DeAlwisCardio Flashcards

1
Q

Why is a detailed history of chest pain important?

A

For diagnosis and risk stratification

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2
Q

What is the positive likelihood ratio (LR) for pain radiating to the right arm or shoulder as an indicator of myocardial infarction?

A

4.7

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3
Q

What does a positive LR of 2.3 indicate?

A

Pain radiating to the left arm

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4
Q

What is the positive LR for pain described as burning or indigestion associated with acute coronary syndrome (ACS)?

A

2.8

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5
Q

Does pain reproducible by palpation exclude ACS or AMI?

A

No

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6
Q

What percentage of patients with AMI will have an initial ECG showing ST segment elevation ≥1 mm in two contiguous leads?

A

Approximately 50%

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7
Q

What is the positive predictive value for diagnosing AMI with ST segment elevation on ECG?

A

> 90%

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8
Q

What is the advantage of high-sensitive troponin assays?

A

Increased sensitivity in early detection of AMI

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9
Q

What is a potential downside of high-sensitive troponin assays?

A

Reduced specificity

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10
Q

In which non-ischaemic conditions can troponin be elevated?

A
  • Sepsis and critically unwell patients
  • Pulmonary embolism
  • Renal failure
  • Myocarditis
  • Stroke
  • Aortic dissection
  • Congestive heart failure
  • Cardiac contusion
  • Pacing, ablation, cardiac surgery
  • Respiratory failure
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11
Q

What is the role of exercise stress testing in coronary artery disease (CAD)?

A

Prognostically useful in predicting adverse events

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12
Q

What does the TIMI score predict?

A

Adverse outcomes and need for early invasive management for NSTEAC syndrome

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13
Q

What factors are included in the TIMI score calculations?

A
  • Age 65 years or over
  • At least 3 risk factors for CAD
  • Aspirin use in the past 7 days
  • At least 2 angina episodes within last 24 hours
  • Known coronary artery disease
  • ST changes of at least 0.5 mm on ECG
  • Elevated serum cardiac biomarkers
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14
Q

What characterizes Wellen’s syndrome?

A

Abnormal T wave inversion or biphasic T waves in leads V2–4

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15
Q

What are the ECG criteria for reperfusion?

A
  • ST segment elevation of ≥1 mm in two or more contiguous limb leads
  • ST segment elevation of ≥2 mm in two or more contiguous chest leads
  • New left bundle branch block (LBBB)
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16
Q

What is the significance of a negative troponin in assessing myocardial infarction?

A

Excludes myocardial infarction but does not exclude ACS

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17
Q

What are some mimics of STEMI?

A
  • Bundle branch block
  • Pacemaker
  • Cardiomyopathy
  • Pericarditis
  • Myocarditis
  • Preexcitation
  • Hyperkalaemia
  • Benign early repolarisation
  • Ventricular hypertrophy
  • Pulmonary embolism
  • Subarachnoid haemorrhage
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18
Q

What is the cumulative sensitivity of the Sgarbossa criteria for AMI diagnosis?

A

93% to 100%

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19
Q

What does ST elevation in leads II, III, and aVF suggest?

A

Inferior infarction

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20
Q

What are the characteristics of posterior myocardial infarction?

A
  • ST depression in V1–V4
  • Tall/wide R waves in V1–V2
  • R/S ratio >1 in V1–V2 without right axis deviation
  • Upright T waves in V1–V2
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21
Q

What are absolute contraindications to thrombolysis?

A
  • Previous intracranial bleeding
  • Ischaemic stroke within past 3 months
  • Known structural vascular lesion in the brain
  • Active internal bleeding
  • Suspicion for aortic dissection
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22
Q

What did the CAPTIM trial suggest about prehospital thrombolysis?

A

Better outcomes than PCI if given within 2 hours

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23
Q

What ECG changes are associated with an inferior wall infarct?

A

ST elevation II, III, aVF

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24
Q

What is the reperfusion treatment of choice for cardiogenic shock associated with AMI?

