MI--STEMI, nonSTEMI, pharm of MI (Johnston) Flashcards
Cardinal symptoms of cardiovascular disease
- Chest pain or discomfort
- Dyspnea, orthopnea, paroxysmal, nocturnal dyspnea, wheezing
- Cough, hemoptysis
- Pain in extremities with exertion (claudication)
ST elevation AMI ECG changes and characteristics of AMI
- ST segment elevation
- “transmural”
- Complete interruption of blood flow (coronary occlusion usually due to thrombus)
Pathobiology of AMI
- Erosion, fissuring or rupture of plaque; thrombus (platelet, fibrin rich thrombus is generated)
- If coronary flow is occluded–STEMI
- If partial occlusion- Unstable angina or NSTEMI
- Most MI caused by atherosclerosis; other causes include vasospasm, vasculitis, dissection, genetics
Typical history of patient with MI
- Chest discomfort (more severe than angina)
- Heavy, pressure, crushing, etc
- Retrosternal, left, across chest; neck, jaw, left arm, epigastrium
- Nausea, vomiting, diaphoresis, dyspnea
- Not reliably relieved by Nitro or rest
- 20% AMI are painless (silent); diabetics elderly woman
Physical Exam findings
- Normal
- S4 gallop–atria contracting forcefully against less compliant, stiff ventricle
- BP variable
Sympathetic hyperactivity (increased HR, increased BP) seen in? Parasympathetic hyperactivity (Bradycardia, decreased BP) seen in?
- Sympathetic=ANTERIOR MI
- Parasympathetic= INFERIOR MI
Heart Failure PE findings
- S3!!!
- Crackles
- Increased JVD
- New murmur
ECG role in MI
-Critical role in stratification, triage, management
STEMI in men vs women
- men: ST elevation of 2mm or more at J point in V2-V3
- women: ST elevation of 1.5 mm or more in absence of LVH or 1 mm or more or in 2 or more contiguous chest or limb leads
Also see what in STEMI ECG?
-New LBBB (obscures ST elevation analysis)
NSTEMI vs Unstable Angina (NSTE ACS) on ECG
-NSTEMI: ST segment depression, T wave inversion
-NSTE ACS: ST segment depression, T wave inversion
so doesn’t help distinguish; key is cardiac enzymes!!
NSTEMI vs Unstable Angina (NSTE ACS) symptoms and cardiac enzymes
- NSTEMI: Chest pain, elevated cardiac enzymes
- NSTE ACS: Chest pain, normal cardiac enzymes
ECG evolution of MI–Early acute phase
- T wave increase amplitude
- Hyper-acute pattern
- Convex upward ST pattern
What are other causes of ST segment elevation?
- Pericarditis–but you will see ST elevation in multiple leads and you won’t see reciprocal depression
- LV aneurysms with J point elevation–ST elevation that does not resolve for weeks–often associated with ANTERIOR WALL infarction
- African Americans have normally elevated ST segments indicating early ventricular depolarizations–this is normal
ECG evolution of MI: Elevated Acute phase–Chronic phase
- Resolution of ST elevation is variable (2 weeks inferior wall; later anterior wall)
- Persistent ST elevation (after 2 weeks) think ventricular aneurysm!!!
QRS complex indicates what? Normal duration? Normal width?
- Ventricular depolarization
- 0.05-0.10 sec duration
- Q waves should not be found more than 0.03 sec in width
Narrow small q waves (1-2 mm) is normal in what leads?
-1, AVL, AVF, V5 and V6
Normal and abnormal morphology of the ST segment
- Observe the level relative to baseline (elevated or depressed) and shape
- Normally ISOELECTRIC
- Sometimes normally elevated not more than 1 mm in standard chest leads
- NEVER normally depressed more than 0.5 mm
ST depression indicates
ST elevation indicates
- depression=Sub endocardial
- ST elevation=sub epicardial or transmural injury or ischemia
T wave is a marker for
ischemia
Normal T wave indicates? Upright in what leads? inverted in which leads? normal morphology/shape?
- indicates ventricular Repolarization
- Upright in 1, 2, V3-V6
- Inverted in AVR
- Variable in 3, AVL, AVF, V1-V2
- Shape: slightly rounded and asymmetrical/height–not greater than 5 mm in standard leads not greater than 10 mm in precordial leads
QT duration reflects
-Ventricular systole!
Ischemia–T wave pattern
-inverted T waves and tall, peaked T waves
Pattern of injury is determined by?
Pattern of necrosis is determined by?
- Pattern of injury determined by ST elevation
- Pattern of necrosis or infarction determined by Q wave or QS complex
In precordial leads V1-V3 what happens to the R wave?
- normally should get larger until it reaches an isoelectric point where positive deflection equals negative deflection
- called transition zone ( between V3 and V4?)
Infarction is? Indicated by what on ECG
- Dead tissue
- Lacks depolarization
- Seen by changes in Q WAVES!
