LO03 - Chest pain and vascular disease Flashcards
Describe the common complications MI and their pathological basis
Complications and prognosis depend of infarct size, location and thickness (transmural or subendocardial). Worse outcome with large, anterior and transmural infarcts
Arrhythmias: myocardial irritability or conduction disturbances following MI → depending on the site of MI can cause sinus bradycardia, heart block, ventricular tachycardia, and ventricular fibrillations
Cardiogenic shock: “pump failure” occurs in 10-15% of patients post MI, generally in those with large infarcts (>40% of left ventricle). Mortality rate ~70%
Pericarditis: Fibrinous or fibrino-haemorrhagic develops 2-3 days post transmural MI (full thickness MI) as a result of underlying myocardial inflammation
Cardiac rupture: softening and weakening of the necrotic inflamed myocardium (3-7 days post MI). 1) Rupture of ventricular free wall causing cardiac tamponade (most common), 2) Rupture of the inter-ventricular septum causing acute ventral-septal defect and left to right shunting, 3) Rupture of papillary muscle leading to severe mitral regurgitation.
Cardiac failure: due to functional decompensation of hypertrophied non-infarcted myocardium
− Non-infarcted segments undergo ventricular remodelling: hypertrophy of Myocytes + dilation of chambers
− Initially beneficial but the heart is eventually overwhelmed by increased O2 demand (to maintain hypertrophied cells) and the reduced compliance of the scarred stiffened ventricle walls
Pulmonary thromboembolism:
What pharmacological treatments are used to limit the extent of a myocardial infarction and what is their mechanism of action?
Immediate: Restoring coronary patency, Thrombolysis (within 12 hrs of symptom onset, St elevation present)
− Choice of drug o tPA (human tissue plasminogen activator): better survival rates than streptokinase o Streptokinase: causes hypotension and allergic reactions (increased chance with repeat administration)
Short term: Maintaining coronary patency and reducing risk of arrhythmias
− Antiplatelet: aspirin
PLUS
− Anticoagulant: Iv heparin for 2-3 days following thrombolysis
− B-blockers: reduce risk of arrhythmias
Long-term prevention
− Antiplatelet: aspirin
− B-blockers: to diminish cardiac oxygen demand and reduce risk of arrhythmias. Avoid in those with heart failure or severe bradycardia
− Statins: decrease LDL, reduce risk of new plaque formation and stabilise already formed plaques
− ACE inhibitors: reduce ventricular dilation post MI by decreasing afterload
Describe the way in which estimation of blood enzyme and protein levels may aid in the diagnosis of myocardial infarction
The following enzymes and proteins are contained within myocardial cells and are released into plasma when they undergo necrosis. Serial measurements are needed because it is the change in plasma concentration over time that is of diagnostic value
- Creatinine Kinase (CK) or CK-MB (cardiac specific CK): starts to rise at 4-6 hrs, peaks at 12, falls to normal within 48-72 hrs. CK is less specific because it can be released with skeletal muscle damage as well
- Cardio-specific proteins (Troponin T, Troponin I): released within 4-6 hours, remain elevated for up to 2 wks. More sensitive
Describe the ECG abnormalities that characterise myocardial infarction
ST elevation: Indicates evolving myocardial infarction secondary to complete occlusion of a coronary artery (“Injury current” moving from the infarcted regions of myocardium to normal myocardium)
Pathological Q waves (>1 small square in width, >2 small squares in depth): “Electric window” created by a full thickness infarction allowing the electrode to record/see septal depolarisation.
T wave inversion: May be due to reperfusion of the area as the artery recannulates spontaneously or in response to treatment (often seen in patients following thrombolysis)
Site of Infarction: ECG changes are seen in the leads overlying the damaged regions of myocardium
− Anterior infarction: V3-V4, (classically), V2-V5
− Inferior infarction: III, VF
− Lateral infarction: I, VL, V5-V6
− True posterior infarction: dominant R waves in V1
Define stable angina, unstable angina and MI. In your answer describe the underlying pathological process in the coronary circulation
Stable Angina: Angina precipitated by exertion or other form of stress (cold, emotion, heavy meals). Ischemia due to fixed atheromatous stenosis of one or more coronary arteries
Unstable Angina: Angina on minimal exertion/rest, rapidly worsening (crescendo angina). Ischemia cause by dynamic obstruction of a coronary artery due to plaque rupture with superimposed thrombus and spasm.
Myocardial Infarction: Myocardial necrosis caused by acute occlusion of a coronary artery due to plaque rupture and thrombosis
Describe the events leading up to an acute coronary syndrome
Acute coronary syndromes result from the loss of integrity of the protective covering over an atherosclerotic plaque. This occurs with plaque rupture, plaque erosion, or calcified nodule. The loss of the protective endothelial covering allows blood to come in contact with the highly thrombogenic contents of collagen and/or necrotic core of the plaque and allows luminal thrombosis to occur. Other mechanisms can cause acute coronary syndromes, including a supply-demand mismatch.
