B P5 C37 ST-Elevation Myocardial Infarction: Pathophysiology and Clinical Evolution Flashcards
1
Q
Type of MI
Demonstration of acute atherothrombosis in the artery supplying the infarcted myocardium
A
Type 1
Acute myocardial infarction should be used when there is acute myocardial injury with clinical evidence of acute myocardial ischemia and with detection of a rise and/or fall of cTn values with at least one value above the 99th percentile URL and at least one of the following:
• Symptoms of myocardial ischemia
• New ischemic ECG changes
• Development of pathologic Q waves
• Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology
• Identification of a coronary thrombus by angiography or autopsy (not for type 2 or 3 MIs)
2
Q
An imbalance between myocardial oxygen supply and demand unrelated to acute atherothrombosis meets criteria for _________
A
Type 2 MI
3
Q
Cardiac death in patients with symptoms suggestive of myocardial ischemia and presumed new ischemic ECG changes before cTn values become available or abnormal meets criteria for ____________
A
Type 3 MI
4
Q
Percutaneous coronary intervention (PCI)-related MI is termed _______________
A
Type 4a MI
5
Q
Type 4b MI ______________
Type 4c MI ______________
A
Type 4 MI include type 4b MI stent thrombosis and type 4c MI restenosis that both meet type 1 MI criteria.
6
Q
Coronary artery bypass grafting (CABG) related MI is termed _______________
A
Type 5 MI
7
Q
Coronary procedure related MI </= 48 hr after the index procedure is arbitrarily defined by an elevation of cTn values > ___ times for type 4a MI and >___ for type 5 MI of the 99th percentile URL in patients with normal baseline values.
A
> 5x: type 4a
> 10x: type 5
8
Q
Patients with preprocedural cTn values, in whom the preprocedural cTn level is stable (<20% variation) or falling, must meet the criteria for a >5 or >10 fold increase and manifest a change from the baseline value of >_____%.
A
> 20%
9
Q
Criteria for prior or silent /unrecognized MI
A
- Abnormal Q waves +/- symptoms in the absence of nonischemic causes.
- Imaging evidence of loss of viable myocardium in a pattern consistent with ischemic etiology.
- Pathoanatomical findings of a prior MI.
10
Q
Management and outcomes of patients with STEMI appear to vary substantially depending on the volume of such patients cared for within a hospital system.
_____ have lower STEMI mortality rates.
Conversely, patients with STEMI _____ have higher mortality rate
A
LOWER STEMI Mortality:
Hospitals with a high clinical volume
High rate of invasive procedures
Top ranking in quality reports
HIGHER MORTALITY RATE:
Not cared for by a cardiovascular specialist
11
Q
The highest risk of ischemic complications following MI occurs within ____ days, after which the risk becomes fairly linear. This pattern is most evident in patients older than 80 years
A
180 days
12
Q
Identify type of MI:
Any one of the following criteria meets the diagnosis for prior or silent/ unrecognized MI:
• Abnormal Q waves with or without symptoms in the absence of nonischemic causes.
• Imaging evidence of loss of viable myocardium in a pattern consistent with ischemic etiology.
• Pathoanatomical findings of a prior MI.
A
Prior or silent/unrecognized myocardial infarction
13
Q
Cause of myocardial injury related to AMI
A
Atherosclerotic plaque disruption with thrombosis
14
Q
Most ACSs result from coronary atherosclerosis, generally with superimposed coronary thrombosis caused by_____
A
Rupture or erosion of an atherosclerotic lesion
15
Q
Thus, equating the lipid-rich, thin-capped plaque with “vulnerability” is a misnomer. Other morphologic characteristics associated with rupture-prone plaque include _____.
A
Expansive remodeling that minimizes luminal obstruction (mild stenosis by angiography)
Neovascularization (angiogenesis)
Plaque hemorrhage
Adventitial inflammation
“Spotty” pattern of calcification
16
Q
Infarction alters the sequence of depolarization ultimately reflected as changes in the QRS-T complex.
The most characteristic change in QRS that develops in most patients with STEMI is the evolution of _____ in leads that interrogate the infarct zone.
A
Q waves
In a minority of patients with ST elevation, no Q waves develop but other abnormalities in the QRS complex occur frequently, such as diminution in R wave height and notching or splintering of the QRS
17
Q
Myocardial injury related to acute myocardial ischemia because of oxygen supply/demand imbalance
Identify causes with reduced myocardial perfusion
A
• Coronary artery spasm, microvascular dysfunction
• Coronary embolism
• Coronary artery dissection
• Sustained bradyarrhythmia
• Hypotension or shock
• Respiratory failure
• Severe anemia
18
Q
Causes of Increased myocardial oxygen demand
A
Sustained tachyarrhythmia
Severe hypertension with or without left ventricular hypertrophy
19
Q
Gross alterations in the myocardium appear _____ hours after the onset of necrosis, but a variety of histochemical stains can identify zones of necrosis after only _____ hours.
