Ischaemic Heart Disease and Hypoxia Flashcards
What is ischaemic heart disease (IHD)?
AKA coronary heart disease (CHD) / coronary artery disease (CAD)
Heart problem caused by narrowed heart (coronary) arteries that supply blood to the heart muscle
Mismatch between demand and supply
Most common cause of death in Western cultures
Manifests clinically as myocardial infarction (MI) and ischaemic cardiomyopathy
Sudden death = acute coronary occlusion
Gradual death = progressive weakening of heart pumping process over several years
What are the signs and symptoms of IHD?
Angina chest pain Heart rhythm issues Nausea, sweating, fatigue, shortness of breath, weakness, dizziness Reduced exertional capacity Leg swelling Diaphoresis
What are the different characteristics of angina chest pain?
Aching, burning, fullness, heaviness, numbness, pressure, squeezing
Radiation of pain to arms, back, jaw, neck, shoulder
High or low BP
Syncope (fainting)
What is IHD often mistaken for and why?
Chest pain may be described by patient in a way that leads to heartburn / indigestion diagnosis
What are the characteristics of different heart rhythm problems?
Palpitations (irregular heartbeats or skipped beats)
Heart murmurs
Tachycardia (Acute coronary syndrome
ACS, Acute myocardial infarction AMI)
Atrial fibrillation
Ventricular tachycardia or ventricular fibrillation
S4gallop: A common early finding of diastolic dysfunction
S3gallop: An indication of reduced left ventricular function and a poor prognostic sign
IHD is the most common cause of death. Where geographically is IHD death rate high?
East Europe
Middle East
Some of Asia
What is a (daily adjusted life year) DALY?
Sum of years a person lost due to death or disability
What are some risk factors of IHD?
Non-modifiable (30%): Age Sex (male) Family history of CVD Ethnicity Genetic evidence Previous history of CVD
Modifiable (70%): Hypertension Hyperlipidaemia (/ high cholesterol) Smoking Diabetes High BMI Diet Exercise Stress / Mental ilness Low socioeconomic state Alcohol abuse Certain medications Social deprivation
Are the modifiable risks/causes of IHD the same around the world?
High income countries = hypertension, cholesterol, tobacco use
Low income countries = poor diet, air pollution, low education
What are the 2 causes of IHD?
Myocardial ischaemia occurs when there is an imbalance between the supply of oxygen and the myocardial demand
1. Coronary blood flow to a region may be reduced due to OBSTRUCTION: Atheroma Thrombosis Spasm Embolus Coronary ostial stenosis Coronary arteritis
- A general decrease of oxygenated blood flow to myocardium:
Anaemia
Carboxyhaemoglobulinaemia
Hypotension causing decreased coronary perfusion pressure
What is atherosclerosis and how does it contribute the IHD?
Complex inflammatory process involving accumulation of lipids, macrophages and smooth muscle cells
Plaque formation is initially stable, but becomes unstable over time - leads to thrombus:
Fibrous cap on vulnerable plaque ruptures and pro-thrombotic components are exposed to pro-coagulation factors leading to thrombus formation
[fibrous cap contains macrophages and smooth muscle cells]
What are some triggers of atherogenesis?
Endothelial dysfunction
Mechanical sheer stresses (HTN)
Biochemical abnormalities (elevated and modified LDL, DM, elevated plasma homocysteine)
Immunological factors (free radicals from smoking)
Inflammation ( infection such as chlamydia, Helicobacter)
Genetic alteration
What is the presentation of IHD depending on the progression of athersclerosis?
Asymptomatic = small, asymptomatic athercosclerotic plaque
Chronic stable angina = stable fixed atherosclerotic plaque (reduced blood flow to heart)
Acute Coronary Syndrome = unstable angina, non ST elevation MI or ST elevation MI
Heart failure
Sudden death
What is the role of hypoxia in acute coronary occlusion?
Happens in people with underlying atherosclerotic disease
Local blood clot = thrombus formation
Atherosclerotic plaque breaks through the endothelium –> direct contact with the flowing blood
This can lead to - blood platelets adhering to it, fibrin being deposited, and/or RBCs entrap to form a blood clot
Either or all of these = clot growth until the artery occludes the vessel OR clot breaks away and blocks a more distal artery (coronary embolus)
What are collateral blood vessels and what is their role in IHD?