A

Percutaneous coronary intervention (PCI)

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25
What is the relative risk reduction in mortality with aspirin alone?
Up to 25%
26
What are the recommendations for beta-blocker therapy in STEMI patients?
Oral beta-blocker therapy during the first 24 hours if no contraindications
27
What is the significance of BNP values between 100–500 pg/mL?
Regarded as non-diagnostic
28
What conditions can promote fluid retention leading to heart failure?
* Uncontrolled hypertension * Atrial fibrillation * Myocardial ischaemia * Renal failure * Use of NSAIDs
29
What are common causes of fluid overload?
Medications (negative inotropes or noncompliance), myocarditis, or progression of disease.
30
What is the mainstay of management for normotensive/hypertensive patients?
Vasodilators and non-invasive ventilation.
31
What is the significance of BNP levels in diagnosing heart failure?
Values <100 pg/mL make acute heart failure less likely; values >500 pg/mL make it more likely.
32
What is the most common cause of cardiogenic shock?
Myocardial infarction (AMI).
33
What percentage of AMI cases complicate with cardiogenic shock?
6–7%.
34
What is preferred over thrombolysis for treating AMI?
PCI or CABG.
35
What is the overall mortality for cardiogenic shock complicating AMI?
About 80%.
36
What are the first-line treatments for acute mitral regurgitation?
Inotropes to improve cardiac contractility and vasodilators to decrease afterload.
37
What effect does endotracheal intubation have in cardiogenic shock?
It nearly always exacerbates hypotension.
38
What does the intra-aortic balloon pump do?
Increases cardiac output by timed inflation during diastole and deflation during systole.
39
What characterizes hypertensive encephalopathy?
Neurological dysfunction from severe hypertension.
40
What is the recommended reduction of MAP in hypertensive encephalopathy?
About 25% over 1–2 hours.
41
What is the initial treatment for aortic dissection?
Rate control and systolic BP reduction.
42
What does hydralazine do?
It is a direct arteriolar vasodilating agent.
43
What are the ECG changes associated with pericarditis?
ST segment elevation and PR depression.
44
What suggests cardiac tamponade on an ECG?
Electrical alternans and low voltage complexes.
45
What is the most common cause of pericardial tamponade?
Malignancy (40% of non-traumatic cases).
46
What are the major pathogens in endocarditis?
Streptococcus species, Staphylococcus aureus, Enterococcus species.
47
What is the Duke criteria used for?
Diagnosing endocarditis.
48
What is the mortality rate for native and prosthetic valve endocarditis?
20–25%.
49
What is the San Francisco syncope rule?
A tool for identifying patients at high risk of adverse outcomes in the following 7 days.
50
What is required to diagnose orthostatic hypotension?
Systolic BP reduction of >20 mmHg upon standing.
51
What characterizes third-degree heart block?
Complete failure of conduction between atria and ventricles.
52
What is Mobitz type I second-degree heart block?
PR interval progressively lengthens until a 'missed' atrial complex occurs.
53
What is the hallmark of VT on an ECG?
AV dissociation.
54
What indicates a supraventricular origin of tachycardia?
A preceding P wave.
55
What are common causes of torsades de pointes?
Drug toxicity, electrolyte abnormalities, congenital prolonged QT syndrome.
56
What is the first-line therapy for stable SVT?
Adenosine.
57
What are the types of tachycardia associated with Wolff-Parkinson-White syndrome?
Reentrant tachycardia with orthodromic conduction, antidromic conduction, rapid conduction of atrial tachycardia.
58
What drugs are contraindicated in AF with preexcitation?
Verapamil, digoxin, adenosine, beta-blockers.
59
What is the efficacy of adenosine in converting SVT to sinus rhythm?
Over 90%.
60
What can increase the dose of adenosine needed?
Patients taking methylxanthines, such as theophylline.
61
What percentage of reentrant SVT in WPW syndrome are orthodromic?
85% ## Footnote Orthodromic conduction passes through the AV node in the usual direction, resulting in a narrow QRS on ECG.
62
What is the approximate breakdown of different types of arrhythmias in WPW syndrome?
* 80%: AV reentrant tachycardia * 15–30%: Atrial fibrillation (AF) * 5%: Atrial flutter ## Footnote Only 1–2% of patients with WPW present with arrhythmias.
63
What are the characteristic ECG features of WPW syndrome?
