Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

1 - Cardiology > Ischemic Heart Disease/Acute Coronary Syndrome > Flashcards

Ischemic Heart Disease/Acute Coronary Syndrome Flashcards

1
Q

Define stable angina

A

1) reproducible chest discomfort
2) occurs on exertion/stress
3) relieved in 5-10 mins by rest
4) relieved by TNG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define unstable angina

A

DEF (duration, limited exercise, frequency)

1) rest angina duration >20 mins
2) limited exertion due to new severe sudden onset angina
3) crescendo pattern of increasing frequency, exertional SOB, and frequency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What diagnoses are included under acute coronary syndrome (ACS)?

A

ACS consists of 3 diagnoses

1) unstable angina
2) NSTEMI
3) STEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

List the 3 diagnostic criteria for ACS

Which combination of diagnostic criteria gives UA, NSTEMI, and STEMI?

A

Patient presents w/2/3 of the following

1) chest pain/angina
2) ECG changes
3) elevated cardiac biomarkers

UA = angina + ECG changes (but not ST elevation) NO CARDIAC BIOMARKERS

NSTEMI = elevated cardiac biomarkers + angina OR ECG changes (but not ST elevation)

STEMI = elevated cardiac biomarkers + angina OR ECG changes (must be ST elevation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How can you distinguish between UA and NSTEMI?

A

Take blood 2x for cardiac biomarkers 4-6h apart (james)

ACS protocols say every 0, 3, 6, 12h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Outline the pathology in STEMI

What is the clinical implication?

A

Normal vessel –> sudden block by thrombus/embolus –> transmural infarct

Implication –> needs urgent revascularization as no collaterals exist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Outline the pathology in NSTEMI

What is the clinical implication?

A

athersclerosed coronary artery –> microthrombi rupture and heal repeatedly –> collateral circulation present

Implication –> urgent revascularization by PCI not necessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are vulnerable plaques and what do they cause?

A

Plaques w/thin fibrous cap
Prone to rupture
Causes complete occlusion –> infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are stable plaques and what do they cause?

A

Plaques w/thick fibrous cap and thin lipod core
Not prone to rupture
Causes stenosis –> ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When is coronary artery stenosis significant?

A

Dependent on lesion location
Left main branch ≥50%
Proximal LAD ≥70%
Proximal LCX ≥70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

List risk factors for IHD

A

metabolic syndrome

1) obesity (central)
2) DM
3) HT
4) DLPD
5) HCHL

smoking
sedentary lifestyle
+ve FHx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Outline SOCRATES for IHD/ACS except associated symptoms

A

Site: retrosternal chest pain
Onset and progression: variable/usually after exertion or stress and progressively worsens

Character: compressive (rock on the chest)

Radiation: to the arms, neck, and jaw (if back consider aortic dissection)

Alleviation: TNG doesn’t help

Severity: very painful…

Levine’s sign –> right arm over chest (left arm hurts from radiating pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Outline associated symptoms of IHD/ACS

A

1) Nausea/vomiting (increased sympathetic drive; suggestive of MI)
2) Sweating (sympathetic)
3) SOB (heart failure induced APO)
4) Dizziness/syncope (VT,VF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

IHD/ACS Emergency DDx

A

1) Aortic dissection (tearing chest pain radiating to back )
2) Pulmonary embolism (leg swelling, long flight, OCP)
3) Tension pneumothorax (SOB, deviated trachea)
4) Perforated peptic ulcer PPU (…forgot)
5) Esophageal rupture (?Mallory-Weiss ?Boerhaave)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

IHD/ACS non-emergency DDx

A

1) Cardiovascular: pericarditis
2) Respiratory: pneumonia, pleuritis
3) Gastrointestinal: GERD, esophagitis
4) Dermatological: herpes zoster
5) Musculoskeletal: costochondritis (most common; tender on palpation at that spot)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List and justify Ix for IHD/ACS

A

1) CBC
- check PLT to consider PCI as cannot PCI if 50>PLT
2) INR and Clotting profile
- check INR to consider PCI cannot PCI if INR>1.7?1.5?
3) Cardiac biomarkers
- troponin (I, T), creatine kinase (CK), myoglobin, LDH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What troponin T result indicates MI?

A

Both of the following

1) Baseline >14
2) 3-6h later >100% increase (…so >28?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How long does TnT remain elevated after MI? What is the implication?

