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Semester 2 - CVS > 17. Acute Coronary Syndromes > Flashcards

17. Acute Coronary Syndromes Flashcards

1
Q

What causes a STEMI?

A

Acute complete obstruction of a coronary artery

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2
Q

What is an aborted STEMI?

A

Rapid early reperfusion of a thrombotic occlusion of an epicardial coronary artery
- no increase in troponin plasma levels to suggest necrosis

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3
Q

What are the criteria for diagnosis of a MI?

A

Detection of increase/decrease in cardiac biomarkers (i.e. troponin) + at least 1 of the following:

  1. Symptoms of ischaemia.
  2. New or presumed new significant ST-T wave changes or left bundle branch block on 12-lead ECG.
  3. Development of pathological Q waves on ECG.
  4. Imaging evidence of new or presumed new loss of viable myocardium or regional wall motion abnormality.
  5. Intracoronary thrombus detected on angiography or autopsy
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4
Q

What is type 1 MI?

A

Atherosclerotic plaque rupture, ulceration, fissure, erosion or dissection with resulting intraluminal thrombus in one or more coronary arteries leading to decreased myocardial blood flow and/or distal embolization and subsequent myocardial necrosis.

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5
Q

What is type 2 MI?

A

Condition other than coronary plaque instability contributes to an imbalance between myocardial oxygen supply and demand

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6
Q

What are some mechanisms of type 2 MI?

A
  • Coronary artery spasm
  • Coronary endothelial dysfunction
  • Tachyarrhythmias, bradyarrhythmias
  • Anaemia
  • Respiratory failure
  • Hypotension
  • Severe hypertension
  • Heart failure
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7
Q

What are the common complications after an MI?

A
  • acute pulmonary oedema
  • complete heart block or dangerous tachyarrhythmia
  • post MI ventricular septal defect developed
  • mitral regurgitation due to papillary muscle rupture or dysfunction
  • Effect on LV function
  • Left ventricular mural thrombus
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8
Q

What needs to be considered in the history of someone with possible acute coronary syndrome?

A 
 Cardiac sounding?
 Radiation?
 Relieved with GTN?
 How long?
 Is it getting worse?
 Pleuritic?

Risk Factors
 Smoker, FH, high cholesterol, HTN, thrombophilia

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9
Q

When examining a patient what haemodynamics do you need to consider

A

 BP (if systolic <90mmHg –Cardiogenic shock)
 Tachycardia or Bradycardia (2:1 Heart block, Complete heart block)
 JVP
 Lungs - clear or wet?
 Heart sounds – this could be life saving – missing a murmur could be costly!
 Cool peripheries?

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10
Q

Which ECG leads are inferior, lateral and anteroseptal?

A

Inferior: II, III, aVF
Lateral: I, aVL, V5, V6
Anterospetal: v1-v4

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11
Q

On an ECG what do the following mean:

ST elevation, St depression, T wave inversion, Heart block, Ventricular dysrhythmia

A

ST elevation: sudden occulsion, also persists long term as a mark of Left ventricle aneurysm

ST depression: implies under supply of blood to myocardial but not sudden coronary occulsion.

T wave inversion: implies under supply of blood to myocardium but not sudden coronary occulsion, there can be other non ischaemia related causes

Heart block: various grades

Ventricular dysrhythmia: Vt, VF and ECTOPICS

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12
Q

What 4 ECG presentations does an ST elevation evolve with and what should be done when an ST elevation is present

A
  • Hyper acute T waves
  • St segment elevation
  • T wave inversion
  • Pathological Q waves

• Need to go directly to the cath lab for emergency percutaneous coronary intervention

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13
Q

With a Non ST elevation MI(NSTEMI), what is present on the ECG and what blood tests should you consider

A

ECG: can be normal, ST depression and T inversion may be present

BLOOD TESTS:
• Haemoglobin (anaemia) – will need to consider antiplatelets
• Renal function (angiograms – contrast, may develop AKI).
• Cholesterol
• HBA1C
• Troponin

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14
Q

What is an echocardiogram?

A

an ultrasound of the heart; noninvasive method for monitoring cardiac performance
Can look at: LV function, wall motion, valvular disease, complication from MI

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15
Q

What questions should be asked in investigation of ACS?

