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Y1 TP2 Cardiovascular (topic 4 Onwards) > 9. Ischaemic Heart Disease > Flashcards

9. Ischaemic Heart Disease Flashcards

1
Q

2 types of chest pain

A
  • Ischaemic

* Non ischaemic

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2
Q

Ischemic chest pain - examples

A

• Acute coronary syndrome
▪ Unstable angina
▪ NSTEMI
▪ STEMI

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3
Q

Non ischaemic chest pain

A
  • Cardiac (non-ischemic)
    • Pulmonary
    • Gastrointestinal – anything causing pain in upper abdomen
    • Musculoskeletal
    • Psychological
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4
Q

Non ischaemic chest pain

• Cardiac (non-ischemic)

A

▪ Aortic dissection = tearing of intima of aorta
▪ Cardiac tamponade = pressure build up in pericardial sac – due to accumulation
▪ Myocarditis = inflammation of heart
▪ Pericarditis

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5
Q

Non ischaemic chest pain

• Pulmonary

A

▪ Pulmonary Embolism
▪ Pneumothorax
▪ Pneumonia
▪ Pleural effusion

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6
Q

Non ischaemic chest pain

• Gastrointestinal – anything causing pain in upper abdomen

A

▪ Gastritis
▪ Peptic ulcer
▪ Esophagitis
▪ Pancreatitis

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7
Q

History Obtain a detailed history of the patient’s chest pain,including:

A 
▪ Site of pain 
▪ Quality of pain 
▪ Intensity 
▪ Timing 
▪ Aggravating factors 
▪ Relieving factors 
▪ Secondary symptoms
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8
Q

Specifics to chest pain as part of history

A

▪ Comorbidities: hypertension, diabetes mellitus, peripheral vascular disease,malignancy
▪ Previous diagnostic studies
▪ Recent events: trauma, major surgery or medical procedures (eg, endoscopy), periodsof immobilization (eg, long plane ride)
▪ Other factors: cocaine use- chemica cause vasospasm, cigarette smoking, familyhistory

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9
Q

History 1. Site of pain

A

▪ Substernal - under sternum or superficial
▪ Central or across the chest
▪ Lateral chest
▪ Localised or general
▪ lower chest/epigastric
▪ Radiates to jaw, neck, shoulder or back - refered pain
▪ Vague

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10
Q

History 2. Quality of pain

A

▪ Pleuritic - [pain originating in pleura – sharp and localsied
▪ Spasmodic
▪ Tightness or heaviness – like someone sitting in cheast
▪ Pressure
▪ Sharp and localized
▪ Visceral (hard to localize)
▪ Tearing /Excruciating

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11
Q

History 2. Quality of pain

Somatic pain

A 
▪ Bones and joints 
▪ Connective tissue 
▪ Muscles
 ▪ Sharp 
▪ Can localize the site 
▪ Worse by movement
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12
Q

History 2. Quality of pain

Visceral pain

A

Organs
▪ Dull
▪ Difficult to localize

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13
Q

History 3. Intensity of pain

A

Rank on a scale

▪ 0 – 10
▪ 0 = “no pain at all”
▪ 10 = “worst imaginable pain”

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14
Q

History 4. Timing

A

▪ Acute vs chronic
▪ Sudden onset vs gradual

Acute coronary syndrome – normally gradually builds over 20 mins

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15
Q

History 5. Aggravating factors

A

▪ Worse on exertion - walking and movement
• occurs in acute coronary syndrome due to occlusion if coronary artery
▪ Worse on deep inspiration – seen in pleuritic type chest pain
▪ Sleeping
▪ Lying down
▪ Lifting heavy object
▪ Coughing – fatigue of intercostal muscles

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16
Q

History 6. Relieving factors

A

▪ Better at rest
▪ Improves on leaning forward
▪ Relieved by analgesia
▪ Lying on one side

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17
Q

History 7. Secondary symptoms

Acute coronary syndrome

A

▪ Sweating

▪ Nausea/vomiting

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18
Q

History 7. Secondary symptoms

Elderly patients withACS

A

▪ Dyspnea, a shortness of breathe
▪ Weakness
▪ Altered mental status
▪ Syncope

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19
Q

History 7. Secondary symptoms

Non-ischemic chest

A

▪ Sweating

▪ Nausea

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20
Q

History 7. Secondary symptoms

Pulmonary embolus, pneumothorax, and pneumonia

A 
▪ Shortness of breath 
▪ Tachypnea - greater respiratory rate than normal
▪ Wheezing 
▪ Low grade fever 
▪ Palpitations
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21
Q