A

1) TnT remains elevated for 10-14w post MI
2) Unable to use it as a marker for MI if patient experience chest pain again in a few days
3) Must resort to CK-MB as it returns to normal in 3d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

In what patients are troponin and CK-MB unreliable markers for MI?

A

1) CKD
2) severe heart failure
3) new onset arrhythmia
4) sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

If cardiac biomarkers return negative do you repeat or not?

A

For cases w/negative cardiac biomakers at repeat at 8-12h post symptom onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What time intervals should serial ECGs be taken?

A

10-15mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What CXR signs in look for in a patient w/chest pain?

A

1) AMI –> heart failure –> APO –> pulmonary congestion
2) Aortic dissection (CI thrombolysis)–> widened mediastinum
3) Tension pneumothorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the 1y risk of death for ACS patients?

A

8-10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Myocardium survival curve indicates that…

A

less than 6h = time is most important factor to save myocardium

more than 6h = time is no longer the most important;
just revascularize to save salvageable myocardium (sounds exactly like time…==)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Outline the progression of ECG changes in acute MI

A

1) 5-30mins hyperacute T wave (local hyperk)
2) minutes to hours ST elevation (>1mm limb leads/>2mm precordial/>2 consecutive leads)
3) 12-24h pathological Q wave (>0.04s wide)
4) 1-2 weeks T wave inversion TWI (but normally present in AVR, V1/2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

ST elevation >1mm limb leads/>2mm precordial/>2 consecutive leads in V1/2/3/4

What area? Which artery?

A

Anteroseptal/Anterior

LAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

ST elevation >1mm limb leads/>2mm precordial/>2 consecutive leads in I, AVL, V4/5/6

What area? Which artery?

A

Anterolateral /Lateral

LCX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

ST elevation >1mm limb leads/>2mm precordial/>2 consecutive leads in II, III, AVF

What area? Which artery?

A

Inferior
RCA –> risk of complete heart block

occasionally LAD if LAD dominant and supplying inferior heart

DDx aortic dissection as Type A can involve ostium of coronary artery –> RCA usually more than LCA

palpate pulse discrepancy, auscultate aortic regurgitation, CXR/echo for widened mediastinum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

ST depression in V1/2/3/4

What area? Which artery?

A

Posterior
RCA

ST depression cause posterior so just flip it around

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

ST elevation in V3/4R

What area? Which artery?

A

Right ventricle

RCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the implication of inferior MI?

A

1) Inferior MI usually means RCA infarct
2) RCA supplies AV node through AV nodal branch
3) Small inferior MIs are enough to cause 3rd degree heart block (complete)
4) Also risk of right sided infarct so check V3/4R for ST elevation
5) Also risk of posterior infarct so check V7/8/9 (on the back)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Signs of right ventricular infarct

A

1) V3/4R ST elevation >2mm
2) low BP/hypotension (CO is preload dependent –> affected in right ventricular infarct) [CI nitrates/morphine as these cause venodilation further reducing preload causing cardiogenic shock]
3) Bezold Jarisch reflex (right ventricular infarct –> stimulates phrenic nerve + vagal resposne –> increased parasympathetic tone –> sinus bradycardia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How does MI affect the SA node?

A

SA node blood supply is more variable
60% LAD/40% RCA (wikipedia)
40% LAD/60% RCA (http://lifeinthefastlane.com/ecg-library/basics/inferior-stemi/)

Depends on the patient and site of infarct…I guess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the implication of any new LBBB?

A

Consider it as acute MI until proven otherwise –> and recall the rest of the ECG findings are no longer reliable

35
Q

Define treatment delay in ACS cases

A

Total time between symptom onset to primary percutaneous coronary intervention (PCI)

36
Q

List the 4 components of treatment delay

A

1) Patient delay
2) Prehospital system delay
3) Door to balloon delay
4) System delay

37
Q

Define patient delay

A

Time between symptom onset and calling 999

38
Q

Define prehospital system delay

A

Time between calling 999 and arrival at the PCI center

39
Q

Define door to balloon delay

A

Time between arrival at PCI center and performing primary PCI

40
Q

Define system delay

A

Time between calling 999 to performing primary PCI

equivalent to prehospital delay + door to balloon delay

41
Q

Explain the rationale for therapeutic hypothermia post MI

A

1) Loss of cerebral circulation autoregulation post MI –> prone to pyrexia further increasing brain damage

42
Q

What temperature range for therapeutic hypothermia post MI? How long is this done for?

