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Cardiology HF

Heart failure is a clinical syndrome where the heart cannot maintain sufficient cardiac output to meet metabolic needs despite normal venous return. It can be left-sided, right-sided, or both. Common causes include ischemic heart disease, hypertension, and left-sided heart failure for right-sided heart failure. Treatment involves identifying and treating the underlying cause, rest, diuretics like furosemide, vasodilators like ACE inhibitors, inotropic agents like digitalis, and beta-blockers. Acute heart failure can result from a sudden rise in pulmonary venous pressure from causes like myocardial infarction or mitral stenosis with aggravating factors.

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0% found this document useful (0 votes)
558 views

Cardiology HF

Heart failure is a clinical syndrome where the heart cannot maintain sufficient cardiac output to meet metabolic needs despite normal venous return. It can be left-sided, right-sided, or both. Common causes include ischemic heart disease, hypertension, and left-sided heart failure for right-sided heart failure. Treatment involves identifying and treating the underlying cause, rest, diuretics like furosemide, vasodilators like ACE inhibitors, inotropic agents like digitalis, and beta-blockers. Acute heart failure can result from a sudden rise in pulmonary venous pressure from causes like myocardial infarction or mitral stenosis with aggravating factors.

Uploaded by

dhayemaru
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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In Capsule Series

Cardiology

Heart Failure
Definition:
It is a clinical syndrome in which the heart cant maintain sufficient cardiac output to meet the metabolic needs of the body inspite of normal venous return.

Classification:
1- Left sided 2- Systolic 3- Acute 4- Low COP Right sided Diastolic Chronic High COP Both (congestive HF) Both Acute on top of chronic

Etiology:
I- Left sided heart failure :
A) Left atrial failure: MS , Myxoma . B) Left ventricular failure: 3 x 3 1- Muscle disease : Myocardial infarction Myocarditis CardioMyopathy 2- Volume (diastolic) overload: ( preload ) Hyperdynamic circulation . Valvular disease: MR, AR Congenital disease: VSD, PDA 3-pressure ( systolic ) overload: ( afterload ) Systemic hypertension . AS . Coarcitation of aorta.

II- Right sided heart failure:


A) Right atrial failure: TS , Myxoma B) Right ventricular failure: 3 3 1- Muscle disease: The same as left . 2- Volume ( diastolic ) overload: Hyperdynamic circulation Valvular disease : TR, PR Congenital disease: VSD, ASD

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In Capsule Series 3- Pressure ( systolic ) over load: pulmonary hypertension . pulmonary stenosis . pulmonary embolism . The most common causes of LSHF are: Ischemic heart disease Systemic hypertension The most common cause of RSHF is: LSHF

Cardiology

Diastolic heart failure: In this type of HF, the decrease in COP is due to inadequate ventricular filling, not impaired systolic contraction. High cardiac output HF: HF with hyperdynamic circulation e.g: Thyrotoxicosis, anemia.

Precipitating factors:

2I, 2P, 2A

Infections: chest infections, infective endocarditis . Iatrogenic: Calcium channel blocker (- ve inotropic ) . Cortisone ( salt & water retension ). Discontinuation of antifailure therapy. Physical & emotional stress. Pregnancy & delivery. Anemia. Arrhythmias (tachy & brady arrhythmias) .

Cardiac reserve (Compensatory mechanism) :


Aim: Aim To maintain normal COP. They are beneficial within limit . If they exceed these limits, they will aggravate HF 1- Reflex tachycardia: due to sympathetic 2- Ventricular Dilatation: Volume load increased length of cardiac muscle fibers contraction within limit (starling's law)

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In Capsule Series 3- Ventricular Hypertrophy: of cardiac muscle fibers Pressure load

Cardiology increased thickness

contraction within limit. (bigger is not better)

4- Redistribution of blood flow: From less vital organs (skin) to more vital organs ( brain & heart ) 5- Activation of renin Angiotensin Aldosterone System: Hypovalemia renin Angiotensin  Aldosterone Na & water retension Hypervolemia . 6- Release of natriuretic peptide: (ANP , BNP) Stretch of cardiac muscle fibers Release of natriuretic peptide VD & increase urinary Na exretion

Clinical Picture:
-Left sided heart failure: 1- Manifestations of LCOP : 7 items
1- CNS : Dizziness, headache, syncope . 2-CVS : Ischemic heart disease. 3-Kidney : Oliguria . 4-Skin : Cold, peripheral cyanosis . 5-Skletal muscle : fatigue , intermittent claudication . 6-Blood pressure: low systolic blood pressure. 7-Pulse : Weak 2-manifestations of pulmonary congestion: 7 items 1-Dyspnea: exertional ,orthopnea, paroxysmal nocturnal dyspnea (PND) or dyspnea at rest . 2- Exertional Cough . 3-Recurrent chest infections. 4-Hemoptysis. 5-Pleural effusion. 6-Pulmonary edema . 7-Bilatera basal cripitation. 3-Features of the cause: - Ischemic heart diseases. - Systemic hypertension.

