Cardiac failure

Definition – impaired cardiac function renders the heart unable to maintain output sufficient for the metabolic requirements of the body

• It is a common result of many forms of heart disease

 

• Regardless of the cause of heart failure the CVS attempts to compensate for inadequate cardiac output in heart failure by;
  • Ventricular dilation – Frank-Starling Law, increased force of contraction with myofibril stretch
  • Blood volume expansion by salt and water retension e.g. via the renin-angiotensin-aldosterone mech
  • Tachycardia

 

• In many cases the onset of cardiac failure is preceded by cardiac hypertrophy, the compensatory response of the myocardium to increased mechanical work
• Most instances of heart failure are the consequence of progressive deterioration of the contractility of the myocardium – systolic dysfunction e.g with hypertension or ischaemic heart disease
• Diastolic dysfunction can occur whereby there is inability of the heart muscle to relax, expand and fill sufficiently during diastole. This can occur with massive left ventricular hypertrophy, myocardial fibrosis, amyloid deposition or constrictive pericarditis

 

• Whatever the cause, heart failure is characterised by diminished cardiac output of accumulation of blood in the venous system of both

 

Cardiac hypertrophy

• Myocytes cant undergo hyperplasia as they cant synthesise DNA so aren’t believed to be able to  divide
• Increased mechanical load causes an increase in the content of subcellular components and a consequent increase in cell size. This results in increased heart size
• The weight of the heart depends on the cause of the hypertrophy, hearts weighing more than 1000g are rare
• The pattern of hypertrophy reflects the nature of the stimulus;
• Pressure-overload – leads to concentric hypertrophy as the deposition of sarcomeres is parallel to the long axis of the cells, therefore the cross section of the cell is expanded by the length is not
• Volume-overload – deposition of new sarcomeres results in increased cell length and width and is characterised by dilation with increased ventricular diameter
• Hypertrophic states results in increased metabolic demand and increased wall tension, this was well as increased heart rate and contractility results in increased oxygen demand

 

• The deleterious alterations associated with hypertrophy are;
  • Decreased capillary to myocyte ratio
  • Increased fibrous tissue
  • Synthesis of abnormal proteins
• This can lead to cardiac failure
• With the exception of myocyte death, the mechanisms of cardiac decompensation are not well understood

 

Left sided heart failure

• Most often caused by;
  • Ischaemic heart disease
  • Hypertension
  • Aortic and mitral valve disease
  • Non-ischaemic myocardial disease
• The morphological and clinical effects are due to progressive damming of blood within the pulmonary circulation and the consequences of diminished peripheral blood pressure and flow

 

Morphology

• Heart
  • Hypertrophy and dilation of the LV
  • There may be fibrosis of the myocardium
  • Secondary enlargement of the atrium and AF (may result in blood stasis and thrombus formation)
• Lungs
  • Pulmonary congestion and oedema
  • Associated with haemosiderin containing macrophages in the alveoli called siderophages or heart failure cells
• Kidneys
  • Reduced renal perfusion results in;
  • Salt and water retension
  • Ischaemic acute tubular necrosis
  • Impaired waste secretion causing impaired prerenal azotemia
• Brain
  • In advance CHF, cerebral hypoxia may give rise to hypoxic encephalopathy with symptoms from irritability to coma

 

Right-sided Heart failure

• Usually occurs as a consequence of left sided heart failure
• Pure right sided heart failure most often occurs with chronic severe pulmonary hypertension and is called cor pulmonale – overload of the right ventricle due to increased resistance in the pulmonary circulation
• It may also be caused by pulmonary and tricuspid valve disease

 

Morphology

• Liver and portal system
  • Hepatomegaly with centrolobular congestion and atrophy of central hepatocytes called a nutmeg appearance
  • With severe hypoxia, centrilobular necrosis can occur
  • With high right sided pressure sinusoidal rupture causes central haemorrhagic necrosis
  • Subsequent central fibrosis causes cardiac sclerosis
  • Elevated pressure in the portal vein can lead to congestive splenomegaly
  • Chronic oedema of the bowel wall can result in impaired nutrient absorption and ascites
• Kidneys
  • Congestion of the kidneys is more marked with right sided failure than left, leading to greater fluid retention, peripheral oedema and more pronounced azotemia
• Brain
  • Similar to left sided failure
• Pleural and pericardial spaces
  • Accumulation of fluid in the pleural and pericardial space may occur
  • Although pulmonary oedema indicates left sided failure, pleural effusions indicate right sided failure
• Subcutaneous tissues
  • Peripheral, dependant oedema

 

Sudden cardiac death

• Defined as unexpected death from cardiac causes, early after symptom onset (within one hour) or without symptoms
• In older people may be the first sign of IHD
• In young people is more likely to be due to other causes;
  • Congenital structural or coronary arterial abnormalities
  • Aortic valve stenosis
  • Mitral valve prolapse
  • Myocarditis
  • Dilated or hypertrophic cardiomyopathy
  • Pulmonary hypertension
  • Hereditary or acquired abnormalities in the conduction system
  • Increased cardiac mass
• The ultimate mechanism is generally a lethal arrhythmia