. • Cardiac computerized tomography (CT) scan or magnetic resonance imaging (MRI). • Coronary angiogram • Myocardial biopsy
- 36. Right ventricular failure •Right heart failure occurs when the output of the right ventricle is less than the input from the systemic venous circuit which results in congestion of venous circuit and decreased output to lungs.
- 37. Causes of RHF/RVF •Left heart failure • Pulmonary embolism • COPD • Congenital heart diseases • Pulmonary hypertension
- 38. Backward effect Peripheral edema,dependent edema, generalized edema Increased pressure at capillary line Increased volume in distendable organs(liver, spleen) Increased volume in systemic venous circulation Increased volume and pressure in the greater veins Increase volume and pressure Increase volume and end diastolic pressure Decrease emptying of rt ventricle
- 39. Clinical manifestations • Peripheraledema& dependent edemas • Venous congestion of organs • Hepatomegaly • Abdominal pain due to Hepatomegaly • Discomfort • Constant aching or a sharp pain in rt upper quadrant • Anoxia leading to necrosis of lobules of liver (cardiac cirrhosis) • Ascites, jaundice • Anorexia, nausea, bloating
- 40. Continue.. • Cardiac cachexia(marked wasting of tissue mass) • Anasarca • Cynosis of nail beds • Anxious, depressed, fear • Insomnia Complication: Death
- 41. DIAGNOSTIC EVALUATION (RHF) PhysicalExamination/ History collection • Serum BPN: Brain natriuretic peptide (BNP) test is a blood test that measures levels of a protein called BPN that is made by heart and blood vessels. BNP levels are higher than normal when heart failure occurs. • S3 or S4 may be heard as early finding. • Blood tests- Like LFT, KFT & TSH, BUN
- 42. continue… • Chest X-ray-heart may appear enlarged cardiac silhouette and congestion of lungs. • Electrocardiogram (ECG) • Echocardiogram with doppler flow studies • Stress test- measure how heart and blood vessels respond to exertion. • ABG ( respiratory alkalosis) • Cardiac computerized tomography (CT) scan or magnetic resonance imaging (MRI). • Coronary angiogram • Myocardial biopsy
- 43. Management 1. Reduce myocardialworkload: • Diuretics are the mainstay of treatment in patients with volume overload. Diuretics act to decrease sodium reabsorption at various sites within the nephrons, thereby enhancing sodium and water loss. • Vasodilators. IV nitroglycerin is a vasodilator that reduces circulating blood volume. It also improves coronary artery circulation by dilating the coronary arteries. Therefore nitroglycerin reduces preload, slightly reduces afterload (in high doses), and increases myocardial oxygen supply. When titrating IV nitroglycerin, monitor BP frequently (every 5 to 10 minutes) to avoid symptomatic hypotension.
- 44. Continue.. • Sodium nitroprusside(Nipride) is a potent IV vasodilator that reduces both preload and afterload. • Morphine. Morphine sulfate reduces preload and afterload. • Positive Inotropes. Inotropic therapy increases myocardial contractility. Drugs include β-adrenergic agonists (e.g., dopamine [Intropin], dobutamine [Dobutrex], epinephrine, norepinephrine [Levophed]), the phosphodiesterase inhibitor milrinone (Primacor), and digitalis.
- 45. DRUG THERAPY • HeartFailure Drug Mechanism of Action • Diuretics: • Loop Diuretics • Decrease fluid volume • Decrease preload • Decrease pulmonary venous pressure • Relieve symptoms of heart failure (e.g., edema) • furosemide (Lasix), bumetanide (Bumex) • Thiazide Diuretics* • hydrochlorothiazide (HCTZ) • metolazone (Zaroxolyn) • Potassium-Sparing Diuretics • spironolactone (Aldactone) • eplerenone (Inspra)
- 46. • Renin-Angiotensin-Aldosterone SystemInhibitors: ACE Inhibitors • captopril (Capoten) • benazepril (Lotensin) • enalapril (Vasotec) Angiotensin II Receptor Blockers • losartan (Cozaar) • valsartan (Diovan)
- 47. Drugs • Renin-Angiotensin- Aldosterone System Inhibitors:ACE Inhibitors • captopril (Capoten) • benazepril (Lotensin) • enalapril (Vasotec) Angiotensin II Receptor Blockers • losartan (Cozaar) • valsartan (Diovan) Action • Dilate venules and arterioles • Improve renal blood flow • Decrease fluid volume • Relieve symptoms of heart failure • Promote reverse remodeling • Decrease morbidity and mortality
- 48. • Vasodilators: • hydralazine (Apresoline)* •isosorbide dinitrate/ hydralazine (BiDil)* • nitrates (e.g., nitroglycerin [Nitro-Bid], isosorbide dinitrate [Isordil]) • nesiritide (Natrecor)† • nitroprusside (Nipride)† • Reduce cardiac afterload, leading to increased CO • Dilate the arterioles of the kidneys, leading to increased renal perfusion and fluid loss • Decrease BP • Decrease preload • Relieve symptoms of heart failure (e.g., dyspnea)
- 49. • β-Adrenergic Blockers* •metoprolol (Toprol XL) • bisoprolol (Zebeta) • carvedilol (Coreg) Positive Inotropes β- Adrenergic Agonists† • dopamine (Intropin) • dobutamine (Dobutrex) Phosphodiesterase Inhibitor† • milrinone (Primacor) Digitalis Glycoside* • digoxin (Lanoxin) Continue.. • Morphine • Antidysrhythmic Drugs • Anticoagulants
- 50. 2. Elevate client'shead 3. Reduce fluid retention 4. Improve ventricular pump performance 5. Supplement with oxygen 6. Control dysrhythmias 7.Reduce stress and risk of injury
- 51. Surgical management • Ventricularassist devices • Heart transplantation • cardiomyoplasty
- 52.