patoloji-ders-notlari

Title

Serdar Balcı

Heart Failure and Arryhtmias

Serdar BALCI, MD

Heart failure

Congestive heart failure

End point for many forms of cardiac disease

Progressive condition

Extremely poor prognosis

Diastolic dysfunction

Inability of the heart to adequately relax and fill

Left ventricular hypertrophy, myocardial fibrosis, amyloid deposition, or constrictive pericarditis

Elderly persons, diabetic patients, and women

Valve dysfunction

Congestive heart failure

Occurs when the heart cannot generate sufficient output to meet the metabolic demands of the tissues
Can only generate sufficient output at higher than normal filling pressures
- Hyperthyroidism
- Poor oxygen carrying capacity as in anemia
- High-output failure
Abrupt
- Large myocardial infarct
- Acute valve dysfunction
Gradually and insidiously
- Most cases
- Effects of chronic work overload
- Progressive loss of myocardium

Cannot efficiently pump the blood returned from venous circulation

Increased end-diastolic ventricular volume

Increased end-diastolic pressures

Elevated venous pressures

Inadequate cardiac output (forward failure) almost always accompanied by increased congestion of the venous circulation (backward failure)

The Frank-Starling mechanism

Increased end-diastolic filling volume

Dilate the heart

Increased cardiac myofiber stretching

Lengthened fibers contract more forcibly

Increase cardiac output

Compensated heart failure

Dilation → increased wall tension → Increase the oxygen requirements→ Decompensated heart failure

Neurohumoral systems

Norepinephrine
- Increases heart rate, myocardial contractility, vascular resistance
Renin-angiotensin-aldosterone system
- Increase circulatory volume, increases vascular tone
Atrial natriuretic peptide
- Balance the renin-angiotensin-aldosterone system
- Diuresis
- Vascular smooth muscle relaxation

Myocardial structural changes

Increased muscle mass
- Increased numbers of sarcomeres
- Myocyte enlargement
Hypertrophy

**pressure-overloaded heart **

**volume-overloaded heart **

Robbins Basic Pathology

Hypertrophy in pressure overload

Hypertension, valvular stenosis

New sarcomeres added parallel to the long axis of the myocytes, adjacent to existing sarcomeres

Muscle fiber diameter results in concentric hypertrophy

Ventricular wall thickness increases without an increase in the size of the chamber

Hypertrophy in volume overload

Valvular regurgitation, shunts

New sarcomeres are added in series with existing sarcomeres

Muscle fiber length increases

Ventricle tends to dilate

Wall thickness can be increased, normal, or decreased

Heart weight is the best measure of hypertrophy in volume-overloaded cases

Compensatory hypertrophy

Myocardium vulnerable to ischemic injury
Altered patterns of gene expression
- Fetal myocytes
- Changes in the dominant form of myosin heavy chain
- Increases in heart rate, force of contraction
Myocyte apoptosis
Cytoskeletal alterations
Increased extracellular matrix deposition

Pathologic compensatory cardiac hypertrophy

Increased mortality

Independent risk factor for sudden cardiac death

Volume-loaded hypertrophy induced by regular aerobic exercise

Physiologic hypertrophy

Increase in capillary density

Decreased resting heart rate and blood pressure

Reduce overall cardiovascular morbidity and mortality

Left-Sided Heart Failure

Ischemic heart disease
Systemic hypertension
Mitral or aortic valve disease
Primary diseases of the myocardium
- Amyloidosis
Diminished systemic perfusion
Elevated back-pressures within the pulmonary circulation

Heart in Left-Sided Heart Failure

The gross cardiac findings depend on the underlying disease process
Left ventricular dilation can result in mitral insufficiency and left atrial enlargement
- Associated with an increased incidence of atrial fibrillation
Microscopic changes are nonspecific
- Myocyte hypertrophy with interstitial fibrosis of variable severity

Lungs in Left-Sided Heart Failure

Congestion
Edema
Pleural effusion
Lungs are heavy
Perivascular and interstitial transudates
Alveolar septal edema
Accumulation of edema fluid in the alveolar spaces
Red cells extravasate from the leaky capillaries into alveolar spaces
- Phagocytosed by macrophages
- Hemosiderin-laden alveolar macrophages
  - Heart failure cells

http://www.pathguy.com/lectures/heart_failure_cells.jpg

Left-Sided Heart Failure

Renin-angiotension-aldosterone axis
Exacerbate the pulmonary edema
Reduction in renal perfusion
- Prerenal azotemia
- Increasing metabolic derangement
Diminished cerebral perfusion
- Hypoxic encephalopathy

Right-Sided Heart Failure

Consequence of left-sided heart failure
- Increase in the pulmonary circulation
- Increased burden on the right side of the heart
Isolated right-sided heart failure
- Severe pulmonary hypertension
- Cor pulmonale
Primary pulmonic or tricuspid valve disease
Congenital heart disease
- Left-to-right shunts
Liver is increased in size and weight
- Congestive hepatomegaly
Passive congestion
- Nutmeg liver
- Congested centrilobular areas, peripheral paler noncongested areas
- When left-sided heart failure is also present, severe central hypoxia produces centrilobular necrosis
- Long-standing severe right-sided heart failure, the central areas can become fibrotic, cardiac cirrhosis

http://www.pathguy.com/lectures/nutmeg3.jpg

Elevated pressure in the portal vein
- Portal hypertension
Vascular congestion, tense, enlarged spleen
- Congestive splenomegaly
Chronic passive congestion of the bowel wall
- Edemas
- Interfere with absorption of nutrients and medications
Effusions in Pleural, Pericardial, and Peritoneal Spaces
Subcutaneous Tissues
- Ankle (pedal) and pretibial edema
- Presacral in bedridden patients
- Anasarca

ARRHYTHMIAS

Arrhythmias

Ischemic injury is the most common cause of rhythm disorders
- Direct damage
- Dilation of heart chambers
- Alteration in conduction system firing.
Inherited causes of arrhythmias
- Mutations ion channels
- Channelopathies

Sudden Cardiac Death

Sustained ventricular arrhythmia

Underlying structural heart disease

Coronary artery disease is the leading cause of death 80-90% of cases

SCD often is the first manifestation of IHD

Autopsy typically shows only chronic severe atherosclerotic disease

Acute plaque disruption is found in only 10% to 20% of cases

Healed remote MIs are present in about 40% of the cases

Robbins Basic Pathology

Nonatherosclerotic causes of SCD

**Younger **

Hereditary (channelopathies) or acquired abnormalities of the cardiac conduction system

Congenital coronary arterial abnormalities

Mitral valve prolapse

Myocarditis or sarcoidosis

Dilated or hypertrophic cardiomyopathy

Pulmonary hypertension

Myocardial hypertrophy

Sudden Cardiac Death

Increased cardiac mass is an independent risk factor for SCD
In some young persons who die suddenly, including athletes
- Hypertensive hypertrophy or unexplained increased cardiac mass is the only pathologic finding

The mechanism of SCD

**Lethal arrhythmia **

Asystole or ventricular fibrillation

Infarction need not occur

80-90% of patients successfully resuscitated do not show any enzymatic or ECG evidence of myocardial necrosis, even if the original cause was IHD

**Most cases of fatal arrhythmia are triggered by electrical irritability of myocardium distant from the conduction system **

Autopsy Pathology: A Manual and Atlas