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

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 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

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 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

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 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 \ _ 2-3 months)

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

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)

Acute Coronary Syndrome II Flashcards by Heather Acuff

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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
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

How well did you know this?

Not at all

Perfectly

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
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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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
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

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Sinus Tachycardia

If complicates AMI, usually has an underlying cause
- Pain, anxiety, low CO, anemai, hypovolemia, infection, etc.
Cause –> proper therapy

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

Systolic LV Dysfunction

Important in pts w/ AMI
Most easily measured variables
Myocyte loss

Important in pts w/ AMI
- Size of infarct & ischemia
- Resulting effects on regional & global systolic LV performance
Most easily measured variables
- Global & segmental systolic LV performance (assessed by cardiac imaging)
- Forward CO
Myocyte loss
- More myocytes lost –> more prfound global LV systolic dysfunction –> larger infarct –> more likely HF & cardiogenic shock

“Stunned Myocardium” w/ ACS

LV dysfunction can be reversed if blood flow is restored promptly
- Brief MI form a short coronary occlusion –> prompt abnormality resolution
Repetitive or prolonged ischemia (UA, MI)
- Ischemic areas may require days to weeks to recover
- Tissue often seen within an infarct zone & at the margin of the infarct zone
- This tissue = “stunned myocardium”

Diastolic LV Dysfunction

Frequency
Testing
PV curves
Chief cause of…
Cardiac relaxation

Frequent during MI (esp in pts w/ LVH &/or DM) due to a stiff LV
Testing is inferoir to testing for systolic dysfunction
PV curves are shifted so LVEDP, LA pressures, & pulmonary venous pressures are elevated
Chief cause of pulmonary edema w/ AMI when systolic funciton is normal
Cardiac relaxation
- Energy requiring
- Affected as quickly as contraction
- Impaired relaxation adds to problems from underlying stiff LV

Therapy of HF & Optimizing Volume Status

All
Mild HF
Severe cases
Pulmonary edema
BP
- Normal or hypertensive
- Hypotensive
Severe HF or hypotension requiring inotropic agents

All: continuous positive pressure administration
Mild HF: conventional diuretic therapy
Severe cases: endotracheal intubation & assisted ventilation
Pulmonary edema: prompt & vigorous diuretics, IV morphine
BP
- Normal or hypertensive: nitroglycerin reduces preload & afterload
- Hypotensive: IV inotropic &/or pressor agents for diuresis w/o compromising arterial BP or CO
Severe HF or hypotension requiring inotropic agents
- Manage volume status w/ indwelling pulmonary artery cathether
- Slightly elevated pulmonary capillary wedge pressure: target value range that optimizes CO & minimizes pulmonary edema risk

Mechanical Complications: Typical Cardiogenic Shock

When typical cardiogenic shock may complicate AMI
Features
Therapy
When to consider early coronary revascularization

When typical cardiogenic shock may complicate AMI
- When >35-40% of LV myocardium has been damaged by AMI or cumulatively from a current + previous MIs
Features
- Severe hypotension
- Elevated LV filling pressure
- Reduced CO
  - Clinical signs: oliguria/anuria, mental obtundation, cold clammy extremities, pallor, sweating, tachycardia
Therapy
- Optomize volume status
- Inotropic & vasopressor agents
- LV assistance device
- Goal of MAP = 60 mmHG & CI = 2.5
When to consider early coronary revascularization
- Large amoutn of stunned but not necrotic myocardium
- Correctable abnromality like acute MR, acute VSD, or a LV

Mechanical Complications: Shock Associated w/ Major RV Involvement in Inferoposterior MI

Acute inferoposterior MI: RV vs. LV
Acute inferoposterior MI
- Occlusion
- Clinical importance
- RV SV
- Electrocardiography
- Echo
- Right-heart cath
- Recovery
- Death rates
Therapy

Acute inferoposterior MI: RV vs. LV
- Thin, low pressure RV is mroe resilient to diminished blood flow than RV
- But RV ischemia, infarction, & stunning can contribute to acute inferoposterior MI
Acute inferoposterior MI
- Occlusion of the proximal right coronray artery prior to its acute marginal branch (major artery to the RV)
- Uncommon clinically important involvement
- Inadequate RV SV –> imapired LV filling –> decreased LV SV & BP
- Right-sided electrocardiography detects RV injury
  - ST elevation compatible w/ a current of injury in V1-V6
- Echo determines RV size & contraction
- Right-heart (Swan-Ganz) cath shows depressed CO & elevated RA pressure
- Most cases have nearly full recovery of RV contraction in ~3 days
- Death rates up to 50%
Therapy
- Fluid administration –> slightly elevate left sided filling pressures
  - Don’t elevate RA (central venous) pressure b/c an overly distended RV can impinge on the LV & decrease LV SV
- Positive inotropic agents to return RV function to normal
- Avoid vasodilator therapy (nitrates & ACE-Is or ARBs) & beta blockers until RV contraction has improved

