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Cardiovascular System > Pathology of Ischemic Heart Disease > Flashcards

Pathology of Ischemic Heart Disease Flashcards

1
Q

Cardiac Failure Definition

A

The clinicopathologic state where the heart is unable to pump blood at the rate required for normal function and metabolism

Cardiac failure may be acute or chronic and may affect one or both ventricles (i.e. called biventricular failure)

This entails increase in the ventricular wall
thickness as well as the mass of the heart

It is only when the hypertrophic ventricles no
longer can compensate for the increased
demand, that the ventricles dilate, i.e. failure

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2
Q

Categories of Cardiac Failure

A
  1. Low-output or high output failure
  2. Systolic or diastolic failure
  3. Right or left heart failure

Low-output, high-output, systolic and diastolic
failure are considered functional definitions

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3
Q

Low-Output Cardiac Failure:

A

The heart itself is incapable of pumping normally and this is seen in cases of abnormal myocardial function or valvular lesions

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4
Q

High-Output Cardiac Failure

A

The heart is pumping normally, but cannot meet the

excessive demand for blood by the body and this is encountered in cases of anaemia or hyperthyroidism

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5
Q

Systolic Failure:

A

The heart is unable to contract forcefully enough in order to pump blood into the systemic circulation

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6
Q

Diastolic Failure:

A

Although the systolic function is normal, the heart cannot relax adequately during diastole to fill with blood, and thus a smaller volume of blood is pumped
into the circulation during systole

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7
Q

Right Ventricular Failure:

A

Can be classifies as either Acute or Chronic

  1. Acute failure occurs after massive pulmonary
    embolism, resulting in sudden death
  2. Chronic failure may be secondary to mitral stenosis
    or lung disease (cor pulmonale), resulting in neck
    vein distention, liver congestion (so-called nutmeg
    liver) and peripheral oedema

Important to note that the normal heart
muscle has a large functional reserve (600%),
allowing the ventricles to compensate for the
increased functional demands, i.e. ventricular
hypertrophy

Causes:

  1. LV hypertrophy: systemic hypertension, aortic stenosis and incompetence, mitral incompetence, coarctation of the aorta, severe anaemia, severe hyperthyroidism.
  2. RV hypertrophy: pulmonary hypertension (lung diseases, mitral stenosis, LV failure), pulmonary stenosis, VSD, ASD, PDA.

CARDIAC FAILURE

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8
Q

Left-Ventricular Failure:

A

Can be classified as either Acute and Chronic:

  1. Acute failure occurs after massive myocardial
    infarction, resulting in severe dyspnoea, pulmonary
    oedema and death
  2. Chronic failure may be secondary to systemic
    hypertension or chronic ischaemic heart disease
    (IHD), which leads to chronic lung congestion (socalled ‘brown induration’ of the lungs) and with
    time, right ventricular failure
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9
Q

The pathological causes of Heart Failure can broadly be categorised as:

A

Ischaemic heart disease (IHD)

Hypertensive heart disease

Valvular heart disease

Primary (non-ischaemic) myocardial disease

Congenital heart disease

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10
Q

Ischemic Heart Disease:

Definition

A

IHD encompasses the conditions that arise owing to an imbalance between the supply and demand of oxygen an nutrients to the heart muscle it is also termed coronary artery disease (CAD)

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11
Q

Ischemic Heart Disease:

Aetiology

A

Coronary artery atherosclerosis

Coronary vasospasm

Narrowing of the coronary ostia

Coronary artery vasculitis

AETIOLOGY OF IHD
• coronary vasospasm
▪ results in the temporary reduction of luminal
caliber
▪ may aggravate the local mechanical forces that
result in plaque fracture

