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Cardio Exam 2 > Lec 21-22 Acute Coronary Syndromes > Flashcards

Lec 21-22 Acute Coronary Syndromes Flashcards

1
Q

What types of coronary syndromes with a partially occlusive thrombus?

A
  • unstable angina

- non-ST elevation MI [NSTEMI]

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2
Q

What distinguishes unstable angina from NSTEMI?

A

NSTEMI = necrosis present

unstable angina = no myocardial necrosis

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3
Q

What type of coronary syndrome with a completely obstructed coronary artery?

A

ST-elevation MI [STEMI]

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4
Q

What is difference intrinsic vs extrinsic coagulation path?

A 
instrinsic = within bloodstream activating coagulation
extrinsic = not in contact with bloodstream
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5
Q

What is action of Factor X?

A

catalyzes conversion prothrombin to thrombin

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6
Q

What is action of fibrin?

A

forms mesh-like network that capture debris like red/white cells; forms actual structure of thrombus

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7
Q

What is the sequence of events leading to thrombin generation?

A
  • activated factor VII binds tissue factor
  • this complex activates factor X
  • activated factor X and factor V together catalyze conversion prothrombin to thrombin
  • thrombin stimulates platelets + increases activation of coagulation cascade
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8
Q

What is action of antithrombin? Where does it come from? What increases its activity

A
  • plasma protein in blood
  • irreversibly binds thrombin [factor IIa] and inactivates
  • increased efficacy by 1000x when its bound to heparan on surface of endothelial cells
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9
Q

What is action of protein C?

A
  • activated protein C [activated by thrombmodulin-thrombin complex]
  • activated C degrades factors Va and VIIIa –> inhibiting coagulation
  • protein S enhances action of protein C
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10
Q

Which 2 other factors needed in protein C action?

A
  • thrombomodulin activates protein C

- Protein S enhances function of protein C

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11
Q

What enhances action of anti-thrombin?

A

heparan

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12
Q

What enhances action of protein C?

A

protein S

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13
Q

What is action of thrombomodulin?

step1

A
  • on surface of endothelial cell
  • binds thrombin and prevents it converting fibrinogen –> fibrin
  • as bound thrombomodulin-thrombin complex it activates protein C
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14
Q

Which factors does protein C inhibit?

step1

A

factors Va and VIIIa

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15
Q

What are 2 principal targets of antithrombin?

step1

A

thrombin and factor Xa

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16
Q

What 6 factors does antithrombin inhibit?

step1

A

activated forms of

- II [thrombin], VII, IX, X, XI, XII

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17
Q

What is action of TFPI?

A

TFPI = tissue factor pathway inhibitor

  • activated by Xa
  • Xa-TFPI complex binds and inactivates TF-VIIa complex that normally triggers extrinsic coagulation path

== negative feedback inhibitor of coagulation

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18
Q

Which endogenous anti-coagulant lyses clots?

A
  • tPA = tissue plasminogen activator secreted by endothelial cells
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19
Q

What is action of tPA?

step1

A
  • secreted by endothelial cells in response to clot formation
  • cleaves plasminogen to plasmin which degrades fibrin clot
  • when bound to fibrin = activity enhanced
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20
Q

What are actions of plasmin?

step1

A
  • cleaves fibrin mesh

- destroys coagulation factors

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21
Q

What is action of prostacyclin? Where does it come from?

Step1

A
  • secreted by endothelial cells
  • increases platelet cAMP –> inhibits platelet activation/aggregation
  • also indirectly inhibits coagulation via vasodilation
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22
Q

How does vasodilation guard against thrombosis?

A

more blood flow = minimize contact between procoagulant factors

less shear stress which is an inducer of procoagulant factors

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23
Q

What is action of NO?

step1

A
  • secreted by endothelial cells
  • inhibits local platelet activation
  • vasodilates
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24
Q

What is major trigger of coronary thrombosis?

A

plaque rupture

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25
Q

What is role of ADP in platelet activation?

A
  • activated platelets have ADP

- endothelial cells convert ADP –> adenosine so inhibit activation of platelets

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26
Q

What are endothelial cell mechanisms of platelet inhibition?

A
  • release prostacyclin and NO that inhibit platelet activation
  • convert ADP –> adenosine to minimize platelet activation
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27
Q

What are endothelial cell mech of vasodilation?

A
  • release prostacyclin and NO that vasodilate
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28
Q

What are the 3 underlying causes of plaque disruption?

A
  • chemical factors that destabilize fibrous cap: T lymphocytes secrete cytokines that inhibit collagen synthesis + MMP proteins in plaque degrade matrix
  • physical stresses: shoulder region of cap due to high stress; high BP; torsion from myocardial contraction [high inotropy]
  • triggers that increase chem or phys stress: emotional upset, physical activity; MI in morning when high BP
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29
Q

How does dysfunctional endothelium increase likelihood of thrombus formation?

