Ischaemic Heart Disease Flashcards
Describe the normal coronary anatomy
RCA: supplies RA, RV and some LV, it originates from the right aortic sinus, it divides into the PDA (posterior descending artery) that supplies the inferior wall of the heart as well as the margianl artery
LCA: originates from the left aortic sinus, it bificates into the left anterior Descending artery & the circumflex artery
LAD: supplies the anterior wall of LV, Interventricular septum & apex of the heart
Circumflex: Supplies lateral & postural regions of LV
Branches of arteries divide further into arterioles & capillaries, providing a microvascular supply to the myocardium
Describe coronary perfusion
Coronary perfusion pressure: this refers to the difference between aortic diastolic pressure & right atrial pressure, optimum CPP occurs during diastole with higher perfusion pressures favouring increased blood supply to myocardium
Describe O2 consumption& demand
O2 delivery & consumption: Oxygen supplied by coronary arteries is extracted and used for myocardium muscle function. The demand for oxygen can be determine by factors such as exercise, increased afterload, increased contractility & heart rate
Describe the circulatory regulators that influence blood flow
Autoregulation: The coronary arteries either dilate or constrict to maintain blood flow despite changes in blood pressure.
Metabolic regulation: increased metabolic demand e.g., exercise, stimulates vasodilation to increase blood flow, due to release of vasodilators e.g., NO
Endothelial regulation: Endothelial cells lining the blood vessels release substances e.g. nitric oxide to control vessel tone & blood flow.
Describe the relationship between supply & demand
Supply & demand: A balance is required between supply & demand as it is vital to maintain healthy myocardial function. Disruption of this balance can lead to ischaemic heart disease.
Describe the determinants of O2 supply
- Heart rate: The heart is supplied with most of the blood during diastole, a faster HR reduces the time spent in diastole, so less blood fills the heart at higher rates, but more is pumped out, this creates an oxygen debt
- Oxygen content in the blood: The volume of oxygen in th blood depends on oxygen saturation levels in haemoglobin, If the Hb is fully saturated then the supply of oxygen will be greater to the heart. The heart will receive less oxygen if a person possesses anaemia (poor oxygen saturation in HB)
- Coronary blood flow: Having healthy coronary arteries with an adequate blood flow with no indicators of disease. Maintaining a high aortic diastole pressure increases the coronary perfusion pressure which increases blood flow to the heart. Having little resistance in the coronary arteries allows for blood to flow easier and deliver more O2
- Vasodilators/Autonomic regulation: : Endothelial cells lining the blood vessels release substances e.g. nitric oxide to control vessel tone & blood flow. Sympathetic & parasympathetic pathways regulate blood flow via constriction & dilation of blood vessels in response to an increase/decrease in HR
Describe the determinants of O2 demand
- Contractility: Strength of myocardial contraction is correlated to O2 demand as increased contractility requires more ATP which increases O2 consumption in myocardial cells. The sympathetic system can also increase contractility and therefore O2 demand
- HR: earts oxygen consumption increases with HR, as the heart requires more energy to beat at a faster rate, maintain rhythm & contract muscle fibers
- Preload & Afterload: Preload is the volume of blood left in the ventricles at end of diastole, as the preload increases the heart works harder to eject more blood, leading to a higher O2 demand, fluid overload (effusions) can increase the preload. Afterload refers to the pressure the heart needs to overcome to eject blood from the ventricles. An increased afterload requires the heart to exert more force during contraction which requires more energy and to produce more energy more oxygen is needed to enable myocardial cells to respire to produce ATP
Describe the pathophysiology of IHD
- Atherosclerosis: evolution of plaque that narrows coronary arteries
- Created reduced coronary blood flow, creates stable angina & risk of thrombus formation
- Myocardial ischaemia: O2 supply decreased to the myocardium, electrical disturbances & lactic acid build-up
- Prolonged ischaemia causes necrosis of the myocardium
- Inflammation of ischaemia leads to more damage, damaged tissue replaced with scar tissue, reduces cardiac function
- leads to arrhythmias, heart failure, cardiogenic shock, gives poor prognosis
Describe the symptoms indicating CAD
- Angina: chest pain with exertion or at rest due to narrowing of CAD
- MI: severe chest pain, SOB due to a complete blockage of CA
- Heart failure: SOB, swelling, fatigue caused by ischemia/infarction
- Arrythmias: sudden dizziness, Cardiac arrest, palpitations caused by disruption of hearts electrical system
- Sudden cardiac arrest: loss of pulse/consciousness due to a fatal arrythmia followed by an infarction
What are the types of investigations used to identify an MI
Blood tests, Echoes, ECG’s & LHC
Describe the purpose of serum markers
Serum marker: it refers to a substance or molecule in the blood that can measured to provide information regarding a pathological condition. They are used in clinical diagnosis to assess the severity, Prescence & progression of disease
Markers: proteins, enzymes, hormones, metabolites, antibodies & genetic markers.
