Chest Pain Flashcards
1
Q
What percentage of chest pain cases are from cardiovascular causes?
A
25%
2
Q
What percentage of cases of chest pain are from non-cardiovascular causes?
A
75%
3
Q
Name the 2 main causes of cardiovascular chest pain and 2 examples of each cause
A
- Myocardial Ischemia (most common) -> coronary artery disease (commonest cause in UK), aortic stenosis
- Cardiovascular non-Ischemia (0.003% of A&E cases) -> aortic dissection, pericarditis
4
Q
Name 6 other causes of myocardial ischemia other than CAD
A
- Aortic stenosis
- Hypertrophic cardiomyopathy
- Tachyarrhythmias
- Cocaine use
- Anemia
- Thyrotoxicosis
5
Q
Name 3 main causes of non-CVS chest pain and examples of each
A
- Upper GI
- GORD
- Gallstones
- Peptic ulcer
- Pancreatitis - Respiratory
- Pneumonia
- Pneumothorax
- PE
- Pleurisy - Musculoskeletal
- Costochondritis
- Herpes Zoster
6
Q
When taking a history from the patient, use SOCRATES to understand their pain.
SITE:
What would diffuse/poorly localised pain pain indicate?
A
Visceral pain (internal organs)
7
Q
What would localised pain indicate?
A
Somatic pain (musculoskeletal)
8
Q
What would sudden onset of pain suggest?
A
PE
9
Q
What character of pain is present in ACS/GORD?
A
- Pressure/heavy/tight
2. Indigestion/belching
10
Q
What character suggests aortic dissection?
A
Severe ripping
11
Q
What character suggests pleuritic pain/musculoskeletal problem?
A
Sharp, stabbing pain
12
Q
Where does the pain radiate in ACS?
A
L arm, both arms, jaw, neck
13
Q
Where does the pain radiate in cholecystitis?
A
R shoulder
14
Q
In what conditions does the pain radiate to the back/intrascapular?
A
Aortic dissection GORD Peptic ulcer Pancreatitis ACS
15
Q
In what conditions does the pain radiate to the epigastrium?
A
Pancreatitis
Peptic ulcer
Gallstones
ACS
16
Q
What associated features present with ACS?
A
- Nausea/vomiting
- Sweating
- Shortness of breath
- Hypotension/syncope
17
Q
What associated features present with PE?
A
- Sweating
- SOB
- Hypotension/syncope
18
Q
What associated features present with GI pathology?
A
Nausea/vomiting
19
Q
What associated features present with aortic dissection?
A
Sweating
20
Q
What associated features present with aortic stenosis?
A
Hypotension/syncope
21
Q
Name conditions where the onset of pain is within seconds?
A
Musculoskeletal
Non-cardiac
22
Q
Name conditions where onset of pain is within minutes?
A
ACS
GORD
Musculoskeletal
23
Q
Name conditions where onset of pain is within hours?
A
All conditions (non-discriminative time frame)
24
Q
Name conditions where onset of pain is within days?
A
Not ACS (dull/persistent pain)
25
Name a condition where the pain gets worse on exertion/emotion?
Angina
26
Name conditions where the pain gets worse when eating?
ACS
GORD
Peptic ulcer
27
Name conditions where the pain gets worse based on position?
Pericarditis
GORD
Musculoskeletal
Pancreatitis
28
What 3 physical examinations should you perform on a patient complaining of chest pain?
1. Cardiovascular
2. Respiratory
3. Abdominal
29
What is the most valuable tool in ACS and shows changes in other conditions (I.e. PE)?
ECG
30
What is angina (pectoris)?
Symptomatic, reversible myocardial ischemia.
Most commonly due to coronary artery disease.
31
What are the features of angina?
1. Constricting/heavy discomfort in chest, jaw, shoulders, neck, or arms
2. Symptoms brought on by exertion
3. Symptoms relieved within 5mins by rest or GTN
32
What is typical angina?
Angina presenting with all 3 features of angina
33
What is atypical angina?
Chest discomfort which meets 2 of the typical angina characteristics
34
What are the most important risk factors for developing CAD?