Collateral blood vessels = small capillary-like branches off an artery formed overtime. Collaterals “bypass” the area of narrowing and help to restore blood flow
Dilate within seconds during an acute episode - doubling by the 2nd/3rd day and often reaching normal coronary flow within 1 month
In chronic atherosclerotic patients = slow occlusion = collaterals open at the same time as atherosclerosis begins, and continue to develop as the atherosclerosis gets worse over time
Why do you get ACS if collaterals are so effective in helping take over the function?
The collaterals are also blood vessels so they can also get atherosclerosis
OR
The damage becomes so intensive the collaterals cannot cope/keep up
OR
Can cause weakening of the heart = eventually heart failure
Why can you restore total heart function after MI?
Collateral formation after acute MI
In about a month - normal coronary flow = normal heart function
What are some cardiac muscle stats?
Cardiac muscle require 1.3ml of oxygen per 100g of muscle tissue
8 ml of oxygen per 100 g delivered to normal resting left ventricle each minute so usually muscle do not die
If 15 to 30 percent of blood supply remains, muscle will not die except in the central portion of a large infarct with no collaterals
What happens during an MI?
During an acute occlusion = area of muscle has either zero or little flow = cannot sustain cardiac muscle function = infarction
What happens soon after infarction? (pathogenesis)
Soon after infarction:
Small amount of collaterals open and blood seeps into the infarcted area
Local blood vessels dilate and area becomes overfilled with stagnant blood
Muscle fibres use all the remaining oxygen, haemoglobin becomes totally deoxygenated giving bluish brown hue & blood vessels appear engorged despite lack of blood flow
What happens in the later stages of an MI?
Vessel walls’ permeability increases, fluid leak and local tissue oedematous (excessive accumulation of serous fluid in the intercellular spaces of tissue)
Cardiac muscle cells swell and due to no blood supply, die within few hours
What are the 4 different causes of death after an MI?
Decreased cardiac output - due to systolic stretch and cardiac shock = normally heart wall pushes back to exert force during systole, but the weak heart muscle is instead stretched outwards during systole = poor CO that cannot meet body’s needs (cardiogenic shock_
Damming of blood in body’s venous system = poor CO = poor blood flow to kidneys = failure to excrete = increase in blood volume = congestive symptoms = pulmonary oedema
Ventricle fibrillation = can happen during first 10 minutes or after 1 hour or so
Rupture of infarcted area =
Early little danger, but after few days infarcted area begins to degenerate and the heart walls become very thin and stretched. Until it finally ruptures during stretch
How does recovery start after an MI?
Tissue is non-functional in the area affected
Small area: little or no death of muscle
Might become non functional temporarily due to lack of nutrients, but recovers
VS
Large area:
Some in the centre die rapidly within 1 to 3 hours due to complete loss of blood supply
Immediately around is non functional area failure of contraction and impulse conduction
But surrounding areas = weak from mild ischaemia, but as collaterals open they go back to functioning
Normal areas of heart gradually hypertrophy to compensate for lost tissue for partial / almost full recovery
Does cardiac output stay the same during ischaemia?
Mild = yes, due to cardiac reserve - normal heart can actually pump 300-400% if it wants to; thats how it increases CO during exercise
So problem = when exercising after MI, as reserve is already being use to meet daily needs
Severe = no
What is the IHD risk assessment?
All aged 40–74 years, who have not been diagnosed with CVD, diabetes, or CKD = free health check every 5 years
Health check includes CVD risk assessment, alcohol consumption, physical activity, BMI, dementia in 65+, DM, CKD
Person’s 10 year CVD risk assessed using QRISK every 5 years - useful for preventative measures to be put in place for the patient
How do you diagnose IHD?
Clinical History:
Symptoms—chest pain type etc, any associated symptoms and signs
Age, sex, Ethnicity, Smoking, Ask about other risk factors, Socioeconomic, family history
Clinical Examination:
Heart auscultation, BP, BMI, GPE
Lab tests:
LDL, HDL, Triglycerides, lipoprotein a, C-reactive proteins etc
Serum markers - esp. in A&E: Troponins(I or T) Creatine kinasewith MB isozymes Lactate dehydrogenase and lactate dehydrogenase isozymes Serumaspartate aminotransferase
Biomarkers for predicting death e.g. presence of raised: B-type natriuretic peptide CRP Homocysteine Renin Urinary albumin-to-creatinine ratio = more likely of death following MI
What are the 3 types of IHD and what are their characteristics?
