Lecture 9: Myocardial infarction and angina Flashcards
1
Q
What is the coronary circulation?
A
- The circulation of blood that supplies the heart muscle (myocardium) with O2 and nutrients
- Coronary arteries: arise from root of aorta, supply O2-rich blood to heart muscle, main arteries on the surface smaller penetrate into muscle
- Coronary veins: collects deoxygenated blood after utilised by the myocardium, drain into the coronary sinus which empties into the right atrium
- Only 1/10 of mm of endocardial surface can obtain nutrients from blood in chambers
2
Q
Why is there phasic blood flow through the coronary circulation?
A
- Little flow of blood during systole to the heart
- During exercise, heart is in systole
- When you need more blood supply to the heart, you are effectively reducing it → getting more time n vessels are compressed
3
Q
How is venous drainage primarily facilitated in the heart?
A
- Venous drainage in the heart is primarily accomplished via the coronary sinus, which empties into the right atrium.
- The return of blood from the heart muscle is aided by small anterior cardiac veins.
- Major venous vessels are located within the epicardial fat layer, lying superficially to their arterial counterparts.
- Blood pathway: aorta → right coronary artery → cardiac veins → coronary sinus → right atrium
- While the heart contracts, it can pose a challenge as the squeezing action may compress or shut blood vessels.
4
Q
What factors can lead to a reduction in coronary blood flow?
A
- Reduction in the diastolic interval, particularly during exercise when the heart rate is increased.
- Increase in ventricular end-diastolic pressure, which occurs when the ventricles are filled with blood from the left atrium. This increased pressure makes it more challenging for blood to be pushed through the coronary arteries.
- Fall in arterial pressure, which can further compromise coronary blood flow.
5
Q
What is the resting coronary blood flow, and how does it relate to cardiac output?
A
The resting coronary blood flow is approximately 225 ml/min, which constitutes about 4-5% of the cardiac output.
6
Q
What percentage of oxygen is typically extracted from the blood as it flows through the heart?
A
Around 70% of the oxygen carried by blood is removed as it flows through the heart.
7
Q
How does the body respond to increased oxygen requirements in the heart?
A
Coronary blood flow is augmented by dilating the coronary arteries.
8
Q
What is the major cause of ischemic heart disease?
A
Atherosclerosis
9
Q
What are some factors contributing to atherosclerosis?
A
Genetic predisposition
Excessive cholesterol intake
Sedentary lifestyle
10
Q
What happens during atherosclerosis?
A
- Cholesterol is deposited beneath the endothelium of arteries
- Arteries are invaded by fibrous tissue and calcified
- Atherosclerotic plaques form, protruding into the arterial lumen and partially or completely blocking blood flow.
11
Q
What is a myocardial infarction?
A
- Occlusive thrombus
- Complete occlusion of coronary artery
- Blood clot attached to plaque completely occludes the blood vessel, resulting in a heart attack.
12
Q
What is stable angina?
A
Caused by plaque causing partial occlusion of a coronary artery.
13
Q
What is unstable angina?
A
- Caused by a combination of plaque and thrombus
- Partially occlusive thrombus allowing some blood flow
- Can occur periodically.
14
Q
What is a myocardial infarction?
A
- Also known as a heart attack.
- Occurs due to the sudden blockage of blood flow to a part of the myocardium (heart muscle).
- Complete occlusion of a blood vessel leads to ischemia (loss of blood supply and nutrients) and subsequent necrosis (cell tissue death).
- It is the most common cause of morbidity and mortality, with approximately 123,000 heart attacks occurring per year.
15
Q
What are the mechanisms that can lead to plaque rupture and subsequent occlusion in coronary artery disease?
A
- Plaque ruptures are more likely to occur when there is a thin fibrous cap.
- Plaque rupture can be triggered by factors such as stress, exertion, or a large meal.
- Hemorrhage within the plaque → blockage of the vessel lumen and subsequent occlusion.
- Release of tissue factor from the plaque → activate the coagulation cascade → occlusion.
- Exposure of collagen underneath the plaque, combined with turbulent blood flow, can activate platelets and the coagulation cascade, resulting in occlusion.
- Dysfunction of the endothelium can lead to impaired vasodilation, increased vasoconstriction, and ultimately, occlusion.
16
Q
What are the consequences of blood vessel occlusion in myocardial infarction?
A
- Occlusion of blood vessels leads to a cessation of blood flow.
- Collateral blood flow may develop to compensate for the occlusion.
- Local dilation and collateral flow can result in overfilling with stagnant blood.
- Depletion of oxygen leads to deoxygenated hemoglobin, causing affected areas to appear blue or brown.
- Highly permeable vessel walls lead to fluid leakage, resulting in edema in the affected area.
- Muscle cells swell due to diminished cellular metabolism.
- Without a blood supply, cardiac muscle cells can die within approximately 20 minutes.
17
Q
What are the cellular consequences of ischemia during myocardial infarction?
A
- Ischemia results in a lack of oxygen and glucose supply to the affected tissues.
- ATP levels decrease due to the inability to undergo glycolysis and oxidative phosphorylation.
