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Cardiovascular System > Session 9 > Flashcards

Session 9 Flashcards

1
Q

How do you diagnose chest pain?

A
  • History
  • Clinical examination
  • Investigations (cardiac troponin, full blood counts, ECG)
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2
Q

How do you take history for chest pain?

A 
SQITARS 
Site: location? radiation?
Quality: how does pain feel?
Intensity: effect, severity?
Timing: sudden? gradual?
Aggravating factors: what makes it worse?
Relieving factors: what makes pain better?
Secondary symptoms: anything else?
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3
Q

What could be the potential causes of respiratory chest pain?

A
  • Will involve the pleura (pleural sac irritated by inflammation)
  • Pneumonia/pulmonary embolism
  • No fever. Shortness of breath. Cough. Sudden chest pain. DVT (PE)
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4
Q

What could be the potential cause of cardiac chest pain?

A
  • Stable and unstable angina (infarction/ischaemia)
  • Myocardial infarction
  • Pericarditis (sharp pain, well localised, worse on breathing + coughing - mimics pleuritic chest pain)
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5
Q

What are the features of cardiac/ischaemic pain?

A
  • Related to the visceral nervous system (eg. sweating, nausea, pallor)
  • Dull and poorly localised but still central
  • Worsened with exertion and may radiate to shoulder and joints
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6
Q

What are the features of pleuritic pain?

A
  • Related to the somatic nervous system (pneumonia + PE)
  • Sharp, well localised
  • Worse with inspiration, coughing or positional movement
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7
Q

What is pericarditis?

A
  • Inflammation of the chest wall
  • More common in men
  • Typically viral
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8
Q

How does pericarditis present?

A
  • Sharp, localised to front
  • Aggravated with inspiration/cough/lying flat
  • Eased with sitting up and leaning forward
  • Pericardial rub*
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9
Q

What are the features of pericarditis on an ECG?

A

Widespread, saddle-shaped ST elevation

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10
Q

What is cardiac/ischaemic chest pain?

A
  • Pain secondary to cardiac pathology (ischaemic heart disease)
  • Potentially life-threatening if occluded
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11
Q

What is atherosclerosis?*

A

The buildup of fatty deposits in the arteries over time, which lead to a lipid-laden core with fibrous plaque formation that can rupture

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12
Q

What are the modifiable risk factors for ischaemic heart disease and atherosclerosis?

A
  • Smoking
  • Hypertension
  • Dyslipidaemia
  • Diabetes
  • Obesity
  • Sedentary lifestyle
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13
Q

What are the non-modifiable risk factors for atherosclerosis/ischaemic heart disease?

A
  • Advanced age
  • Family history
  • Male sex
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14
Q

What is stable angina?

A
  • Fixed occlusion where the atherosclerotic plaque is stable (not ruptured)
  • Ischaemia occurs only when metabolic demand of muscle is more than what can be delivered (exertion)
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15
Q

What is the typical history of a patient with angina?

A
  • Pain only on exertion
  • Relieved by rest/GTN spray
  • Does not last very long
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16
Q

What includes acute coronary syndrome?

A
  • Unstable angina
  • Non-ST elevation MI
  • ST elevation MI
  • MI
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17
Q

What are acute coronary syndromes?

A

Acute myocardial ischaemia caused by atherosclerotic coronary artery disease

Plaque rupture with thrombus formation causing acute increased occlusion that can lead to ischaemia and potential infarction.

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18
Q

What is the mechanism of acute coronary syndrome?

A
  1. Atherosclerotic plaque rupture
  2. Platelet aggregation + thrombus formation
  3. Partially occlusive thrombus developing into a completely occlusive one
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19
Q

How to differentiate between unstable angina and myocardial infarction?*

A

UA: the lumen is narrowed so less O2 is delivered, leading to ischaemia. There is no cardiac enzyme leak as tissue does not die

MI: Tissue is very starved of O2 and does die (infarction), which lead to cardiac enzymes (Troponin I + T) leaking from the necrosed cardiac muscle cells

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20
Q

What are the features of unstable angina?

A
  • Pain occurs at rest as well
  • Pain may be more intense and last longer
  • Risk of further deterioration will increase likelihood of MI
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21
Q

What ECG findings and tests would indicate unstable angina?

A

ECG: ST depression and T wave inversion, BUT may be normal

Blood tests: negative for troponin and cardiac enzymes

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22
Q

What is the typical patient history of a patient with MI?

A
  • Dull and crushing chest pain in the middle of the chest which may radiate to shoulder and jaw (dermatomes/myotomes)
  • Severe pain
  • Pain not relieved by rest or GTN spray
  • Likely to have occurred while at rest
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23
Q

What are the ECG and blood tests features in a MI?

A
  • Cardiac myocyte death affects whole thickness of muscle
  • IMMEDIATE ANGIOPLASTY
  • Blood tests WILL show cardiac troponins/enzymes
24
Q

What are the ECG changes that occur in a STEMI?*

A
  • ST segment elevation in the leads that correspond to which area the occlusion has occurred in
  • Hyperacute T waves
  • Q waves that are pathological
25
Q

What are the ECG changes seen in a NSTEMI and unstable angina?*

A
  • ST segment depression
  • T wave flattening/inversion
  • Differentiate between them by checking cardiac enzymes in blood
26
Q

What is acute myocardial infarction?*

A

Cardiomyocyte necrosis in a clinical setting consistent with acute myocardial ischaemia.

