Acute Coronary Syndrome II Flashcards
ACS Demographics & Statistics
- Middle age: men > women
- Elderly: men = women
- 1/2 of patients who die w/ AMI do so due to sudden death before they reach the hospital
- Up to 10% of survivors die in the year after hte MI
Unstable Angina Pectoris
- Symptoms of MI or impending MI
- Physical exam
- Symptoms of MI or impending MI
- New onset of chest discomfort suggestive of MI occuring at rest or w/ ordinary activities
- Angina changes
- –> more frequent, severe, prolonged, or difficult to relieve w/ rest or nitroglycerin
- Occurs at rest for the first time
- Chest discomfort suggestive of MI in a pt w/ coronary heart disease that’s unrelieved by rest or nitroglycerin
- Physical exam
- Less valuable in ACS than history & ECG
- S4 sometimes present form stiff LV
- If S3 is present, indicates LV dysfunction
- Short systolic murmurs may suggest MR from ischemic papipllary muscle dysfunction
ECG
- Places pt into 1 of 2 categories
- Transmural injury
- Subendocardial injury/ischemia
- Infarction patterns
- Leads
- “Strictly” / “True” posterior wall
- Silent MI
- Caution
- Places pt into 1 of 2 categories
- ST elevation MI (STEMI)
- Unstable angina pectoris (UA) / Non-ST elevation MI (NSTEMI)
- Transmural injury
- ST elevation + injury pattern
- J-point elevation w/ an ST segment that’s lost its normal concave upward appearance & has a straight or concave downwards appearance
- Subendocardial injury/ischemia
- ST segment depression or T wave inversion or both
- Infarction patterns
- Pathological Q wave / QS complex (old = prior infarction)
- Likely to develop after ST elevation
- Leads
- V1-V5: anterior wall
- V1-V4: anteroseptum
- V3-V6: anterolateral
- V3 &/or V4: apex
- I, aVL, & V6: lateral wall
- II, III, & aVF: inferior wall
- “Strictly” / “True” posterior wall
- Inferred in the presence of deep ST depression in leads V1 & V2
- Silent MI
- Not associated w/ classical symptoms
- > 25% of Q-wave infarctions
- In pts at risk for coronary heart disease, presentation w/ pulmonary edema or stroke should be considered as due to AMI
- Caution
- ECG is near normal in some cases early in the event
- Esp when the circumflex coronary artery is the “culprit”
- In pts w/ ongoing symptoms, ST depression, & T wave changes in lateral leads: NSTEMI may mask an STEMI
- ECG is near normal in some cases early in the event
Cardiac Biomarker Measurements for Myocardial Necrosis
- Cardiac markers
- Cardiac troponins I (inhibitory) & T (tropomyosin-binding)
- CK & CK-MB (its subunit)
- Using cardiac markers
- Cardiac markers
- Measrued in the peripheral blood to document MI & determine infarct size
- Cardiac troponins I (inhibitory) & T (tropomyosin-binding)
- Appear in the bloodstream 8 hours after MI, peak at 24 hours, & gradually decline over a week
- Highly sensitive & specific for myocardial necrosis
- Useful for detecting MI in patients who present early & late
- Caution: MI damage from any cause –> troponin elevation, so doesn’t diagnosis ACS
- CK & CK-MB (its subunit)
- CK naturally occurs in 3 forms
- MM: skeletal muscle (100%) & cardiac muscle (80-85%)
- BB: CNS (100%)
- MB: cardiac muscle (15-20%), presence in serum –> AMI
- Appear in bloodstream 8 hours after MI, peak in 24-48 hours, return to normal in 3-5 days
- Diagnosis of MI w/ CK requires elevated CK/CK-MB w/ characteristic peaking pattern
- CK naturally occurs in 3 forms
- Using cardiac markers
- Toponin I or T: measure at admission, 8-12 hours later, & 24 hours later
- Most reasonable & cost-effective
- CK & CK-MB: measure every 8 hours for > 3 samples until (trending values) until peak CK is established
- Reserved for pts w/ suspected recurrent MI w/ known troponin elevation
- Negative troponin or CK in first 6-8 hours doesn’t rule out MI
- Toponin I or T: measure at admission, 8-12 hours later, & 24 hours later
General Pathophysiologic, Diagnostic, & Therapeutic Considerations