History 7. Secondary symptoms

Pericarditis, myocarditis

A

▪ Fever Pulmonary embolism or valvular heart disease
▪ Cough
▪ Syncope,
▪ Hemoptysis - coughing up blood

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22
Q

History 7. Secondary symptoms

Gastrointestinal causes

A

▪ Nausea/vomiting

▪ Belching

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23
Q

History

Differentiating chest pain

ACS

A

▪ Discomfort from ACS typically starts gradually and may worsen withexertion

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24
Q

History

Differentiating chest pain

Stable angina

A

▪ With stable angina, discomfort occurs only when activity creates an increased oxygen demand

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25
Q

History

Differentiating chest pain

Unstable angina

A

▪ Unstable angina represents an abrupt change from baseline, which may manifest as discomfort that begins at lower levels of exercise or at rest

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26
Q

History

Differentiating chest pain

aortic dissection, pneumothorax, and pulmonary embolism

A

▪ Pain that starts suddenly and is severe at onset is associated with aortic dissection, pneumothorax, and pulmonary embolism

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27
Q

History

Differentiating chest pain

pulmonary embolism

A

▪ Chest pain associated with pulmonary embolism can begin suddenly, but may worsen overtime
▪ Pain in pulmonary embolism and pneumothorax is normally pleuritic

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28
Q

History

Differentiating chest pain

ruptured esophagus and mediastinitis

A

▪ A history of forceful vomiting preceding symptoms raises concern for a ruptured esophagus and mediastinitis

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29
Q

History Risk factors

Acute coronary syndrome

A 
▪ Male sex 
▪ Age over 55 years 
▪ Family history of CAD 
▪ Diabetes mellitus 
▪ Hypercholesterolemia 
▪ Hypertension 
▪ Tobacco use 
▪ Cocaine or amphetamine use
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30
Q

History Risk factors

Aortic dissection

A

▪ Inherited connective tissue diseases
▪ Bicuspid aortic valve
▪ Cocaine use
▪ Hypertension

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31
Q

History Risk factors

Pulmonary embolus

A 
▪ History of prolonged immobilisation
 ▪ Recent surgery
 ▪ Trauma 
▪ Pregnancy 
▪ Cancer 
▪ Obesity 
▪ COCP
 ▪ Hypercoagulability e.g. sepsis 
▪ Previous VTE  - has the same thing happened before
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32
Q

History Risk factors

Pneumothorax

A

▪ Smoking
▪ COPD
▪ Tall slim males
▪ Trauma

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33
Q

Typical cardiac chest pain

A

Characterized as discomfort/pressure rather than pain
▪ Time duration >2 mins
▪ Provoked by activity/exercise
▪ Radiation (i.e. arms, jaw)
▪ Does not change with respiration/position
▪ Associated with sweating/nausea
▪ Relieved by rest/nitroglycerin - spray under tongue

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34
Q

Atypical cardiac chest pain

A

▪ Pain that can be localized with one finger
▪ Constant pain lasting for days
▪ Fleeting pains lasting for a few seconds
▪ Pain reproduced by movement/palpation
▪ No Pain
• Elderly, female or diabetic patients more often present atypically

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35
Q

ECG - cardiac chest pain

A

▪ ECG should be obtained and interpreted within 10 minutes of patient presentation in the ED. - with cest pain
▪ Can be repeated as frequently as every 10 minutes if the initial ECG is not diagnostic but the patient remains symptomatic.
▪ Prior ECGs are important for determining whether abnormalities are new or a chronic change

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36
Q

Use of an ECG allows

A

–> Allows initial categorization of the patient with a suspected myocardial infarction into one of three groups based on the pattern:

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37
Q

▪ ST elevation MI (STEMI)

A

▪ ST elevation MI (STEMI): ST elevation or new left bundle branch block [LBBB] new LBBB managed same as stemi
• Complete occlusion consistent of coronary artery – myocardial infarction

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38
Q

▪ Non-ST elevation ACS:

A

May or may not have ecg changes, e.g. inverted t waves
▪ Non-ST elevation MI (NSTEMI) – cardiac enzyme positive
▪ Unstable angina – cardiac enzyme negative
▪ Undifferentiated chest pain syndrome (non-diagnosticECG)= not sure whats going on

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39
Q

ECG —> Localisation of ischemia:

A

The anatomic location of a transmural infarct is determined by which ECG leads showST elevation and/or increased T wave positivity:

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40
Q

▪ Anterior wall ischemia:

A

Two or more of the precordial leads(V1-V6) = chest leads on front of chest

41
Q

▪ Anteroseptal ischemia

A

Leads V1 to V3 – middle anterior and interventricular septum

42
Q

Apical or lateral ischaemia

A

Leads aVL and I, and leads V4 to V6

43
Q

Inferior wall ischaemid

A

Leads II, III, and aVF

44
Q

Right ventricular ischaemia

A

V1 or change to right-sided precordial leads

45
Q

Posterior wall ischaemia

A

ST depression in V1-V2

46
Q

Leads II, III, AVF cure supplied by

A

• Supplied by right coronary artery or left cicrumflex artery

47
Q

V1-V4 supplied by

A

• Supplied by left anterior descending artery

48
Q

V5 and V6 supplied by

A

• Left circumflex coronary afert or diagonal branch of left anterior descending artery

49
Q

Lead I supplied by

A

Lead I – left circumflex artery pr diagonal branch of left anterior descending artery

50
Q

Cardiac Biomarkers – enzymes

A
  • Troponin I and T

* Elevate after about 3 levels of injury

51
Q

Troponin I and T

A

▪ Troponin I and T are cardiac enzymes measured in the blood and used to aid diagnosis in suspected ACS – they are sensitive and specific to cardiac muscle

▪ Troponin is released from the myocardium during ischaemic injury

52
Q

MB isoenzyme of creatine kinase(CK-MB)

A

▪ The MB isoenzyme of creatine kinase(CK-MB) is also a cardiac enzyme although less commonly used due to poor specificity

53
Q

Interpreting elevation of cardiac troponins

A

▪ Elevation in cardiac troponins must be interpreted in the context of the clinical history and ECG findings since it can be seen in a variety of clinical settings and is therefore not specific for an acute coronary syndrome(ACS) - interpret levels in context of patients history

54
Q

Three points should be kept in mind when using troponin to diagnose acute MI:

A

▪ With contemporary troponin assays, most patients can be diagnosed within 2-3 hours of presentation of chest pain
▪ A negative test at the time of presentation, especially if the patient presents early after the onset of symptoms, does not exclude myocardial injury.
▪ Acute MI can be excluded in most patients by six hours, but the guidelines suggest that if there is a high degree of suspicion of an ACS, a 12-hour sample should be obtained. However, very few patients become positive after eight hours

55
Q

Serial cardiac troponins (I or T)

A

Serial cardiac troponins (I or T) should be obtained at presentation and 3–6 hoursafter symptom onset
• Repeat troponin levels

56
Q

Guidance for taking troponin levels

A

Hospitals have different protocols for troponin levels

* Take levels when patient arrives alongside ecg 
* If toponin is normal and so is ecg may be discharged
* If troponin elvels are slightly high test again 3-6 hours later
57
Q

Ischameia heart disease: Stable angina

A
  • Small and fixed narrowing of coronary artery
    • Only becomes and issue upon exertion
    • No ecg changes
    • No ischemic or infarction
    • No rise in troponins
    • Managed by gp and cardiologists
58
Q

Ischameia heart disease: Acute coronary syndrome

A

• ST segment elevation MI = comlete occlusion of coronary artery
• Non-ST segment elevation MI – partial occlusion
• Unstable Angina
- New onset angina (<24hrs)
- Abrupt deterioration of angina symptoms
- Pain at rest or minimal effort
- Rapidly progressing angina

59
Q

Unstable angina - signs

A
  • No injruy to myocardium

* No negative cardiac enxymes

60
Q

NSTEMI -signs

A
  • Injury of mhyocarduym
    • Rise in troponin
    • Positive cardiac enzymes
    • ST elevation, T wave inversion
61
Q

STEMI - signs

A
  • ST elevation

* Positive cardiac enzymes due to mycocardial injru and necrosis

62
Q

Pericarditis -what is it

A
  • Inflammation of the pericardium +/- accumulation of pericardial fluid
    • Viral
    • Bacterial
    • Autoimmune inflammatory disease
    • Idiopathic
63
Q

Pericarditis - signs

A

• Pericardial friction rub on auscultation

64
Q

Pericarditis - symptoms

A
  • Chest pain, often retrosternal and pleuritic
    • Fever
    • Nausea/vomiting
    • Positional pain (may improving on leaning forwards)
65
Q

