Heart Failure

Kalaiselvan ot
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
 It is a common end point for many
diseases of cardiovascular system
 It can be caused by :

-Inappropriate work load (volume or pressure

overload)

-Restricted filling
-Myocyte loss
Causes of left ventricular

failure
• Volume over load: Regurgitate valve
High output status
• 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

 From hemodynamic stand point HF can

be secondary to systolic dysfunction or

diastolic dysfunction
Neurohormonal changes
N/H changes Favorable effect Unfavor. effect

 HR , contractility, Arteriolar constriction 

 Sympathetic activity vasoconst.   V return, After load  workload
 filling  O2 consumption

 Renin-Angiotensin – Salt & water retention VR Vasoconstriction 

 after load
Aldosterone
 Vasopressin Same effect Same effect

 interleukins &TNF May have roles in myocyte Apoptosis

hypertrophy

Vasoconstriction VR  After load

Endothelin
 Cellular changes
 Changes in Ca+2 handling.
 Changes in adrenergic receptors:
• Slight  in α1 receptors
• β1 receptors desensitization  followed by down regulation

 Changes in contractile proteins

 Program cell death (Apoptosis)
 Increase amount of fibrous tissue
Symptoms
• SOB, Orthopnea, paroxysmal nocturnal
dyspnea

• Low cardiac output symptoms

• Abdominal symptoms: Anorexia,nausea,

abdominal fullness,
Rt hypochondrial pain
Physical Signs
 High diastolic BP & occasional decrease in
systolic BP (decapitated BP)
 JVD
 Rales (Inspiratory)
 Displaced and sustained apical impulses
 Third heart sound – low pitched sound that is heard
during rapid filling of ventricle
Physical signs (cont.)
 Mechanism of S3 sudden deceleration of blood
as elastic limits of the ventricles are
reached

 Vibration of the ventricular wall by blood

filling

 Common in children
Physical signs (cont.)
 Fourth heart Sound (S4)
- Usually at the end of diastole
- Exact mechanism is not known
Could be due to contraction of
atrium against stiff ventricle

 Pale, cold sweaty skin

Framingham Criteria for
Dx of Heart Failure
 Major Criteria:
 PND
 JVD
 Rales
 Cardiomegaly
 Acute Pulmonary Edema
 S3 Gallop
 Positive hepatic Jugular reflex
 ↑ venous pressure > 16 cm H2O
Dx of Heart Failure (cont.)
 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
 Pregnancy, anemia, thyrotoxisis, A/V fistula,
Beriberi, Pagets disease
 Low Output Failure
 Acute
 large MI, aortic valve dysfunction---
 Chronic
Forms of heart failure
( cont.)
 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 run)
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
 Ischemia
 Valvular heart disease
 Thyrotoxicosis and other high output status
 Shunts
 Arrhythmia
 A fib, flutter, PJRT
 Medications
 Ca channel blockers, some antiarrhythmics
Diet and Activity

 Salt restriction
 Fluid restriction
 Daily weight (tailor therapy)
 Gradual exertion programs
Diuretic Therapy
 The most effective symptomatic relief
 Mild symptoms
 HCTZ
 Chlorthalidone
 Metolazone
 Block Na reabsorbtion in loop of henle and distal
convoluted tubules
 Thiazides are ineffective with GFR < 30 --/min
Diuretics (cont.)
 Side Effects
 Pre-renal azotemia
 Skin rashes
 Neutropenia
 Thrombocytopenia
 Hyperglycemia
 ↑ Uric Acid
 Hepatic dysfunction
Diuretics (cont.)
 More severe heart failure → loop
diuretics
 Lasix (20 – 320 mg QD), Furosemide
 Bumex (Bumetanide 1-8mg)
 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

 Renin-angiotensin-aldosterone system is activation

early in the course of heart failure and plays an
important role in the progression of the syndrome
 Angiotensin converting enzyme inhibitors
 Angiotensin receptors blockers
 Spironolactone
Angiotensin Converting
Enzyme Inhibitors
 They block the R-A-A system by inhibiting the
conversion of angiotensin I to angiotensin II
→ vasodilation and ↓ Na retention
 ↓ Bradykinin degradation ↑ its level → ↑ PG
secretion & nitric oxide
 Ace Inhibitors were found to improve survival
in CHF patients
 Delay onset & progression of HF in pts with
asymptomatic LV dysfunction
 ↓ cardiac remodeling
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
 Reduction in hospitalization

 Reduction in symptoms of HF
Digitalis (cont.)
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
Digitalis Toxicity
 Cardiac manifestations
 Sinus bradycardia and arrest
 A/V block (usually 2nd degree)
 Atrial tachycardia with A/V Block
 Development of junctional rhythm in patients with
a fib
 PVC’s, VT/ V fib (bi-directional VT)
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
 Reduction of afterload by arteriolar
vasodilatation (hydralazin)  reduce LVEDP, O2
consumption,improve myocardial perfusion,  stroke
volume and COP
 Reduction of preload By venous dilation
( Nitrate)  ↓ the venous return ↓ the load on
both ventricles.
 Usually the maximum benefit is achieved by
using agents with both action.
Positive inotropic agents
 These are the drugs that improve myocardial
contractility (β adrenergic agonists, dopaminergic
agents, phosphodiesterase inhibitors),
dopamine, dobutamine, milrinone, amrinone
 Several studies showed ↑ mortality with oral
inotropic agents
 So the only use for them now is in acute
sittings as cardiogenic shock
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
Antiarrhythmics (cont.)
 Patients with non sustained ventricular
tachycardia
 Correction of electrolytes and acid base imbalance
 In patients with ischemic cardiomyopathy → ICD
implant is the option after r/o acute ischemia as
the cause
 In patients wit non ischemic cardiomyopathy
management is ICD implantation
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
 1 year 80% - 90%
 5 years 70%
Prognosis
 Annual mortality rate depends on patients
symptoms and LV function
 5% in patients with mild symptoms and mild
↓ in LV function
 30% to 50% in patient with advances LV
dysfunction and severe symptoms
 40% – 50% of death is due to SCD