A
  • less secretion of NO/prostacyclin that normally inhibits platelets + vasodilate
  • less able to fight against platelet products [thromboxane, serotonin] + thrombin promoting vasoconstriction
  • –> reduces coronary blood flow and normal clearance of procoagulant factors
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30
Q

What happens to contractility in MI? 3 different types?

A

impaired contractility

  • hypokinesis = reduced contraction
  • akinesis = loss of contraction, larger infarct
  • dyskinesisa = outward bulging during contraction, aneurysm, very large infarct
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31
Q

Why do you get impaired relaxation and thus diastolic dysfunction in MI? consequences?

A

relaxation is ATP dependent; less ATP in ischemia –> less compliance and thus increased filling pressures

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32
Q

What is stunned myocardium?

A
  • after MI get prolonged but reversible period of contractile dysfunction
  • restored days to wks after episode
  • usually in areas adjacent to region of MI
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33
Q

What is ischemic preconditioning?

A

after episodes of ischemia –> get physiologic adaptations that render you resistant to further episodes = “warm up” phenomenon

  • walk a few blocks, get chest pain, stop, now can walk longer w/o pain
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34
Q

If ST segment depression or T wave inversion and positive serum biomarkers with partially occlusive thrombus

what is it?

A

non-ST-elevation MI

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35
Q

If ST segment depression or T wave inversion and negative serum biomarkers with partially occlusive thrombus

what is it?

A

unstable angina

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36
Q

When should you suspect that ACS due to reason other than acute thrombus formation?

A
  • young patient

- no coronary risk factors

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37
Q

What are some causes of acute coronary syndrome other than thrombus formation?

A
  • vasculitic syndrome
  • coronary embolism [from endocarditis or artificial heart valve]
  • congenital anomaly of coronary arteries
  • trauma or aneurysm
  • severe coronary artery spasm [cocaine]
  • increased blood viscosity
  • coronary artery dissection
  • severe aortic stenosis increasing O2 demand
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38
Q

What happens in early and late remodeling after MI?

A

early: thinning and elongation of fibrous scar within infarcted zone
late: dilation, transition elliptical to spherical configuration due to myocyte hypertrophy and increase interstitial collagen

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39
Q

What is a transmural infarct?

A

spans entire thickness of myocardium within zone of perfusion

results from total prolonged occlusion of coronary artery

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40
Q

What is a subendocardial infarct?

A

exclusively involves innermost layers of myocardium but may expand beyond zone of perfusion

subendocardium = susceptible to highest pressure and has few collateral + farthest from blood supply

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41
Q

What factors determine how much tissue is infarcted?

A
  • mass of myocardium that is perfused by the occluded vessel
  • magnitude and duration of impaired coronary blood flow
  • oxygen demand of affected region
  • presence of collateral vessels
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42
Q

When does irreversible cell injury occur following occlusive thrombosis?

A

w/in 20 min

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43
Q

What are the earliest histological changes of MI?

A

wavy myofibers = intercellular edema separates myocardial cells that are being tugged about by surrounding functional myocardium

start to occur in 4-12 hrs

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44
Q

What are contraction bands?

A
  • see near border of infarct
  • sarcomeres are contracted and consolidated and appear as bright eosinophilic belts
  • can see w/in 12-24 hr
45
Q

WHen does acute inflammatory response to MI occur?

A

approx 4-24 hrs after MI

46
Q

What is hallmark of subendocardial ischemia on EKG?

A

ST depression

47
Q

What is most sensitive and specific marker for MI?

A

troponin I

48
Q

What types of ventricular remodeling in early post MI period?

A

infarct expansion

- infarcted ventricular segment enlarges = thinning and dilatation of necrotic zone

49
Q

What are effects of infarct expansion in early post MI period?

A
  • increases ventricular size which increases wall stress, impairs systolic contractile function, increases likellihood of aneurysm formation

higher mortality + risk of heart failure and ventricular aneurysm

50
Q

What are clinical findings in infarct expansion?

A
  • impaired systolic function
  • new/louder S3 gallop sounds
  • new/worsening pulm congestion
51
Q

What happens in late ventricular remodeling post MI? What initiates it?

A

myocyte hypertrophy to minimize wall stress

initiated by: neurohormonal activation, myocardial stretch, activation of local tissue RAAS, paracrine/autocrine factors

52
Q

What are some non-atherosclerotic causes of acute coronary syndrome?

A
  • embolus due to mechanical valve or infective endocarditis
  • vasculitis
  • spontanoueous coronary dissection in peripartum female]
  • cocaine abuse
53
Q

How does cocain cause ACS?

A
  • potent vasoconstrictor
  • increases HR, inotropy, Ox demand
  • causes vasospasm which reduces ox supply
  • associated with increase risk atherosclerosis
54
Q

What is MI type 1?