Myocardial injury is? indicated by what on ECG?
- Deficient blood supply
- Inability to fully polarize
- ST segment shifts
Ischemia is? Indicated by what on ECG?
- Deficient blood supply
- Impaired repolarization
- T wave changes!
LAD associated with
- ANterior wall infarction
- Leads V1-V7
RCA associated with
- Inferior wall infarction (RV infarction)
- II, III and AVF
- V3R-V6R
Circumflex artery associated with
Lateral wall
-I, AVL
V5-V6
Posterior descending artery
- Posterior wall infarction
- V1-V3
Indicative vs reciprocal changes
- Indicative changes happens on the side where changes are taking place (example LV)
- Reciprocal changes happens on the opposite side of where change is taking place (RV)
Ischemia changes
- Inversion of T wave due to altered repolarization
- reciprocal changes on opposite side (upright T waves)
- Muscle injury causes elevation of ST segment; on opposite side see ST depression
- Death (infarction) of muscle causes Q or QS waves due to absence of depolarization current from dead tissue and opposite currents from other parts of heart
During recovery from ischemia (subacute and chronic stages)–what ECG changes are seen?
-S-T segment often is first to return normal, then T wave, due to disappearance of zones of injury and ischemia
Typically the q wave/ qs complex should not be greater than
1/3 of the whole qrs complex
-if its greater, its pathological
Chronic ischemia (from Old MI) indicated by
-DEEP QS complexes
Onset and first several hours of transmural infarction
- Subendocardial injury and myocardial ischemia
- No cell death yet
- R wave is normal or nearly normal
- Peaked T wave
- ST segment elevated
First day after transmural infarction
- Ischemia and injury extend to epicardial surface; subendocardial muscle dying in area of most severe injury
- R wave amplitude diminishing
- ST elevation more marked
First and second days of transmural infarction
- Transmural infarction nearly complete
- Some ischemia and injury may be present at borders
- R wave gone or nearly gone
- Significant Q wave
- ST elevation may decrease
- T wave inversion beginning
After 2-3 days of transmural infarction
- Transmural infarction complete
- No R wave
- Marked Q wave
- ST may be at baseline
- Deep T wave inversion
After several weeks or months of transmural infarction
- Infarcted tissue replaced by fibrous scar, sometimes bulging (ventricular aneurysm)
- Some R wave may return
- Significant Q wave usually persists
- T wave often less inverted
- ST elevation may persist if aneurysm develops
With inferior infarction (leads II, III, AVF) you see reciprocal changes in which leads?
- Laterally
- I, AVL
Tall, broad, peaked T waves in precordial leads indicates
- ischemic pattern
- Most likely LAD (V1-V6)
- Marker for person ready to have STEMI
- Anterior wall infarction
Lost r wave voltage, and Large QS voltage and inverted T waves
-Progression into myocardial necrosis
Persistent ST segment elevation after weeks after having MI think_____
-ventricular aneurysm
Posterior wall infarction
- IF we know posterior wall is infarcted inscribing a q wave in that area, the reciprocal change of a q wave (which is down) will be a positive strong R wave (which will be up) and see these in V1 and V2
- Reciprocal changes of ST segments that shows current of injury posteriorly, we would see anteriorly as ST segment depression
- must really have index of suspicion for posterior wall infarction
To diagnose posterior wall infarction, need to look at what leads?
- V1 and V2 and look for reciprocal changes
- Since no leads reflect posterior electrical faces, changes are reciprocal of those in anterior leads
- V1 shows unusually large R wave (reciprocal of posterior Q wave) and upright T wave (reciprocal of posterior T wave inversion)
First few hours after SUBendocardial infarction (NONSTEMI)
- subendocaridal muscle ischemic and injured but not dead
- ST depressed or elevated
- T wave inversion
Lab findings associated with MI
- Increased WBC
- Increased CRP
- BNP is increased in ventricular wall stress and fluid overload
Cardiac biomarkers of necrosis–when detected and when peak?
- Troponin I (cTnI) or T(cTnT)
- 1-4 hours detectable after onset AMI
- 10-24 hours peak
- Persist 5-14 days
What can cause false positive cTnT?
-Renal failure
What are non-myocardial infarction causes and elevated troponin levels? Heart causes:
- Myocardial injury: cardiac contusion, surgery, ablation, shocks
- Myocardial inflammation: myocarditis, pericarditis
- Heart failure
- Cardiomyopathies: infiltrative, stress, hypertensive, hypertrophic
- Aortic dissection
- Severe aortic stenosis
- Tachycardia
elevated troponin levels–pulmonary causes
- Pulmonary Embolism
- Pulmonary hypertension
- Respiratory failure
Neurologic causes of elevated troponin levels
Other causes
- Stroke
- Intracranial hemorrhage
-Other causes: shock (septic, hypovolemic, cardiogeninc), Renal failure
Majority of deaths from AMI happen when and how?