27
Q

What is required to meet an acute MI diagnosis?

A

1) Cardiac biomarker
And at least one of the following:

  • Symptoms of ischaemia
  • New ST-T wave changes or LBBB
  • Pathological Q waves
  • Imaging evidence of myocardium loss
  • Intracoronary thrombus on angiography
28
Q

What is a type I MI?

A

Caused by atherosclerotic plaque rupture, ulceration, fissure, erosion or dissection with intraluminar thrombus in one/more coronary arteries leading to ischaemia and subsequent myocardial necrosis.

29
Q

What is a type II MI?

A

A condition other than atherosclerotic plaque instability that contributes to a reduced O2 supply:

  • Coronary artery spasm
  • Tachy/bradyarrythmias
  • Hypotension (severe)
30
Q

What is involved in the assessment of a patient with MI symptoms?

A
  • Is the problem cardiac sounding?
  • Does the pain radiate?
  • Relieved with GTN?
  • How long?
  • Getting worse?
  • Pleuritic?
  • Does the patient have any risk factors?
31
Q

What do you examine in a patient with suspected MI?

A
  • Haemodynamics
  • BP
  • Tachy/bradycardia
  • Jugular venous pressure (will tell fluid balance)
  • Lungs (crackling? pulmonary oedema?)
  • Heart sounds and murmurs
  • Peripheries (are they cool?)
32
Q

How to tell if a patient is in cardiogenic shock?

A

(Condition caused by a severe heart attack when the heart suddenly can’t pump a lot of blood)
- Systolic BP <90 mmHg

33
Q

What is the inferior territory of the ECG?

A

II, III, aVF

34
Q

What is the anteroseptal territory of the ECG?

A

V1, V2, V3, V4

35
Q

What is the lateral territory of the ECG?

A

I, aVL, V5, V6

36
Q

Where will the infarct/change in ECG be seen if it’s septal?

A

V1 + V2

37
Q

Where will the infarct/change in ECG be seen if it’s anterior?

A

V1 - V6

38
Q

Where will the infarct/change in ECG be seen if it’s lateral?

A

V5 + V6

39
Q

Where will the infarct/change in ECG be seen if it’s anteroseptal?

A

V1 - V4

40
Q

Where will the infarct/change in ECG be seen if it’s anterolateral?

A

V3 - V6

41
Q

Where will the infarct/change in ECG be seen if it’s inferior?

A

II, III, aVF

42
Q

Where will the infarct/change in ECG be seen if it’s high lateral?

A

I, aVL

43
Q

What does ST elevation in 2 or more leads imply?

A
  • Sudden occlusion

- LV aneurysm (pathological Q waves)

44
Q

What does ST depression imply?

A

Under supply of blood to the myocardium, but not a sudden coronary occlusion (can be from sudden if in anterior leads/ posterior STEMI)

45
Q

What does T wave inversion imply?

A

Under supply of blood to the myocardium but not sudden coronary occlusion

46
Q

What is seen in an ECG during a STEMI?*

A
  • ST elevation that evolves with:
  • Hyperacute T waves
  • ST elevation
  • T wave inversion
  • Pathological Q waves
47
Q

What is the treatment for ST elevation?

A

Need to immediately go to the cath lab for emergency percutaneous coronary intervention (angioplasty)

48
Q

How can a NSTEMI appear on an ECG?

A
  • Can be normal OR
  • ST depression
  • T wave inversion

Must do cardiac marker enzyme tests to confirm (can also use cholesterol, HbA1C, haemoglobin)

49
Q

What is troponin?

A
  • Cardiac muscle contractility
  • T and I are of specific cardiac origin
  • Peaks at 24-48h after damage, remains elevated for 2+ weeks
50
Q

What would you see on a CXR of someone with MI?*

A
  • Pulmonary oedema

- Widened mediastinum

51
Q

What will an echocardiogram show?

A
  • LV function
  • Wall motion
  • Valvular disease (eg. regurgitation)
  • Ventriculo-septal defects
52
Q

How do you manage a STEMI?*

A
  • 300mg aspirin
  • Ticagrelor 180mg
  • Morphine 5-10mg IV
  • Nitrate 2 puffs under tongue (vasodilator so low BP)
  • O2 (sats < 92%)
  • PCI
53
Q

How do you manage a NSTEMI?*

A
  • Antiplatelets/antithrombotics (aspirin and clopidogrel, enoxaparin via subcutaneous injection)
  • Anti-ischaemic (bisopolol, GTN infusion)
  • Statins
  • ACE inhibitors for prevention
54
Q

When should a patient be sent for an urgent percutaneous coronary intervention?

A
  • If ongoing CP (constrictive pericarditis) with dynamic ECG changes
  • Arrythmias with compromise
55
Q

What does invasive coronary angiography do?*

A
  • Establish type of lesion and location

Works by giving local anaesthetic and inserting a catheter into radial/femoral artery to use a stent with a metal scaffold to keep vessel open.

56
Q

How do you manage people after acute coronary syndrome?

A
  • Lifestyle (low fat and low salt diet)
  • Dual antiplatelets for 12 months
  • Aspirin for LIFE
  • Atorvastatin (reduced cholesterol levels)
  • Birsoprolol (low HR)
  • Echo at 3 months showing an ejection fracture of under 35% = high risk of arrhythmia, needs a cardiac defibrillator implanted

Cardiovascular System (11 decks)

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