Mechanical Complications: Shock Associated w/ Rupture of the Papillary Muscles or the Interventricular Septum

Papillary muscle involvement
Interventricular septum involvement
Both conditions
Therapy
- First line
- If BP allows it
- Surgical candidates

~10% of myocardial rupture cases involve papillary muscles
- Immediate acute MR
~10% of myocardial rupture cases involve the interventricular septum
- Immediate VSD w/ left to right shunt
Both MR & VSD –> HF –> murmur & cardiogenic shock
- Echo or right heart cath –> prompt differentiation b/n these murmurs
Therapy
- First line: LV assistance w/ inotropic agents & vasopressors
- If BP allows it: ACE-Is, ARBs, or nitrates + hydralazine for LV unloading
- Surgical candidates: early (<24 hours) coronary bypass surgery
  - Prognosis: poorer for VSD than MR, better than w/o surgery

Mechanical Complications: Free Wall Rupture of the LV

Frequency
Risk factors
Casue
Features
Sub-acute rupture (“pseudo-aneurysm in evolution”)

~90% of myocardial ruptures are of the free wall
Risk factors: elderly, women, HTN
Cause: dissection through the myocardium at the junciton of infarcted & normal myocardium
Features: hemopericardium –> pericardial tamponade –> death within minutes
Sub-acute rupture (“pseudo-aneurysm in evolution”): rare
- Clot, fibrous tissue, & surrounding structures provid ethe “walls” for the pseudoaneurysm
- Eventual rupture of a pseudoaneurysm occurs w/o surgery

Mechanical Complications: “Atypical” Shock Patterns that must be Distinguished from More Serious Cases

Atypical Cardiogenic Shock due to the Neurocardiac Reflex
- Mechanism
- Associations
- Therapy
Atypical Cardiogenic Shock due to Hypovolemia
- Mechanism
- Associations
- Therapy

Atypical Cardiogenic Shock due to the Neurocardiac Reflex
- Neurocardiac reflex –> transietn (few hours to a day) peripheral vascular dilation –> acute inferior & posterior wall MI
- Pattern of hypotension is associated w/ normal or low right- & left-sided ventricular filling pressures
  - Absence of findings indicates low CO & pulmonary edema
- Therapy
  - Vasoconstriction w/ dopamine, phenylephrine, or NE until systemic vascular resistance returns to normal
Atypical Cardiogenic Shock due to Hypovolemia
- MI –> volume depletion –> LV deteriorates w/ under-filling –> atypical cardiogenic shock
- Usually associated w/…
  - Normal or low right- & left-sided filling pressures
  - Little to no pulmonary edema
  - Decreased CO
  - Increased systemic vascular resistance
- Therapy
  - Volume support until hemodynamic state improves
  - Voluem repletion until pulmonary capillayr wedge pressure is normal

Mechanical Complications: LV Aneurysm & Thrombus * LV aneurysm * LV thrombus

* LV aneurysm * LV anuerysm formation & LV dilation occur in 12-15% of MIs * Almost always a STEMI (90% are anterior or apical) * True aneurysms never rupture * Cause problems by soaking up contractile energy & contributing to HF * Early aneurysms are associated w/ LV thrombus & thromboemoblism * Via stagnant blood flow within the aneurysm & inflamed myocardium * LV thrombus * Complicates the healing in 30% of acute evolving Q wave MIs involving the atnerior wall &/or apex * Main risk: thromboembolism & stroke * Time of risk: greatest in first few days, subsides over next 3 months

Emergency Reperfusion Therapy * STEMI * UA/NSTEMI

* STEMI * All patients within 12 hours of STEMi onset should be considered * Percutaneous coronary interventions w/ angiopasty & stenting --\> protective effect superior to IV thrombolytic therapy * Esp in pts at high risk for adverse outcomes * Fewer side effects (ex. intracranial hemorrhage) except for other bleeding (ex. at the cath site) * Alternate approaches * IV thrombolytic therapy if door-to-dilation time \> 100 minutes * Primray angioplasty if pts present \> 3 hours post-MI * UA/NSTEMI * Not beneficial b/c these pts don't have persistent total occlusion of a coronary artery * Similarly not beneficial for emergency primary angioplasty therapy