- occur within 1 hour of onset of symptoms
- Most deaths related to V. Fib
- Greatest time lag to repercussion therapy is patients delay in calling for help
E.D standard of care–STEMI
- 12 lead ECG with continuous cardiac monitoring
- IV lines inserted
- Cardiac enzymes (cTnI), CBC, CMP, PT, PTT
Repercussion strategy choices
- Primary percutaneous coronary intervention with angioplasty and stunting
- Cath lab within 90 minutes (goal)
- Fibrinolysis: fibrinolytic or thrombolytic
- Begun in ED within 30 min
Dangers of fibrinolytic agents
-Bleeding
Reperfusion therapy
- Accelerates changes over minutes to hours
- Failure of ST elevation to resolve by >50-70% within 1-2 hours, suggests failure of fibrinolysis
- If hospital doesn’t have cath lab (non PCI capable), transfer within 120 min
Primary PCI preferred for
- STEMI with symptoms <12 hours
- Lower mortality and ICH (intracerebral hemorrhage)
Fibrinolytic therapy useful for
- Useful for STEM or new left BBB within 12 hours of onset of symptoms
- Major risk is ICH (0.5-1.0%)
Absolute contraindication for fibrinolytic therapy
- Active bleeding or bleeding diathesis (menses EXcluded)
- Prior hemorrhagic stroke, ischemic stroke within 3 months, except acute ischemic stroke within 3-4.5 hours
- Intracranial or spinal cord neoplasm or AV malformation
- Suspected or known aortic dissection
- Closed head or facial trauma within 3 months
Initial medical management STEMI
-ASA (162-325mg) po–given on presentation unless contraindicated
IV heparin or exoxaparin
- Adenosine diphosphate receptor (p2Y12) inhibitor
- Antiplatelet agent (clopidogrel prasugrel or ticagrelor)
- Use for 1 year after PC1 for STEMI with stenting to prevent stent stenosis
Treatment for STEMI–meds and uses
- Nitro: relieve vasoconstriction, relieve pain, reduce pre and after load
- Morphine: persistent pain
- Beta blocker: esp if BP increase or HR increases; DONT use in decompensated HF, decreased HR, decreased BP or MCO2
- Oxygen
- Stool softener
- ACEI helpful in EF is reduced, increased BP; prevent remodeling statin
- Coronary ICU–AHA diet
Beta blocker contraindicated in which kind of heart block?
-greater than 1st degree
Complications of MI and treatment
- Recurrent chest pain after MI
- Acute pericarditis–2 to 4 days post MI
- 2-10 weeks after MI could be Dressler syndrome (immune mediated)–hurts to breathe, feels better learning forward
- Tx: ASA and NSAID
rhythm disturbances associated with MI
-Ventricular: occur early–
-VF (3-5% in 1st 4 hours)–Tx is elective cardioversion
-VT
-VT (polymorphic VT)—some are going up and some down on ECG bc coming from different foci
VF
-Afib– 5-10% in 1st 24 hrs
-Sinus bradycardia–inferior MI
-2nd degree AV block (Wenkebach)–inferior MI
Accelerated idioventricular rhythm (AIVR)–rate and see when?
- Show VT (60-100 BPM)
- After fibrinolytic therapy
- Benign
Leading cause of in hospital death from AMI
-Heart failure
Heart failure PE findings
- LV dysfunction–S3 and S4, crackles
- RV infarction–10-15% of inferior STEMI–decreased BP, clear lungs, increased JVP, Kussmaul sign, treat with IV fluids
- Cardiogenic shock–decreased BP, decreased CI
- Increased PCWP>18 mm Hq
- Mortality 70-80
Mechanical complications associated with MI
- Acute mitral valve regurg–infarction related rupture or dysfunction of papillary muscle
- New holosystolic murmur associated with inferior wall MI
- Rx=surgery
Septal rupture with VSD associated with
- ANterior wall infarction
- LV free wall rupture causes tamponade
LV aneurysm associated with Anterior MI
-Rx=surgery
Thromboembolic complications with AMI
- Arterial emboli from LV aneurysm
- Cause stroke, ischemic bowel
RV infarction
- Proximal occlusion of RCa before acute marginal branch; can cause acute inferior wall MI in 30% of cases
- Use R precordial chest leads
- ST elevation or 1mm or more in V40V6
- Pericarditis, myocarditis, stress induced (takotsubo) syndrome, early depolarization
Differential diagnosis of a STEMI
- Pericarditis
- Myocarditis
- Stress induced (takotsubo) syndrome–broken heart syndrome
- Early repolarization
Uses for echocardiogram
- Global and RWM abnormalities
- Murmur
- Papillary muscle dysfunction
- VSD
- LV free wall rupture
- LV aneurysm
- Mural thrombosis