A

32-34 degrees is known as therapeutic hypothermia

less than 36 degrees is known as temperature control

needed for 24-48h post PCI

43
Q

Outline prehospital Mx of ACS

A

1) Resucitation
2) O2
3) Aspirin [chewed] (160mg loading then 300mg)
4) Nitroglyecrin [sublingual] (max 3 doses Q5min)
5) Morphine (w/nitrates have venodilating effect to reduce preload –> CI in right ventricular infarct?)
6) ECG monitor –> if STEMI seen go to PCI center!!!

MONAH BAH

44
Q

Outline acute hospital treatment for ACS

Drugs to be tested later

A

1) Arrange CCU bed then DAVID
2) NPO for initial 12h
3) Bed rest for at least 24h
4) Vitals (RR, HR, BP, SaO 2 ) + continuous ECG monitoring
5) Ix –> CBC for PLT, clotting profile and INR to determine if patient can undergo PCI
6) Drugs –> MONAH (heparin) BAH

45
Q

Outline the drugs used in acute hospital Mx of ACS

Antiplatelets tested later

A

MONAH BAH

1) Morphine –> pain relief and venodilation to reduce preload (caution in right ventricular infarcts)
2) O2 –> 4-6L/min by nasal cannula
3) Nitrates –> dilates coronary vessels but also venodilation (same risk as morphine)
4) Antiplatelets (aspirin, clopidogrel, prasugrel, ticagrelor, IV eptifibatide, IV tirofiban)
5) Heparin –> type of heparin depends on subsequent Mx (UFH –> primary PCI; LMWH –> thrombolysis)

46
Q

Outline the antiplatelets used in acute hospital treatment of ACS

A

Double antiplatelet therapy (DAPT) as aspirin + P2Y12 receptor blocker is recommended (clopidogrel, prasugrel, ticagrelor) for all patients regardless of Mx; for patients using aspirin + ticagrelor combination use a lower dose of aspirin (less than 100mg aspirin)

1) Aspirin (loading 160-325mg chewed then up to 325mg)

2) Clopidogrel (loading 600mg PO for primary PCI; loading 75mg PO for other Mx)
3) Prasugrel (loading 60mg)
4) Ticagrelor (loading 180mg)
[P2Y12 receptor blocker CI]
- active GI bleed
- intracerebral bleed
- avoid concurrent omeprazole as it inhibits CYP2C19 needed to metabolize clopidogrel into its active form

5) IV Glycoprotein IIb/IIIa inhibitors (IV eptifibatide, tirofiban, abciximab)
- used w/primary PCI if no P2Y12 receptor blocker has been used –> PO not useful…?

47
Q

What special Mx is needed in cases of right ventricular MI?

A

1) CI nitrates and morphine as these reduce preload but CO is preload dependent so w/impaired right ventricular function already there is risk of cardiogenic shock
2) Give IV fluid (?e.g. 200mL Gelofusine [James notes says won’t pulmonary edema…?]

48
Q

Outline the types of anticoagulant regimens used in Mx of ACS

A

All of the following are on the assumption patients will be on aspirin + P2Y12 receptor blocker (e.g. ticagrelor)

1) primary PCI –> UFH better than bivalirudin
2) fibrinolytic therapy –> LMWH (enoxaparin [Clexane] or fondaparinux)
3) no reperfusion therapy –> LMWH or UFH

49
Q

Explain the rationale of beta blockers post MI

A

1) Reduces short term complications and improves long term survival
2) Initiate within 24h of MI if no contraindications
3) Reduces O 2 demand –> drops HR, BP, and contractility –> relieves ischemia
4) Lower HR prolongs diastole –> improves diastolic perfusion to myocardium

50
Q

Outline the types of beta blockers used post MI

A

1) metoprolol/atenolol (loading 12.5mg daily then up to 200mg daily) [extended release is better]
(PO 25mg bd/ IV 5mg slowly state 3 doses at 5 min intervals)

2) carvedilol (loading 3.125mg daily then up to 50mg bd) (use in left systolic heart failure)
3) bisoprolol (loading 1.25mg daily then up to 5-10mg daily) (use in left systolic heart failure)

