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4th Year Cardiology > Ischaemic heart disease > Flashcards

Ischaemic heart disease Flashcards

1
Q

Define angina pectoris

A

Symptomatic reversible myocardial ischaemia

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2
Q

Features of angina pectoris

A
  1. Constricting/heavy discomfort to the chest, jaw, neck, shoulders, or arms
  2. Symptoms brought on by exertion
  3. Symptoms relieved within 5 minutes by rest or GTN

All features = typical angina; 2 features = atypical angina, 0-1 features = non-anginal chest pain

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3
Q

Precipitates of angina

A
  • Exertion
  • Emotion
  • Cold weather
  • Heavy meals
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4
Q

Symptoms associated with angina (other than chest discomfort)

A
  • Dyspnoea
  • Nausea
  • Sweatiness
  • Faintness
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5
Q

Pathophysiology of stable angina

A
  • Coronary artery narrowing by an atherosclerotic plaque reduces blood flow and oxygen delivery to the myocardium
  • The atheroma also causes endothelial dysfunction, reducing vasodilator release (eg nitric oxide and prostacyclin)
  • The demand for increased myocardial oxygen supply (eg by walking uphill) is unable to be met due to the stenosic lesion, resulting in myocardial ischaemia
  • Ischaemia causes acidosis, decreased ATP production and release of lactate and other chemokines, which stimulate nerve cells in myocytes, producing the sensation of pain
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6
Q

Risk factors for angina

A
  • Men affected twice as much as women
  • South Asians more likely to be affected
  • Modifiable risk factors:
    • diabetes mellitus
    • hypertension
    • hyperlipidaemia
    • smoking
    • obesity
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7
Q

Investigations for angina

A
  1. Obtain and ECG
  2. Blood tests - FBC, U&Es, LFTs (required for statin therapy), glucose, HbA1c, cholesterol, HDL, LDL and triglycerides
  3. Consider echo and chest X-ray
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8
Q

Management of stable angina

A
  • Optimise diet and lifestyle
  • Prescribe aspirin and a statin
  • Pharmacological therapy (GTN, beta blocker, calcium channel blocker)
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9
Q

Pharmacological therapy in stable angina

A
  • Glyceryl trinitrate (GTN) should be used as and when necessary, repeating a second time after 5 minutes if the pain persists; call an ambulance if the pain persists 5 minutes after a second dose
  • First line: beta blocker or calcium channel blocker (rate limiting eg verapamil)
  • Increase the dose of monotherapy if still symptomatic
  • Second line: beta-blocker and calcium channel blocker combination therapy (use a non-rate limiting agent, eg nifedipine)
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10
Q

How would you institute lipid modification therapy?

  1. Which blood tests would you require?
  2. What liver values would indicate it is safe to start statins?
  3. When should LFTs be measured after commencing statins?
  4. Which values give the best prediction of CVD risk? What is the role of LDL?
  5. What dose and which statin would you prescribe?
A
  1. Measuere a full lipid profile, including total cholesterol, HDL, LDL, triglycerides and liver function tests
  2. Statins are safe to start as long as liver transaminase results are less than 3 times the upper limit of normal
  3. LFTs should be measured within 3 months of starting treatment and at 12 months
  4. Ratio of total cholesterol to HDL cholesterol is the best predictor of CVD risk, while LDL cholesterol helps guide goals of lipid therapy
  5. Atorvastatin 20 mg for primary prevention if 10 year cardiovascular risk is >10%; atorvastatin 80mg for secondary prevention in patinets with pre-existing CVD
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11
Q

Indications for coronary artery bypass grafting in angina:

A
  • Significant left main disease
  • Three vessel disease
  • Two vessel disease in diabetics
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12
Q

What are the criteria for metabolic syndrome?

How does this syndrome affect risk of cardioembolic events?

A

Metabolic syndrome is characterised by having 3 of the following 5 criteria:

  • Hyperinsulinaemia (elevated fasting plasma glucose)
  • Decreased HDL
  • Central obesity
  • Hypertriglyceridaemia
  • Hypertension (>130/85)

This syndrome confers a threefold increase in the risk of cardioembolic event

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13
Q

Define acute coronary syndrome

A

ACS refers to a group of conditions that result from a sudden and unpredictable disruption in coronary blood flow. This includes unstable angina and myocardial infarction.