A
6-12 hours: Gross alterations
2-3 hours: Histochemical stains
20
Q
Within hours of death from MI, the presence of an infarct can often be detected by immersing slices of myocardium in triphenyltetrazolium chloride (TTC), which turns noninfarcted myocardium a _____ color due to preserved lactate dehydrogenase activity while the infarcted area _____
A
Birck-red color: NONINFARCTED
Unstained: INFARCTED
21
Q
An MI can often be identified at _____ hours as a red-blue area of disco-oration caused by edema and extravasated blood.
By day ____, an infarct is rimmed by a zone of granulation tissue as it eventually evolves into a fibrous scar.
A
12-24 hours: RED-BLUE AREA
DAY 7
22
Q
Approximate time of onsent of key events in ischemic cardiac myocytes
Onset of ATP depletion:
Loss of contractility:
ATP reduced
to 50% of normal:
to 10% of normal:
Irreversible cell injury:
Microvascular injury:
A
Onset of ATP depletion: Seconds
Loss of contractility: <2 min
ATP reduced
to 50% of normal: 10 min
to 10% of normal: 40 min
Irreversible cell injury: 20–40 min
Microvascular injury: > 1 hr
23
Q
Myocardial relaxation-contraction is compromised within a minute after the onset of severe ischemia with loss of systolic function, and irreversible cell injury begins within as early as _____________
A
20 minutes
24
Q
Irreversible cell death usually occurs in the ischemic region in _____ hrs in the absence of reperfusion or sufficient collateral circulation
A
6 hours
25
ECG criteria for ST Elevation
New ST elevation at the J point in two contiguous leads with the following cut points:
• ≥0.1 mV in all leads (except V2 –V3 )
• In leads V2 –V 3 the following cut points apply:
• ≥0.2 mV in men ≥40 years
• ≥0.25 mV in men <40 years
• ≥0.15 mV in women
26
ECG manifestations of ST Depression and T Wave Changes
• New horizontal or downsloping ST depression ≥0.05 mV in two contiguous leads
• T wave inversion ≥0.1 mV in two contiguous leads with a prominent R wave or R/S ratio >1
27
Electrocardiographic Manifestations of Ischemia in the Setting of Left Bundle Branch Block
Electrocardiographic Criterion
ST-segment elevation ≥1 mm and concordant with the QRS complex (5 points)
ST-segment depression ≥1 mm in lead V1 , V2 , or V3 (3 points)
ST-segment elevation ≥5 mm and discordant with the QRS complex (2 points)
A score of ≥3 had a specificity of 98% for acute MI
28
Electrocardiographic Changes Associated With Previous Myocardial
Infarction (in the Absence of Left Ventricular Hypertrophy and Left Bundle Block)
Any Q wave in leads V2 –V 3 ≥0.02 sec or a QS complex in leads V 2 and V3
Q wave ≥0.03 sec and ≥0.1-mV deep or QS complex in leads I, II, aVL, aVF, or V4 –V 6 in any 2 leads of a contiguous lead grouping (I, aVL; V1 –V6 ; II, III, aVF)
R wave ≥0.04 sec in V1 –V 2 and R/S ≥1 with a concordant positive T wave in absence of a conductions defect
29
Ultrastructural changes appear within several minutes after the onset of ischemia. If reperfusion occurs, these early changes can reverse.
Irreversible damage usually requires a reduction of flow to less than ___% of normal for _____ minutes.
<10% of normal for 20-30 minutes
30
In experimental infarction, the earliest ultrastructural changes in cardiac muscle after ligation of a coronary artery, noted within _____ minutes, is a reduction in the size and number of glycogen granules, myofibrillar relaxation, intracellular edema, and swelling and distortion of the transverse tubular system, sarcoplasmic reticulum, and mitochondria.
Changes after _____ minutes of occlusion include myocyte swelling,swelling and internal disruption of mitochondria, development of amorphous (flocculent) aggregation and margin- ation of nuclear chromatin, and relaxation of myofibrils.
