Core conditions 2 Flashcards
Ischaemic heart disease definition
Caused by atheromatous plaques that cause blocking/narrowing of the coronary arteries. Causes ischaemia and death of heart muscle. Can be temporary or permanent. Split into angina pectoris and ACS.
Angina
Occurs on exertion, due to narrowing of a coronary artery causing less oxygen to reach the heart muscle resulting in anaerobic respiration. Lactic acid builds up in the heart muscle causing pain, on rest pain stops
Angina clinical features
- A syndrome of reversible myocardial ischaemia
- 1= Constriction/heavy discomfort in the chest which may radiate to the jaw, neck, shoulders or arms
- 2= Symptoms are present on exertion
- 3= Symptoms are relieved within 5mins by rest or GT
- All 3 features = typical angina, 2/3 features = atypical angina, 0-1 features = non-anginal chest pain
- Associated symptoms: dyspnoea, nausea, sweatiness and faintness
Angina investigations
- Bloods – FBC, U&Es, TFTs, lipids, HbA1c, Troponin (if unstable)
- ECG – usually normal, but may show ST depression, flat or inverted T-waves or signs of a past MI
- Echo or CXR
To confirm IHD diagnosis
- Exercise ECG – assess for ischaemic ECG changes
- Angiography – either using cardiac CT with contrast, or transcatheter angiography
- Functional imaging: myocardial perfusion, scintigraphy, stress echo, cardiac MRI
Complications of angina
- Main complication of angina is progression to ACS
- Risk stratification is caried out using the QRISK 2 tool, calculates risk of stroke or MI within 10 years. If risk >10% take statin
Management of angina
- Short acting nitrates: GTN spray
- Beta blocker or calcium channel blocker
- Information, lifestyle modification
- Second line: long acting nitrates, Ivabradine, Nicorandil
- Symptomatic: beta blocker and dihydropyridine
Investigations ACS
- Bloods: FBC, U&E, glucose, lipids, troponin
- CXR: look for cardiomegaly, pulmonary oedema or widened mediastinum
- Echocardiogram: regional wall abnormalities
ACS treatment: STEMI and NSTEMI
- STEMI patients and very high-risk NSTEMI patients (e.g. haemodynamically unstable) should receive immediate angiography with or without PCI (inserting a stent into the coronary artery to open it up)
- NSTEMI patients who are high risk should have angiography within 24 hours; immediate risk within 3 days; low-risk patients may be considered for non-invasive testing
Treatment for ACS: symptoms and multivessel disease
- Patients with multivessel disease may be considered for CABG (involves harvesting a vessel from elsewhere in the body and bypassing the blockage of the coronary artery) instead of PCI
- Symptom control: PRN GTN and opiates, if insufficient give GTN infusion (monitor BP)
Post ACS cardioprotective treatment
- Antiplatelets: aspirin (75mg OD) and a second antiplatelet agent (e.g. clopidogrel) for at least 12 months to decrease vascular events (e.g. MI, stroke). Consider adding a PPI (e.g. lansoprazole) for gastric protection
- Anticoagulate, until discharge
- Beta-blockers If contraindicated, consider verapamil or diltiazem
- ACE-Iin patients with LV dysfunction, hypertension, or diabetes unless not tolerated (consider ARB). Titrate up slowly, monitoring renal function
- High-dose statin, e.g. atorvastatin 80mg
- Do an echo to assess LV function.Eplerenoneimproves outcomes in MI patients with heart failure (ejection fraction <40%)
Common co-morbidities with ACS
- Stroke, TIA and peripheral vascular disease
- Heart failure: diagnosis requires symptoms of HF and evidence of cardiac dysfunction at rest. For example: fatigue, breathlessness and oedema
- Depression, stress, anxiety, PTSD: recommend CBT and yoga
Driving and ACS
- The patient should stop for; 1 week if they have had a successful angioplasty, 4 weeks if they have an unsuccessful angioplasty and 4 weeks again if they didn’t have an angioplasty
- Bus, coach or lorry: inform DVLA and stop driving for 6 weeks, must be assessed by doctor before they can start driving again
ACS investigations
- Bloods: FBC, U&E, BNP
- CXR
- ECG: may show cause (MI, ischaemia or ventricular hypertrophy), rare to be normal
- Echocardiogram: can indicate cause and confirm presence or absence of LV dysfunction. If either ECG or BNP is abnormal then echocardiography is required
- Endomyocardial biopsy is rarely needed
Main physical symptoms of heart failure at end of life
- Fatigue
- Breathlessness: usually caused by pulmonary oedema. Management is sitting patient up and improving oxygen flow. Maintain good oral hygiene
- Peripheral oedema: manage with diuretics i.e. furosemide
- Pain: opiates
- Nausea and vomiting: anti-emetics and changing position when eating
- Cardiac cachexia or anorexia: loss of appetite and weight loss
- Anxiety and depression
Ischaemic stroke
When blood flow to part of the brain is disrupted due to blockage in the blood vessel. Can be thrombotic where the blood clots forms within the artery or Embolic where the blood clots travels from another part of the body
Haemorrhagic stroke
When a blood vessel ruptures and bleeds into the brain tissue. Intracerebral haemorrhage is in the brain parenchyma and is due to hypertension, cerebral amyloid angiopathy or vascular malformation. A subarachnoid haemorrhage is due to a rupture of an intracranial aneurysm or arteriovenous malformation in the subarachnoid space
Bamford stroke classification rules
- unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
- homonymous hemianopia
- higher cognitive dysfunction e.g.[dysphasia]
Total anterior circulation infarct (TACS)
- involves middle and anterior cerebral arteries
- all 3 of the above criteria are present: unilateral sensory loss of face, arms and legs, homonymous hemianopia, higher cognitive impairement i.e. dysphasia
Partial anterior circulation infarcts (PACI, c. 25%)
- involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery
- 2 of the above criteria are present: unilateral sensory loss of face, arms and legs, homonymous hemianopia, higher cognitive impairement i.e. dysphagia