Outline the principles of history-taking.
- Site: location of the pain and if it radiates
- Quality: how the pain feels (sharp, dull, etc)
- Intensity: effect on patient, severity score
- Timing: when it started (sudden or gradual onset)
- Aggravating factors: what makes pain worse
- Relieving factors: what makes the pain better?
- Secondary symptoms: other symptoms
What are the manifestations of Myocardial Ischaemia?
- Stable angina
- Unstable angina
- Myocardial infarction
- Left ventricular contractile impairment
What are the different causes of chest pain?
- Cardiac causes
- Non-cardiac causes:
I. Upper gastro-intestinal causes
II. Respiratory causes
III. Musculoskeletal causes
What are the respiratory causes of chest pain?
- E.g. Pneumonia – temperature, cough, breathlessness
- E.g. Pulmonary embolism – chest pain; sharp; well localised, worse with inspiration/cough
- E.g. Pleurisy - inflammation of the pleura; breathlessness, cough, pyrexia, dull pain
What are the cardiac causes of chest pain?
I. Dull, retrosternal, central
II. Radiate (jaw, neck, arms, shoulders)
III. May be worse with exertion
I. Central (retrosternum), sharp
II. Eased with sitting up / leaning forward
What are the upper gastro-intestinal causes of chest pain?
I. Burning pain
II. Can be felt centrally
III. Worse after food, worse on lying flat
- Peptic ulcer disease
What are the musculoskeletal causes of chest pain?
- Rib fracture
- Costochondritis – inflammation of the costal cartilages
I. Sharp, well localised
II. Tender to palpate
III. Worse with movement of chest wall – rough inspiration
Distinguish pleural/pericardial pain with cardiac ischaemic chest pain.
- Visceral pain: Cardiac ischaemic
I. Dull, poorly localised
II. Worsened with exertion
- Somatic pain: Pleural/pericardial
I. Sharp pain, often well localised
II. Worse with inspiration, coughing or positional movement
Outline Cardiac (Ischaemic) Chest Pain.
- Pain secondary to pathology involving the heart – Ischaemic heart disease
- Initial primary concern is to rule out urgent, potentially life-threatening causes of chest pain
- Heart tissue ischaemia occurs only when the metabolic demands of cardiac muscle are greater than what can be delivered via coronary arteries.
Explain the pathophysiology of ischaemic heart disease.
Describe the risk factors for atherosclerosis.
- Risk factors for atherosclerosis = risk factors for ischaemic heart disease.
VI. Sedentary lifestyle
I. Advanced age
II. Family history
Describe the features of stable angina.
- Atherosclerotic plaque is 'stable'
- Typical patient history:
I. Dull, retrosternal chest pain
II. Triggered by exertion
III. Relieved completely by rest
IV. NO chest pain at rest
V. GTN spray - relieve pains
What are the features of unstable angina?
- Many similarities to stable angina
I. Pain occurs at rest
II. Pain may be more intense
II. Pain may last longer
- Risk of deteriorating further – NSTEMI/ STEMI
Briefly describe the presentation of stable angina.
- Chest discomfort of almost any character but often pressure like
- Wide range of anatomical locations
- Usually brought on by increased cardiac work and relieved by rest
- Usual causes: coronary artery stenosis (poor perfusion of myocardium), spasm, anaemia, severe aortic valve stenosis
Briefly describe the presentation of unstable angina.
- Rapidly deteriorating symptoms control
- Increasingly frequent, severe, prolonged symptoms over short time course
- Location and character of discomfort as for stable
- Usual causes: coronary plaque rupture
What are the investigations for Stable Angina?
- Bloods: Full blood count (anaemia), high cholesterol (risk factor), renal and thyroid function (hyperthyroidism can cause angina)
- ECG: rhythm disturbance, atrial fibrillation, pathological Q waves
- Chest X Ray
- When to test for ischaemia?
I. Treadmill test
ii. Dibutamine stress echo
iii. Myocardial perfusion stress test
iv. MR Stress test
vi. Nuclear scan
vii. Coronary angiography
Describe the signs and symptoms of Myocardial infarction.
- Dull, retrosternal chest pain, central
- More severe
- Radiate neck, shoulders
- Chest pain at rest
- Look unwell
- Sweaty, pallor, nauseous, dyspnoea
- Pain last longer than 15 minutes
- Can be painless (e.g. Some diabetics)
What are the causes of myocardial infarction?
- Coronary heart disease (CHD) is the leading cause of heart attacks. CHD is a condition in which the major blood vessels that supply the heart get clogged up with deposits of cholesterol, known as plaques.
- Before a heart attack, one of the plaques ruptures (bursts), causing a blood clot to develop at the site of the rupture. The clot may block the supply of blood to the heart, triggering a heart attack.
Explain the concept of Acute Coronary Syndrome.