Non-modifiable:
1. Age
2. Gender
3. Family history of CAD (MI in 1st degree relative < 55yrs)
Modifiable:
1. Smoking
2. Hypertension
3. Diabetes
4. Hyperlipidemia
5. Obesity
6. Sedentary lifestyle
7. Cocaine use
35
What other parts of the history are relevant to diagnosing CAD?
1. Concurrent diagnosis of CAD (I.e. stable angina, previous MI)
2. Concurrent diagnosis of other atherosclerotic arterial disease (I.e. Ischemic stroke, peripheral vascular disease, renovascular disease)
3. Family history of CAD or atherosclerotic arterial disease
36
What are the 3 main points in managing stable angina?
1. Info + support
2. Offer short-acting nitrate to prevent/treat episodes of angina
3. Offer optimal drug treatment
37
What are the side effects of short-acting nitrates?
Flushing
Headache
Light-headedness
38
Name 3 drug classes used in the treatment of stable angina
1. B-blocker or calcium channel blocker
2. Combination of #1 (I.e. dihydropyridine calcium channel blocker)
3. Long-acting nitrate
39
Name 2 drugs used for 2º prevention of cardiovascular disease?
1. Aspirin (75mg daily)
| 2. ACE inhibitors (for those at increased risk - angina + diabetes)
40
What 2 procedures are used for revascularization of the heart?
1. Coronary Artery Bypass Graft (CABG)
| 2. Percutaneous Coronary Intervention (PCI)
41
When is a CABG indicated?
When the patient is stable with medication but a coronary angiograph indicates L main stem disease/proximal 3-vessel disease
42
Does CABG or PCI have a better outcome in terms of patient survival?
CABG
43
Explain the CABG procedure
Attaching grafted vessels (usually from chest, leg, arm) to coronary arteries beyond the narrowing
44
Explain PCI procedure
Stent placement via the femoral or radial artery to open the narrowing of the coronary vessel affected
45
How many seconds does 1 little square on an ECG represent?
0.04s
46
What is the normal speed of an ECG?
25mm/s
47
What plane do the limb leads look at the heart in?
Vertical plane
48
What leads look at the heart from an inferior view?
aVF, II, III
49
What leads look at the heart from a lateral view?
aVL, I
50
What plane do the chest leads look at the heart in?
Horizontal plane
51
Which leads look at the septal part of the heart?
V1 + V2
52
Which leads look at the anterior view of the heart?
V3 + V4
53
Which leads look at the lateral view of the heart?
V5 + V6
54
What does the p-wave represent?
Depolarisation of the atria (pulse of electrical activity from SA to AV node)
55
What does the QRS complex represent?
Impulse from AV node causing depolarisation of ventricles
56
What does the T-wave represent?
Ventricular depolarisation
57
Why can’t you see atrial repolarization on the ECG?
It is hidden by the QRS complex
58
How long is the PR interval normally?
0.12-0.2s (3-5 small squares)
59
How long is the QRS complex normally?
< 0.12s (<3 small squares)
60
How do you measure the QT interval?
From the beginning of the Q wave to the end of the T wave
61
How long is the QT interval normally?
Varies inversely to HR (as HR increases, QT interval decreases)
I.e. HR 60 = 0.35-0.46s
62
How do you calculate the rate on an ECG?
300/(# of large squares between adjacent R waves)
63
How do you determine the axis of an ECG?
Normal: Both leads I and II are positive in QRS
L axis deviation: Lead I is negative, Lead II is positive
R axis deviation: Lead I is positive, Lead II is negative
64
Where is it normal to see deeper Q waves?
Leads III and aVR
65
Which leads normally don’t show Q waves?
V1-V3
66
Name 2 important features of normal T waves
1. Upright in all leads except aVR and V1
| 2. Height is < 5mm in limb leads and < 15mm in chest leads
67
What is a normal QT interval?
QTc should be less than 1/2 the preceding RR interval
68
What are ECG changes that indicate CAD?
1. Pathological Q waves (current/prior MI)
- >40ms (1mm) wide
- > 2mm deep
- > 25% depth of QRS complex
- > Seen in leads V1-V3
2. LBBB
- Broad QRS (>0.12s)
- Deep S wave in V1
- No Q wave in V5/V6
3. ST segment + T wave abnormalities
- ST depression
- T wave flattening/inversion
69
What is cardiovascular disease?