51
Q

Explain the rationale of ACEIs/ARBs post MI

A

1) Initiate within 24h of MI if no contraindications
2) These benefits are mediated through attenuation of cardiac remodeling by slowing the rate of left ventricular dilatation that occurs post MI
3) Benefits greater in
- reduced LVEF
- heart failure
- anterior MI
- recurrent MI
- elderly

4) ACEI/ARB improves LVEF at 1m and 1y post MI
5) ACEI/ARB prolongs survival for at least 1y

52
Q

Outline the contraindications for beta blocker therapy post MI

A

Any patients w/risk of cardiogenic shock

1) >70y/o
2) SBP less than 120
3) HR >110 or less than 60

Other contraindications

1) COPD
2) Asthma
3) Any degree of heart block

53
Q

Outline the types of ACEIs/ARBs used post MI

What is 1st dose hypotension?
What must be monitored while on ACEI/ARBs?

A

Maintain SBP >90mmHg when using ACEI therapy

1) Captopril (loading 6.25mg then increase Q6/8h up to 50mg tds)
2) Lisinopril (loading 2.5mg/d then up to 10mg/d)
3) Enalapril (loading 2.5mg/d then up to 20mg bd)

IV ACEIs have risk of hypotension and are not used

1st dose hypotension –> fall in BP when moving from supine to erect

  • risk of syncope occurring w/ACEIs and alpha blockers
  • avoid diuretics for 24h prior to 1st dose

Monitor RFT for hyperkalemia while on ACEI

54
Q

Outline the contraindications for ACEI/ARB therapy post MI

A

1) ACEI/ARB allergy
2) SBP less than 90-100mmHg
3) Shock
4) Hx RAS
5) Hx impaired RFT w/ACEI/ARB

55
Q

Indications for revascularization therapy (PCI or fibrinolytic therapy)

A

1) Typical chest pain >30mins
2) Onset chest pain less than 12h
3) 20-80y/o patient
4) 3 ECG findings
1. ST elevation >2mm chest leads/>1mm limb leads + in 2 consecutive leads
2. Posterior infarct (ST depression V1/2)
3. New onset LBBB
5) Killip Class 3/4 or TIMI score >5 (STEMI) >3 NSTEMI

56
Q

When is primary PCI preferred over fibrinolysis?

A

1) less than 90mins predicted door to balloon time
2) less than 120mins predicted symptom onset to balloon time
3) STEMI diagnosis in doubt
4) hemodynamically unstable (e.g. cardiogenic shock)
5) mechanical problem (e.g. refractory HF)
6) electrical problem (e.g. VT/VF)
7) patient CI fibrinolytic therapy

57
Q

When is fibrinolysis preferred over primary PCI?

A

1) >90mins predicted door to balloon time
2) >120mins predicted symptom onset to balloon time
3) aim fibrinolysis to be done within 3h symptom onset
- benefit plateaus after this time
- by 6h clot becomes organized and fibrinolysis becomes ineffective; PCI becomes preferred again

58
Q

What is the TIMI flow grade?

A

Classification to assess fibrinolytic efficacy (TIMI = thrombolysis in myocardial infarction trial)

Measured at 60-90mins post fibrinolysis
0 –> absence of antegrade flow beyond occlusion
1 –> faint antegrade flow beyond occlusion + incomplete filling of distal territory
2 –> delayed/sluggish antegrade flow + complete filling of distal territory
3 –> normal flow + complete filling of distal territory

59
Q

What is the Killip classification system?

A

Risk stratification system for survival in initial 30d post MI

I –> no clinical heart failure
II –> rhonchi and crackles + elevated JVP + S3
III –> frank APO
IV –> hypotension/cardiogenic shock (SBP less than 90mmHg)

The higher the grade the higher the 30d mortality
Killip class 3/4 is indication for revascularization
60
Q

What is the TIMI risk score?

A

7 Points (AMERICA)

1) Age >65y/o
2) Markers (cardiac) elevated
3) ECG (ST changes >0.5mm in contiguous leads)
4) Risk factors >3 (HT, DM, low HDL, smoking, FHx)
5) Ischemic >2 anginal episodes in last 24h
6) Coronary ischemic heart disease (>50% stenosis)
7) Aspirin use in last 1w

TIMI >5 indication for revascularization in STEMI
TIMI ≥3 indication for revascularization in NSTEMI

61
Q

Distinguish between fibrinolysis followed by PCI vs. facilitated PCI

A

Fibrinolysis followed by PCI aka pharmacoinvasive strategy involves routine PCI done 3-24h post fibrinolytic therapy. Adjunctive PCI done hours after; early elective PCI done days after. Rationale is the presence of persistent flow reduction despite fibrinolysis is a risk for reinfarction.