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In Capsule Series

Cardiology

4-Cardiac signs: 1-Left ventricular enlargement . 2-Tachycardia. 3-Pulsus alternans: alternating strong & weak beats(In advanced stage) 4-Gallop on the apex: due to flabby ventricle. NB : ventricular gallop = S3 + tachycardia 5-murmure of functional MR: pansystolic murmure due to LV dilatation .

Clinical picture of right sided heart failure: 1-manifestations of LCOP: see before 2-manifestations of systemic congestion:
1-Insomnia. 2-Sweating on slight activity: due to sympathetic activation. 3-Congested neck vein. 4-Edema lower limb, later on ascites. 5-Liver: enlarged , tender. 6-GIT: dyspepsia, malabscorption may lead to cardiac cachexia. 7-Pleural effusion. 3-Features of the cause: e.g: - LSHF . -Pulmonary hypertension .

4-Cardiav Signs:

( the same as left pulsus alternans )

1-Right ventricular enlargement . 2-Tachycardia 3-gallop (over tricuspid area). 4-murmure of functional TR . N.B:

LSHF
RSHF

Lung Congestion .
Systemic Congestion .

Differential Diagnosis :
LSHF RSHF -Causes of dyspnea &orthopnea. -Pericardial effusion -COPD -Obesity -Liver cirrhosis

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In Capsule Series

Cardiology

Investigations:
1- X ray:
o Chamber enlargement . o Pulmonary congestion in LSHF. o Pleural effusion

2-ECG:
o Chamber enlargement . o Detect the cause e.g: MI 3-Echo Cardiography: (key investigation) o Chamber enlargement. o Detect the cause. o Paradoxical movement of the myocardium. o measures COP & Ejection fraction (EF) strok volume Ejection fraction = End diastolic volume EF < 40% systolic HF (n = 50%)

4-cardiac catheterization:
Chamber enlargement . Detect the cause . 5-BNP: (if normal, HF is unlikely) o o

Treatment of heart failure:


A. Treatment of underlying cause e.g: valve replacement . B. Treatment of precipitation factors e.g: anemia..

C. Specific treatment of CHF:


1-Rest: until signs of HF disappear. semisitting rather than lying down to decrease the venous return. complications of prolonged bed rest: -pyschosis . -bed sores. -DVT . -pulmonary embolism. -constipation . -retention of urine.

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In Capsule Series 2-Diet: Salt restriction is essential. Fluid restriction: in severe cases. Low calories. Small frequent meals. 3-Sedation: as diazepam.

Cardiology

4-Diuretics:
Aim: a. They increase salt & water excretion decrease the work of the heart . b. Edema & visceral congestion . blood Volume So,

Types: - Loop diuretics: -act on loop of henle ( reabsorption of Na, H2O, K, Cl) -e.g: - Furosemide (Lasix) : 40-160 mg/d (oral, IV, IM). - Bumetanide (Burinex) - Thiazides: d -act on distal tubules ( reabsorption of Na, H2O, K, Cl) -e.g: - Hydrochlorothiazide: 25-100 mg/d - Chlorothalidone. - potassium sparing diuretics: - e.g: Spirnolactone (aldosterone antagonist) -can be combined with lasix or thiazide to avoid hypokalemia. Side effects of lasix & thiazides: 4 hypo: -4 hyper ( glucose ) -hypokalemia -hyperglycemia -hypovolemia -hyperlipidemia -hyponatremia -hyperurecemia - hypochloremic alkalosis -hypercalcemia (Thiazide only) Lasix Spironolactone Ototoxicity & nephrotoxicity . Hyperkalemia & gynecomastia.

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In Capsule Series -

Cardiology

In HF: lasix is more better than thiazide . Better given in the morning . Its better to combine diuretics with ACEIs . Diuretics are the most effective treatment for symptoms of CHF .

5-Vasodilators:
- They are classified into: Arteriolar Venous Both - Reduce afterload Reduce preload Reduce both . - Hydralazine Nitrates - ACEIs. - Diazoxide - Na nitroprusside. - Pharmacological details: see systemic hypertension N.B: ACE inhibitors are the best vasodilator in the cases of CHF especially in LV failure .

6- Inotropic agents:
Digitalis . Dopamine . Dobutamine . Milrinone: phospho diastrase inhibitors, used in emergency .

Digitalis
Action: o Contractility of the ventricles . o Excitability . o Conductivity . o HR : by direct action & vagal stimulation . o On ECG: sagging depression of ST segment . Mechanism of action : ( contractility )

Inhibition of Na - K ATPase (Na pump) intracellular Na intracellular Ca increase muscle contraction by sliding of actin & myosin .