After 20 minutes to 2 hours of ischemia, the changes in some cells become irreversible
20 minutes
Reduction in the size and number of glycogen granules
Myofibrillar relaxation
Intracellular edema
Swelling and distortion of the transverse tubular system, sarcoplasmic reticulum, and mitochondria
60 minutes
Myocyte swelling
Swelling and internal disruption of mitochondria
Development of amorphous (flocculent) aggregation and margination of nuclear chromatin
Relaxation of myofibrils.
31
_____ necrosis results from severe, persistent ischemia and is usually present in the central region of infarcts.
Coagulation necrosis
The tissue exhibits:
Stretched myofibrils
Many cells with pyknotic nuclei
Congested microvessels
Phagocytosis of necrotic muscle cells
Mtochondrial damage occurs, but no calcification is evident
32
This form of myocardial necrosis, also termed ______________________, results primarily from severe ischemia followed by reflow
The entire infarct may show this form of necrosis after reperfusion
Contraction band necrosis or coagulative myocytolysis
It is characterized by:
Hypercontracted myofibrils with contraction bands and mitochondrial damage, frequently with calcification
Marked vascular congestion
Healing by lysis of muscle cells
33
Ischemia without necrosis generally causes no acute changes visible on light microscopy, but severe prolonged ischemia can result in myocyte vacuolization, often termed _____.
Myocytolysis
Prolonged severe ischemia, which is potentially reversible, causes cloudy swelling, as well as hydropic, vascular,and fatty degeneration.
34
An additional pathway of myocyte death involves ______, a form of programmed cell death. In contrast to coagulation necrosis, myocytes undergoing apoptosis exhibit shrinkage, and fragmentation of DNA without the usual cellular infiltrate indicative of inflammation.
Apoptosis
35
Early reperfusion of the myocardium evolving from ischemia to infarction (i.e., within _____ minutes) can prevent necrosis. Beyond this early stage, the number of salvaged myocytes—and therefore the amount of salvaged myocardial tissue (area of necrosis/area at risk)— relates directly to the duration of coronary artery occlusion, the level of myocardial oxygen consumption, and collateral blood flow
Within 15-20 mins
36
While all patients who achieve reperfusion as soon as possible to preserve viable, but at risk, myocardium, the reperfusion of tissue per- fusion can induce arrhythmias and potential for “reperfusion injury,” which has been estimated to account for up to _____% of the ultimate infarct size.
50%
37
The physiology of reperfusion injury is likely multifactorial and includes:
Pathologic findings of reperfusion injury include widespread myocardial hemorrhage and contraction bands.
Release of cytotoxic mitochondrial content
Myocyte hypercontractility due to Ca2+ excess
Reactive oxygen species
Leukoyte aggregation
Platelet and complement activation
38
Approximately _____% of STEMI cases will have a total occlusion of the infarct-related vessel on initial angiogram
90%
39
Factors that influence the viability of myocardial cells distal to the occlusion:
Collateral blood flow
Level of myocardial metabolism
Presence and location of stenoses in other coronary arteries
Rate of development of the obstruction, and quantity of myocardium supplied by the obstructed vessel
40
Approximately ________ of patients with inferior infarction have some involvement of the right ventricle
Isolated ______
30% to 50%
3% to 5%
41
The classic presentation of an RV infarct:
Hypotension, clear lung fields, and elevated jugular venous pressures
Acute management of RV infarction complicated by cardiogenic shock includes judicious volume replacement, early revascularization, maintenance of atrioventricular synchrony, and in refractory cases, mechanical circulatory support.
In contrast to the left ventricle, the right ventricle can sustain long periods of ischemia but still demonstrate excellent recovery of contractile function after reperfusion.
42
Infarction of the atria occurs in up to 10% of patients with STEMI if ______________ is used as the criterion
Isolated atrial infarction?
In conjunction with ventricular infarction?
PR segment displacement
<5%
Approx 15%
43
Atrial infarction is more common on the _____ side, occurs more frequently in the _____ of the atrium, and can result in thrombus formation
Right than the left
Atrial appendages than in the lateral or posterior walls
44
The _________________ is a principal determinant of the infarct size
Magnitude of coronary collateral flow
45
_______________ defined as evidence of MI (positive cardiac b marker and corroborative clinical evidence of infarction due to ischemia) with angiographically normal or near-normal coronary arteries (the absence of obstructive CAD on angiography [i.e., no coronary artery stenosis ≥50%] in any potential infarct-related artery), and no other explanation for the presentation
Myocardial infarction with nonobstructive coronary arteries (MINOCA)
46
_______________, _______________, ______________ are common MINOCA etiologies affecting the epicardial arteries, as are plaque erosion and plaque rupture not discerned by standard angiography
Coronary artery spasm, plaque erosion or rupture, and coronary dissection
47
Two most common myocardial or microvascular mimickers of MI
Myocarditis
Takotsubo CMP
48
Compared to patients with atherosclerotic-mediated MI, patients with MINOCA tend to be younger, and more often ____________, black Maori or Pacific race, or Hispanic, with relatively few coronary risk factors except a ___________________
Female
History of cigarette smoking
49
In general, patients who have survived STEMI without evidence of significant CAD have a ________________ and better long-term outlook than those with atherosclerotic-mediated STEMI; in-hospital mortality is approximately 60% lower, and 1-year mortality, 40% lower.