- Acute Coronary Syndrome: Acute myocardial ischaemia caused by atherosclerotic coronary artery disease – atheromatous plaques rupture with thrombus formation causing an acute increased occlusion (in an already partially occluded lumen) leading to ischaemia.
- Acute Coronary Syndromes: a spectrum of increasing occlusion from a common pathophysiologic mechanism
What does Acute Coronary Syndrome include?
Acute Coronary Syndrome includes:
- Unstable angina
- Myocardial infarction
- Non-ST elevation myocardial infarction (NSTEMI)
- ST elevation myocardial infarction (STEMI)
- NOT STABLE ANGINA
Further elaborate on Acute coronary syndrome.
Acute Coronary syndromes: a spectrum of increased occlusion following a plaque rupture
Differentiate the Clinical Examination Findings of stable angina and acute coronary syndromes.
- Stable angina
I. Clinical examination often normal
II. Will be chest pain free at rest
- Acute coronary syndromes (UA, NSTEMI, STEMI)
I. Clinical examination is often normal
II. But may appear sweaty, anxious, pale
III. +/- Clinical signs secondary to complications of cardiac tissue death (NSTEMI/STEMI) E.g. Acute heart failure, heart murmurs
Describe the investigations of myocardial infarction.
- Type one:
I. Spontaneous myocardial infarction
II. Plaque rupture, fissuring, ulceration, or dissection with resulting intraluminal thrombus leading to decreased myocardial blood flow or distal platelet emboli and myocardial necrosis
- Type two:
I. Myocardial infarction secondary to ischaemia imbalance
II. A condition other than CAD contributes to an imbalance between myocardial oxygen supply/demand – e.g. Coronary spasms, coronary embolism, tachy or Brady arrhythmia, anaemia, respiratory failure
- Type three:
I. MI resulting in death before biomarkers obtained
II. Cardiac death with symptoms of myocardial ischaemia and presumed new ischaemic changes Orr new LBBB on ECG without biomarker availability
- Type four A and B: Myocardial infarction due to coronary intervention or stent thrombosis
- Type five: MI related to CABG (Coronary Artery Bypass Grafting)
Describe the use of the investigations in the diagnosis of MI, distinguishing STEMI from an NSTEMI.
I. Changes suggestive of current ischaemia or infarct
II. Look at ST segments, T waves, +/- pathological Q wave
- Blood tests – Troponin – presence indicates cardia myocyte death
- Other investigations
I. To exclude potential diagnoses
II. To identify potential complications
Describe the use of ECG changes in the STEMI.
- Patterns of infarct
I. ST segment elevation
II. Hyperacute T waves
- Localisation of changes helps to determine anatomical site
E.g. Inferior STEMI: ST elevation seen in II, III, avF
- New left bundle branch block (LBBB)
Describe the ECG changes in Unstable angina and NSTEMI.
- Patterns of ischaemia
I. ST segment depression
II. T wave flattening or inversion
- Differentiate between the two diseases – blood tests – there is troponin release in NSTEMI
- Initially thought to be highly sensitive and specific for acute coronary syndrome
- Marker of myocardial damage often
- However, released in almost any condition
- Specificity poor
- Troponin elevation outside of ACS – general medical, elderly frail patients.
Which cardiac conditions result in the release of Troponin?
- Acute coronary occlusion or severe stenosis
- Acute heart failure with or without valvular heart disease
- Prolonged tachycardia
- Cardiac amyloidosis
- Cardiac trauma
- Takotsubo syndrome
- Defibrillation, CPR
- Aortic dissection
Which non-cardiac conditions call for the release of troponin?
- Acute PE
- Pulmonary hypertension
- Haemodynamic challenge
- Systemic illness (“cellularly sick”)
- Severe anaemia
- Catecholamine release
- SAH, intracranial haemorrhage
- Kidney failure
Outline Stable angina treatment.
- Aspirin – prevent heart attack, prevent blood clots
- Beta blocker – reduces blood pressure and slows heart rate
- Statin – reduce LDL cholesterol
- ACE inhibitor – lower BP
- Oral nitrate – ease angina pains, includes GTN
- Nicorandil – causes vasodilation
- CCB – prevent calcium from entering into heart muscle cells, prevent vasoconstriction. (calcium channel blockers)
- PCI – percutaneous coronary intervention
- CABG – Coronary artery bypass surgery
Outline unstable angina treatment.
- Optimise general condition
Outline Myocardial Infarction treatment.
- Pain relief
- GTN sublingual
- Second antiplatelet
Describe the signs and symptoms of acute pericarditis.
- Inflammation of the pericardium
- Often secondary to a viral illness
- Present with chest pain
II. Sharp pain, localised to front of chest
III. Aggravated with inspiration, cough, lying flat
IV. Eased with sitting up and leaning forward
V. Pericardial rub may be heard on auscultation
How do you account for the pallor, nausea and vomiting that is accompanied with MI?
In terms of anatomical sites, leads and coronary arteries,