HEART FAILURE

ACQUAAH-ARHIN GODWIN, MBCHB (CLASS OF 2025)

 PREVIEW

• The heart is a four chambered structure that pumps blood around the body
• Ventricles( left and right)
• Atrium ( left and right)
• Arterial supply by the Right and left coronary arteries
• Venous drainage by the coronary sinus
• Normal weight 250-300 in females
300-350 in males
 PREVIEW

• LV thickness 13-15mm
• RV thickness 3-5mm
 HISTOLOGY/PHYSIOLOGY

• The heart has three layers from internal to external

• Endocardium
• Myocardium (main functional unit of the heart)
• Epicardium
• Ventricular myocytes are the most specialized cells
• They are arranged circumferentially in a spiral orientation
• Contractile unit are sarcomere
 HISTOLOGY / PHYSIOLOGY

• Sarcomeres are composed of thick and thin filaments

• Contractile proteins are troponin and tropomyosin
• Valves ensure unidirectional flow of blood
• Composed of Tricuspid and Mitral leaflets
• Pulmonary and semilunar valves, have cusps
CASE

A 62 year old hypertensive and diabetic man presents with stupor, 3 months hsitory of
cough, orthopnoea, PND and bidpedal swelling.
• Explain the pathophysiology of his condition
• What are the pathologic basis of his condition
• 3 days on admission, patient died. State the morpholgic changes of the various organs
you would expect to see on autopsy
 HEART FAILURE

• Heart failure is a clinical syndrome that results from structural and functional abnormality
of ventricular filling or ejection of blood, leading to inadequate cardiac output to meet the
metabolic needs of the tissues and organs of the body.
• Epidemiology
• Prevalence in the United States is 1%-2%
• Prevalence in African Americans is 25% higher than in whites
• Most common cause of hospitalization in 60 years and above
 HEART FAILURE
ETIOLOGY
• Hypertension
• Valvular heart disease
• Coronary artery disease
• Cardiomyopathy
• Constrictive pericarditis
• Amyloidosis
• Myocardial infarction
ETIOLOGY

• Hemochromatosis
• Cor pulmonale
• Congenital heart diseases
• Substance abuse
• Cardiotoxic drugs
• Renal failure
PATHOPHYSIOLOGY

• When cardiac workload increases or cardiac function is compromised several physiologic

mechanisms swing in to compensate
• a) Neurohormonal activation
• i)SNS
• ii) RAAS
• b) Cardiac remodelling , concentric and eccentric LEFT VENTRICULAR
HYPERTROPHY
PATHOPHYSIOLOGY

• Cardiac remodelling
• sustained increase in mechanical work of either ventricle due to pressure overload, volume
overload and trophic signals(those actiavted through the activation of beta adrenergic receptors
• leads to cellular hypertrophy
• lead to increase in the size and weight of the heart
• pressure overload new sarcomeres are assembled in parallel to the long axes of cells hence
expanding the cross sectional area of myocytes and a concentric increase in wall thickness
PATHOPHYSIOLOGY

• voolume overload new sarcomeres are assembled in series within existing sarcomeres
leading to ventricular dilation
PATHOPHYSIOLOGY

• Left ventricular dysfunction

• Left ventricular systolic dysfunction
• Impaired myocyte contractility and dilated heart reflected by LV ejection fraction less
than or equal to 40%
• Left ventricular diastolic dysfunction
• Inadequate relaxation and filling of the ventricle but normal myocyte contractility
reflected by LVEF greater or equal to 50%
PATHOPHYSIOLOGY

• LEFT SIDED HEART FAILURE

• CAUSES
• hypertension
• Ischemic heart disease
• valvular heart disease
• clinical and morphologic effects of left-sided heart failure are pimary due tp
• i) pooling of blood in the pulmonary circulation
PATHOPHYSIOLOGY

• stasis of bood in left sided chambers

• inadequate perfusion of downstream tissues leading to organ dysfunction
ORGAN CHANGES

• Heart
• Gross
• depends on the disease process but the left ventricle is mo hypertrophied and often dilated
• myocardial infarcts
• stenotic valves
• Microscopic changes
• myocyte hypertrophy and interstitial fibrosis
ORGAN CHANGES

• lung
• pulmonary edema and congestion
• heart failure cells
ORGAN CHANGES

• Kidneys
• stimlulation of RAAS
• prerenal azotaemia
• acute tubular necrosis
• Brain
• cerebral hypoperfusion
• hypoxic encephalopathy which can lead stupor and coma with ischemic cerebral injury
 LEFT SIDED HEART FAILURE

• Clinical manifestations
• cough
• exertional dyspnea
• orthopnea
• paroxysmal nocturnal dyspnea
• dyspnea at rest
• fatigue
• basal crackles on ausculation of chest
CONT....

• tachypnea
• tachycardia
• apex beat may be displaced
• a murmur may be heard
RIGHT SIDED HEART FAILURE
CAUSES

• left sided heart failure

• cor pulmonale
• congenital heart disease associated with left to right shunt
• tricuspid and pulmonic valve lesions
ORGAN CHANGES

• LIVER
• congestive hepatomegaly
• nutmeg appearance, congested red-brown pericentral zones with relatively normal-
colored tan periportal regions.
• cardiac cirrhosis
• congestive splenomegaly
 ORGAN CHANGES

• fluid accumulation in the pleural, pericardial and peritoneal spaces

• subcutaneous tissue pitting pedal edema and anasarca
CLINICAL MANIFESTATIONS
• pedal swelling
• right hypochrondiac pain
• abdominal distension
• anorexia
• raised JVP
CONT...

• smooth, soft tender hepatomegaly

• pitting oedema
• gallop rhythm
INVESTIGATIONS
• ECG
• ECHPCARDIOGRAPHY
• FBC
• Chest X-ray
• BUN and Creatinine
• LFT
• TFT
• lipid profile
• genetic testing
• cardiovascular MRI
TREATMENT

• Diuretics
• ACE INHIBITORS
• ARB
• BETA BLOCKER
• MINERALOCORTICOID RECEPTOR ANTAGONIST
• SGLT2 INHIBITOR
COMPLICATIONS

• CARDIORENAL SYNDROME
• CONGESTIVE HEPATOPATHY
• PLEURAL EFFUSION which can lead LUNG ATELECTASIS
• PREDISPOSITION TO THROMBOEMBOLISM
PROGNOSIS

• 30 -40% mortality rate within 1 year of diagnosis

• 60-70% die within 5 years
• survival worsens with age
• women, in general have a better prognosis
• lower socioeconomic status reduces survival rate
REFERENCES

• ROBBINS AND CONTRANS PATHOLOGIC BASIS OF DISEASES

• wikidoc.com
• cardofmich.com
DANKE
BIS SPATER