Smaller infarct sizes
50
_______________ can result from embolization into a coronary artery.
_______________ of coronary arteries can occur secondary to chest wall trauma or hypercoagulable states.
Embolic/Thrombotic coronary arterial occlusions
The causes of coronary embolism are numerous: infective endocarditis and nonbacterial thrombotic endocarditis (see Chapter 80), prolapsed mitral valve, or myxoma, mural thrombi, prosthetic valves, neoplasms, air introduced at cardiac surgery, and calcium deposits from manipulation of calcified valves at surgery.
In situ thrombosis
51
___________________ medial dissection or rupture in the vasa vasorum, often in the setting of some physical or emotional stress in patients with some predisposition, that leads to intramural hemorrhage and subsequent coronary occlusion by the hematoma itself or a dissection flap.
SCAD
may account for 25% to 33% of MIs in women younger than 50 years old
52
Type of SCAD
_____________ classic appearance of contrast dye staining of arterial wall with multiple radiolucent lumen
Type 1
53
Rarer causes include _____, which can produce marked narrowing or occlusion of one or both coronary ostia, whereas Takayasu arteritis can result in obstruction of the coronary arteries
Syphilitic aortitis
54
Additional causes MI in the setting of normal-appearing coronary arteries include _____.
(1) CAD in vessels too small to be visualized on coronary arteriography
(2) Coronary arterial thrombosis with subsequent recanalization;
(3) Hematologic disorder (e.g., polycythemia vera, cyanotic heart disease with polycythemia, sickle cell anemia, disseminated intravascular coagulation, thrombocytosis, thrombotic thrombocytopenic purpura) causing in situ thrombosis in the presence of normal coronary arteries
(4) Anatomic variations, such as anomalous origin of a coronary artery, coronary arteriovenous fistula, or a myocardial bridge
55
Type of management for SCAD with occlusive lesions with ongoing ischemia, shock, or associated arrhythmias, recognizing a higher risk of complications.
Revascularization with PCI or coronary artery bypass grafting (CABG)
Conservative management with oral and IV antithrombotic therapy alone is recommended if coronary flow is preserved because of high rates of PCI-related complications
56
________________ involves transient wall motion abnormalities involving the LV apex and midventricle
Occurs in the absence of obstructive epicardial CAD and can mimic STEMI, but should not be considered a subtype of MINOCA as it has a specific pathophysiology that likely reflects neurocardiogenic myocardial stunning
Acute stress cardiomyopathy, also termed transient LV apical ballooning syndrome or takotsubo cardiomyopathy
Typically, an episode of physical or psychological stress precedes the development of takotsubo cardiomyopathy, although some cases lack an evident precipitant. More than half of patients presenting with takotsubo cardiomyopathy have an active or history of a neurologic or psychiatric disorder, potentially linking neurologic-mediated vasoconstriction.
57
Diagnostic criteria for Takotsubo CMP
Presence of transient regional wall motion abnormalities
Frequent (but not required) preceding stressful trigger
Absence of culprit CAD lesion, abnormal electrocardiographic and biomarker findings
Absence of myocarditis or pheochromocytoma
Recovery of ventricular function over subsequent weeks or months
58
Most patients with stress cardiomyopathy will recover v tricular function rapidly, although more than _________ of patients do suffer inhospital complications, including heart failure (HF), arrhythmias, and death, at rates similar to patients with ACS
20%
59
A clinical score (InterTAK Diagnostic Score) assigns points for _____ that can provide good specificity for stress myopathy or ACS in patients with high and low score, respectively.