- Evaluation & ECG monitoring
- IV access
- Oxygen therapy
- Pain relief
- Evaluation & ECG monitoring
- Immediate ECG monitoring
- High incidence of life-threatening rate & rhythm disorders in early ACS
- Chest pain –> ECG interpretation within 10 mins
- Determines ACS &, if so, ST elevation vs. depression &/or T wave abnormalities
- Immediate ECG monitoring
- IV access
- Facilitates immediate pharmacological therapy
- Oxygen therapy
- For all MI pts until normal oxygen saturation is documented
- Hypoxia w/ AMI is common & caused by ventilation-perfusion abnormalities & LV failure
- Pain relief
- High priority b/c ongoing pain can worsen ischemia & necrosis
- (1) Sublingual nitroglycerin (unless contraindicated) b/c difficult to distinguish ischemia from infarction
- (2) Opiate analgesics if chest pain & ECG abnormalities don’t resolve w/ 3 nitroglycerin administrations
Assessing Risk w/ ACS: Determinants of Mortality
- Determinants of mortality following AMI
- Why mortality risk is important
- Intermediate/high risk category
- Includes…
- Intervention
- Intermediate
- High
- Both
- Determinants of mortality following AMI
- LV size & function
- Hemodynamic status (HR, BP, CHF, CVP, PCW/PA diastolic pressure, CO)
- Size of infarct
- Gender (women worse)
- Age (older worse)
- Ventricular rhythm disorders
- Spontaneous or provoked (stress-test) ischemia
- Why mortality risk is important
- Place UA/NSTEMI pts in low, intermediate, or high risk categories to dermine need for early coronary arteriography & coronray revascularization therapy
- Higher risk –> greater benefit of interventions
- Continue risk eval for > 24 hours after admission b/c low risk can –> high risk
- Intermediate/high risk category
- Includes…
- CAD
- Unstable angina
- Ongoing chest discomfort
- New or dynamic ST changes or T wave changes
- Positive biomarkers for MI
- Hemodynamic instability
- Ventricular rhythm abnormalities (“electrical instability”)
- Intervention
- Intermediate: admission to hospital in a step-down monitored unit
- High: admission to coronary intensive care unit
- Both: strong consideration for early (24-48 hours) but not emergency coronary arteriography
- Includes…
Ventricular Tachyarrhythmias: Early VT, VF, & Sudden Cardiac Death (First 2 Days)
- AMI associated w/…
- VT abnormalities
- Likelihood of these abnormalities
- Prognosis w/ VT or VFib in the first two days of MI
- AMI associated w/…
- Increased incidence of VT
- Decreased threshold for VFib
- Most common causes of SCD in 1st day of ACS
- VT abnormalities
- “Warning” premature ventricular complexes (PVCs) –> higher risk for VFib
- Frequent, coupled, multiform, or falling on the T wave of the proceeding complex (“R on T phenomenon”)
- “Primary” VFib w/o warning PVCs
- (Non)-Sustained VT
- Esp polymorphic VT w/o torsades de pointes
- VFib due to deterioration from VT
- “Warning” premature ventricular complexes (PVCs) –> higher risk for VFib
- Likelihood of these abnormalities
- Highest risk in the first minutes after AMI onset
- Increased risk for ventricular rhythm disorders persists for 24-48 hours & can return w/ recurrent MI
- Prognosis w/ VT or VFib in the first two days of MI
- Doesn’t worsen long term prognosis as long as the rhythm disorders are promptly reversed w/ antiarrhythmic therapy for 6-24 hours –> watchful waiting
Ventricular Tachyarrhythmias: Later VT & VF (After First 2 Days)
- Prognosis of VFib or sustained VT after first 2 days
- Scar VT
- Important differentiations in late VT following MI
- Antiarrhythmic therapy
- Pts after MI that have a better outcome if treated w/ an ICD
- Prognosis of VFib or sustained VT after first 2 days
- Substantially worsens long term prognosis
- Scar VT
- Life-threatening ventricualr rhythm disorder that MI survivors are at risk for
- Monomorphic VT due to micro-reentrant circuits in the LV
- Develop b/n infarcted & viable myocardium
