Heart Failure

DR.LIU LIXIN
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 vasoconst. → ↑ V return, After load →↑ workload
activity ↑ filling →↑ O2 consumption
↑ Renin- Salt & water retention→↑ Vasoconstriction →
Angiotensin – VR ↑ after load
Aldosterone
↑ Vasopressin Same effect Same effect

↑ interleukins May have roles in myocyte Apoptosis

&TNFα 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
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