Female sex
Physical or emotional trigger
Absence of ST-segment depression
Known neurologic or psychiatric disorder
QTc prolongation
60
Most common variant of stress cardiomyopathy
Apical ballooning (75-80%)
Others:
Midventricular (10-20%) - severe LVD, acute HF
Basal or inverted (5%)
Biventricular (<0.5%)
Focal dysfunction (Rare) - benign, more associated with chest pain
61
An abnormal contraction patterns in ACS
Dissociation of the time course of contraction of adjacent segments
Dyssynchrony
62
A reduction in the extent of shortening
Hypokinesia
63
Cessation of shortening,
Akinesia
64
Paradoxical expansion, and systolic bulging
Dyskinesis
65
Give the correct sequence of abnormal LV patterns after MI
Dyssynchrony
Hypokinesis
Akinesis
Dyskinesis
66
______________ of the remaining normal myocardium initially accompanies dysfunction of the infarct.
Hyperkinesis
The early hyperkinesis of the noninfarcted zones probably results from acute compensation, including increased activity of the sympathetic nervous system and the Frank-Starling mechanism.
67
The increased motion of the noninfarcted region subsides within____________ of infarction, during which some degree of recovery often occurs in the infarct region as well, particularly if reperfusion of the infarcted area occurs and myocardial stunning diminishes.
2 weeks
68
Patients with STEMI may also have reduced myocardial contractile function in noninfarcted zones.
This finding may result from previous obstruction of the coronary artery supplying the noninfarcted region of the ventricle and loss of collaterals from the freshly occluded infarctrelated vessel, a condition termed _________________
Ischemia at a distance
69
The degree to which ___________________ is perhaps the most powerful hemodynamic predictor of mortality following STEMI.
End-systolic volume increases
Paradoxical systolic expansion of an area of ventricular myocardium further decreases LV stroke volume
70
The earliest abnormality in LV function is ___________________
Ventricular stiffness in diastole
71
Percentage of abnormally contracting myocardium will produce the ffg:
Decrease in EF, increase in LVEDP and LVEDV
Clinical HF
Cardiogenic shock
>15%
>25%
>40%
72
Changes in diastolic function in AMI
Decrease in the peak rate of decline in LV p sure (peak—dP/dt), an increase in the time constant of the fall in LV pressure, and an initial rise in LV end-diastolic pressure
73
Dilation of the left ventricle elevates ________________ and elevates ________________
Ventricular wall tension
Myocardial oxygen consumption
74
The changes in LV size, shape, and thickness involving both the infarcted and the noninfarcted segments of the ventricle occur and are collectively referred to as ____________________
Ventricular remodeling
75
An increase in the size of the infarcted segment, known as _________________, is defined as “acute dilation and thinning of the area of infarction not explained by additional myocardial necrosis.”
Infarct expansion
76
The thinnest region of the left ventricle
Apex
77
Infarct expansion associates with both higher mortality and a higher incidence of nonfatal complications, such as _____ and _____________
HF
Ventricular aneurysm
Infarct expansion is best recognized by elongation of the noncontractile region of the ventricle on echocardiography or CMR. When the expansion is severe enough to cause symptoms, the most characteristic clinical findings are deterioration of systolic function, new or worsening pulmonary congestion, and development of ventricular arrhythmias.
78
An increase in the size of the infarcted segment, known as _____, is defined as “acute dilation and thinning of the area of infarction not explained by additional myocardial necrosis.
Infarct expansion
79
__________________ and ________________ given early after MI can cause scar thinning and greater infarct expansion, whereas ___________ attenuate the ventricular enlargement.
Glucocorticoids
Nonsteroidal antiinflammatory drugs (NSAIDs)
RAAS inhibitors
80
Despite these metabolic considerations, the most contemporary data indicate that maintaining glucose levels _________________, while avoiding hypoglycemia, is the safest post-MI glucose management strategy
Below 180 mg/dL
81
Although patients with STEMI are generally euthyroid clinically, _______________ levels can decrease transiently, a fall that is most marked on approximately the _____________ after the infarct.
Serum triiodothyronine (T3 )
Third day
82
The time of onset of STEMI has a pronounced circadian periodicity, with the peak incidence of events in the _____________
Morning
Circadian rhythms affect many physiologic and biochemical variables; plasma catecholamines and cortisol and platelet aggregability increase in the early morning hours.
83
.Clinicians should not be complacent about ongoing plausibly ischemic pain. In some patients—particularly _____—STEMI can manifest clinically not by chest discomfort but rather by symptoms of acute LV failure and chest tightness or by marked weakness or frank syncope.
Older adults
Diabetes
Heart transplant recipients
84
Recurrent pain after initial reperfusion should prompt consideration of ________________ of the culprit lesion.
