9. Ischaemic Heart Disease Flashcards
1
Q
2 types of chest pain
A
- Ischaemic
* Non ischaemic
2
Q
Ischemic chest pain - examples
A
• Acute coronary syndrome
▪ Unstable angina
▪ NSTEMI
▪ STEMI
3
Q
Non ischaemic chest pain
A
- Cardiac (non-ischemic)
- Pulmonary
- Gastrointestinal – anything causing pain in upper abdomen
- Musculoskeletal
- Psychological
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
5
Q
Non ischaemic chest pain
• Pulmonary
A
▪ Pulmonary Embolism
▪ Pneumothorax
▪ Pneumonia
▪ Pleural effusion
6
Q
Non ischaemic chest pain
• Gastrointestinal – anything causing pain in upper abdomen
A
▪ Gastritis
▪ Peptic ulcer
▪ Esophagitis
▪ Pancreatitis
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
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
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
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
11
Q
History 2. Quality of pain
Somatic pain
A
▪ Bones and joints ▪ Connective tissue ▪ Muscles ▪ Sharp ▪ Can localize the site ▪ Worse by movement
12
Q
History 2. Quality of pain
Visceral pain
A
Organs
▪ Dull
▪ Difficult to localize
13
Q
History 3. Intensity of pain
A
Rank on a scale
▪ 0 – 10
▪ 0 = “no pain at all”
▪ 10 = “worst imaginable pain”
14
Q
History 4. Timing
A
▪ Acute vs chronic
▪ Sudden onset vs gradual
Acute coronary syndrome – normally gradually builds over 20 mins
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
16
Q
History 6. Relieving factors
A
▪ Better at rest
▪ Improves on leaning forward
▪ Relieved by analgesia
▪ Lying on one side
17
Q
History 7. Secondary symptoms
Acute coronary syndrome
A
▪ Sweating
▪ Nausea/vomiting
18
Q
History 7. Secondary symptoms
Elderly patients withACS
A
▪ Dyspnea, a shortness of breathe
▪ Weakness
▪ Altered mental status
▪ Syncope
19
Q
History 7. Secondary symptoms
Non-ischemic chest
A
▪ Sweating
▪ Nausea
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
21
Q
History 7. Secondary symptoms
Pericarditis, myocarditis
A
▪ Fever Pulmonary embolism or valvular heart disease
▪ Cough
▪ Syncope,
▪ Hemoptysis - coughing up blood
22
Q
History 7. Secondary symptoms
Gastrointestinal causes
A
▪ Nausea/vomiting
▪ Belching
23
Q
History
Differentiating chest pain
ACS
A
▪ Discomfort from ACS typically starts gradually and may worsen withexertion
24
Q
History
Differentiating chest pain
Stable angina
A
▪ With stable angina, discomfort occurs only when activity creates an increased oxygen demand
25
History
Differentiating chest pain
Unstable angina
▪ Unstable angina represents an abrupt change from baseline, which may manifest as discomfort that begins at lower levels of exercise or at rest
26
History
Differentiating chest pain
aortic dissection, pneumothorax, and pulmonary embolism
▪ Pain that starts suddenly and is severe at onset is associated with aortic dissection, pneumothorax, and pulmonary embolism
27
History
Differentiating chest pain
pulmonary embolism
▪ Chest pain associated with pulmonary embolism can begin suddenly, but may worsen overtime
▪ Pain in pulmonary embolism and pneumothorax is normally pleuritic
28
History
Differentiating chest pain
ruptured esophagus and mediastinitis
▪ A history of forceful vomiting preceding symptoms raises concern for a ruptured esophagus and mediastinitis
29
History Risk factors
Acute coronary syndrome
```
▪ Male sex
▪ Age over 55 years
▪ Family history of CAD
▪ Diabetes mellitus
▪ Hypercholesterolemia
▪ Hypertension
▪ Tobacco use
▪ Cocaine or amphetamine use
```
30
History Risk factors
Aortic dissection
▪ Inherited connective tissue diseases
▪ Bicuspid aortic valve
▪ Cocaine use
▪ Hypertension
31
History Risk factors
Pulmonary embolus
```
▪ History of prolonged immobilisation
▪ Recent surgery
▪ Trauma
▪ Pregnancy
▪ Cancer
▪ Obesity
▪ COCP
▪ Hypercoagulability e.g. sepsis
▪ Previous VTE - has the same thing happened before
```
32
History Risk factors
Pneumothorax
▪ Smoking
▪ COPD
▪ Tall slim males
▪ Trauma
33
Typical cardiac chest pain
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
34
Atypical cardiac chest pain
▪ 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
35
ECG - cardiac chest pain
▪ 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
36
Use of an ECG allows
--> Allows initial categorization of the patient with a suspected myocardial infarction into one of three groups based on the pattern:
37
▪ ST elevation MI (STEMI)
▪ 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
38
▪ Non-ST elevation ACS:
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
39
ECG ---> Localisation of ischemia:
The anatomic location of a transmural infarct is determined by which ECG leads showST elevation and/or increased T wave positivity:
40
▪ Anterior wall ischemia:
Two or more of the precordial leads(V1-V6) = chest leads on front of chest
41
▪ Anteroseptal ischemia
Leads V1 to V3 – middle anterior and interventricular septum
42
Apical or lateral ischaemia
Leads aVL and I, and leads V4 to V6
43
Inferior wall ischaemid
Leads II, III, and aVF
44
Right ventricular ischaemia
V1 or change to right-sided precordial leads
45
Posterior wall ischaemia
ST depression in V1-V2
46
Leads II, III, AVF cure supplied by
• Supplied by right coronary artery or left cicrumflex artery
47
V1-V4 supplied by
• Supplied by left anterior descending artery
48
V5 and V6 supplied by
• Left circumflex coronary afert or diagonal branch of left anterior descending artery
49
Lead I supplied by
Lead I – left circumflex artery pr diagonal branch of left anterior descending artery
50
Cardiac Biomarkers – enzymes
* Troponin I and T
| * Elevate after about 3 levels of injury
51
Troponin I and T