- Most common after large, anterior wall MIs w/ LVEF < 40%
- Can deteriorate to VF
- Account for many SCDs in MI survivors
- Important differentiations in late VT following MI
- Polymorphic VT: indicates ongoing ischemia, non-torsade
- Monomorphic VT: indicates development of a reentrant “scar” VT
- Antiarrhythmic therapy
- Not helpful, can be harmful
- Pts after MI that have a better outcome if treated w/ an ICD
- Most benefit: sustained monomorphic VT + poor LV contraction
- Moderate benefit: non-sustained monomorphic VT + inducible VT + LVEF < 35%
- Least benefit: LVEF < 35% + full recovery from MI (> 2-3 months)
Accelerated Idioventricular Rhythm (AIVR)
- Commonly seen soon after MI
- May be a “reperfusion” arrhythmia
- Rate = 50-120 bpm
- AIVR stpos immediately when sinus rhythm exceeds its rate
- Rarely deteriorates to VT
Sinus Bradyarrhythmias
- Frequency
- Neurocardiac reflex
- Effect on AMI
- Treatment options
- Frequent following MI (esp of posterior & inferior walls)
- Usually due to neurocardiac reflex
- State of predominantly parasympathetic tone
- Short-lived phenomenon (few hours to a day)
- Simulation of mechano-receptors in the infero-posterior wall –> decrease sympathetic tone –> parasympathetic predominance
- Mixed effect on AMI
- Decrease CO
- Increase likelihood of serious ventricular rhythm disorders
- Decreases myocardial oxygen demand –> protects jeopardized myocardium
- Rarely warrants therapy (only when associated w/ hemodynamic consequences)
- Treatment options
- Atropine
- Temporary pacer if atropine fails
Bradyarrhythmias Associated w/ AV & Intraventricular Conduction Delays:
Block at the Level of the AV Node (Supra-Hisian)
- Frequency
- Cause
- Duration
- Heart block
- QRS
- Hemodynamic compromise
- Therapy
- Most common w/ inferior & posterior MIs
- Usually due to the neurocardiac reflex
- Usually short-lived (few hours to a day)
- Heart block
- 2nd degree block is usually Mobitz Type I
- 3rd degree (complete) block
- Often preceeded by 1st or 2nd degree (Motibtz type I) block
- Often not associated w/ hemodynamic compromise
- Normal QRS
- Hemodynamic compromise is usually HR related
- Therapy
- No hemodynamic compromise: not required
- Hemodynamic compromise or persistunacceptable bradycardia: temporary pacing
Bradyarrhythmias Associated w/ AV & Intraventricular Conduction Delays:
Block Below the AV Node (Infra-Hisian, within the His-Purkinje System)
- Heart block
- Hemodynamic compromise
- Heart block
- Block is usually associated w/ a large anterior infarction
- Frequently associated w/ a prolonged QRS &/or BBB/fasicular block
- 2nd degree block is usually Mobitz type II
- 3rd degree (complete) block may occur precipitously w/o warning w/ lesser degree block
- Severe hemodynamic compromise is almost always associated w/ complete heart block
Bradyarrhythmias Associated w/ AV & Intraventricular Conduction Delays
- 2nd degree heart block, Mobitz type II &/or trifasicular block within the His-Purkinje system
- Associated w/ AMI
- Frequent harbinger of 3rd degree heart block
- ECG evidence
- 2nd degree heart block, Mobitz type II
- RBB or LBBB + 1st degree AV block
- RBBB + left anterior or posterior fasicular block
- Alternating BBB
- Treatment
- Temporary ventricular pacer
Sinus Tachycardia
- If complicates AMI, usually has an underlying cause
- Pain, anxiety, low CO, anemai, hypovolemia, infection, etc.
- Cause –> proper therapy
Atrial Tachyarrhythmias
- Types
- Cause
- Mortality
- Therapy
- Types: AFib, atrial flutter, & supraventricular tachycardia
- Usually due to larger infarcts & increased atrial pressure (not atrial damage)
- Associated w/ higher mortality w/ MI due to abnormal rhythm
- Therapy
- Type III antiarrhythmic for 6-12 weeks (period of greatest recurrence risk)
- Conventional therapies for rate control & anti-thrombin therapy to prevent stroke & thromboembolism (for AFib & atrial flutter)