Acute re-occlusion
85
Unrecognized or silent infarction occurs more often in patients without antecedent angina pectoris and in patients with ______________ and ______________ and typically manifests as new wall motion abnormalities, fixed perfusion defects, or pathologic Q waves.
Diabetes and hypertension
86
Nausea and vomiting may occur, presumably because of activation of the vagal reflex or stimulation of LV receptors as part of the _____ reflex.These symptoms occur more frequently in patients with inferior STEMI than with anterior STEMI.
Bezold-Jarisch Reflex
87
They often massage or clutch their chests and frequently describe their pain with a clenched fist held against the sternum ______________
Levine sign
88
________________ at presentation associates with a higher risk for fatal complications of MI.
Tachycardia
Typically, the pulse is rapid and regular initially (sinus tachycardia at 100 to 110 beats/min) and slows as the patient’s pain and anxiety are relieved; premature ventricular contractions are common.Tachycardia at presentation associates with a higher risk for fatal complications of MI.
89
Most patients with uncomplicated STEMI are _____, although the reduced stroke volume accompanying the tachycardia can cause declines in systolic and pulse pressure and elevation of diastolic BP.
Normotensive
90
In previously normotensive patients, a hypertensive response is occasionally seen during the first few hours, presumably because of _____.
Adrenergic discharge due to pain
Anxiety
Agitation
91
Patients in cardiogenic shock by definition have systolic pressure below 90 mmHg and evidence of end-organ hypoperfusion.
Hypotension alone does not necessarily signify cardiogenic shock; some patients with inferior infarction and activation of the _____reflex may also transiently have a systolic BP below 90 mmHg.
Their hypotension eventually resolves spontaneously, although _____ can accelerate recovery.
Bezold-Jarisch reflex
IV atropine (0.5 to 1 mg) and adopting the Trendelenburg position
92
Previously hypertensive patients may become normotensive without treatment after STEMI, although many of them eventually regain their elevated BP levels, generally _________________ after infarction.
3 to 6 months
93
Fever, mediated by cytokine release from tissues undergoing necrosis, develops in most patients with extensive STEMI within _____ hours after the onset of infarction.
Body temperature often begins to rise within _____ hours after onset of infarction, and rectal temperature may reach 38.3°C to 38.9°C (101°F to 102°F).
The fever usually resolves by the ____ day after MI.
Within 24 to 48 hours
4-8 hrs after onset
4th or 5th day after MI
94
The a-wave may be _____ in patients with pulmonary hypertension secondary to LV failure or reduced compliance.
In contrast, RV infarction (regardless of whether it accompanies LV infarction) often results in marked jugular venous distention and, if complicated by necrosis or ischemia of RV papillary muscles ,in _____ waves of tricuspid regurgitation
Prominent a-wave: Pulmonary hypertension sec to LV failure
Tall c-v waves: TR
95
______________ often results in marked jugular venous distention and, if complicated by necrosis or ischemia of RV papillary muscles, in tall c-v waves of tricuspid regurgitation.
RV infarction (regardless of whether it accompanies LV infarction)
96
In patients with STEMI, hypotension, and h fusion (findings that may resemble those of patients with cardiogenic shock) without elevated jugular venous pressures, the depression in LV performance may be related to _________________
Hypovolemia
97
A,small pulse suggests reduced ________________
Sharp, brief upstroke often occurs in patients with ______________
________________ reflects severe LV dysfunction.
Stroke volume
Mitral regurgitation or a ruptured ventricular septum with a left-to-right shunt
Pulsus alternans
98
A,small pulse suggests reduced ________________
Sharp, brief upstroke often occurs in patients with ______________
________________ reflects severe LV dysfunction.
Stroke volume
Mitral regurgitation or a ruptured ventricular septum with a left-to-right shunt
Pulsus alternans
99
Enumerate Killip classification and describe each
Class I patients have no rales and third heart sound (S3 )
Class II patients have rales, but only to a mild to moderate degree (<50% of lung fields), and may or may not have an S3
Class III patients have rales in more than half of each lung field and frequently have pulmonary edema
Class IV patients have cardiogenic shock.
100
Palpation of the precordium may be normal,but in patients with transmural STEMI, it more often reveals a presystolic pulsation synchronous with an audible ______, a finding reflecting vigorous left atrial contraction filling a ventricle with reduced compliance. Patients with LV systolic dysfunction may have a diffuse or dyskinetic LV impulse, or an outward movement of the left ventricle palpable in early diastole, coincident with an _____.
Fourth heart sound (S4)
S3
101
An _______ is almost universally present in patients in sinus rhythm with STEMI, but it has limited diagnostic value because it is usually audible in most patients with chronic ischemic heart disease and is recordable, although not often audible, in many normal individuals older than 45.