Generally due to low blood flow to the heart, brain, or body caused by atheroma or thrombosis.
Plaques of fatty atheroma build up in different arteries over life and can eventually cause narrowing of arteries, or trigger a local thrombosis (blood clot) which completely blocks blood flow.
70
List the 3 main types of cardiovascular disease
1. Coronary heart disease
2. Stroke
3. Peripheral arterial disease
71
Name 9 risk factors for cardiovascular disease
1. Smoking
2. Poor diet
3. Hyperlipidemia
4. Hypertension
5. Physical inactivity
6. Obesity
7. Diabetes
8. Psychological stress
9. Excess alcohol consumption
72
Name 3 diagnostic investigations for CAD
1. 64-slice CT coronary angiography
2. Non-invasive functional testing (i.e. Myocardial perfusion scintigrapy with single photon emission CT, stress ECHO, 1st pass contrast-enhanced magnetic resonance perfusion, MRI for stress-induced wall motion abnormalities
3. Invasive coronary angiography
73
Name systolic heart murmurs
1. Aortic stenosis
2. Mitral regurgitation
3. Mitral valve prolapse
74
Name diastolic murmurs
1. Aortic regurgitation
| 2. Mitral stenosis
75
For aortic stenosis, name the type, sound and loudest areas where the murmur can be heard
1. Ejection systolic murmur
2. Crescendo-decrescendo murmur (with ejection click)
3. Loudest over aortic area + carotids (b/c branch of aorta)
76
For mitral regurgitation, name the type, sound and loudest areas where the murmur can be heard
1. Pansystolic murmur
2. Intensity of murmur sound stays consistent throughout systole
3. Radiates to axilla
77
For mitral valve prolapse, name the type, sound and loudest areas where the murmur can be heard
1. Mid-systolic click with late systolic murmur
2. Non-ejection click
3. Best heard over apex + associated with mitral regurgitation
78
For aortic regurgitation, name the type, sound and loudest areas where the murmur can be heard
1. Early diastolic murmur
2. Decrescendo murmur
3. Best heard at L eternal border (blood flowing backwards)
79
For mitral stenosis, name the type, sound and loudest areas where the murmur can be heard
1. Opening snap + mid-diastolic rumble
2. Opening snap + pansystolic excentuation
3. Heard best over apex
80
Name 4 extra heart sounds
1. Systolic clicks
2. Opening snap
3. S3 -> Volume overload condition
4. S4 -> Pressure overload condition
81
What position can you best hear S3 and S4?
Heard best in apex when in L lat decubitus position (pt turns to L side)
82
Explain the sound heard in S3 and the physiology behind the condition
Ventricular gallop
Occurs in rapid filling phase of diastole when chordate tendenae are tensed b/c increased volume in ventricle. Usually normal in adolescence. Congestive heart failure can cause this in the elderly
83
Explain the sound heard in S4 and the physiology behind the condition
Aortic gallop
Occurs when atria contracts into very stiff hypertrophied ventricle. Always bad news.
84
Does a normal ECG exclude ACS?
NO
85
What treatment would you give for suspected ACS?
Loading dose of aspiring 300mg
| Morphine, Oxygen, Nitrates, Aspirin - MONA
86
How will you monitor the patient until ACS is excluded?
Use clinical judgement to decide how often this should be done:
1. Exacerbates of pain/other symptoms
2. Pulse + BP
3. Heart rhythm
4. O2 sat
5. Repeated ECG
6. Checking pain relief is effective
87
Name 3 changes in the ECG in a STEMI
1. ST depression = cardiac tissue is “hurting” for O2 -> Ischemic endocardium
2. ST elevation = cardiac tissue is dying -> infarcting endocardium
3. Inverted T waves = previous/current cardiac event (MI)
88
How can you visualise the posterior aspect of the heart on an ECG?
V1-V3 represent the posterior of the heart (V7-V9) when inverted
I.e. ST depression in V1-V3 = ST elevation in V7-V9
89
When and why don’t you give GTN as treatment for an MI?