Indications : long term control of : 1- Heart failure : contractility . 2- Atrial fibrillation : conductivity of AV node . Contraindications: o Absolute contraindications : - Digitals toxicity . - Ventricular tachycardia (VT).

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In Capsule Series

Cardiology

o Relative contraindications : - Partial heart block . - Peptic ulcer . Administration : o Digitalistion : (to reach optimum therapeutic level ) 2 tablets daily for 5 days (oral). o Maintenance dose : (compensates for daily urinary excretion ) 0.5 1 tablets daily (oral) Preparations : o Digoxin (Lanoxin):excreted mainly by the kidney (tab=0.25mg , amp=0.5mg ) o Digitoxin : metabolised mainly in the liver (digitoxine hepatic). o Ouabain (IV) . DIGITALIS TOXICITY : o Precipitating factors: Old age. Renal failure. Hypokalemia. Hypercalcemia. Thyroid disorders. Drugs : quinidine. o Clinical picture: Non cardiac : GIT : Anorexia , nausea, vomiting (1STsymptom) Neurological: Psychosis , yellow vision . Gynecomasteia . Cardiac : (most life threatening ) excitability Arrhythmias . AVN conduction heart block. N.B: Almost any arrhythmia can be a manifestation of digitalis toxicity
except type 2 second degree heart block .
(MCQ)

o Treatment : Stop digitalis. Stop diuretics. Give K. Digitalis antibodies (Digibind). Anti-arrhythmic drugs (e.g: phenytoin , lidocaine ) .

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In Capsule Series

Cardiology

o To avoid toxicity : Decrease the dose. Drug holiday. Routine estimation of serum level of digitalis(N=0.5-2ng/ml).

7- -blockers :
Historically , blockers were contraindicated in HF due to their -ve inotropic effect. Recently: blockers are indicated in HF because they were found to : Reduce mortality & improve the prognosis. Prevent arrhythmia. Decrease blood pressure. e.g: Metoprolol ( 2nd generation 1 blocker ) Carvedilol (3rd generation 1 blocker). Start with low doses with gradual increase .

8- Aminophylline :
Action : Bronchodilator . Diuretic effect . Vasodilator . +Ve inotropic .

Administration : Oral , suppositories , IV. IV injection must be very slowly to avoid arrhythmia .

9- Oxygen therapy :
Especially in acute pulmonary edema , MI & hypoxic cor pulmonale

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In Capsule Series

Cardiology

ACUTE HEART FALIURE (Acute Cardiogenic Pulmonary Edema)


Etiology : (sudden
in pulmonary venous pressure) Acute left sided heart failure e.g : myocardial infarction. MS with aggravating factor as AF.

Clinical picture :
Severe dyspnea at rest & orthopnea. Sense of impending death. Cyanosis. Cripitations . Cough with expectoration of frothy pink sputum .

Treatment :
1) Hospitalization in ICU : bed rest in sitting position . 2) High dose oxygen correct hypoxia . 3) Morphine (IV) Reduce anxiety. Reduce preload (venodilator). 4) Furosemide (IV) Decreases pulmonary congestion (venodilator) Diuresis. 5) vasodilators (IV): Na nitroprusside IV infusion (0.5 5 mg / kg/ min) Nitroglaycrin IV infusion (S/E: tolerance). 6) Inotropics : Dobutamine ( receptor agonist): +ve inotropic & vasodilatation (inodilator) Milrinone (phosphodiesterase inhibitor): inodilator. :Milrinone is preferred to dobutamine in patients receiving blocker NB : because its mechanism of action does not involve receptors. 7) Aminophylline : 250 500 mg / IV infusion very slowly . 8) Treatment of the cause & the precipitating factors . 9) Advanced management : in refractory conditions Mechanical ventilation . Mechanical assist devices : Intra-aortic balloon counter pulsation.

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In Capsule Series

Cardiology

Refractory ( Intractable ) Heart Failure


ETIOLOGY :
Diagnostic error : the case may be pericardial effusion rather heart failure . Improper management : Inadequate salt restriction . Discontinuation of treatment . presence of a precipitating factor :e.g : infection . presence of the cause : uncontrolled hypertension. mechanical factor :AS . Terminal cases of heart failure .

TREATMENT :
Reassess the cause. Removal of mechanical factor : valve replacement . Removal of precipitating factor. Proper management : Strict bed rest. Salt & even fluid restriction. Proper doses. For terminal cases : IV Lasix , morphine , dobutamine , nitrate may be used . Mechanical ventilation . cardiac transplantation .

Medicine cannot, except over a short period, increase the population of the world.

Bertrand Russell

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