S4
102
An ______ in patients with STEMI reflect severe LV dysfunction with elevated ventricular filling pressure. It reflects rapid deceleration of transmitral blood flow during protodiastolic filling of the left ventricle and is typically heard in patients with large infarctions.
S3
An S3 may result not only from LV failure but also from increased inflow into the left ventricle, as occurs when mitral regurgitation or a ventricular septal defect complicates STEMI.
103
A new, prominent, apical holosystolic murmur accompanied by a thrill may represent ____________________
Rupture of a head of a papillary muscle
104
________________ produces murmur and thrill are usually most prominent along the left sternal border and may be audible at the right sternal border as well.
Rupture of the interventricular septum
105
The systolic murmur of _________________ (from RV failure caused by pulmonary hypertension or RV infarction, or from infarction of an RV papillary muscle) is also heard along the left sternal border. It is characteristically intensified by inspiration and is accompanied by a prominent c-v wave in the jugular venous pulse and an RV fourth sound
Tricuspid regurgitation
106
Friction rubs can be heard within 24 hours or as late as 2 weeks after onset of infarction, they occur most frequently on the ________________
2nd or 3rd day
107
Delayed onset of the rub and the associated discomfort of pericarditis (as late as 3 months after infarction) characterizes the ___________________
Post-MI (Dressler) syndrome
108
True or False
All patients with suspected MI should undergo measurement of cardiac specific troponin as soon as possible at the initial encounter
True
In patients with STEMI, the results of biomarker assessment should not delay interventions.
109
Because of continuous release from a degenerating contractile apparatus in necrotic myocytes, elevations in cTnI may persist for 7 to 10 days after MI; elevations in cTnT may persist for up to _________________
10 - 14 days
The prolonged time course of the elevation in cTnT and cTnI is advantageous for the late diagnosis of MI.
110
Detecting reinfarctions should be based on the clinical scenario, ECG, and at least two serial tests.
If the cTn concentrations are elevated but stable or declining at the time of the recurrent symptoms, then an elevation of _________________ indicates a reinfarction.
Greater than 20%
Measuring concurrent CKMB may help identify early reinfarction because CKMB levels decline much faster than cTn.
111
During the first 24 to 48 hours after admission, ______________ and _____________ levels remain at or near baseline values, but they generally fall after that.
Total cholesterol and highdensity lipoprotein (HDL) cholesterol
The fall in HDL cholesterol after STEMI is greater than the fall in total cholesterol; thus, the ratio of total cholesterol to HDL cholesterol is no longer useful for risk assessment unless measured early after MI
112
All patients with STEMI admitted within 24 hours of symptom onset should have a lipid profile, although regardless of lipid levels and unless contraindicated, all patients with STEMI should receive _________________
High-intensity statin therapy
113
Elevation of the white blood cell count usually develops within ________ after the onset of chest pain, reaches a peak __________ after infarction, and returns to normal in ___________; the peak leukocyte count generally ranges between 12 and 15 × 103/mL but occasionally rises to as high as 20 × 103/mL in patients with large STEMI.
2 hours
2 to 4 days
1 week
12-15 x10^3
114
Cardiovascular mortality increases progressively as the initial hemoglobin value falls below _____ g/dL; conversely, it also rises as the hemoglobin level increases above _____ g/dL
< 14-15 g/dL
> 17 g/dL
115
The _________ remains the most important diagnostic test in the evaluation of patients with suspected ischemic symptoms
ECG
116
Because the right bundle is supplied by the septal perforators off the LAD, evidence of a new RBBB with a Q-wave in V1 in setting of STEMI is a specific but non-sensitive sign of an _____ MI
Anteroseptal MI
117
Instead of “posterior,” the descriptor “inferobasal” may be more appropriate given the segmental anatomy of the heart as it sits in the thorax and can often be identified with adding leads in the _____ position
V7 and V8
118
Patients with an abnormal R wave in V 1 (0.04 second in duration and/or R/S ratio ≥1 in the absence of preexcitation or RV hypertrophy) and inferior or lateral Q waves have an increased incidence of ____________________ without collateral circulation
Isolated occlusion of a dominant left circumflex coronary artery
119
ST-segment elevations in _________, reflecting the basal i tricular septum, can be observed in up to 30% of STEMIs and identifies patients with a higher likelihood of left main coronary artery or multivessel disease and worse outcomes
aVR
120