* Short PR interval (<0.12 seconds) * Slightly prolonged QRS complex (>0.1 seconds) * Slurring of the upstroke of the R wave (delta wave) ## Footnote WPW may also produce a tall R wave in V1.
64
Which IV agents are recommended to control heart rate in patients with AF and heart failure without an accessory pathway?
* Amiodarone * Digoxin ## Footnote Dihydropyridine calcium channel blockers do not reduce heart rate and may cause reflex tachycardia.
65
Why is cardioversion not recommended after 48 hours?
Increased risk of thromboembolism ## Footnote Patients with chronic AF carry a significant risk of embolic events if cardioverted without proper anticoagulation.
66
What can happen in patients with WPW when AF is present with a very short antegrade refractory period?
Very rapid ventricular rates may occur ## Footnote This can lead to rapid ventricular response and potential degeneration into ventricular fibrillation (VF).
67
True or False: In AF not related to preexcitation syndromes, the AV node protects the ventricle from achieving very high rates.
True ## Footnote The relatively long refractory period in the AV node prevents AF from degenerating into VF.
68
Which medications should not be used in WPW AF due to the risk of precipitating VF?
* Calcium channel blockers * Beta-blockers * Digoxin ## Footnote These medications are beneficial in non-WPW AF but dangerous in WPW AF.
69
What is the appearance of atrial flutter on a 12-lead ECG?
Saw-tooth appearance of atrial complexes (flutter waves) ## Footnote Flutter waves are regular and typically visible in one lead system only.
70
What does the letter 'T' indicate in pacemaker terminology?
'T' stands for triggered ## Footnote It indicates pacing is triggered in response to sensed cardiac activity.
71
What are some reasons for failure to capture in a patient with a pacemaker?
* Insufficient energy from pacemaker * Local inflammatory reaction * Lead problems (fracture, dislodgement) * High levels of antiarrhythmic drugs * Electrolyte abnormalities ## Footnote These factors can prevent successful depolarization of the myocardium.
72
What is the ideal position for children with Tetralogy of Fallot during a 'tet' spell?
Squatting position ## Footnote This position increases afterload and decreases right to left shunting.
73
What is the mainstay treatment for ductal-dependent shock in neonates?
Prostaglandin E1 (PGE1) infusion ## Footnote This treatment is crucial for neonates who rely on a patent ductus arteriosus for oxygenated blood.
74
What does a failed hyperoxia test indicate in a neonate?
Right to left shunt due to a cyanotic congenital heart lesion ## Footnote A PaO2 < 100 mmHg suggests a significant structural heart lesion.
75
How is childhood hypertension defined?
Systolic or diastolic BP ≥95th percentile for age and height ## Footnote BP between 90–95th percentile is defined as prehypertension.
76
What are common causes of hypertension in neonates?
* Renal vascular thrombosis * Stenosis * Coarctation of the aorta ## Footnote These causes are important to consider before essential hypertension is diagnosed in older children.
77
How do you do a hyperoxia test?
Pulse oxymetry alone may be unreliable during this test and arterial blood gas (ABG) sampling is advised. PaO2 is obtained first with the neonate on room air (if not tolerated with a low tolerable amount of supplemental oxygen). PaO2 is then assessed after 100% oxygen supplement for 15 minutes. If PaO2 is >250 mmHg (‘passed hyperoxia test’) on the second ABG it usually excludes hypoxia secondary to congenital heart disease. Another cause for the child’s hypoxia should be sought. PaO2 < 100 mmHg (‘failed hyperoxia test’) is considered to be caused by a right to left shunt due to a cyanotic congenital heart lesion. PaO2 100–250 mmHg range may be due to intracardiac mixing as a result of a structural heart lesion. A neonate with a failed hyperoxia test needs urgent evaluation for an anatomical diagnosis and should immediately be treated with prostaglandin E1.
78
What are the duct dependent cyanotic cardiac lesions?
*tetralogy of Fallot *tricuspid atresia and Ebstein’s anomaly *hypoplastic left heart syndrome *interrupted aortic arch and transposition of great arteries without a mixing lesion (e.g. ventricular septal defect, or VSD
79
What are the acyanotic duct dependent cardiac lesions?
*pulmonary stenosis *severe coarctation of the aorta.