CVS session 10: ischaemic heart disease Flashcards
What might cause chest pain and what sort of pain would be felt?
CARDIAC:
- myocardial ischaemia (tightening, diffuse radiation pain)
- pericarditis (sharp)
- aortic dissection (tearing)
RESPIRATORY: lateral chest pain, “pleuritic” pain (worse on inspiration and coughing), other respiratory symptoms
- infection
- pulmonary embolism
- pneumothorax
GI: chest and epigastric pain, reflux causes burning pain, other GI symptoms
- reflux oesophagitis
- gastric/gall bladder/pancreatic
MSK: history of trauma/excessive use, often localised, movements may make pain worse
- trauma
- muscle pain
- bone metastases
Why are sub-endocardial areas most vulnerable to ischaemia?
Coronary blood flow is from epicardium to endocardium, so during diastole when the coronary arteries can perfuse they will perfuse this area last, so if they can’t perfuse as well this area will suffer
Why does tachycardia worsen ischaemia?
At a rapid heart rate diastole is shortened so less time for coronary blood flow
What is the most common cause of ischaemic heart disease?
Atherosclerosis which causes a fixed narrowing of a coronary artery:
- no collaterals between major arteries
- some collaterals between smaller coronary arteries & arterioles
- some development during ischaemia but this takes time
What does myocardial O2 demand and supply depend on?
Demand: HR, wall tension (preload and after load) and contractility
Supply: coronary blood flow (perfusion pressure [diastolic BP] and coronary artery resistance) and the oxygen carrying capacity of blood
What are the modifiable and non-modifiable risk factors for ischaemic heart disease?
Non-modifiable: increased age, male sex (females catch up after menopause), family history of IHD
Modifiable: hyperlipidaemia, hypertension, diet low in fruit and veg, diabetes, obesity, smoking, lack of exercise, stress
Pathological difference between stable and unstable angina
Stable angina: stable fixed plaque with a small necrotic core and a thick fibrous cap, so is unlikely to rupture
Unstable angina: plaque disruption and platelet aggregation, fibrous cap can undergo erosion which exposes blood to the thrombogenic material in the necrotic core
Describe the progression of atherosclerosis in the acute coronary syndromes
Unstable angina: plaque disruption and platelet aggregation. Occlusion of coronary artery but not enough to cause infarction
NSTEMI: platelet clot is followed by a fibrin thrombus which causes obstruction in a coronary artery leading to infarction
STEMI: plaques can fissure causing a sudden worsening of symptoms with complete obstruction; can quickly cause death
How is stable angina diagnosed?
Symptoms: no pain at rest and moderate pain on stress/exertion that is relieved by rest or nitrates within 5 minutes
Signs: related to risk factors (e.g. hypertension, corneal arcus), signs of atheroma elsewhere (e.g. absent pulses)
Investigations:
-resting ECG normal but may show signs of previous MI
-stress perfusion scan
-exercise stress ECG (not normally used anymore but used to be): patient connected to ECG then graded exercise on treadmill until target HR reached/ECG changes/chest pain/other problems
What are the ECG changes seen on an exercise stress test in a patient with stable angina?
Exercise induces transient sub-endocardial ischaemia, so see ST segment depression that returns to baseline with rest. Test is positive if ST depressions are >1 mm (horizontal or down sloping), and is negative if the target heart rate is reached without any ECG changes
How might stable angina be treated?
- Patient education and lifestyle changes
- Acute episodes: sublingual nitrates
- Mediations to modify risk factors:
- long acting nitrates for venodilation to reduce preload
- beta blockers to decrease HR and contractility
- Ca2+ channel blockers: decrease after load by peripheral vasodilation
- statins: decrease LDL cholesterol by inhibition of HMG-CoA reductase and up regulate LDL receptors in the liver (decreases atherosclerosis and increases plaque stability)
- aspirin: decreases platelet aggregation so decreases thrombus formation if plaques disrupted - Revascularisation: coronary angiography to identify the sites of occlusion and decide technique to restore blood flow, which will be either:
- Percutaneous Coronary Intervention: angioplasty and stenting (inflate balloon, guide wire, stent)
- Coronary Artery Bypass Grafting: internal thoracic artery, radial artery or reversed great saphenous vein grafts
What causes acute coronary syndrome?
Fissuring or rupture of an atheromatous plaque, which stimulate a thrombotic response. Causes variable obstruction to flow in a coronary artery lumen with downstream ischaemic myocardial injury.
UA and NSTEMI: obstruction to flow usually incomplete/collaterals present
STEMI: obstruction complete
Why does total occlusion of a coronary artery appear as ST segment elevation on ECG?
Transmural (full thickness) injury extending to the subepicardial area appears as ST elevation in electrodes facing the damaged area.
Ischaemic region depolarised and generates electrical currents traveling away from the recording electrode so baseline voltage prior to the QRS complex will be depressed. All the muscle becomes depolarised during the ST segment so that zero voltage is recorded by the electrode. Followiing repolarisation after the T wave, the baseline is again negative as in the resting state. Therefore, ST segment appears elevated relative to the baseline.
Why do some MIs and unstable angina cause ST depression on an ECG?
Ischaemic region is depolarised and so generates electrical currents; if traveling toward a positive electrode, the baseline voltage prior to the QRS complex (which is normally isoelectric) will be elevated. When the normal parts of the ventricle become depolarised, all myocardium is depolarized so that zero voltage is recorded by the electrode. After repolarization, the voltage following the T wave remains positive as in the resting state. So the elevated baseline voltage causes the ST segment to appear depressed compared to the baseline
Why are unstable angina and NSTEMIs initially treated in the same way?