AETIOLOGY OF IHD
• narrowing of coronary ostia
▪ aortic atherosclerosis
▪ syphilitic mesaortitis (a form of tertiary syphilis)
AETIOLOGY OF IHD
• other rare causes include
▪ shock (diffuse subendocardial infarction)
▪ aortic stenosis
▪ embolism
▪ dissecting aneurysm
▪ congenital abnormalities of coronary arteries
▪ severe anaemia
CLINICAL FEATURES OF IHD
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12
Q

Aetiology of IHD:

Coronary Artery Atherosclerosis

A

Coronary artery atherosclerosis:

  • fixed coronary atherosclerosis
  • progressive coronary atherosclerosis

acute disruption of the atherosclerotic plaque
causing partial or total occlusion of the coronary
artery lumen, i.e.:

❑rupture or ulceration of plaque with superimposed
thrombosis (‘crack’ or ‘facture’ theory) or

❑haemorrhage into a plaque

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13
Q

Aetiology of IHD:

Coronary Vasospasm

A

Results in the temporary reduction of luminal

caliber and may aggravate the local mechanical forces that result in plaque fracture

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14
Q

Aetiology of IHD:

Narrowing of Coronary Ostia

A

Aortic atherosclerosis

Syphilitic mesaortitis (a form of tertiary syphilis)

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15
Q

Aetiology of IHD:

Rare causes

A

Aortic stenosis

Embolism

Shock-Diffuse subendocardial infarction

Dissecting Aneurysm

Congenital abnormalities of coronary arteries

Severe anaemia

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16
Q

The clinical manifestations that an individual

develops is determined by:

A

Cause of the ischaemia

The degree of ischaemia

The collateral circulation

The mass of the ventricle

17
Q

Clinical Features of IHD

A

The clinical manifestations of ischaemic heart
disease include the following

  • Angina pectoris
  • Acute myocardial infarction
  • Chronic ischaemic heart disease
  • Sudden cardiac death
18
Q

Angina Pectoris

A

Defined as a sudden transient retrosternal
chest pain usually elicited by physical exertion
and relieved with rest

No myocardial pathology demonstrable

19
Q

Acute Myocardial Infarction

A

Acute myocardial infarction can be defined as
a localized area of ischaemic necrosis in heart
muscle resulting from a sudden reduction in
coronary blood flow

The lay term is ‘heart attack

20
Q

Acute Myocardial Infarction:

Incidence

A

Very common

Responsible for approximately 25% of deaths in Western countries

In South Africa, mainly White and Indian
population, and mostly males

Age incidence in males after 40 years, and females
after 55 years

Sometimes familial

21
Q

Acute Myocardial Infarction:

Aetiology

A

Coronary atherosclerosis with acute disruption of
the atherosclerotic plaque, i.e. usually
superimposed thrombosis or sometimes
haemorrhage into plaque

The result is total occlusion of the vascular lumen
with interruption of blood flow to the cardiac
muscle, which undergoes ischaemic necrosis (i.e.
infarction)

ACUTE MYOCARDIAL INFARCTION
• infarcts may be classified as
▪ diffuse subendocardial
❑as a complication of shock, i.e. hypoperfusion which
results in ischaemic necrosis of subendocardial region of
the heart (watershed area)
❑involves the entire subendocardial region
❑rare
ACUTE MYOCAR

22
Q

Classification of Infarcts

A

Diffuse subendocardial

Regional

23
Q

Diffuse Subendocardial

A

As a complication of shock, i.e. hypoperfusion which
results in ischaemic necrosis of subendocardial region ofthe heart (watershed area)

Involves the entire subendocardial region

Rare

24
Q

Regional

A

Involves only a part of the ventricular wall

-May be either transmural, i.e. almost the entire
ventricular wall thickness or regional subendocardial

-Transmural infarction is most common

25
Q

The position of the regional infarct is determined by the anatomical pattern of coronary blood supply and the position of the occlusion

A

Left anterior descending artery:
-approximately 50% of cases
-anterior and anterior part of the septum (anteroseptal
infarction)

Right coronary artery

  • approximately 35% of cases
  • posterior (inferior) and posterior part of the septum

Circumflex artery

  • approximately 15% of cases
  • lateral infarction
26
Q

Macroscopic appearance of Myocardial Infarctions

A

For 24 hours after the occlusion the muscle looks normal. It then becomes pale and swollen and after 3 - 4 days is yellow with a hemorrhagic border.

