Hypoxic Damage to the Heart

Question 1

Define ischaemia

Answer 1

a condition where in an organ or tissue has perfusion (blood flow) lowered relative to its metabolic needs. (reduced blood Supply)

Question 2

Define infarction

Answer 2

Localized area of tissue necrosis as a result of ischaemia

Examples: MI, stroke, limb gangrene

Question 3

mechanisms of hypoxic damage

Answer 3

Ischaemic and Hypoxic Injury

1. First point of attack → cell’s aerobic respiration → reduced ATP generation
   a) → membrane transport defect → calcium & Na gain + water with K loss → cell swelling
   b) → anaerobic glycolysis → increased lactic acid → fall in intracellular pH → clumping of chromatin
2. Disrupt interaction between ER and ribosomes → ribosomal detachment

Question 4

HYPOXIC DAMAGE IN THE HEART =

Answer 4

= ISCHAEMIC HEART DISEASE

Question 5

Factors influencing o2 demand and supply by heart

Answer 5

demand: cardiac work
- HR
- BP
- myocardial contractility
- LVH
- valve disease

supply: coronary blood flow
- duration of diastole
- coronary perfusion pressure
- coronary vasomotor tone
- oxygenation = Hb and O2 saturation

Question 6

Describe the causes of hypoxic damage in the heart

Answer 6

90% of causes:
reduced coronary blood flow due to obstructive atherosclerotic lesions in the epicardial coronary arteries

Non-artherosclerotic causes (10 %)

1. increased demand e.g., tachycardia or hypertension
2. Diminished blood volume e.g., hypotension or shock
3. Diminished oxygenation e.g., pneumonia or CHF
4. diminished oxygen-carrying capacity e.g., anemia or carbon monoxide poisoning

Question 7

IHD clinical syndromes:

Answer 7

1. Myocardial infarction
2. Angina pectoris
   Stable
   Unstable
   Variant
3. Chronic IHD with heart failure.
4. Sudden cardiac death.

Question 8

MI can be of 3 types

Answer 8

1. Stable angina
2. ACS = STEMI
3. ACS = NSTEMI + Unstable angina

Question 9

Describe causes of myocardial infarction

Answer 9

causes
majority - caused by acute disruption of coronary atherosclerotic plaque and superimposed thrombosis
10% - coronary artery vasospasm, embolization from mural thrombi (atrial fibrillation) or valve vegetations
Rare causes– vasculitis, Amyloid deposition, Sickle cell disease, aortic stenosis, shock

suddenly disrupted atheromatous plaque exposing subendothelial collagen and necrotic plaque contents  Platelets adhere, aggregate, and are activated, releasing substances causing further aggregation and vasospasm

tissue factor –> Activation of coagulation –> thrombus formation –> thrombus completely occlude the coronary artery lumen Within minutes

Question 10

Describe consequences of myocardial infarction

Answer 10

• impaired contracitliiy –> stroke embolism / cardiogenic shock / congestive heart failure
• tissue necrosis –> congestive heart failure / cardiac tmponade
• electrical instability –> arrthythmias
• preicardial inflammation –> pericarditis

Question 11

Describe the epidemiology of ischaemic heart disease

Answer 11

Age : Any age
rises progressively with increasing age
10% -  occur before age 40
45% - before age 65
Race : Blacks and whites are equally affected. 
Sex: Men > women (before menopause)
Women > men (after menopause)

Question 12

Describe the pathophysiology of ischaemic heart disease

Answer 12

1) MI
i. stable angina
= stable fixed atherosclerotic plaque

ii. unstable angina = plaque disruption and platelet aggregation, unstable plaque –> thrombus –> NSTEMI or STEMI

Question 13

Describe the pathophysiology of ischaemic heart disease #2

Answer 13

2) ANGINA PECTORIS:
paroxysmal and recurrent attacks of substernal or precordial chest discomfort

transient (15 seconds to 15 minutes) myocardial ischemia (except Unstable angina)