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14
Q

Clinical features of ACS

A
  • Chest pain which is acute, central, crushing and retrosternal in nature, with or without radiation to the jaw, neck or arm
  • Other symptoms include shortness of breath, sweating, nausea and vomiting
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15
Q

Risk factors for ACS

A

Non modifiable:

  • Male sex
  • South Asian ethnicity
  • Age
  • Familiy history of cardiovascular disease (<55 in men, <65 in women) in a first degree relative
  • Dyslipidaemia

Modifiable:

  • Diabetes mellitus
  • Hypertension
  • Hyperlipidaemia
  • Smoking
  • Obesity and sedentary lifestyle
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16
Q

Acute coronary syndrome immediate investigations

A
  • Obtain ECG - compare with olde ECGs if possible
  • Blood tests - Trooponin T or I (serial, 6 hours apart, looking for a peak in the measured values), FBC, U&Es, LFTs
  • Chest X-ray
    • assess cardiomediastinal contours (eg the presence of cardiomegaly, mediastinal widening in aortic dissection)
    • lung fields (eg signs of heart failure)
    • exculde non-cardiac causes of chest pain (eg pneumothorax, pneumonia)
17
Q

Apart from myocardial infarction, which conditions can cause elevated troponin?

A
  • Acute heart failure
  • Myocarditis
  • Pericarditis
  • Pulmonary embolism
  • Renal failure
  • Sepsis
18
Q

Initial management of acute coronary syndrome

A
  • Continuous cardiac monitoring
  • Administer aspirin 300mg, plus another antiplatelet agent (eg clopidogrel)
  • Oxygen - only if SpO2 <94%
  • GTN - avoided if systolic BP <90mmHg
  • IV morphine for pain eg 2.5mg blouses, 5 minutes apart
  • IV metoclopramide - ischaemia and morphine are both emetogenic
  • Tight glucose control - glucose should be monitored regularly
19
Q

Advanced management of STEMI

A
  • Primary percutaneous coronary intervention (PPCI)
    • Gold standard repercussion strategy in STEMI
    • Indicated if symptoms onset occurd within 12 hours
    • Procedure should be performed within 90-120 minutes of diagnosis
    • Bivalirudin (direct thrombin inhibitor) in combination with aspirin and clopidogrel, is recommended for patients with STEMI undergoing PPCI
  • Thombolysis
    • Should only be performed if patients are unable to receive PCI within 90-120 minutes of diagnosis, or where PPCI is contraindicated
    • ECG should be performed 90 minutes after thromolysis
      • Look for 50% reduction in ST elevation
      • If inadequate response, consider PCI within 6 hours of thombolysis
20
Q

Features of STEMI on ECG

A
  • ST elevation of ≥1mm in at least 2 adjacent limb leads or ≥2mm in contiguous precordial leads
  • New onset of LBBB (less specific for STEMI)
21
Q

How to establish diagnosis of NSTEMI or UA

A
  • NSTEMI: positive troponin +- ischaemic changes on ECG (eg ST depression, T wave inversion)
  • Unstable angina negative troponin +- ischaemic changes on ECG
22
Q

Management of NSTEMI/UA

A

NICE recommends the GRACE score to predict 6 monthly mortality

  • If low risk (predicted 6 month mortality <3%)
    • Offer patients anticoagulation (fondaparinux 2.5mg SC is recommended for 8 days or until discharge) without early angiography and proceed to post acute management
  • If intermittent (3-6%) or high risk (>6%)
    • Offer IV glycoprotein IIb/IIIa inhibitors and anticoagulation (bivalirudin or unfractionated heparin recommended)
    • Arrange coronary angiography within 96 hours of admission and consider PCI
23
Q

Post acute management of acute coronary syndrome

A
  • Anitplatelet agents
    • Aspirin 75mg lifelong following ACS
    • P2-Y12 inhibitors eg clopidogrel for 12 months
  • Statin therapy lowers mortality; atorvastatin 80mg
  • Beta blockers lowers mortality and provides symptomatic relief
  • Nitrates regular (if required) and PRN for all patients
  • ACE inhibitors lowers mortality, and prevents ventricular remodelling and subsequent heart failure
24
Q

Complications of acute coronary syndrome

A

Sudden death on PRAED street

  • Sudden death
  • Pump failure or Pericarditis
  • Rupture (eg of LV free wall, septum or papillary muscle)
  • Aneurysn or Arrhythmia
  • Embolism
  • Dressler syndrome
25
Q

Right ventricular failure

  1. Associated with which type of MI?
  2. Suspect if:
  3. Treatment
  4. Why should nitrates and diuretics be avoided?
A
  1. Associated with inferior wall MI
  2. Suspect if clear lung fields, elevated JVP and systemic hypotension
  3. Fluid boluses that augment RV preload (eg 250ml 0.9% NaCl over 10 minutes)
  4. Nitrates and diuretics reduce preload, which will worsen the condition of right ventricular failure, as filling of the right side of the heart is already impaired

4th Year Cardiology (12 decks)

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