Download Free Medical Clinical Approach and Management of CHF PowerPoint Presentation

Clinical Approach and Management of CHF PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Congestive Heart Failure, which is titled "Clinical Approach & Management of CHF", to know about the clinical approach and management Congestive heart failure (CHF).

Tags : Congestive Heart Failure, Clinical Approach, Management, CHF

Published on : Jul 01, 2021 | Views : 2942 | Downloads : 5

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Dr Sarika Gupta (MD,PhD) Asst. Professor CLINICAL APPROACH & MANAGEMENT OF CHF
Slide 2-

DEFINITION A clinical syndrome Occurs when The heart is unable to pump enough blood to the body to meet its needs The heart is unable to dispose of systemic or pulmonary return adequately Or a combination of the two
Slide 3-

PATHOPHYSIOLOGY Systemic oxygen transport = cardiac output X systemic oxygen content Cardiac output = heart rate X stroke volume The primary determinants of stroke volume: afterload (pressure work) preload (volume work) contractility (intrinsic myocardial function)
Slide 4-

PATHOPHYSIOLOGY The heart can be viewed as a pump with an output proportional to its filling volume and inversely proportional to the resistance against which it pumps
Slide 5-

PATHOPHYSIOLOGY As ventricular end-diastolic volume increases, a healthy heart increases cardiac output until a maximum is reached The increased stroke volume obtained in this manner is due to stretching of myocardial fibers Resulting in increased wall tension, elevating myocardial oxygen consumption Cardiac muscle with compromised intrinsic contractility requires a greater degree of dilatation to produce increased stroke volume & does not achieve the same maximal cardiac output as normal myocardium does
Slide 6-

PATHOPHYSIOLOGY Lesion causing increased preload (left-to-right shunt or valvular insufficiency) Cardiac chamber is already dilated Little room for further dilatation as a means of augmenting cardiac output Lesions that result in increased afterload to the ventricle (aortic or pulmonic stenosis, coarctation of the aorta) decreases cardiac performance
Slide 7-

PATHOPHYSIOLOGY Abnormalities in heart rate: compromise cardiac output Tachyarrhythmias shorten the diastolic time interval for ventricular filling. High-output failure: NO basic abnormality in myocardial function Cardiac output is greater than normal Alterations in the oxygen-carrying capacity of blood (anemia or hypoxemia) & increased oxygen demands (secondary to hyperventilation, hyperthyroidism, or hypermetabolism)
Slide 8-

PATHOPHYSIOLOGY
Slide 9-

ETIOLOGY
Slide 10-

ETIOLOGY
Slide 11-

ETIOLOGY
Slide 12-

ETIOLOGY
Slide 13-

ETIOLOGY
Slide 14-

CLINICAL FEATURES Depend on the degree of the child's cardiac reserve A critically ill infant or child who has exhausted the compensatory mechanisms- symptomatic at rest Other patients may be comfortable when quiet but are incapable of increasing cardiac output in response to even mild activity without experiencing significant symptoms
Slide 15-

CLINICAL FEATURES History: Poor feeding, poor weigh gain, tachypnea (worsening during feeding), cold sweat on the forehead- CHF in infants Shortness of breath, specially with activities, easy fatigability, puffy eyelids or swollen feet-older children
Slide 16-

CLINICAL FEATURES Examination: Tachycardia, gallop rhythm, weak & thready pulses Growth failure, perspiration, cold & wet skin Cardiomegaly Tachypnea Dyspnea on exertion Orthopnea Wheezing & pulmonary crackles COMPENSATORY RESPONSE PULMONARY VENOUS CONGESTION
Slide 17-

CLINICAL FEATURES Examination: Hepatomegaly Puffy eyelids Distended neck veins Ankle edema SYSTEMIC VENOUS CONGESTION Clinical assessment of jugular venous pressure in infants may be difficult because of the shortness of the neck & the difficulty of observing a relaxed state; palpation of an enlarged liver is a more reliable sign Edema may be generalized & involves the eyelids & sacrum & less often the legs and feet
Slide 18-

CLINICAL FEATURES
Slide 19-

INVESTIGATION X-RAY Study:
Slide 20-

INVESTIGATION X-RAY Study:
Slide 21-

INVESTIGATION ECG: not helpful ECHO: Standard technique for assessing ventricular function The most commonly used parameter in children is fractional shortening (impaired LV systolic function) Difference between end-systolic & end-diastolic diameter divided by end-diastolic diameter (N=28%-42%) Ejection fraction (impaired LV systolic function) Enlargement of ventricular chambers Doppler tissue imaging (impaired LV systolic & diastolic function)
Slide 22-

INVESTIGATION Magnetic resonance angiography Cardiac catheterization-evaluation of biopsy specimens Decreased arterial oxygen levels; respiratory or metabolic acidosis Hyponatremia Serum B-type natriuretic peptide (BNP) Cardiac neurohormone released in response to increased ventricular wall tension Elevated in patients with heart failure due to systolic dysfunction (cardiomyopathy) Elevated in children with volume overload (left-to-right shunts such as ventricular septal defect)
Slide 23-

MANAGEMENT PRINCIPAL: Elimination of the underlying causes Treatment of the precipitating or contributing causes (infection, anemia, arrhythmias, fever) Control of the heart failure state
Slide 24-

MANAGEMENT Control of the heart failure– GENERAL MEASURES Bed rest Humidified oxygen Adequate calories & fluid 1. Calorie dense food 2. Frequent small feeding 3. Nasogastric feeding 4. Salt restrictions Patients with pulmonary edema- positive pressure ventilation Daily weight measurement in hospitalized children
Slide 25-

MANAGEMENT Control of the heart failure state- Drug therapy Inotropic agents Diuretics Afterload reducing agents DIURETICS: interfere with reabsorption of water & sodium by the kidneys results in a reduction in circulating blood volume thereby reduces preload & control pulmonary & systemic venous congestive symptoms
Slide 26-

MANAGEMENT INOTROPIC AGENTS: Rapidly acting Inotropic agents Dopamine, dobutamine, isoproterenol, epinephrine & amrinone Additional vasodilator actions Used for critically ill infants with CHF, those with renal dysfunction & postoperative cardiac patients with CHF Digoxin
Slide 27-

MANAGEMENT AFTERLOAD REDUCING AGENTS: Arteriolar vasodilator Augments cardiac output by acting primarily on the arteriolar bed Reduction of afterload Hydralazine Venodilators Dilate systemic veins & redistribute blood from the pulmonary to the systemic circuits Decrease in pulmonary symptoms Nitriglycerine, isosorbide dinitrate
Slide 28-

MANAGEMENT AFTERLOAD REDUCING AGENTS: Mixed vasodilator Act on both arteriolar & venous beds ACE inhibitors, nitroprusside & prazosin ACEIs have additional beneficial effects on cardiac structure & function that may be independent of their effect on afterload
Slide 29-

MANAGEMENT AFTERLOAD REDUCING AGENTS: Afterload reducers: especially useful in children with heart failure secondary to cardiomyopathy & in patients with severe mitral or aortic insufficiency Effective in patients with heart failure caused by left-to-right shunts Not used in the presence of stenotic lesions of the left ventricular outflow tract because of concern over coronary perfusion
Slide 30-

MANAGEMENT β-ADRENERGIC BLOCKERS: β-Blockers are used for the chronic treatment of patients with heart failure who were symptomatic despite being treated with standard anticongestive drugs
Slide 31-

MANAGEMENT
Slide 32-

MANAGEMENT