▪ 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
MB isoenzyme of creatine kinase(CK-MB)
▪ The MB isoenzyme of creatine kinase(CK-MB) is also a cardiac enzyme although less commonly used due to poor specificity
53
Interpreting elevation of cardiac troponins
▪ 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
Three points should be kept in mind when using troponin to diagnose acute MI:
▪ 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
Serial cardiac troponins (I or T)
Serial cardiac troponins (I or T) should be obtained at presentation and 3–6 hoursafter symptom onset
• Repeat troponin levels
56
Guidance for taking troponin levels
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
Ischameia heart disease: Stable angina
* 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
Ischameia heart disease: Acute coronary syndrome
• 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
Unstable angina - signs
* No injruy to myocardium
| * No negative cardiac enxymes
60
NSTEMI -signs
* Injury of mhyocarduym
* Rise in troponin
* Positive cardiac enzymes
* ST elevation, T wave inversion
61
STEMI - signs
* ST elevation
| * Positive cardiac enzymes due to mycocardial injru and necrosis
62
Pericarditis -what is it
* Inflammation of the pericardium +/- accumulation of pericardial fluid
* Viral
* Bacterial
* Autoimmune inflammatory disease
* Idiopathic
63
Pericarditis - signs
• Pericardial friction rub on auscultation
64
Pericarditis - symptoms
* Chest pain, often retrosternal and pleuritic
* Fever
* Nausea/vomiting
* Positional pain (may improving on leaning forwards)
65
Pericarditis - investigations and management
* 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
Pathogenesis of ACS
- Imbalance between myocardial oxygen supply and demand
| - A reduction in oxygen supply is more commonly the principle cause
67
Risk factors: ACS
* Unmodifiable: Age, Gender, Ethnicity, family history
* Modifiable Major: Dyslipidemia, hypertension, cigarette smoking, obesity
* Modifiable Contributing: Diabetes Mellitus, stressful lifestyle
68
ACS
3 types
* Unstable angina – no rise in troponin
* NSTEMI – rise in troponin
* STEMI – rise in troponin
69
Stable angina - plaque
* Fixed atherosclerotic plaque
| * Completely occludes
70
Unstable angina - plaque
* Disruption of plaque
| * Narrows coronary
71
NSTEMi -plaque
• Thrombus – partially occludes
72
Risk stratification
---> At initial presentation of ACS:
▪ Clinical history + examination + bedside observations
▪ ECG to decide– STEMI vs NSTEMI
▪ Renal function
▪ Cardiac troponin
73
2 risk calculators for ACS
* 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
Initial Anti-ischemic and AnalgesicTherapies
| When should patients receive them
• All patients should receive anti-ischemic and analgesic medications early in care
75
Acronym for Anti-ischemic and Analgesic Therapies
```
MONA
M = Morphine or other analgesia
O = Oxygen
N = Nitroglycerin
A = Aspirin
```
β-Blocker
76
M = Morphine or other analgesia
▪ 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
O = Oxygen
▪ 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
N = Nitroglycerin
▪ Facilitates coronary vasodilation
▪ Analgesic effects also
▪ E.g. glyeryltrinitrate (GTN) – administered as a sublingual spray under the tongue
79
A = Aspirin
▪ Loading dose of 300mg orally unless clear evidence of allergy
▪ Inhibits platelet activation
▪ Mortality reducing therapy
▪ Clopidogrel if aspirin allergy
80
β-Blocker
▪ 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
Oral β-blocker should be initiated within 24 hr in patients who do not have:
▪ 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
Revascularization
Invasive therapy
* Stents
* Coronary angiograms
* High risk NSTEMI
83
Decision for Invasive Management NSTE-ACS – non st elevation infarcts
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
Decision for Invasive Management
Ischaemia guided therapy
▪ 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
Decision for Invasive Management STEMI
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
Fibrinolytic Therapy - what is it
• 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
Fibrinolytic Therapy - contraindications
* May cause catastrophic bleeding for some patients
| * Check contraindication before adminsitering drug
88
Stemi - treatment
• Cath lab – PCI or clot busting drug based on time
89
NSTEMI - treatment
* Measure troponins to determine unstable angina or NSTEMI
* Moderate to high risk = early invasive
* Low risk = ischaemic guided therapy
90
Antiplatelet Therapy
▪ 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
Dual antiplatelet therapy (DAPT)
---> 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
4 Antithrombotic agents in aCS
Aspirin
P2Y12 inhibitors e.g. clopidogrel, ticagrelor
GP IIb/IIIa Inhibitors
Anticoagulants e.g. fondaparinux
93
Aspirin
▪ Well established first line therapy in ACS
| ▪ Cyclooxygenase 1 inhibitor blocking the formation of thromboxane A2 mediated platelet aggregation
94
P2Y12 inhibitors e.g. clopidogrel, ticagrelor
▪ 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
GP IIb/IIIa Inhibitors
▪ 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
Anticoagulants e.g. fondaparinux
▪ 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
PPCI – primary PCI - what is it
--> The preferred reperfusion therapy in many patients with STEMI
98
Primary PCI preferred in
▪ Diagnosis in doubt
▪ High bleeding risk – can't give fibrolytic therapy
▪ Very high-risk patients (severe heart failure, pulmonary edema)
99
No reperfusion therapy
--> 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.
