269 STEMI Flashcards
Classification of Myocardial infarction. Troponin I positive. Post 2 vessel stentt
Tupe 4A: PCI
Type 4B: Stent Thrombosis
Type 5: CABG
Not associated with CAD A. Age B. Inflammation C. Systemic huper D. Metabolic syndrome
Age
OASIS 7. Superior to placebo in STEMI not receiving reperfusion therapy
Fondaparinux
Less common presentations of STEMI
Loss of consciousness Confusional state Sensation of profound weakbess Appearance of arrhythmia Evidence of peripheral embolism Unexplained drop in arterial pressure Breathlessness
Pain in STEMI typically radiates in what areas but never in what area?
Pain may radiate to occipital area but not below umbilicus and the trapezius
Temporal stages in STEMI
Acute: hours to days
Healing: 7-28 days
Healed: more than 29 days
*Pathologic change in myocardial infarction 24 hours from onset
band necrosis
*still to find actual page in Harrison
CK rises within and returns to normal by?
CK rises in 4 to 8 hours and returns to normal by 48 to 72 hours
Cardiac Troponin remains elevated for how long after STEMI
7 to 10 days
Universally present in STEMI on cardiac imaging
Abnormalities in wall motion
ECG findings candidate for reperfusion
ST segment elevation at least 2 mm in two contiguous precordial leads and 1 mm in two adjacent limb leads
Time from FMC to device time in PCI capable hospital
less than 90 minutes
Door in Door out time from non PCI capable hospital
less than 30 minutes
FMC to device time in non PCI capable hospital
less than 120 minutes
When to administer fibrinolysis when anticipated FMC to device is long
within 30 minutes of arrival
Reason why glucocorticoids and NSAIDS not given to STEMI patients
They can impair infarct healing and increase risk of myocardial rupture
Treatment of choice of ventricular tachycardia if heart failure is present
Digoxin
Cause of LV wall rupture
*Few hours from myocardial infarction
When goes LV aneurysm occur in patients with STEMI
Weeks to months after STEMI
Dykinesia or local expansile paradoxical wall motion; composed of scar tissue; most common location
ventricular aneurysm; apical aneurysm is most common
Class 1 A recommendation for …
Sustained Vtach
Recurrent chest pain
*from exam; still to find actual Harrison page
Pivotal diagnostic and Triage tool because it is at the center of the decision pathway for management
12 Lead ECG
Stages of STEMI
Acute few hours to 7 days
Healing 7- 28 days
Healed more than 29 days
Laboratory test for confirmation of STEMI
ECG
Serum cardiac biomarkers
Cardiac imaging
Nonspecific indices of tissue necrosis and inflammation
Why does slowly developing high grade coronary artery stenoses do not typically precipitate STEMI
development of rich collateral network over time
what causes STEMI in most cases
atherosclerotic plaque becomes disrupted and conditions favor thrombogenesis
characteristic of plaque prone to rupture
rich lipid core and thin fibrous cap
the amount of myocardial damaged caused by coronary occlusion depends on what factors
- territory supplied 2. whether or not the vessel becomes totally occluded 3. duration of coronary occlusion 4. quantity of blood supplied by collateral vessels 5. demand of oxygen of the myocardium whoes blood supply has been limited 6. endogenous factors that produce spontaneous lysis of occlusive thrombus 7. adequacy of myocardial perfusion in the infarct zone when flow is restored in occluded epicardial coronary artery
most common presenting symptom in STEMI
pain
cluster where STEMI often commence
morning within a few hours of awakening
typical pain in STEMI
central portion of the chest and or epigastrium and on occasion it radiates to the arms
pain in STEMI can radiate as high as where but not below the what?
radiate as high as the occipital area but not below the umbilicus
differentials of the pain in STEMI
acute pericarditis, pulmonary embolism, acute aortic dissection, costochondritis, and gastrointestinal disorders
True or false. Radiation of discomfort to the trapezius is not seen in patients with STEMI
True.
Proportion of painless STEMI is greater in what subset of patients
elderly, patients with diabetes mellitus
less common presentation of STEMI
loss of consciousness, confusional state, sensation of profound weakness, appearance of an arrhythmia, evidence of peripheral embolism or a merely unexplained drop in arterial pressure
duration of substernal chest pain and diaphoresis that strongly suggest STEMI
more than 30 mins
manifestation of anterior infarction
sympathetic nervous system hyperactivity like tachycardia and or hypertension
manifestation of inferior infarction
parasympathetic hyperactivity like bradycardia and or hypotension
True or false. In patients with anterior wall infarction, an abnormal systolic pulsation casued by dyskinetic bugin fo the infarcted myocardium amy develop in the periapical area within the first days of the illness and then may resolve
True.
decline in systolic pressure in patients with transmural infarction
systolic pressure declines by 10-15 mmHg from the preinfarction state
True or false. Most patients initially presenting with ST segment elevation ultimately evolve Q waves on the ECG
True.
Levels of cardiac troponin may remain elevated for how many days after STEMI
7-10 days
CK rises within how many hours and generally returns to normal by how many hours
CK rises within 4-8 hrs and generally returns to normal by 48-72 hr
True or false. Nonspecific reaction to myocardial injury is associated with polymorphonuclear leukocytosis with WBC count reaching levels of 12,000- 15, 000/ uL
True.
Elevated WBC and ESR may occur for how long in STEMI
leukocytosis for 3-7 days, and ESR may remain elevated for 1-2 weeks
universally present on cardiac imaging for patient with STEMI
abnormalities of wall motion
True or false. Although perfusion scanning is extremely sensitive, it cannot distinguish acute infarcts from chronic infarcts
True.
technique to detect MI on high resolution cardiac MRI
late enhancement
two general classes of complications for STEMI
electrical complications (arrhythmias) and mechanical complications (pump failure)
most common cause of death in the first 24 hr of STEMI
ventricular fibrillation
greatest cause of delay for the treatment of STEMI
onset of pain and patient’s decision to call for help
criteria for AMI
detection of a rise and or fall of cardiac biomarker values, symptoms of ischemia, new ST wave changes of new LBBB, development of pathologic Q waves on ECG, imaging evidence of new loss of viable myocardium, or new regional wall motion abnormality, identification of intracoronary thrombus by angiography or autopsy
AMI in PCI
cTn 5x in patients with normal baseline or rise of cTn values 20% from baseline if elevated
AMI in CABG
cTn 10x in patient with normal baseline
Criteria for prior myocardial infarction
any one of the ff. 1. pathologic Q waves with or without symptoms in the absence of nonischemic causes 2. imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract, in the absence of nonischemic cause, 3. pathologic findings of a prior MI
goal of initiating PCI
Within 120 mins of first medical contact
Classification of Myocardial infarction. Spontaneous
Type 1
Classification of Myocardial infarction. Secondary to an ischemic imbalance
Type 2
Classification of Myocardial infarction. Resulting in death when biomarker values are unavailable
Type 3
Classification of Myocardial infarction. Related to PCI
Type 4a
Classification of Myocardial infarction. Related to stent thrombosis
Type 4b