Pericarditis - investigations and management

A
  • Investigations: ECG – concavr up ST elevation, saddle shaped - , echocardiogram, cardiac enzymes, CXR, pericardiocentesis (nedle placed into pericaridal sac and fluid taken to be tested)
  • Management: analgesia, NSAIDs
66
Q

Pathogenesis of ACS

A
  • Imbalance between myocardial oxygen supply and demand

- A reduction in oxygen supply is more commonly the principle cause

67
Q

Risk factors: ACS

A
  • Unmodifiable: Age, Gender, Ethnicity, family history
    • Modifiable Major: Dyslipidemia, hypertension, cigarette smoking, obesity
    • Modifiable Contributing: Diabetes Mellitus, stressful lifestyle
68
Q

ACS

3 types

A
  • Unstable angina – no rise in troponin
    • NSTEMI – rise in troponin
    • STEMI – rise in troponin
69
Q

Stable angina - plaque

A
  • Fixed atherosclerotic plaque

* Completely occludes

70
Q

Unstable angina - plaque

A
  • Disruption of plaque

* Narrows coronary

71
Q

NSTEMi -plaque

A

• Thrombus – partially occludes

72
Q

Risk stratification

—> At initial presentation of ACS:

A

▪ Clinical history + examination + bedside observations
▪ ECG to decide– STEMI vs NSTEMI
▪ Renal function
▪ Cardiac troponin

73
Q

2 risk calculators for ACS

A
  • TIMI risk score is useful in predicting 30-day and 1-year mortality in patients with NSTE-ACS.- non sst elevation – unstable angina and NSTEMI
    • The GRACE score predicts in-hospital and post-discharge mortality.
74
Q

Initial Anti-ischemic and AnalgesicTherapies

When should patients receive them

A

• All patients should receive anti-ischemic and analgesic medications early in care

75
Q

Acronym for Anti-ischemic and Analgesic Therapies

A 
MONA 
M = Morphine or other analgesia 
O = Oxygen 
N = Nitroglycerin 
A = Aspirin

β-Blocker

76
Q

M = Morphine or other analgesia

A

▪ Provides analgesia and decreased pain-induced sympathetic/adrenergic tone. -reduce vasoconstriction and workload on heart, demand
▪ Induce vasodilation and mediate some degree of after load reduction

77
Q

O = Oxygen

A

▪ Can help attenuate anginal pain secondary to tissue hypoxia.
▪ Oxygen is indicated only in patients with hypoxia (SaO2 < 94%)
▪ Routine oxygen is not recommended in patients with ACS (evidence of free radical release) - can casue worse damage – so only give if they are hypoxic

78
Q

N = Nitroglycerin

A

▪ Facilitates coronary vasodilation
▪ Analgesic effects also
▪ E.g. glyeryltrinitrate (GTN) – administered as a sublingual spray under the tongue

79
Q

A = Aspirin

A

▪ Loading dose of 300mg orally unless clear evidence of allergy
▪ Inhibits platelet activation
▪ Mortality reducing therapy
▪ Clopidogrel if aspirin allergy

80
Q

β-Blocker

A

▪ Decrease myocardial ischemia, reinfarction, and frequency of dysrhythmias and increase long-term survival.
▪ Does not form part of the immediate management but is ideally given within 24 hours of myocardial infarction if no contraindication

81
Q

Oral β-blocker should be initiated within 24 hr in patients who do not have:

A

▪ Signs of HF
▪ Evidence of low-output state
▪ Increased risk of cardiogenic shock
▪ Other contraindications to β-blockade (e.g., heart block or active asthma)

be careful of which patients require a beta blocker as they may need a higher heart rate to maintain their cardiac output

82
Q

Revascularization

Invasive therapy

A
  • Stents
    • Coronary angiograms
    • High risk NSTEMI
83
Q

Decision for Invasive Management NSTE-ACS – non st elevation infarcts

A

prevent total occlusion of the related artery and to control chest pain and associated symptoms.
▪ Patients with NSTE-ACS are treated on the basis of risk (TIMI, GRACE) with either:
a. Early invasive strategy (interventional approach) or
b. Ischemia-guided strategy
▪ The majority will undergo a coronary angiogram within several days
▪ Revascularisation with stenting can be performed based on findings
▪ Invasive therapy is generally superior to ischemia-guided strategy in patients with one or more of the following risk features: advanced age (older than 70 years), previous MI or revascularization, ST deviation, HF, LVEF less than 40%, high TIMI or GRACE scores, markedly elevated troponins, and diabetes.

