Heart Failure

Heart Failure
By:S. Soliman MD

Definition:
* A state in which the heart cannot provide sufficient cardiac output to satisfy the metabolic needs of the body
* It is commonly termed congestive heart failure (CHF) since symptoms of increase venous pressure are often prominent
Etiology
-Inappropriate work load (volume or pressure overload)
-Restricted filling
-Myocyte loss

Causes of left ventricular failure

• Volume over load: Regurgitate valve
• Pressure overload: Systemic hypertension

Outflow obstruction
• Loss of muscles: Post MI, Chronic ischemia
Connective tissue diseases Infection, Poisons
(alcohol,cobalt,Doxorubicin)
• Restricted Filling: Pericardial diseases, Restrictive
cardiomyopathy, tachyarrhythmia

Pathophysiology
* Hemodynamic changes
* Neurohormonal changes
* Cellular changes

Hemodynamic changes
Neurohormonal changes
Cellular changes
Symptoms
Physical Signs
Framingham Criteria for Dx of Heart Failure
* Major Criteria:
o PND
o JVD
o Rales
o Cardiomegaly
o Acute Pulmonary Edema
o S3 Gallop
o Positive hepatic Jugular reflex
o ↑ venous pressure > 16 cm H2O
* Minor Criteria
LL edema,
Night cough
Dyspnea on exertion
Hepatomegaly
Pleural effusion
↓ vital capacity by 1/3 of normal
Tachycardia 120 bpm
Weight loss 4.5 kg over 5 days management

Forms of Heart Failure
* Systolic & Diastolic
* High Output Failure
o Pregnancy, anemia, thyrotoxisis, A/V fistula, Beriberi, Pagets disease
* Low Output Failure
* Acute
* Chronic
* Right vs Left sided heart failure:

Right sided heart failure :
Most common cause is left sided failure
Other causes included : Pulmonary embolisms
Other causes of pulmonary htn.
RV infarction
MS
Usually presents with: LL edema, ascites
hepatic congestion
cardiac cirrhosis (on the long
Differential diagnosis
* Pericardial diseases
* Liver diseases
* Nephrotic syndrome
* Protein losing enteropathy

Laboratory Findings
* Anemia
* Hyperthyroid
* Chronic renal insuffiency, electrolytes abnormality
* Pre-renal azotemia
* Hemochromatosis

Electrocardiogram
* Old MI or recent MI
* Arrhythmia
* Some forms of Cardiomyopathy are tachycardia related
* LBBB→may help in management

Chest X-ray
* Size and shape of heart
* Evidence of pulmonary venous congestion (dilated or upper lobe veins → perivascular edema)
* Pleural effusion

Echocardiogram
* Function of both ventricles
* Wall motion abnormality that may signify CAD
* Valvular abnormality
* Intra-cardiac shunts

Cardiac Catheterization
* When CAD or valvular is suspected
* If heart transplant is indicated

TREATMENT
* Correction of reversible causes
Diet and Activity
* Salt restriction
* Fluid restriction
* Daily weight (tailor therapy)
* Gradual exertion programs

Diuretic Therapy
* The most effective symptomatic relief
* Mild symptoms
* Side Effects
* More severe heart failure → loop diuretics
o Lasix (20 – 320 mg QD), Furosemide
o Bumex (Bumetanide 1-8mg)
o Torsemide (20-200mg)

Mechanism of action: Inhibit chloride reabsortion in ascending limb of loop of Henle results in natriuresis, kaliuresis

and metabolic alkalosis

Adverse reaction:
pre-renal azotemia
Hypokalemia
Skin rash
ototoxicity

K+ Sparing Agents
* Triamterene & amiloride – acts on distal tubules to ↓ K secretion
* Spironolactone (Aldosterone inhibitor)
recent evidence suggests that it may improve survival in CHF patients due to the effect on renin-angiotensin-aldosterone

system with subsequent effect on myocardial remodeling and fibrosis

Inhibitors of renin-angiotensin- aldosterone system

o Renin-angiotensin-aldosterone system is activation early in the course of heart failure and plays an important

role in the progression of the syndrome
o Angiotensin converting enzyme inhibitors
o Angiotensin receptors blockers
o Spironolactone

Angiotensin Converting Enzyme Inhibitors
Side effects of ACE inhibitors
* Angioedema
* Hypotension
* Renal insuffiency
* Rash
* cough
Angiotensin II receptor blockers
* Has comparable effect to ACE I
* Can be used in certain conditions when ACE I are contraindicated (angioneurotic edema, cough)
Digitalis Glycosides (Digoxin, Digitoxin)
* The role of digitalis has declined somewhat because of safety concern
* Recent studies have shown that digitals does not affect mortality in CHF patients but causes significant

Mechanism of Action
* +ve inotropic effect by ↑ intracellular Ca & enhancing actin-myosin cross bride formation (binds to the Na-K ATPase →

inhibits Na pump → ↑ intracellular Na → ↑ Na-Ca exchange
* Vagotonic effect
* Arrhythmogenic effect

Digitalis Toxicity
* Narrow therapeutic to toxic ratio
* Non cardiac manifestations
Anorexia,
Nausea, vomiting,
Headache,
Xanthopsia sotoma,
Disorientation
* Cardiac manifestations

Digitalis Toxicity Treatment
* Hold the medications
* Observation
* In case of A/V block or severe bradycardia → atropine followed by temporary PM if needed
* In life threatening arrhythmia → digoxin-specific fab antibodies
* Lidocaine and phenytoin could be used – try to avoid D/C cardioversion in non life threatening arrhythmia

β Blockers
* Has been traditionally contraindicated in pts with CHF
* Now they are the main stay in treatment on CHF & may be the only medication that shows substantial improvement in LV

function
* In addition to improved LV function multiple studies show improved survival
* The only contraindication is severe decompensated CHF

Vasodilators
Positive inotropic agents
Anticoagulation (coumadine)
* Atrial fibrillation
* H/o embolic episodes
* Left ventricular apical thrombus

Antiarrhythmics
* Most common cause of SCD in these patients is ventricular tachyarrhythmia
* Patients with h/o sustained VT or SCD → ICD implant
* Patients with non sustained ventricular tachycardia

New Methods
* Implantable ventricular assist devices
* Biventricular pacing (only in patient with LBBB & CHF)
* Artificial Heart

Cardiac Transplant
* It has become more widely used since the advances in immunosuppressive treatment
* Survival rate
Prognosis
Heart Failure