A

MI due to plaque rupture with thrombus

55
Q

What is MI type 2?

A

MI due to supply/demand imbalance w/o rupture

56
Q

What is MI type 3?

A

cardiac death

57
Q

What is MI type 4/5?

A

MI in setting of revascularization procedure

58
Q

Which type of MI has historical Q wave?

A

transmural [vs subendocardial = non-Q wave MI]

59
Q

What are 3 different types of patterns of symptoms that could represent unstable angina?

A
  • rest angina: at rest w/o provocation
  • new onset: angina < 2 mo very severe
  • crescendo/increasing: pt with chronic stable angina sudden increase in frequency/ duration/ intensity of episodes
60
Q

What are clinical symptoms of MI vs unstable angina?

A

MI: more severe chest pain, radiates, longer duration, will no improve with rest or nitroglycerine, sympathetic response [tachy, nausea, diaphoresis, clammy cool skin], SOB, fever

unstable angina: may get better w/ rest, improves with nitroglycerine

61
Q

What specific pt population do you worry about asymptomatic MI?

A

diabetics

62
Q

What are physical findings [sounds] in MI?

A
  • S4 due to atrial contraction against non-compliant LV
  • S3 due to volume overload/HF
  • systolic murmur –> MR if papillary muscle dysfunction or VSD
63
Q

What are 2 examples of times you hear an S4?

A
  • myocardial infarction
  • hypertrophic obstructive cardiomyopathy

= sign of ventricular hypertophy

64
Q

How do you distinguish pleuropericardial syndrome [pericarditis or pleuritis] from MI clinically?

A

pleuropericardial syndrome = pain worse w/ inspiration or position; diffuse elevated ST

65
Q

How do you distinguish aortic dissection from MI clinically?

A

aortic dissection = tearing/ripping discomfort; BP asymmetry; widened mediastinum

66
Q

What is order of EKG changes in STEMI?

A

before = normal
minutes/hrs = ST elevation
hrs/days = ST elevation, T inversion + Q wave
1 wk = coronary inverted T + Q wave deeper
mos = normal ST/T + Q wave

67
Q

What is management for STEMI vs NSTEMI?

A

STEMI = immediate reperfusion with preferred door to balloon time < 90 min

NSTEMI = depends on risk stratification score

68
Q

What are markers of myocardial necrosis?

A
  • troponin [troponin-I]

- creatine kinase -MB

69
Q

What is action of troponin?

A

controls Ca-mediated interactions between actin and myosin in cardiac and skeletal muscle

70
Q

Where does troponin come from in cardiac injury?

A
  • released from cytosolic pool and muscular pools as necrotic cell membranes degrade
71
Q

What are normal values troponin I?

A

not normally detected in blood!

72
Q

When can you detect troponin I in blood after MI?

A
  • starts to rise after 4 hours and peaks in 24ish hrs

- declines slowly over 7-10 days

73
Q

What will be values of troponin I and CK-MB at time 0 of infarct?

A

both may be 0; need a little time to rise up

74
Q

What is creatine kinase?

A

enzyme involved in generation of ATP

75
Q

When can you detect CK-MB in blood after infarct?

A
  • peaks slightly faster than troponin [~24 hr] and returns to normal before troponin [~48 hr]
76
Q

What do positive biomarkers tell you?

A

that MI occurred –> either STEMI or NSTEMI

77
Q

Why is it important to measure CK-MB?

A

useful in diagnosis reinfarction following acute MI b/c should be totally normal w/in 48 hrs

78
Q

What is general medical treatment for all ACS patients [NSTEMI and STEMI]?

A
  • anti-ischemic [Bblocker, nitrates]
  • general [pain control = morphine, give O2]
  • antiplatelet [aspirin or clopidogrel]
  • anticoagulant [heparin]
  • adjunct [statin, ACE-I]
79
Q

Why do you give B-blockers for ACS pts?

A
  • relieve ischemia + ischemic pain
  • reduce risk of arrhythmia
  • mortality benefit; usually give w/in 24 hr

avoid in: bardycardia, bronchospasm, decompensated HF, hypotension

80
Q

Why do you give nitrates for ACS pt?

A
  • venodilation –> lower O2 demand/wall stress
  • improve coronary flow/vasodilation, decrease risk vasospasm
  • no mortality benefit = just symptomatic
  • don’t give long acting due to changes in hemodynamic status
81
Q

Who should not get nitrates in ACS?

A
  • if hypotensive
  • if STEMI pt w/ inferior MI and suspected RV infarction –> change in volume status could influence CO a lot and worry about hypotension
82
Q

What is use of Ca channel blockers in ACS?

A
  • nondihydropyridines [verapamil, diltiazem] reduce HR and contractility = anti-ischemic
  • no mortality benefit
  • use if contraindicated to BBlockers
83
Q

What is use of aspirin in ACS?