84
Q

Decision for Invasive Management

Ischaemia guided therapy

A

▪ Ischemia-guided therapy used to avoid the routine early use of invasive procedures unless patients experience refractory or recurrent ischemic symptoms or develop hemodynamic instability.

a. Recommended for patients with a low risk score (TIMI 0 or 1, GRACE less than 109)
b. Indicated for those with acute chest pain with a low likelihood of ACS who are troponin negative

Wait with lower risk patients to see if they have ischaemia

85
Q

Decision for Invasive Management STEMI

A

restore coronary artery patency and minimize infarct size
▪ Secondary goals include prevention of complications such as arrhythmias or death as well as to control chest pain and associated symptoms.
▪ Requires urgent revascularization either interventionally or with drug therapy
▪ Primary PCI is preferred to lytic therapy
▪ Performance measure includes goal of primary PCI – percutaneous coronary intervention – urgent stent- within 90 minutes of first medical contact (‘door to balloon time’)
▪ Fibrinolytic therapy (e.g. alteplase) is indicated for patients with STEMI in whom PCI cannot be performed.
▪ If PCI cannot be performed within 120 minutes, performance measure for lytic administration includes a door to needle time of 30 minutes.

86
Q

Fibrinolytic Therapy - what is it

A

• Clot busting mechanism
Normally for those who can’t have stents or they are put in fat enough within 2 hours
Drugs that breakdown clot

87
Q

Fibrinolytic Therapy - contraindications

A
  • May cause catastrophic bleeding for some patients

* Check contraindication before adminsitering drug

88
Q

Stemi - treatment

A

• Cath lab – PCI or clot busting drug based on time

89
Q

NSTEMI - treatment

A
  • Measure troponins to determine unstable angina or NSTEMI
    • Moderate to high risk = early invasive
    • Low risk = ischaemic guided therapy
90
Q

Antiplatelet Therapy

A

▪ Patients with ACS should be treated with antiplatelet therapy .
▪ aspirin is normally given first bt Combination therapy with several antiplatelet agents plus a concomitant anticoagulant is the mainstay of acute ACS management, which targets the underlying pathophysiology of thrombus formation inACS.
▪ All patients should receive aspirin and P2Y12 receptor antagonists, and some patients derive benefit from adding GP IIb/IIIa inhibition in the acute management ofACS.

91
Q

Dual antiplatelet therapy (DAPT)

A

—> Dual antiplatelet therapy (DAPT) with aspirin (75mg) plus a P2Y12 receptor inhibitor (e.g. ticagrelor) is indicated for all patients after ACS for at least 12months.

92
Q

4 Antithrombotic agents in aCS

A

Aspirin
P2Y12 inhibitors e.g. clopidogrel, ticagrelor
GP IIb/IIIa Inhibitors
Anticoagulants e.g. fondaparinux

93
Q

Aspirin

A

▪ Well established first line therapy in ACS

▪ Cyclooxygenase 1 inhibitor blocking the formation of thromboxane A2 mediated platelet aggregation

94
Q

P2Y12 inhibitors e.g. clopidogrel, ticagrelor

A

▪ Well established first line therapy in ACS
▪ Inhibit the effect of adenosine diphosphate on the platelet, a key mediator resulting in amplification of platelet activation

95
Q

GP IIb/IIIa Inhibitors

A

▪ Block the final common pathway of platelet aggregation
▪ More likely to be given in those who display high risk features e.g. very high troponin level
• Not a standard drug may be goven later to high risk patients

96
Q

Anticoagulants e.g. fondaparinux

A

▪ Example: fondaparinux, enoxaparin, UFH
▪ Often given to patients with NSTEMI or unstable angina as a prophylactic anticoagulant (SC injection) for up to 8 days
▪ Commonly used in PCI

97
Q

PPCI – primary PCI - what is it

A

–> The preferred reperfusion therapy in many patients with STEMI

98
Q

Primary PCI preferred in

A

▪ Diagnosis in doubt
▪ High bleeding risk – can’t give fibrolytic therapy
▪ Very high-risk patients (severe heart failure, pulmonary edema)

99
Q

No reperfusion therapy

A

–> Despite the benefits of reperfusion for STEMI, a decision to not attempt reperfusion may be made on occasion:
▪ Serious comorbidities
▪ End-of-life status
▪ Percutaneous coronary intervention not available and an absolute contraindication to fibrinolytic therapy present.

Y1 TP2 Cardiovascular (topic 4 Onwards) (8 decks)

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