Patients with new Q waves and ST-segment elevation diagnostic of STEMI in one territory often have ST-segment depression in other territories. These additional ST-segment abnormalities, which imply a poor prognosis, result either from ischemia in a territory other than the area of infarction, termed ________________, as noted above, or from __________________
Ischemia at a distance
Reciprocal electrical phenomena
121
ST-segment elevation in the _____________________ is a moderately sensitive and specific sign of RV infarction
Right precordial leads (V1 , V3 R through V6R)
Occasionally, ST-segment elevation in V2 and V3 results from acute RV infarction; this appears to occur only when injury to the left inferior wall is minimal
122
Criteria that can be used to improve the diagnostic accuracy of STEMI in LBBB:
Concordant ST-segment elevation at least 1mm in leads with a positive QRS
Concordant ST-segment depression at least 1mm in V1 and V1
Discordant ST-segment elevation at least 5mm in leads with a negative QRS complex
123
The presence of RBBB may confound the diagnosis of STEMI
During RV pacing, the ECG also shows LBBB, and the above rules also apply for the diagnosis of myocardial infarction during pacing: however, they are less specific
Isolated ST -depression at least 0.5mm in leads V1 and V2 and ST-segment (at least 0.5 mm) in posterior chest wall leads
ST depression ≥1 mm in eight or more surface leads, coupled with ST- segment elevation in aVR and/or V1, suggests left main-, or left main equivalent-coronary obstruction, or severe three vessel ischemia
124
_____________ estimated from an echocardiogram correlates well with measurements from angiography and is useful in establishing prognosis after MI.
LV function
125
_________ permits exact localizing and sizing the area of i tion and a quantitative assessment of the severity of the ischemic insult
CMR
CMR imaging has limited application during the acute phase because of long scan-times and the need to transport patients with MI to the scanner, but it is a useful imaging technique during the subacute and chronic phases of MI.
This modality is attractive because of its ability to assess perfusion of infarcted and noninfarcted tissue, as well as reperfused myocardium; identify areas of jeopardized but not infarcted myocardium; identify myocardial edema, fibrosis, wall thinning, and hypertrophy; assess ventricular chamber size and segmental wall motion; and identify the temporal transition between ischemia and infarction
CMR may be particularly u ful in the diagnostic assessment of possible etiologies in MINOCA
126
True or False
Radionuclide angiography, perfusion imaging, infarct-avid scintigraphy, and positron emission tomography (PET) can all evaluate patients with suspected ACS but have no role in the acute management of STEMI
True
Nuclear cardiac imaging techniques can assess infarct size, collateral flow, and jeopardized myocardium (“myocardium at risk”); determine the effects of the infarct on ventricular function; and establish the prognosis of patients with STEMI
127
Relationship exists between the number of ECG leads showing ST-segment elevation and the mortality rate: patients with ________ of 12 leads showing STsegment elevation have three to four times the mortality of those with ST elevations in only 2 or 3.
8 or 9
128
True or False
Serial measurements of proteins released by necrotic myocardium can help to determine MI size. Clinically, the peak troponin or CK-MB level provides an approximate estimate of infarct size.
True
129
______________ remains the most frequently used modality for assessing infarct size and LV function,
Echocardiography
130
Unrecognized or silent infarction occurs more often in patients without antecedent angina pectoris and in patients with __________ and _____________ and typically manifests as new wall motion abnormalities, fixed perfusion defects, or pathologic Q waves. Silent ischemia often follows silent STEMI
Diabetes
Hypertension
131
Chest imaging should not delay primary reperfusion strategies, unless there is a reason to evaluate a particular suspected pulmonary pathology. When present, prominent pulmonary vascular markings on the radiograph reflect elevated LV end-diastolic pressure, but significant temporal discrepancies can occur because of diagnostic and post-therapeutic lags. _____ hours can elapse before pulmonary edema accumulates after ventricular filling pressure has increased.
Up to 12 hours
132
The post-therapeutic phase lag represents a longer interval; up to____ days is required for pulmonary edema to resolve and the radiographic signs of pulmonary congestion to clear after ventricular filling pressure have returned toward normal.
Up to 2 days
133
The best predictor of return to normal ventricular wall thickening is less than ___% transmurality of LGE.
25%
134
The sum of ST-segment elevations measured from multiple precordial leads correlates with the extent of myocardial injury in patients with anterior MI. Moreover, a relationship exists between the number of ECG leads showing ST-segment elevation and the mortality rate: patients with 8 or 9 of 12 leads showing ST- segment elevation have ____- times the mortality of those with ST elevations in only 2 or 3.
3-4x