BUT insufficient to induce myocyte necrosis

3 types of angina pectoris: Prinzmetal, stable/fixed stenosis, thrombus/unstable angina

Question 14

describe the 3 types of angina pectoris

Answer 14

i. vasospasm = supply ischaemia
ii. fixed stenosis = typical or stable angina = demand ischaemia
iii. thrombus = unstable angina = crescendo angina = supply ischaemia

Question 15

Common sites of coronary artery obstruction

Answer 15

1. proximal (LAD) artery – 40-50%
   anterior LV, anterior portion of ventricular septum, and apex
   2.Right Coronary Artery – 30-40%
   RV , posterior portion of septum and posterior LV
2. Left Circumflex artery ( 15% - 20%)
   lateral wall of left ventricle

Question 16

Morphology patterns of MI

Answer 16

1. Transmural infarction -nearly full ventricle thickness
2. Subendocardial infarction - partial
3. Multifocal Microinfarction - small intramural vessel occlusions

Question 17

Morphology changes - Evolution of the appearances from the time of onset

Answer 17

depends on age of the injury.

sequence of microscopic changes:
1. coagulative necrosis (+24 hours —- wavy fibres —— 12 hours after = pallor of myocardium)
2. acute inflammation (3 days —- Necrosis and acute inflammation)
3. chronic inflammation (1 week—- removal of necrotic myocytes by phagocytosis ;
10 days - Granulation tissue characterized by loose collagen and abundant capillaries)
4. fibrosis and scar formation. (8th weeks —— dense fibrous scar)

Question 18

explain why the actual early diagnosis and treatment is important.

Answer 18

four hours after symptom onset, there is significant damage to your heart muscle, with only limited ability for treatment to reduce this damage
after six hours the damage to your heart will be permanent and cannot be reversed
after 12 hours there is unlikely to be any benefit from treatment.

Question 19

explain why the actual early diagnosis and treatment is important.

Answer 19

four hours after symptom onset, there is significant damage to your heart muscle, with only limited ability for treatment to reduce this damage
after six hours the damage to your heart will be permanent and cannot be reversed
after 12 hours there is unlikely to be any benefit from treatment.

Question 20

What is the difference between an infarct where ST elevation is demonstrated on the ECG (STEMI) and one where it is not (Non-STEMI)?

Answer 20

Depends on pattern of infarction
1. Transmural infarctions - ST elevated MI (STEMIs)
ST segment elevations / Left bundle branch block (LBBB)
2. Subendocardial (Nontransmural) Infarct - NSTEMI
ST-depression, T wave inversions, or transient ST-elevation
3. Multifocal Microinfarction - Nonspecific changes

Question 21

serum cardiac biomarkers

Answer 21

Measuring blood levels of proteins that leak out of injured myocardial cells -
troponin I and troponin T = are most specific and sensitive . also CK-MB and Myoglobin.

Question 22

MYOCARDIAL INFARCTION COMPLICATIONS / CONSEQUENCES

EARLY PHASE [<10 days]

Answer 22

Reinfarction [extension MI]
Arrhythmia (Paul has a bradycardia due to heart block)
Acute cardiac failure [cardiogenic shock]
Acute Pericarditis
Aneurysm
Thrombosis/Embolism
Cardiac rupture
Free wall
Interventricular septum
Papillary muscle

Question 23

MYOCARDIAL INFARCTION : COMPLICATIONS / CONSEQUENCES

LATE PHASE [>10 days]

Answer 23

Aneurysm

Recurrent M.I.

Chronic cardiac failure (Paul is heading to this.. the next morning Paul’s chest felt tight and he felt breathless (dyspnea) walking to the toilet and especially when lying down(orthopnea) .The Medical Officer Rosie told him that he had signs of fluid on his chest confirmed by a further CXR…

Dressler syndrome =
Pericarditis 2-10 months post MI
Immunological mechanism
Elevated ESR