- Impaired Na, K ATPase function leads to decreased membrane potential, causing depolarization and potentially resulting in arrhythmias.
- Intracellular edema occurs due to ion imbalance, leading to cell death.
- Increased intracellular calcium levels activate proteases and lipases, contributing to cell death.
- Anaerobic metabolism leads to an increase in intracellular hydrogen ions and protein denaturation.
18
Q
What is collateral circulation in the context of cardiovascular health?
A
- Development of new blood vessels in response to blocked or narrowed arteries.
- It occurs when there is partial occlusion in a blood vessel, leading to the growth of heart vessels around the occlusion.
- These collateral vessels slowly narrow due to conditions like atherosclerosis but provide an alternative pathway for blood to reach tissues.
- Collateral vessels may reroute blood flow around obstructions, ensuring some level of blood supply to the affected area.
- This process involves the formation of branches between veins and arteries, gradually building up around atherosclerotic plaques.
19
Q
Causes of death in myocardial infarction
A
○ Decreased in cardiac output (cardiac shock)
§ Can’t supply enough blood to the organs
○ Pulmonary oedema
§ Fluid in the lungs
○ Ventricular fibrillation
§ Completely chaotic rhythm in the heart -> no ejection of blood
* Occasionally
○ Heart rupture
Wall thins -> blood flows out [hole in heart]
20
Q
What is cardiac shock, and what are its potential causes and consequences?
A
- Cardiac shock occurs when there is insufficient force to pump blood into the peripheral arterial tree.
- CAUSE: Systolic stretch, where the heart wall bulges out due to thinness or damage, impairing its ability to contract effectively.
- EFFECT: severe hypotension, with systolic blood pressure dropping below 90 mm Hg, resulting in the death of peripheral tissues.
- Decreased cardiac perfusion → increased ischemia → perfusion of the heart itself down the coronary artery.
- In severe cases, blood may accumulate in the pericardial space, leading to cardiac tamponade.
- The mortality rate for cardiac shock is high, estimated at around 70%.
21
Q
What is pulmonary oedema?
A
- Buildup of fluid in the lungs
- Reduced systemic blood circulation -> blood pools in the atria n in blood vessels of lungs -> can’t breathe
- Less reabsorption n more filtration
- Increased capillary pressure in the lungs
- Little difficulty in first few
- But reduced circulation to kidney -> reduced urine output -> increased total blood volume
- Congestive symptoms
22
Q
What is cardiac arrhythmia, and why is it particularly dangerous following a myocardial infarction?
A
- Cardiac arrhythmia refers to abnormal heart rhythms, which can be dangerous, especially after a myocardial infarction.
- It can cause changes in the ECG and electrical properties of the heart, potentially leading to ventricular fibrillation.
- Several factors contribute to arrhythmias post-myocardial infarction:
- Potassium depletion [inadequate perfusion]
- Injury current generated by dying cells → depolarization.
- Sympathetic reflexes triggered by a fall in blood pressure → activating the sympathetic nervous system and altering the heart’s electrical properties.
- Muscle weakness and ventricular dilation → abnormal conduction pathways around the infarcted area.
23
Q
How is myocardial infarction diagnosed?
A
- History
○ Heavy, crushing, chest, pain radiating down arm but some Mis are silent- Unrelated to exercise
○ Pain exists after exertion - Associated w nausea, vomiting, sweating
- ECG changes
Biochemical markers
- Unrelated to exercise
24
Q
We cannot normally feel our heart, so why do we feel pain with a MI?
A
- Ischemia of cardiac muscle can cause severe pain
- Causes unclear, probably release of acidic substances lactic acid or pain mediators
- Histamine, kinins, proteolytic enzymes
- RESULT: Stimulate nerve endings in cardiac muscle
25
Q
What is the characteristic change in ECG during a heart attack?
A
- ST segment elevation: ST interval abv baseline
- QRS: onset of depolarization of ventricles when they contract
- T: when they depolarize
- ECG goes back to flatline before T
- STEMI: ST - segment elevation MI
26
Q
What causes the ECG changes during a heart attack?
A
- We are measuring flow of current
- No current flow → line is at baseline
- Normally at plateau of AP → ventricular AP is wide n has long plateau
- During plateau, no current flow
- If the heart is not depolarized / short AP → current will flow
- Bc of damage to heart, there is a flow during plateau period
- After period of time, Q wave
- This can be present throughout life (Q wave infarctions)
27
Q
What are the differences between ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (non-STEMI), and unstable angina in the ECG?
A
- Occlusive thrombus → prolonged ischemia -? ST elevation (ECG) -> STEMI
- Transient ischemia → no ST elevation → non-STEMI
- May still hv serum biomarkers
- Partially occlusive thrombus → no ST elevation + no serum biomarkers → unstable angina
- TLDR: transient ischemia won’t produce ST elevation but prolonged will
28
Q
What are the biochemical markers of MI?