Facilitated PCI involves PCI done less than 3h post fibrinolytic therapy. Not recommended as there are significant increases in mortality, reinfarction, stroke, and major bleeds. No improvement in survival.

62
Q

List the absolute contraindications for fibrinolytic therapy

A

1) Hx hemorrhagic stroke
2) Ischemic stroke less than 3m ago
3) Known malignant intracranial tumour
4) Known structural cerebrovascular lesion (AVM)
5) Known active internal bleed or bleeding disorder
6) Known pericarditis
7) Suspected aortic dissection

63
Q

List the relative contraindications for fibrinolytic therapy

A

1) BP >180/110
2) Current anticoagulant use
3) Known bleeding disorder
4) In last 2-4w à internal bleed, biopsy, surgery, trauma, non-compressible vascular puncture
5) In last 6m à GI bleed
6) Active PUD
7) Traumatic prolonged >10min CPR
8) DM proliferative retinopathy
9) Prior exposure (>5d) or allergic reaction to streptokinase (only for streptokinase)

64
Q

List the types of fibrinolytic agents used in fibrinolytic therapy for ACS. How are these agents administered?

A

1) Tenecteplase (TNK-tPA) [give w/LMWH]
- single bolus 0.5mg/kg in 10s based on body weight
- 90kg 50mg
- less noncerebral bleed than tPA
- single bolus makes it easier to administer than tPA

2) Alteplase (tPA) [always w/24h IV heparin infusion]
- 15mg bolus then
- 0.75mg/kg (max 50mg) over 30mins then
- 0.5mg/kg (max 35mg) over next 60mins

3) Reteplase (rPA)
- 10 units over 2mins then
- 10 unit bolus at 30mins
- similar to tPA just easier to administer

4) Streptokinase [never w/IV heparin]
- 1.5 million units over 60mins
- inferior outcomes versus others but cheaper
- neutralizing antibodies develop –> impairs repeated use

65
Q

What must be monitored after administration of antifibrinolytics?

A

Monitor for reperfusion response

1) At 90 mins –> resolution of pain
2) At 90mins –> >50% resolve of ST elevation
- check w/serial ECG Q8h 3x
3) Early biomarker peak –> CK-MB peaks 4-8h post reperfusion
- check w/serial biomarkers Q8h 3x
- CK-MB normally peaks at 12h w/out reperfusion
4) Accelerated Idioventricular Rhythm (AIVR) = reperfusion arrhythmia = aka monomorphic slow VT –> HR 60-110bpm
- ventricular rate exceeds sinus rate due to slow sinus rate or SA/AV nodal block

Rescue PCI indicated if patients fail to reperfuse by 90mins post fibrinolytic therapy as evidenced by lack of the changes above or diagnostic angiography.

66
Q

What to avoid after fibrinolytic therapy?

A

Any injections/punctures

67
Q

List the side effects of fibrinolytic therapy

A

1) Allergic reaction/anaphylaxis (treat w/IV chlorpheniramine + hydrocortisone) –> risk of shock
2) Nausea and vomiting
3) Bleeding (1% risk of hemorrhagic stroke)
4) Arrhythmia
5) Emergent CABG
6) Reinfarction (requires rescue PCI)

68
Q

Mx of shock post fibrinolytic therapy

A

Ix and address the underlying cause of shock

1) Allergic reaction/anaphylaxis –> give IV chlorpheniramine + hydrocortisone
2) Bleeding induced hypovolemic shock –> IV fluids
3) Cardiogenic shock –> mechanical or non-mechanical
- mechanical: chordae rupture from acute MR (listen for PSM)
- mechanical: perforated ventricle
- mechanical: hemopericardium
- non-mechanical: reinfarction

1) Inotrope
2) Intra-aortic balloon pump (IABP) –> reduces afterload and increases coronary blood flow
3) Rescue PCI if non-mechanical

