HEART FAILURE

NORMAL CIRCULATION
SVC,IVC

RIGHT ATRIUM

RIGHT VENTRICLE

PULMONARY ARTERY

LUNGS

PULMONARY VEINS

LEFT ATRIUM

LEFT VENTRICLE

TISSUES
HEART FAILURE:
A clinical syndrome that develops when heart cannot maintain an
adequate cardiac out put or can do it only at the expense of an
elevated filling pressure.

 DEFNITION:
 An abnormality when cardiac output is
inadequate to meet the metabolic
demands of the tissues of the body
during exercise ultimately also at rest
in the presence of normal filling
pressures.
 In mild to moderate forms- CO
adequate at rest inadequate when
metabolic demands increase.
 eg exercise
PATHOPHYSIOLOGY
PATHOPHYSIOLOGY OF PULMONRY EDEMA
TYPES:

Left, Diastolic and

Right ,Biventricu systolic
lar dysfunction
Heart
Failure
High output Acute and
and Low output Chronic failure
falure
CLINICAL FEATURES OF HEART
FAILURE:
 SYMPTOMS:
 Right heart failure:
 Dyspnea
 Pedal oedema right upper quadrant
discomfort
 Severe cases- acites, decreased
renal perfusion(oliguria, uremia)
 Left heart failure:
 Orthopnea
 Paroxysmal noctornal dyspnea
 hemoptysis
 dd pic tu r e
ic o n to a First symptom of
Click failure in both-
FATIQUE
EXERTIONAL
DYSPNEA

FEVER suggests
infectious/ embolic
complication.
Severe failure
cutaneous
vasoconstriction
impairs heat loss so
fever may occurs.
 SIGNS
 General examination:
 Exhausted, ill looking patient,
cachexia , resting dyspnea ,
peripheral cyanosis ,cold
extremities with confusion/ severe
mental distress in severe cases.
 Pulse: pulses alterens’ feeble pulse,
narrow pulse pressure, pulses
paradoxus.
 Right heart failure Left heart failure

 pedal edema  Pulmonry edema

 Raised JVP  Raised JVP
 Third and fourth  Third heart sound
heart sounds at the apex (lvf)
 Basal  Inspiratory
crepitations crepitations
 Hepatomegaly  Cardiac cachexia
 Pleural effusion  Pleural effusion
 Ascites  Low BP
 Hepatojugular  Poor renal
reflex perfusion
COMPLICATONS:
 Renal failure – low CO poor renal
perfusion, exacerbated diuretic, ACE
inhibitors and ARBs
 Hypokalemia – trt wth potassium losing
diuretics.
 Hyperkalemia – comb of ACE inhibitors
and spironolactone , renal dysfunction.
 Hyponatremia – is a feature of severe
heart failure and is poor prognostic
sign, due to diuretic therapy, high ADH,
failure of cell membrane ion pump.
 Impaired liver function – hepatic
venous congestion and poor arterial
perfusion.
 Thromboembolism – low CO & enforced
mobility deep vein thrombosis& pulm
embolism systemic emboli AF,
arrithmia
 Atrial & ventricular arrithmias – very
common, related to ventricular arrithmia.
INVESTIGATIONS
 Chosen on the basis of history & clinical
exam
 In all patients- total count, hemoglobin,
ectrolytes, creatinine , liver function
studies, urine analysis.
 Chest X-ray: PA lateral view-detects
increased transverse diameter of the heart,
pulmonary venous congestion, pulmonary
edema, Kerley B lines, pleural effusion.
 ECG: for evidence of underlying LVH; sinus
tachycardia, intraventricular conduction
defects, non specific STT changes.
 ECHOCARDIOGRAPHY : most useful
diagnostic test, distinguishes systolic and
 diastolic dysfunction , detects regional wall
motion abnormalities, gives prognostic
information.
 Can dignose valvular, congenital disease or
cardiomyopathy.
 MRI:
 BNP LEVELS: useful diagnostically; levels
correlates with severity of HF, falls as
patient reaches compensatory phase.
 IN SELECTED PATIENTS: blood
culture(inf endocarditis)
 Exercise test(coronary ds)
 Metabolic exercise test( diff cardiac
exertional dyspnea from ventilatory defect
causing dyspnea)
 Lung scan(pulmonary embolism)
 Cardiac catheterisation
 Pulmonary angiography
 Thyroid function tests
 Liver function may be abnormal due to
congestion
TREATMENT OF HEART FAILURE
 Aim of treatment:
 In acute stage : to stabilize the patient
 In chronic stage:
 a) to improve quality of life by
releiving symptoms.
 b) to lengthen survival
 C) to prevent the progression of
myocardial remodeling.
 Three major aspects of therapy:
 i Management of acute or chronic
condition
 ii treatment of any underlying cardiac
disease.
 iii treatment of precipitating factors
 Modalities of therapy:
 i Non-drug general measures
 ii pharmacological
 iii Surgical
 NON-DRUG GENERAL MEASURES:
 Bed rest: increases renal flow, initiates
diuresis.
 Chronic stable failure- exercise training is
recommended.
 Avoid- lifting heavy weights
 high dietary salt
 alcohol , smoking
 In obese patients- weight to be shed
 Drugs- negative inotropes,
verampamil,diltiazem, beta blokers.
MANAGEMENT OF PULMONARY EDEMA
 Oxygen- maintain saturation above 90%
 Upright posture- back rest
 If not contraindicated morphine IV 1-4
mg each 10-30min initially.
 Frusemide 40-80mg slow IV bolus over
1-2 min. frusemide causes
venodilatation even before diuretic
response starts.
 If there is no response to above further
drug management as follows
 If systolic BP is more than 100mm
 Give further bolus of furosemide
 Increased to maximum of 200 mg in
subsequent doses based on response.
 If systolic BP is less than 100mm
 Start inotrophic support
 A) IV Dopamine to be used primarily in
case of hypotension.
 B)IV dobutamine if cardiac output is low.
 c)IV infusion of vasodilators
 In MI addnitroglycerine infusion if BP
permits.IV route is preffered to oral
 For severe hypertension
 IV Nitroprusside0.5-8mcg/kg/min
 Intubation /mechnical ventilation for
severe hypoxia or respiratory acidosis
 In severe renal failure/diuretic resistance
acute hemodialysis and ultrafiltration.
 Intra aortic ballon counter pulsation
THANK YOU