In transmural infarcts: fibrinous pericardial exudate. After 5 days a mural thrombus may begin to form. After 10 days the infarct becomes pale and after 3 - 6 weeks becomes a hard, grey-white scar.

27
Q

Microscopic appearance of Myocardial Infarctions

A

0 - 12 hours :Looks normal

12 - 24 hours :Fibres eosinophilic, striations lost, nuclear changes

1 - 4 days :Neutrophils

4 - 14 days :Macrophages and granulation tissue

14 days + : progressive fibrosis with scarring

28
Q

Complications of Myocardial Infarctions

A

Can be classified as Early(within the first 10 days) and Late

29
Q

Early complications of Myocardial Infarctions

A
  1. Arrhythmias, especially VF
  2. Cardiogenic shock, seen in cases of massive
    infarction
  3. Softening of the heart muscle (called myomalacia
    cordis) maximal at day 5 with:

-Ventricular rupture resulting in haemopericardium and
cardiac tamponade

-Tearing of the posterior papillary muscle resulting in
acute mitral incompetence

-Rupture of the IV septum causing an acquired VSD
ventricular rupture

  1. Mural thrombosis (also seen at day 5) with
    subsequent systemic embolism

5.DVT with pulmonary thromboembolism (decreased
cardiac output and patient bedridden)

30
Q

Late complications of Myocardial Infarction

A
  1. Ventricular aneurysm resulting in heart failure,
    mural thrombi and arrhythmias (remember scar
    tissue stretches, cannot contract, and does not
    rupture)
  2. Chronic heart failure
  3. Dressler syndrome (possibly autoimmune-related)
    and characterized by fever, pericarditis and
    effusions
31
Q

Complications of myocardial infarcts with the mechanism involved in each:

A

Sudden death = Ventricular fibrillation

Arrhythmias = Ventricular fibrillation

Persistent pain = Progressive myocardial necrosis

Angina = Ischaemia of non-infarcted
cardiac muscle

Cardiac failure =Ventricular dysfunction
following muscle necrosis / arrhythmias

Mitral incompetence =Papillary muscle dysfunction,
necrosis or rupture

Pericarditis = Transmural infarct with inflammation of pericardium

Cardiac rupture = Weakening of wall following muscle necrosis and acute inflammation

Mural thrombosis = Abnormal endotheleal surface
following infarction

Ventricular aneurysm = Stretching of newly formed
collagenous scar tissue

Dressler’s syndrome = Autoimmune

Pulmonary emboli = Deep venous thrombosis in lower
limbs

32
Q

Prognosis of Myocardial Infarction

A

Mortality is approximately 20%

Prognosis depends on the following:

  • Size of the infarct
  • Position of the infarct (anterior most dangerous)
  • Complications
  • Availability of specialized medical assistance
33
Q

Chronic Ischemic Heart Disease

A

This is characterized by chronic left ventricular failure

Causes are:

-Previous infarct(s) that impair the ability of the
heart to function adequately as a pump

-Progressive coronary atherosclerosis that results
in interstitial myocardial fibrosis (which also
impairs the heart function)

34
Q

Sudden Cardiac Death

A

This is defined as the sudden unexpected
death of a previously healthy individual

Almost always the result of ventricular
fibrillation caused by the following:

-Coronary atherosclerosis with or without
thrombosis

Coronary vasospasm

  • Aortic stenosis
  • Cardiomyopathy or myocarditis
  • Cocaine abuse

-SADS – Sudden Adult (arrhythmic) Death Syndrome:
biochemical abn in sodium or potassium channels –
channelopathies - heritable

Cardiovascular System (12 decks)

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