A
  • What happened? (occlusion, narrowing?)
  • When did it happen?
  • Where did it happen? (right, left coronary?)
  • How bad is it? (complications of MI)
  • Why did it happen? (plaque rupture, dissection? risk factors?)
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16
Q

How can we assess what happened in an ACS?

A

ECGs:

  • ST elevation (STEMI, occlusion)
  • ST depression (NSTEMI/unstable angina, narrowing)

Invasive coronary angiogram can also tell us if there is narrowing or complete blockage

Troponin levels indicates presence of necrosis

17
Q

How can we assess when a ACS occurred?

A

An ECG can be helpful in this as you can follow the ST segment to identify what point of time the MI took place.
Q waves will be useful as they imply an established MI.
Troponin markets can be used in addition.

It can give an indication of the type of condition as well as the severity.

18
Q

How can we assess where a ACS occurred?

A

ECG: 12 leads
• Inferior changes imply right coronary
• Anterior changes imply left anterior descending
• Lateral changes imply diagonal, obtuse marginal, or circumflex

Invasive angiogram
• Identifies the stenosis / occlusion / dissection in the specific vessel

Echocardiogram
• Regional wall motion abnormalities can correlate with the occlusion / stenosis territory

19
Q

How can we assess how bad a ACS is (how do we look for complications)?

A
  • Chest X-ray: Pulmonary oedema
  • Urea and Electrolytes: Acute kidney injury - eg cardiogenic shock
  • ECG and associated cardiac monitoring (bedside, telemetry): AV conduction block (heart block), VT, VF
  • Echocardiogram: Ventricular septal defect due to septal infarction, Mitral regurgitation, Left ventricular impairment
20
Q

How can we assess why a ACS occurred?

A
  • Invasive coronary angiogram: Plaque rupture? Vs dissection etc
  • CT aorta if worried about aortic dissection into RCA
  • FBC - Anaemia? Polycythaemia? Sepsis?
  • Lipid profile - Triggering factors - eg CHD risk factors
21
Q

What are the typical bloods for assessing ACS?

A
  • FBC
  • U&E
  • Lipids
  • Troponin
  • Others as needed according to rarer conditions
22
Q

Which troponin used to assess ACS and why?

A

Troponin I and T

  • highly sensitive
  • specific to cardiac origin
23
Q

How long does troponin levels take to rise, when does it peak and how long does it remain elevated?

A
  • 3 hrs to ride
  • peaks at 24 to 48 hrs
  • remains elevated for 2+ weeks
24
Q

What is a possible issue with using troponin assays?

A

Raised in many conditions, not just coronary syndromes

25
Q

What is regional wall motion abnormality and what is used to detect it?

A

Motion of a region of the heart muscle is abnormal

- detected using echocardiogram

26
Q

What is the management pathway for STEMI

A
  1. Aspirin
  2. Antiplatelets - Ticagrelor
  3. Morphine with anti-nausea
  4. Nitrate if highBP
  5. Oxygen if sats lower then 92%
  6. Time is muscle so act fast
  7. Cath labs
27
Q

What is the management pathway for NSTEMI

A

Antiplatelets and antithrombotics
•Aspirin and Clopidogrel/Ticagrelor
•Enoxaparin

Anti-ischaemia
• Bisopolol
• GTN infusion

Secondary prevention
•Statin
•ACE inhibitors

But

If patients ongoing chest pain with dynamic changes in eCG or develops arrhythmias then go straight to cath lab

28
Q

What is a good way to remember management of STEMI?

A

BROMANCE

Beta blocker
Rate
Oxygen
Morphine
Aspirin
Nitrate
Clopidogrel (antiplatelet)
Enoxaprin (anticoagulant)
29
Q

Explain invasive coronary angiograms method

A

Establishes type of lesion and its location
 Local anesthetic
 Radial or femoral artery access
 30 min procedure
 Wire the occluded vessel
 Predilate the narrowed sections with balloons
 Stent with metal scaffold to keep vessel patent
 Option to include intravascular ultrasound or optical coherence tomography

30
Q

After coronary angiogram stents what is the management given to the patients

A
  • Lifestyle changes (low fat, regular exercise, low salt)
  • Dual antiplatelets for 12months then aspirin
  • Statin aiming for reduced cholesterol
  • Bisproplol aiming for reduced hr
  • Ace inhibitor for reduced bp
  • Possible implantable cardiac defib

Semester 2 - CVS (20 decks)

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