Stable angina = angina symptoms during moderate physical activity
Unstable angina / NSTEMI = angina symptoms while doing very little / at rest
Acute MI / STEMI = angina symptoms while
at rest
How does the ECG change is the 3 types of IHD:
Stable angina
Unstable angina / NSTEMI
Acute MI / STEMI
Stable Angina =
Pretty much normal ECG if you want to see the changes do an exercise stress test
During stress test might see ST depressions indicating IHD
Unstable Angina/ NSTEMI =
ST depressions and T wave inversion, non-Q-wave MI
[NSTEMI = positive cardiac markers, unstable = negative cardiac markers]
Acute MI/ STEMI =
ST segment elevation with T wave inversion, and Q-wave MI
[positive cardiac markers]
What are some types of echocardiography, what can they detect and what can they diagnose?
Transthoracic echo = helps to assess:
Left ventricular function
Wall-motion abnormalities in the setting of ACS
Mechanical complications of ACS
Transoesophageal echo = most often used for assessing possible aortic dissection in the setting of ACS.
Stress echo = used to evaluate haemodynamically significant stenoses in stable patients who are thought to have CAD
What is coronary angiography and why is it used?
In vivo assessment of coronary arteries
Iodinated contrast agent injected through catheter placed at the ostium of the coronaries - contrast agent is visualized through radiographic fluoroscopic examination of the heart
Used to detecting stenoses that may be revascularized through percutaneous or surgical intervention
Coronary CT angiography = used to detect presence and extent of CAD, and independent predictors of significant coronary stenosis and other cardiovascular events
What is ultrasonography and why might it be used?
Ultrasonography (AKA Doppler US) of the common and internal carotid arteries = non-invasive measure of arterial wall anatomy
Can be performed repeatedly and reliably in asymptomatic individuals
Combined thickness of intima and media of the carotid artery = associated with prevalence of CVD and risk factors, and increased risk of MI and stroke
What are doppler velocity probes and why might they be used?
Doppler Velocity probes = measures coronary flow
Doppler guidewire measures phasic flow velocity patterns and tracks flow rates in small, straight coronary arteries
Doppler velocity probe = used to determine the severity of intermediate stenosis (40-60%)
Helps evaluate whether normal blood flow has been restored after percutaneous transluminal coronary angioplasty (PTCA)
What is the pharmacological treatment in stable or some unstable anginas?
HMG-CoA reductase inhibitors =
Lower LDL-C and triglyceride levels, and raise serum HDL levels
e.g. Atorvastatin (Lipitor)
Bile Acid Sequestrants =
Block enterohepatic circulation of bile acids and increase the fecal loss of cholesterol
e.g. Cholestyramine (Questran, LoCholest, Prevalite)
Calcium channel blockers =
Relaxes coronary smooth muscle and produces coronary vasodilation = improved myocardial oxygen delivery
e.g. Amlodipine (Norvasc)
ACE Inhibitors =
Helps hypertension = reduces vascular endothelial dysfunction
e.g. Captopril (Capoten), enalapril (Vasotec), and lisinopril (Zestril)
Beta-blockers =
Inhibit sympathetic stimulation of heart = reduced HR and contractility; decreased myocardial oxygen demand
Antianginal Agents =
Inhibition of late sodium current of cardiac action potential = reduced myocardial cellular sodium and calcium overload
Platelet aggregate inhibitors = Inhibition of platelet function = protection against atherosclerosis e.g. Clopidogrel, Aspirin
Nitrates =
Decrease myocardial oxygen demand by producing systemic vasodilation
Which of these is useful in treating acute angina pain?
Nitrates = very helpful for acute angina pain
What are some revascularisation therapies?
Percutaneous coronary Intervention
(PCI) - given to all patients with stable CAD who have areas that can be revascularised - use angiography to place stent, which compresses plaque and improves blood flow
Coronary Artery Bypass Graft (CABG) - graft from vessel from vein in leg = placed on heart to bypass narrowed artery
Recommended to those with several narrowed coronary arteries
What are some recommendations to help prevent CAD and IHD?
Moderate physical activity for a total of 30 minutes on most days of the week
Avoid tobacco use and exposure to environmental smoke; make plans to quit if you already smoke
Choose a diet rich in fruits, vegetables and potassium, and avoid saturated fats and calorie-dense meals
Maintain a normal body weight; if you are overweight, lose weight by increasing physical activity and reducing calorie intake
Reduce stress at home and at work