Routine Early (within 48 hours) Revascularization Therapy for Patients w/ UA/NSTEMI * High risk UA/NSTEMI * Low risk UA/NSTEMI

* High risk UA/NSTEMI * Pts treated w/ conventional therapy (anti-thrombin, anti-platelet) followed by routine cath & revascularization * --\> improved outcome compared to non-interventional therapy * Low risk UA/NSTEMI * Did not benefit from this strategy * Treat w/ non-invasve initial approach & watch for development of high-risk features & postivie findings on stress test before --\> coronary arteriography

Beta Adrenergic Blocking Agents * Beta blockers for survivors of MI (begun weeks to months post-MI) * Early beta blocker IV therapy followed by long term oral therapy post-MI * Beta blockers w/ intrinsic sympathomimetic activity (ISA) * Carvedilol in post-MI pts w/ LV dysfunciton (LVEF \< 40%) * Contraindications

* Beta blockers for survivors of MI (begun weeks to months post-MI) * --\> moderate reduction in recurrent MI & cardiac death * Early beta blocker IV therapy followed by long term oral therapy post-MI * --\> small additional reduction in in-hospital mortality * Beta blockers w/ intrinsic sympathomimetic activity (ISA) * --\> little to no protective effect following MI --\> avoid * Carvedilol in post-MI pts w/ LV dysfunciton (LVEF \< 40%) * --\> superior results compared to metoprolol * Contraindications * Severe HF * Cardiogenic shock * Severe bronchospasm * 2nd & 3rd degree AV block Bradycardia * HoTN

Nitrates & Calcium Channel Blockers * Nitrate use * Calcium channel blocker use * General * Strongly vasodilating dihydropyridines * HR-limiting & negatively inotropic verapamil & diltiazem

* Nitrate use * Standard anti-ischemic doses as long as needed for active ongoing ischemia * Gradually remove or continue as needed as therapy for chornic MI * Calcium channel blocker use * Therapy to prevent ischemia * Strongly vasodilating dihydropyridines * Adjunctive tehrapy w/ beta blockers (otherwise harmful) * HR-limiting & negatively inotropic verapamil & diltiazem * Replacement for beta blockers in pts who don't tolerate beta blockers & who have good LV function (LVEF \< 40% --\> worse outcome)

ACE-I or ARB Therapy * ACE-Is in high risk pts * ACE-Is in low risk pts post-MI * ARBs * Current guidelines * General * High risk pts * Low risk pts

* ACE-Is in high risk pts * Pts: large infarctions, poor LV contraciton, &/or persistent HF * --\> moderate benefits on limiting HF endpoints & cardoivascular death * --\> moderate reduction in recurrent coronary events * ACE-Is in low risk pts post-MI * --\> small benefit * ARBs * Equivalent to ACE-Is in post-MI pts w/ LV dysfunction or CHF * Current guidelines * Give ACE-Is or ARBs to all pts after ACS * High risk pts w/ large MI, poor LV, or HF: start therapy asap following acute reperfusion therapy & recovery of hemodynamic stability * Low risk pts: start therapy asap prior to discharge

Angiotensin Blocking Therapy * Addition of angiotensin blocking therapy to ACEIs in pts w/ large infarctions, LV dysfunction or DM * Limited to pts w/... * Therapy begins...

* Addition of angiotensin blocking therapy to ACEIs in pts w/ large infarctions, LV dysfunction or DM * --\> additional small protective effect to ACE-Is alone * Limited to pts w/... * Minimal or no renal failure * No hyperkalemia * Therapy begins... * Following establishment of ideal dose of an ACE-I or ARB * Often delayed until outpatient setting

"Plaque Stabilization" w/ Lipid-Lowering Therapy * Cholesterol-lowering therapy * LDL-cholesterol lowering therapy * Effect on preventing coronary syndromes due to... * Guidelines

* Cholesterol-lowering therapy * Prevents progression of atheroslcerosis * Moderate reduction in ACS 7 cardiac death * LDL-cholesterol lowering therapy * Improved survival & fewer ACS * Esp w/ earlier & more aggressive statins * Effect on preventing coronary syndromes due to... * Re-stabilization of coronray plaques (decreased cholesterol content in the plaque & anti-inflammatory actions) * Prevention of endothelial dysfunction --\> decreased risk of future plaque destabliziation & recurrent ACS * Guidelines * All pts w/ ACS & w/o contraindications should be treated asap w/ statins * Pts needing additional agents: elevated triglycerides, elevated VLDL, low HDL