ECGs will show ST depression/T wave inversion/normal, both symptoms suggestive of acute MI. Only differentiating factor is blood enzymes due to necrosis of myocytes in an MI, however these can’t be discovered immediately so treat UA the same
What are the biochemical markers of myocyte damage?
- Cardiac troponins: cTnI and cTnT
- proteins present in myocytes that are important for actin/myosin interactions and released on myocyte death
- elevated in STEMI and NSTEMI (changing levels with more than 1 value above the 99th percentile of the upper limit)
- not in UA as ischaemia but no necrosis
- preferred as highest specificity and sensitivity marker
- peak 18-36 hours and return to normal over 5-14 days, so may not be detected until 4-6 hours after injury so need to repeat but can detect if present late - Myoglobin
- most sensitive early marker as is released ~2 hours after MI
- high sensitivity but poor specificity - Creatine kinase (CK-MB)
- increases 3-12 hours after onset, peak at 24 hours, return to normal 48-72 hours so can observe if late onset or new episodes of pain
- lower specificity and sensitivity than troponins
Describe the typical presentation of MI
Pain: in 50% there is pain at rest which is not relieved by nitrates. Pain is severe, persistent, central crushing pain with typical radiation
Distress, feeling of impending death
Sympathetic features: sweating, pallor, cold skin
Parasympathetic features: nausea, vomiting
Breathlessness due to LV dysfunction, may faint
Arrhythmia, low BP
S3/S4 heart sounds and lung base may be present, indicating heart failure
What are the ECG changes in a fully-evolved STEMI, in leads facing the infarcted area?
Pathological Q waves: wide and deep, due to necrosis area
ST segment elevation: from injury zone
T wave inversion: 2-5 days, recovery weeks/months
How would a posterior MI appear on an ECG, given that there are no leads viewing posteriorly?
May show as ST depression in anterior leads, or tall R waves rather than pathological Q waves in V1 and V2 (due to occlusion of RCA)
Where would an occluded right coronary artery cause an MI and in which leads would ECG changes show up in?
Inferior
II, aVF, III
Where would an occluded LAD cause an MI and in which leads would ECG changes show up in?
Anteroseptal
V1 and V2
Distal LAD would be anteroapical MI showing in V3 and V4
In an anterolateral MI which coronary artery is likely to have been occluded and where would the ECG changes be?
Circumflex
V5, V6, I and aVL
What coronary artery has been occluded in an extensive anterior MI and where are the ECG changes?
The proximal left coronary artery
Seen in leads V1-V6, I and aVL
How are NSTEMIs and STEMIs differentiated by ECG?
NSTEMI: ST segment depression and/or T wave inversion OR no ECG changes
STEMI: ST elevation in two or more leads facing the same area (elevation 1mm in limb leads or 2mm in chest leads) OR new left bundle branch block
How are all acute coronary syndromes initially managed?
Aspirin
IV opioids/other analgesia
O2 IF sats
How is a STEMI treated?
Dual anti platelet therapy: aspirin and ticagretor to prevent more thrombosis
If emergency PCI in the next 2 hours is available then this will be done first; if not give fibrinolytics thrombolysis and PCI later
Anti-ischaemic therapy: IV nitrates, beta blockers
ACE inhibitors (Esp. if LV failure) to decrease harmful remodelling
Statins
How is an NSTEMI treated?
Dual anti platelet therapy: aspirin and ticagretor to prevent more thrombosis; anti-ischaemic therapy: IV nitrates, beta blockers; ACE inhibitors (Esp. if LV failure) to decrease harmful remodelling; statins
then
Prevent progression of thrombus with anti platelets and anticoagulants (e.g. LMW heparin): NOT THROMBOLYTICS
Risk assess using GRACE score: high risk needs a PCI or CABG soon; low risk initially medical then elective angio
What long term treatments are used following MI?
Aspirin, beta blockers and statins to decrease mortality and re-infarction
ACE inhibitors
Management of risk factors
What are the long term complications of myocardial infarction?
- sudden cardiac death: VF or asystole
- arrythmias: sinus tachycardia (pain, anxiety, heart failure), sinus bradycardia (SA node ischaemia)
- heart block: AV node ischaemia
- VT or VF: ventricle ischaemia causing re-entry circuits or increased automaticity
- heart failure: loss of myocardium decreases contractility
- cardiogenic shock: when >40% infarcted cardiac output decreases with inadequate tissue perfusion
What are the signs and symptoms of acute pericarditis?
Symptoms:
- pain: dull/sharp/burning/pressing in substernal/precardial area. ranges in severity
- pain radiates to neck or shoulders
- pain worsened by inspiration, swallowing, coughing, lying flat, relieved by sitting up and forward
- non productive cough
- chills
- weakness
Signs:
- pericardial friction rub on auscultation
- tachypnoea
- tachycardia
- fever
Why does referred pain occur?
Heart is usually insensitive to touch, heat etc; ischaemia and associated metabolic products stimulate pain endings in the myocardium and afferent pain factors enter the spinal cord at ~T1-T4 especially on the left.
Cardiac referred pain is a phenomenon where stimuli in the heart are perceived by a person as pain arising from a superficial part of the body, e.g. skin of the left shoulder. Spinal cord segments of cutaneous nerves are also common to the visceral afferent terminations for the coronary arteries
Why could anaemia worsen angina?
Reduced oxygen capacity of blood so ischaemia worsens and heart has to work harder. Therefore may cause a “flow” murmur due to increase CO and a forceful apex beat
Signs of aortic stenosis with LVH and how this worsens angina?
Loud systolic murmur and forceful apex beat
Blood can’t get through aortic valve to circulate oxygenated blood to body, so less O2 perfuses coronary arteries