Describe the microscopic and macroscopic changes occurring in the myocardium after an acute MI (include a timeline)
Macroscopic
6-12hrs: No/minimal changes
12-24 hrs: Dark mottling due to stagnated trapped blood
1-7 days: Progressively sharply defined, yellow/tan coloured, soft
7-10 days: Yellow center bordered by red tan margins (highly vascularised hyperemic granulation tissue)
2-8 wks: Grey-white scar progressing from border to center of infarct
>2 months: Scarring complete
Microscopic
6-12hrs: Early coagulative necrosis; oedema; haemorrhage; wavy fibres (non contractile dead fibres which have been stretched by adjacent contractile myocardium)
12-24hrs: Coagulative necrosis; pyknosis of nuclei, neutrophil infiltrate
1-7 days: Coagulative necrosis: loss of nuclei and striations, disintegration of myofibrils, dead neutrophils
7-10 days: Phagocytosis of dead cells, Ingrowth of granulation tissue
2-8 wks: Collagen deposition
>2 months: Dense collagenous scar
Common causes of aortic dissection?
The initial tear in the intima is usually spontaneous or iatrogenic, but can be due to primary haemorrhage in the media (from the vasa vasorum – the blood vessels supplying the blood vessels). Risk factors include things that can damage the vessel wall: • CVD risk factors o Hypertension (80% of cases) o Aortic atherosclerosis • Aortic o Non-specific aortic aneurysm (aneurysms can predispose to aortic dissection, but chronic aortic dissection can cause aneurysms – hard to identify primary pathology) o Aortic coarctation • Collagen disorders o Marfan’s syndrome o Ehlers-Danlos syndrome • Iatrogenic o Previous aortic surgery o Iatrogenic • Pregnancy • Smoking • Trauma
Pathological changes in aortic dissection?
• Cystic medial degeneration:
o Smooth muscle layer dropout and necrosis
o Elastic tissue fragmentation
o Accumulation of amorphous proteoglycan-rich ECM
o Inflammation absent
Clinical consequences of aortic dissection?
On history you might expect:
• Chest pain: acute onset, severe, ‘ripping’ or ‘tearing’, can change location as the dissection extends, eg to back between shoulder blades as the descending aorta is involved
• Syncope
• Dyspnoea
• Symptoms reflecting ischaemia to areas of the body eg altered mental state, hemiparesis/paraesthesia, renal failure, abdominal pain, limb pain/pallor
On examination you might see signs that more blood is going to one side than the other:
• Left/right arm BP differential: a hallmark feature
• Pulse differential between the 2 legs
In proximal dissections you might also see a diastolic murmur indicating aortic regurgitation.
Causes of pericarditis
Pericarditis is inflammation of the pericardium – the sac surrounding the heart – and as such, causes are things that can induce inflammation: • V: damage from acute MI • I: viral infection (eg Coxsackie B), bacterial, TB • T: chest wall trauma • A: CT disease (eg SLE) • M: uraemia • I • N: malignancy • D
Clinical features of pericarditis
You would expect clinical features that represent inflammation in the mediastinum:
• Chest pain: retrosternal, radiating to shoulders and neck, relieved by sitting forward, exacerbated by lying supine, movement, deep breathing, exercise, swallowing
• Low-grade fever
• Pericardial rub: caused by movement of the inflamed pericardium
• ECG changes: can be confused with AMI. Initially ST segment elevation (upward concave rather than convex like in MI) followed by a period where that elevation disappears, then T wave inversion, which then disappears.
Complications of pericarditis
Inflammation causes exudation, which can lead to
• Pericardial effusion: the usual volume in the pericardial sac is 30-50mL. Pericarditis can cause volumes to accumulate much higher than this. (The effusion could also be haemorrhagic eg if pericarditis was caused by malignancy). When the fluid in the pericardium compresses the heart and restricts ventricular relaxation and filling, this is cardiac tamponade. This usually occurs if the effusion builds up quickly, as over a longer period of time the heart can adjust for it. Beck’s triad for cardiac tamponade is hypotension, soft/absent heart sounds, and jugular venous distension with prominent x descent but absent y descent. Pulsus paradoxus is also a common feature (but seriously who measures that).
With chronic inflammation, healing by fibrosis can occur, which can lead to
• Chronic constrictive pericarditis: fibrosis of the pericardium occurs, leading to adhesions or dense, fibrotic scars in the pericardial space – when the heart is completely encased by dense fibrosis it can’t expand normally during diastole.