Do not give for posterior or inferior MI
Heart is depending on preload (how much blood V in ventricles at end of diastole). GTN vasodilates + lowers V of blood being pushed into R side of heart = decreased total blood pumped = decreased cardiac cell survival b/c less blood thru aorta
90
What are the top 4 lines of treatment for an acute STEMI?
1. PCI -> pt presents within 12hrs of onset of symptoms + within 120min of time when fibrinolysis could have been delivered
2. Fibrinolysis -> if patient doesn’t get PCI within 120mins of when fibrinolysis could have been delivered
3. Antiplatelet agents -> ticagrelor, prasugrel, cangrelor
4. Antithrombin agents -> heparin, bivalirudin
91
What 6 medications would you offer post-MI?
1. Antiplatelet -> aspirin 75mg (+ clopidogrel for 12mo)
2. Anticoagulant -> with fondaparinux
3. B-blocker -> -OLOL
4. ACE inhibitor -> -PRIL
5. High-dose statin -> atorvastatin
6. Echo for LV function (LVEF)
92
Explain the pathophysiology of ACS
1. Acute thrombosis induced by ruptured atherosclerotic plaque
2. Vasoconstriction
3. Critical reduction in blood flow
4. Clinical sequelae (angina, heart failure, pump failure, arrhythmia)
93
How often should an ECG be performed in a patient with chest pain?
3, 6, 24hr after presentation + immediately if chest pain recurs
94
What is the gold standard of heart biomarkers?
Troponin T and I
95
How do the levels of Troponins act?
Levels rise within 2-4hrs and may stay elevated for 2wks
96
What is the gold standard for chest pain investigations?
Coronary angiography
97
What substance is an early marker of CAD?
Calcium
98
What does ST elevation in aVR indicate?
L main stem/3-vessel disease (CABG to treat)
99
Name 2 risk scores in ACS
GRACE score -> Ischemic risk
| CRUSADE score -> bleeding risk
100
What is the treatment of ACS?
1. Anti-Ischemic agents -> B-blockers, Ca-channel blocker, Nitrates
2. Antiplatelet -> Aspirin, P2Y12 receptor inhibitors, clopidogrel
3. Anticoagulation
- Indirect anticoagulation: heparin, LMWH, Factor Xa (fondaparinux)
- Direct anticoagulation: Bivalirudin, Factor Xa (rivaroxaban)
101
What is the long-term management of ACS?
1. Aspirin (for life) + clopidogrel (12mo)
2. Statins (LDL < 1.8mmol/L)
3. B-blocker (for LVEF < 40%)
4. ACE inhibitor/ARB (for LVEF < 40%)
5. Aldosterone antagonists (LVEF < 35%)
6. Enrolment in 2º prevention lifestyle programs (I.e. diet, exercise)
102
Where do the coronary arteries run?
Within the pericardial layers of the heart
103
When does coronary flow occur?
During diastole when the myocardium is relaxed and the smaller coronary vessels are not squeezed by the contracting myocardium
104
What happens to oxygen demand with tachycardia?
Tachycardia increases myocardial oxygen demand (as the heart has to beat faster and do more work) and decreases coronary blood flow (as the duration of diastole is shortened)
105
Where do the coronary arteries originate from?
Aortic sinuses (small bulges in the aorta above the aortic valve)
106
What are the key branches of the right main coronary vessel?
1. Right marginal artery
| 2. Posterior descending artery
107
What are the main branches of the left main coronary vessel?
1. Left anterior descending artery
2. Left marginal artery
3. Left circumflex artery
108
Where does venous drainage occur in the heart?
Coronary sinus
109
What is the coronary sinus?
A collection of veins joined together to form a large vessel that collects blood from the myocardium. It delivers deoxygenated blood to the R atrium.
110
What do increased levels of Troponins and Creatinine Kinase indicate?
Myocardial necrosis
111
Where can creatine kinase be released from?
Any muscle
112
What are the levels of Troponins and creatine kinase in unstable angina?
Not raised as the condition is not associated with myocardial necrosis
113
What are the troponin and creatine kinase levels like in NSTEMI and STEMI
Increased. The levels increase as severity increases leading to increased chances of mortality.
114
When do troponin levels peak?
24-48hrs
115
What are Troponins associated with physiologically?
Actin myofilaments.