Types of markers:
Diagnostic: Used to diagnose a specific disease or condition.
Prognostic markers: provide information about the likely outcome of the disease,
Describe the presence of elevated troponin & CK in blood
A CK-MB level greater than 5-10 ng/mL is generally considered elevated, indicating myocardial injury or infarction. However, CK-MB is less specific than troponin because it can also be elevated in skeletal muscle injury or other conditions (e.g., stroke, heavy exercise).
MI is suggested if troponin levels are above the 99th percentile of the upper reference limit (typically > 0.1 ng/mL for troponin T and > 0.1-0.2 ng/mL for troponin I) within 3-6 hours of symptom onset.
Levels often peak 12-48 hours after the infarction and can remain elevated for 7-10 days.
Troponin is highly specific to cardiac muscle.
Describe the importance of serum markers
Early detection: serum markers allow early detection and therefore diagnosis of a disease, before symptoms may appear
Prognosis: enables the diseases pathway to be monitored, whether the disease is under control
Treatment decisions: serum markers can guide therapeutic treatments e.g., medication, need for surgery or chemotherapy
Describe the use of ECG’s when identifying MI’s
Changes in the ECG can give information regarding the location, severity & extent of damage.
Define a STEMI
STEMI (ST elevation): an ST elevation indicates an acute STEMI (ST-elevated MI), the ST segment needs to elevate by more than 1-2mm in 2 or more continuous leads. It reflects ongoing MI injury and ischaemia. Typically seen in leads that correspond to the region of the heart affected (e.g., V1-V4 for anterior wall, II, III, aVF for inferior wall, I, aVL for lateral wall). In the first hours to days after the infarction, the ST elevation may be prominent. After 24-48 hours, the ST elevation may begin to normalize as the infarction evolves.
Define a NSTEMI
ST depression: Indicates MI ischaemia, Downward displacement of the ST segment by more than 0.5 mm in two contiguous leads.
Often seen in reciprocal leads (the opposite side of the infarction), such as: Inferior infarction (leads I, aVL, lateral leads may show ST depression). Anterior infarction may show ST depression in the inferior leads (II, III, aVF). ST depression can also be a sign of subendocardial ischemia or non-ST-elevation MI (NSTEMI).
Define a T-wave inversion
T wave inversion seen in both STEMI & NSTEMI, inverted T waves in the leads corresponding to the area of ischemia or infarction. T-wave inversion may appear shortly after the onset of chest pain or ischemia and can last for days to weeks. Deep, symmetric T-wave inversion is more suggestive of severe ischemia or an evolving infarction. Evolution: In the acute phase, T-wave inversion is common and reflects myocardial injury. In the subacute phase, T-wave inversion may persist or evolve into pathological Q waves.
Define pathological Q waves
Pathological Q waves develop after the death of myocardial tissue (necrosis), indicating irreversible damage to the heart muscle. ECG Findings: A Q wave is considered pathological if it is > 0.04 seconds in duration and more than 1/3 of the height of the R wave in the same lead.
Describe the changes to an ECG pre & post infarction
- Pre-infarction
- During infarction, tall hyperacute T wave
- ST elevation
- within hours of MI, Loss or R wave, appearance of Q waves & T wave inversion
- Week later ST returns to normal
- Months after T wave returns to normal
Describe the use of echo when detecting an MI
Echocardiography is essential for assessing the functional consequences of myocardial infarction.
It provides real-time visualization of wall motion abnormalities, left ventricular function, and complications such as mitral regurgitation, thrombus formation, and pericardial effusion.
