Hypoxic Damage to the Heart Flashcards
Define ischaemia
a condition where in an organ or tissue has perfusion (blood flow) lowered relative to its metabolic needs. (reduced blood Supply)
Define infarction
Localized area of tissue necrosis as a result of ischaemia
Examples: MI, stroke, limb gangrene
mechanisms of hypoxic damage
Ischaemic and Hypoxic Injury
- 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 - Disrupt interaction between ER and ribosomes → ribosomal detachment
HYPOXIC DAMAGE IN THE HEART =
= ISCHAEMIC HEART DISEASE
Factors influencing o2 demand and supply by heart
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
Describe the causes of hypoxic damage in the heart
90% of causes:
reduced coronary blood flow due to obstructive atherosclerotic lesions in the epicardial coronary arteries
Non-artherosclerotic causes (10 %)
- increased demand e.g., tachycardia or hypertension
- Diminished blood volume e.g., hypotension or shock
- Diminished oxygenation e.g., pneumonia or CHF
- diminished oxygen-carrying capacity e.g., anemia or carbon monoxide poisoning
IHD clinical syndromes:
- Myocardial infarction
- Angina pectoris
Stable
Unstable
Variant - Chronic IHD with heart failure.
- Sudden cardiac death.
MI can be of 3 types
- Stable angina
- ACS = STEMI
- ACS = NSTEMI + Unstable angina
Describe causes of myocardial infarction
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
Describe consequences of myocardial infarction
- impaired contracitliiy –> stroke embolism / cardiogenic shock / congestive heart failure
- tissue necrosis –> congestive heart failure / cardiac tmponade
- electrical instability –> arrthythmias
- preicardial inflammation –> pericarditis
Describe the epidemiology of ischaemic heart disease
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)
Describe the pathophysiology of ischaemic heart disease
1) MI
i. stable angina
= stable fixed atherosclerotic plaque
ii. unstable angina = plaque disruption and platelet aggregation, unstable plaque –> thrombus –> NSTEMI or STEMI
Describe the pathophysiology of ischaemic heart disease #2
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
describe the 3 types of angina pectoris
i. vasospasm = supply ischaemia
ii. fixed stenosis = typical or stable angina = demand ischaemia
iii. thrombus = unstable angina = crescendo angina = supply ischaemia
Common sites of coronary artery obstruction
- 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 - Left Circumflex artery ( 15% - 20%)
lateral wall of left ventricle
Morphology patterns of MI
- Transmural infarction -nearly full ventricle thickness
- Subendocardial infarction - partial
- Multifocal Microinfarction - small intramural vessel occlusions
Morphology changes - Evolution of the appearances from the time of onset
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)
explain why the actual early diagnosis and treatment is important.
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.
explain why the actual early diagnosis and treatment is important.
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.
What is the difference between an infarct where ST elevation is demonstrated on the ECG (STEMI) and one where it is not (Non-STEMI)?
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
serum cardiac biomarkers
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.
MYOCARDIAL INFARCTION COMPLICATIONS / CONSEQUENCES
EARLY PHASE [<10 days]
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
MYOCARDIAL INFARCTION : COMPLICATIONS / CONSEQUENCES
LATE PHASE [>10 days]
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