A
  • inhibits platelet synthesis of thromboxane A2 = mediator of platelet activation
  • huge mortality benefit in all forms ACS
  • give immediately on presentation
84
Q

What is use of clopidogrel in ACS?

A

irreversible inhibitor platelet P2Y12 ADP receptor = anti-platelet
use in pt allergic to aspirin

can use in all pts with USA/NSTEMI unless surgery planned

85
Q

What is treatment-risk balance of antithrombotics?

A
  • helpful preventing clot formation or dissolving existing thrombus
  • can cause thinning blood and bleeding risk –> higher risk for complications and death over time
86
Q

What is use of prasugrel in ACT?

A

newer generation of clopidogrel
irreversible inhibitor P2Y12 platelet ADP receptor = more selective
use only if pt undergoing PCI

87
Q

What is use of glycoprotein IIb/IIIa receptor inhibitors?

A

bind glycoprotein receptor IIb/IIIa on activated platelets and prevent aggregation

use primarily in pt undergoing PCI

88
Q

What is use of heparin in ACS?

A

anticoagulant –> inhibit coagulation factor Xa

89
Q

What are 2 alternative to heparin in ACS treatment?

A

direct thrombin inhibitors = only use w/ PCI

factor Xa inhibitir

90
Q

What is difference unfractionated vs low molecular weight heparin?

A

UF-heparin = can bind factor Xa or thrombin

LMW heparin = binds preferentially factor Xa

91
Q

What is conservative vs early invasive approach to USA/STEMI?

A

conservative: give meds alone; if clinical worsening or evidence of ischemia do angiography/revascularization
invasive: do urgent cardiac catheterization

do more invasive in higher risk pts

92
Q

What is TIMI risk score calculator?

A
  1. age > 65
  2. > 3 risk factors for CAD
  3. known CAD w/ stenosis > 50%
  4. ASA used in past 7 days
  5. severe angina [> 2 episodes in 24 hrs]
    • cardiac markers

more factors you have –> worse you do

early invasive recommended in score >=3

93
Q

What is goal of STEMI treatment?

A

reperfusion via fibrinolysis or mechanical revascularization

94
Q

What is optimal door to balloon time?

A

< 90 min

95
Q

How effective is fibrinolysis vs primary PCI?

A

fibrinolysis –> 70-80% flow
PPCI –> 90% flow

greater benefit in PPCI esp if pt are sicker = good for elderly and tohse at risk for bleeding complications

96
Q

Any mortality benefit to PCI?

A

depends on the scenario

  • no benefit in stable ischemic heart disease
  • clear benefit with STEMI
97
Q

When do you prefer fibrinolysis over invasive strategy in STEMI pt?

A
  • early presentation [< 3 hrs from symtpoms onset]
  • invasive strategy not an option
  • delay to invasive strategy [> 1 hr to invasive vs fibrinolysis now]
98
Q

When do you prefer invasive strategy over fibrinolysis for STEMI pt?

A
  • skilled PCI lab available
  • door to balloon < 90 min
    high STEMI risk [risk of cardiogenic shock]
  • contraindications to fibrinolysis
  • later presentation
  • diagnosis of STEMI is in doubt
99
Q

What medical treatments for STEMI?

A
  • antiplatelet [ASA, clopidogrel]
  • anticoagulant [heparin]
  • ACEI
  • Statins
100
Q

What type of MI has greatest benefit w/ ACE inhibitor?

A

anterior MI and systolic dysfunction

101
Q

WHat is most cause of sudden cardiac death in early MI?

A

ventricular fibrilation

102
Q

What do you do if you see signs of right heart failure in MI?

A

treat with volume expansion to correct hypotension

RV infarct wil cause high JVP and LV underfilling b/c of lack of RV compliance

103
Q

What types of arrhythmias in MI?

A

supraventricular

  • bradycardia
  • tachycardia
  • atrial fibrillation

ventricular fibrillation

104
Q

What happens in free wall rupture?

A

happens in first 2 wks after MI = surgical emergency

get tamponade and die

105
Q

What happens in pseudoaneurysm after MI?

A

get a contained myocardial rupture that is plugged by mural thrombus = at risk for rupture and thus tamponade

106
Q

What happens in LV aneurysm in MI?

A

happens wks to mos after MI
no communication between LV cavity and pericardium

tissue bulges with cardiac contractions
can manifest on EKG as ST elevation

107
Q

What happens in papillary muscle rupture in MI?

A

happens days to wks after MI
complete rupture –> severe MR –> HF or death

partial –> moderate MR and symptoms of HF

happens with RCA infarct usually

108
Q

What is dressler syndrome?

A

autoimmune pericarditis happens wks to mos after MI

Cardio Exam 2 (19 decks)

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