69
Q

List the conduction complications of MI

A

Conduction Problems
1) Sinus bradycardia –> 1st: atropine, 2nd: pacing

2) Sinus tachycardia –> Ix underlying cause; beta blockers
3) SVT –> 1st: adenosine, 2nd: verapamil
4) Atrial fibrillation/flutter –> HF: digoxin, not HF: beta blocker OR diltiazem

5) Premature ventricular ectopic (PVC) –> MOST COMMON post MI arrhythmia –> risk of VF
- VF occurs if R on T phenomenon occurs
- IV amiodarone

6) Ventricular tachycardia/fibrillation
- medical cardioversion by: amiodarone, lignocaine, procainamide
- emergent electrical cardioversion if hemodynamically unstable
- can cause sudden cardiac death!!!

7) Heart Block
1st Degree + 2nd Degree Mobitz Type 1 –> medical
2nd Degree Mobitz Type 2 + 3rd Degree –> pace

70
Q

What are the differences in 3rd degree heart block found in inferior MI versus anterior MI?

A

Inferior MI –> RCA –> supplies AV node

  • conservative Mx if there is narrow QRS escape rhythm w/adequate HR
  • this is usually from transient RCA ischemia + increased vagal tone + adenosine release

Anterior MI –> 60% RCA; 40% LAD
- permanent pacing usually as LAD infarction to the extent of 3rd degree heart block indicates extensive infarct

71
Q

List the endocardial complications of MI

A

Endocardial Problems

1) Mitral regurgitation
- from ruptured chordae tendinae
- from ruptured papillary muscles

2) Left Ventricular Mural Thrombus (LVMT)
- common in anterior infarct of left ventricular wall
- LV dyskinesia/akinesia + injury/inflammation to endocardial tissue facilitates thrombus formation

72
Q

List the 4 types of complications in post MI

A

1) Conduction
1. Sinus bradycardia
2. Sinus tachycardia
3. Suprventricular tachycardia (SVT)
4. Atrial fibrillation/flutter (AF)
5. Premature ventricular ectopic (PVC) [most common post MI arrhythmia]
6. Ventricular tachycardia/fibrillation (VT/F)
7. Heart block

2) Endocardial
1. Mitral regurgitation (MR)
2. Left Ventricular Mural Thrombus (LVMT)

3) Myocardial
1. Systolic dysfunction (left/right)
2. Left ventricular aneurysm
3. Ventricular wall rupture

4) Pericardial
1. Post MI Pericarditis/ Dressler Syndrome

73
Q

List the myocardial complications of MI

A

Myocardial Problems

1) Systolic dysfunction (left/right)
2) Left ventricular aneurysm
3) Ventricular wall rupture
- ventricular free wall rupture (VFWR) –> cardiac tamponade
- ventricular septal rupture (VSR) –> VSD

74
Q

List the pericardial complications of MI

A

Pericardial Problems

1) Dressler Syndrome [MUST HAVE LATENT PERIOD IN BETWEEN MI and PERICARDITIS/PERICARDIAL EFFUSION]
- manfiests 2-10w post MI as triad of pleuritic chest pain + fever + pericardial rub
- develops pericardial effusion and sometimes pleural effusion
- ?distinguish from reinfarction by radiation to trapezius
- ECG –> diffuse ST elevation in all leads
- rule out cardiac tamponade by echocardiography
- Ix –> elevated CRP/ESR
- due to inflammation of pericardial tissue overlying infarcted myocardium
- autoimmune component w/myocardiocyte injury stimulating autoantibodies aginst myocardiocytes –> responsive to NSAIDs, steroids, even colchicine
- Mx: rest + aspirin 650mg QDS + NSAIDs ± steroids

75
Q

List the non-pharmacological management on discharge post MI

A

1) Smoking cessation
2) Alcohol abstinence
3) Diet control (low oil, low salt, low sugar, high fibre)
4) Regular exercise (at least 30min/d 5d/w)
5) Educate regarding signs/symptoms of reinfarction and stroke –> seek medical attention
6) Do not exercise or drive till 2 weeks post PCI
7) Do not go on flights or return to work until 2 months post PCI

76
Q

List the pharmacoogical management on discharge post MI

A

Anticoagulants –> stopped on discharge

  • PCI cases –> UFH stopped at end of procedure
  • fibrinolytic therapy –> LMWH at least 48h up to 8d or discharge whichever earlier
  • no revascularization –> LMWH