A
- Troponin is part of muscle that couples actin to myosin
- Troponin C binds calcium
- Cardiac muscle cells dying → release troponin into blood stream
- Biomarker bc they can only come from damaged muscles in the heart
- There are 2 isoforms specific to myocardium: T n I
- T: structural n maybe expressed in skeletal muscle in utero
- I: catalytic n only ever in myocardium
- This is what is measured
- Pros: sensitive so can detect v small infarctions
- Measured 12h after infarction
- Problem: long time for levels to drop back to normal so cannot detect re-infarction
29
Q
What are the initials aims for MI treatment?
A
- Confirm diagnosis (ECG n biomarkers)
- Relieve ischemic pain
- Stabilize hemodynamic abnormalities
- Save as much myocardial tissue as possible
30
Q
How is MI treated in the short and long term?
A
- Short term
- Oxygen (if hypoxic, oximetry not routine)
- Test hypoxia via oximetry
- Diamorphine (+ antiemetic) for the pain
- Aspirin 300mg (clopidogrel if allergic)
- GTN: vasodilator
- Thrombolytic drugs
- Breaks clots -> restore blood flow
- Administer as early as possible (within 2h)
- Angioplasty/coronary artery bypass graft
- Oxygen (if hypoxic, oximetry not routine)
- Long term
- Aspirin
- β-blockers
- ACE inhibitors
- Statins
31
Q
Describe the recovery from MI
A
- MI causes dead figures and non functions sections of myocardium
- Area of dead fibres enlarges
- Non-functional muscle recovered - collateral blood flow
- Respiration of dead tissue by macrophages
- Fibrous tissue develops
- Gradual progressive contraction of fibrous tissue over years
- Hypertrophy of normal areas to compensate
- Recovers either partially/completely within a few months
32
Q
Describe cardiac function after recovery
A
- Often pumping capacity permanently reduced
- Normal cardiac reserve 300 - 400% more blood per minute than at rest
- Reserve maybe reduced to 100% but can still function normally
33
Q
What is angina pectoris (stable angina)?
A
- Insufficient blood supply to the heart during increased load (e.g. exercise)
- Similar pain to MI
- Pain felt beneath upper sternum over the heart also referred to other areas (e.g. left arm, shoulder, neck even side of the face,
- What makes it different from MI?
- Pain can last from 2-10 minutes after exercise
- Common in the cold n after large meals
- Relieved by rest n GTN
- Often described as pressure, tightness, burning n heaviness
34
Q
What is the difference b/w stable and variant angina?
A
- Fibrous obstructive atheromatous plaques in one or more arteries
- If narrowed by more than ~70%+, reduced flow capacity is sufficient at rest but insufficient when there is increased oxygen demands
- Stable angina: pattern of chronic predictable transient angina during exertion / emotional stress
- Imbalance between myocardial oxygen supply n demand (demand > supply) → ischemia
- When you stop exercising, reduce demand
- This is the difference between stable n variant angina
35
Q
How is angina diagnosed?
A
- Patient history
- During attack
- Increased HR n BP
- Changes in ECG (gone after attack has finished)
- Stress test
- Treadmill
- Might precipitate angina
- Pharmacological (dobutamine, adenosine, dipyridamole)
- Preferential leakage of blood away from the plaque which reduces blood flow -> pain
- Treadmill
- Angiography
- Put dye in coronary artery
- See where occlusion is
- Nuclear imaging
36
Q
How is angina treated?
A
- Vasodilators
- No donors
- Calcium channel blockers
- β-blockers
- Block sympathetic enhancement of heart rate n cardiac metabolism during exercise
37
Q
How do vasodilators like glyceryl trinitrate affect myocardial oxygen demand and coronary blood flow?
A
- Do not work in coronary artery
- Reduce myocardial oxygen demand
- Dilate blood vessel
- Less blood comes back to heart
- Heart does less work n also reduce afterload
- Afterload: pressure heart is pushing against
- Reduce amt of blood coming back to the heart so oxygen demand of myocardial goes down
- Not much increase in oxygen supply, just reduction in demand
- Little effect in coronary artery but major effect is in venorelaxation reduce preload -> reduce stroke volume
- Some coronary artery dilation increases coronary blood flow
- Nitric oxide
- Griciltrinitrate work by releasing nitrous oxide which is a vasodilator
38
Q
Provide 4 examples of surgical intervention to treat coronary artery disease
A
- Aortic-coronary bypass surgery
- Cut artery out of leg n replace
- Coronary angioplasty
- Inflating balloon catheder inside vessel
- Push plaque back inside the wall of the lumen
- Successful but after a while plaque would relax back into the lumen
- Stents
- Metal cage that goes into artery n around w where you put your ballon, you insert stent
- It keeps the artery open so it can’t recollapse back
- Stent also contains drugs that blocks cell growth to prevent cells growing around the stem
- Sirolimus
- Paclitaxel
39
Q
What distinguishes angina not triggered by exercise from exercise-induced angina, and how is it relieved?
A
- Angina not associated w exercise
- No real pattern
- Plaque that partially occludes blood vessel
- Periodically blood vessel is attaching to that plaque
- Lasts for a while n thrombus comes away from the plaque n blood flow is resumed → pain disappear
- Relieved by GTN
- Get enough oxygen
- Non-STEMI → short lived