Thin filament (actin) and in relaxed muscle myocytes troponin prevents cross-bridging and contraction of muscle. But in depolarisation there’s increased levels of Ca2+ that inhibit Troponins allowing cross-bridging and cardiac contraction.
Troponins will leak out into the blood into the dead cell membrane where they can be detected in cases of myocardial cell death.
116
How do you know that the ventricle is contracting properly in an ECHO?
Overall appearance of ventricle -> are all walls the same thickness? Moving at the same time? Is everything contracting at the same time?
117
What is the most common complication post-MI?
Arrhythmias
118
What is ventricular fibrillation?
Ventricles lose the ability to contract and circulate blood throughout the body.
Rapid, random signalling in ventricles from AV node through the septum = poor contractibility
119
What does ventricular fibrillation look like on an ECG?
Coarse, squiggly lines
Pt will be unconscious and pulseless
120
What are risk factors for ventricular fibrillation
1. Irritable ventricular cells (over-firing)
- Coronary artery disease = decreased blood flow to ventricles
- Increased potassium, decreased calcium, decreased magnesium
2. Scar tissue
- MI = tissue death -> scar tissue + decreased conduction of electrical signal
- Cardiomyopathy = decreased function of heart tissue (I.e. infection, genetics, CAD)
3. Electrocution
121
What is ventricular tachycardia?
Up to 250bpm = heart has difficulty circulating blood to the rest of the body (decreased filling of ventricles with blood)
122
What are the two types of VT?
1. Focal VT = irritated cells
- Cells in ventricle irritated by hormones, decreased O2, stretch
- Caused by CAD, electrolyte abnormality
2. Reentrant = scarring
- Reentry circuit around dead tissue spreading into ventricles = increased HR
- Caused by MI, hypertrophic cardiomyopathy, dilated cardiomyopathy
123
What does the ECG look like for VT?
Coarse wide QRS complex + tachycardia
124
What is supraventricular tacycardia?
- Start from atria/AV node
- ECG may be normal
- COPD, CAD, and Heart failure are all risk factors
125
What is atrial fibrillation?
- Supraventricular tachycardia
- Irregularly irregular heart rhythm of atria
- No distinct p-waves
- Electrical impulses fire off from different places in the atria
126
What are the complications post-MI?
1. Decreased contractibility
- Hypotension
- Decreased coronary perfusion
- Ischemia
- Cardiogenic shock
2. Tissue necrosis
- Inflammation
- Pericarditis
- Ventricular septal defect
- Hypoxemia + stress on lung vessels
- Ventricular rupture -> cardiac tamponade
- Papillary muscle rupture -> mitral regurgitation
3. Electrical instability
- Arrhythmias
127
How does coronary artery disease present?
1. Silent ischemia
2. Stable angina
3. Unstable angina
4. NSTEMI
5. STEMI
6. Heart failure
7. Sudden death
128
What are the clinical presentations of ACS?
1. Prolonged chest pain (>20min) at rest
2. New onset angina
3. Worsening of existing angina
4. Angina followed by MI
5. Atypical presentations are common over 75yrs of age
129
How could the ECG be normal in ACS?
1. Ischemia in circumflex territory
2. Isolated RV ischemia
- These are detected using V7-V9 and V3R and V4R leads
3. Transient episodes of bundle branch block (either RBBB or LBBB)
130
How do you image non-invasively in NSTEMI ACS?
1. 12-lead ECG
2. Transthoracic (TTE) echocardiography
3. Stress echocardiography
4. Cardiac magnetic resonance
5. Nuclear myocardial perfusion imaging
6. CT coronary angiography (gold standard)
131
What are the ECG criteria to diagnose a STEMI?
1. >/= 1mm ST elevation in leads V4 + V5
| 2. New LBBB
132
Which murmur is best heard over the aortic area radiating to the carotids and is characterised as an ejection systolic murmur?
Aortic stenosis
133
Mid-diastolic rumbling murmur, heard best with the bell of the stethoscope at the apex with the patient in the left lateral position?
Mitral stenosis
134
Pansystolic murmur heard loudest at the apex of the heart radiating to the axilla
Mitral regurgitation
135
Early diastolic murmur heard best at the L 4th intercostal space with the patient sat forward in expiration
Aortic regurgitation