It is particularly useful in acute settings to assess the extent of damage and guide management decisions, including the need for interventions like surgery or medical treatment.
Define RWMA (regional wall motion abnormalities)
Description: One of the most important findings on echo that suggests myocardial infarction is regional wall motion abnormality.
Indication of MI:
Hypokinesis: Reduced motion of the affected area of the heart muscle.
Akinesis: Absence of movement in the area of the infarction, suggesting that part of the heart muscle is no longer contracting due to loss of function.
Dyskinesis: Abnormal movement of the infarcted area, where the wall moves outward during systole instead of inward.
Location: The specific wall motion abnormality depends on the location of the infarction (e.g., anterior, inferior, lateral, or posterior wall of the heart).
Define LVEF, LVD & mitral regurgitation
LVEF: a decreased ejection fraction based on a decreased pumping ability
LVD: Increased EDV that indicates heart failure
Mitral regurgitation: Papillary dysfunction which worsens MR
How to diagnose an MI?
Present diagnosis based on history & ECG
Final diagnosis involves: raised cardiac enzymes, structural wall abnormalities
Describe left heart catheterisation
A diagnostic procedure carried out to assess the hearts’ structure & function, able to determine underlying cause of MI, assess extent of disease in vessels e.g., CAD
Describe the complications of an MI
- Arrhythmias due to damage of the conduction system e.g., AFIB
- Cardiogenic shock, decreased CO leads to loss of function of myocardium, causing hypotension & organ failure
- Heart failure as LV becomes impaired resulting in reduced CO, causing SOB, fatigue, oedema
- Myocardial wall rupture leading to cardiac tamponade, severe chest pain, shock & hypotension
- Thromboembolism where blood clots in infarcted area break off and cause stroke/PE
Describe the treatments used for a STEMI & NSTEMI
STEMI: PCI if available within 90 mins if not, fibrinolytic therapy e.g., IPA which destroys clots
NSTEMI: decide if high/low risk, if low go to cath lab only if angina is consistent or exercise test is positive
If high invasive procedure of PCI and perhaps CABG
Describe PCI
A non-surgical procedure which involves opening up of narrowed/blocked arteries via a catheter, sometimes catheter is followed via balloon or stent, suitable for patients with angina, NSTEMI, STEMI & significant stenosis.
It is less invasive than CABG & provides immediate relief of ischemia, with a shorter recovery time than surgery.
Risk of bleeding, vessel damage & arrythmias
Post-op care involves anti-platelet therapy to prevent thrombosis at site of PCI
Describe stenting
A procedure normally performed during a PCI where a stent is placed in the artery to keep it open wide and prevent restenosis. For patients with STEMI, NSTEMI & stable angina. It provides prevention of restenosis & reduces risk of other cardiovascular events. However there is always a risk of in stent restenosis, bleeding complications & infection
Describe the use of 2 different types of stents
Drug eluting stent: releases medication that helps prevent restenosis by inhibiting normal tissue growth at site of stent, used for patients with significant blockages & provides a better long-term outcome compared to BMS, with lower rates of restenosis
BMS: Bare metal stents, less commonly used due to higher likelihood of restenosis, however may be used during emergencies or high-risk patients for bleeding, it is a simpler procedure with less concern for long-term meds,
Describe balloon angioplasty
A procedure where a balloon is inflated within the narrowed vessel using a catheter, it compresses plaque against arterial wall, widens the artery & improves blood flow, used when stenting is not possible or needed,
It is a less invasive procedure, but there is the risk of vessel rupture, restenosis & embolism, with fragments of plaque breaking off
A patient may have a balloon when having had an NSTEMI or unstable Angina. Post-op care involves anti-platelet therapy to prevent clot formation
Describe CABG
CABG is a surgical procedure known as a coronary bypass, surgeons take BV’s from a patients less important arteries and create a graft to bypass narrow/blocked arteries, this occurs where there is severe CAD involving the LAD, able to treat lesions PCI cannot
There is a risk of infection, stroke, MI, graft failure, however it provides lower risk of recurrent events and promotes long-term survival & benefits for those with severe CAD
Rehab, statins & beta-blockers are needed to be taken post-op