Antiplatelets –> continued on discharge
- 12m double antiplatelet (80mg aspirin + 75mg clopidogrel) then aspirin indefinitely

Nitrates –> PRN for symptomatic relief; no survival benefit

Beta blockers –> metoprolol, bisoprolol, carvedilol; survival benefit by reducing heart workload and alleviating myocardial ischemia

  • metoprolol 12.5mg daily loading up to 25mg bd
  • carvedilol 3.125mg daily loading up to 50mg bd
  • bisoprolol 1.25mg daily loading up to 10mg bd

ACEI –> captopril, lisinopril, enalapril, ramipril; survival benefit by attenuating cardiac remodeling

  • captopril 6.25mg daily loading up to 50mg tds
  • lisinopril 2.5mg daily loading up to 10mg daily
  • enalapril 2.5mg daily loading up to 20mg bd

HLPD lowering therapy –> statins, niacin, fibrate, ezetimibe; stablizes plaque

  • simvastatin/rosuvastatin 5-40mg daily; atorvastatin/pravastatin 10-80mg daily
  • ezetimibe 10mg daily
  • gemfibrozil 600mg bd (triglyceride lowering)
  • fenofibrate 145mg daily (triclyeride lowering)
  • target LDL ezetimibe –> bile acid sequestrants (cholestyramine 4-24g/d) [bile acid sequestrants reduce fat soluble vitamine absorption!!!]
  • avoid statins + fibrates as risk of rhabdomyolysis
77
Q

Explain the antiplatelet mechanism of clopidogrel

A

1) Clopidogrel itself is a prodrug that requires modification by CYP2C19 to become the active metabolite
2) It irreversibly inhibits the P2Y12 subtype of ADP receptor necessary in platelet activation and cross linking fibrin

78
Q

Outline the rationale for avoiding combined administration of clopidogrel and omeprazole

A

1) Omeprazole is a prominent P450 inhibitor especially of CYP2C19
2) Inhibition of CYP2C19 means clopidogrel is not transformed into its active metabolite
3) This reduces the antiplatelet protection provided by clopidogrel increasing risk of MI

79
Q

What genetic genotype should be considered before administration of clopidogrel?

A

1) Different CYP2C19 genotypes exist some metabolize effectively while others metabolize poorly.
2) CYP2C19 poor metabolizing patients have no antiplatelet benefit from clopidogrel and thus require other antiplatelet medication

80
Q

Outline the major differences in management for NSTEMi compared to STEMI

A

1) Emergent PCI not necessary; early PCI can be done after coronary angiography within 48h post symptom onset
2) Fibrinolytic therapy is contraindicated in NSTEMI as it increases mortality

ALL NSTEMI should undergo early PCI if coronary arteries stenosed as this improves survival

81
Q

Outline the 4 major contributing mechanisms to unstable angina

A

1) Dynamic obstruction e.g. coronary spasm
2) Plaque rupture/erosion w/superimposed non-occlusive thrombus
3) Progressive mechanical obstruction (e.g. rapidly advancing atherosclerosis OR neointimal hyperplasia in stent)
4) Increased myocardial oxygen demand (e.g. anemia, thyrotoxicosis)

82
Q

List the diagnostic criteria for Wellens’ syndrome

A

1) Deeply inverted (Type B) or biphasic T waves (Type A) in V2-3 [may extent to V1-6] indicating critical stenosis of LAD
2) No precordial Q waves
3) Preserved precordial R wave progression
4) Recent Hx angina

83
Q

Explain the progression of T wave changes in Wellens’ syndrome –> applies to all other leads with occlusion, reperfusion, and re-occlusion

A

1) Sudden LAD occlusion causes transient anterior STEMI
2) Patient develops chest pain + diaphoresis
3) Spontaneous LAD reperfusion occurs and chest pain resolves –> ST elevation improves and T waves become biphasic or inverted (identical to those who reperfuse after successful PCI)
4) If artery remains patent T waves evolve from biphasic to deeply inverted
5) If re-occlusion occurs, T wave pseudonormalization is the first sign on ECG where T waves switch from biphasic/inverted to upright and prominent
6) T wave pseudonormalization indicates hyperacute STEMI and is accompanied by recurrence of chest pain

1 - Cardiology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions