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6902 test 2 > Myocardial Injury > Flashcards

Myocardial Injury Flashcards

1
Q

Venous drainage of the heart occurs through

A

coronary sinus - RA btwn IVC and tricuspid valve

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2
Q

Major epicardial vessels

A

RCA
LCA - divides into the LAD and circumflex
LAD divides into the diagonal branches
Circumflex divides into the obtuse marginal arteries

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3
Q

Ischemia occurs when . . .

A

Supply/demand of oxygen to the heart is not balanced

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4
Q

Nerves from the heart

A

T1-T5

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5
Q

What % of atherosclerosis in CA causes pain

A

when 70% of vessel is occluded

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6
Q

Vulnerable plaques characteristics

A
  • lipid cores with thin fibrous cap
  • Have reduced smooth muscle cells
  • increased macrophage activity
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7
Q

Chronic stable angina

A

Predictable chest pain

Lasts 2 or more hours

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8
Q

Unstable angina

A

At rest
New onset
Increasing severity or frequency

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9
Q

Etiology of CAD

A

endothelia damage with cholesterol deposition
LDL formation
Macrophage infiltration - Foam cells causing ROS, causing cellular damage

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10
Q

Revascularization

A

CABG when:

  1. Severe left main
  2. 3 vessel disease
  3. Diabetic with 2 or 3 vessel disease
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11
Q

ACS

A

Acute worsening or destabilizing angina
Usually from plaque break off
STEMI or NSTEMI

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12
Q

Atherosclerosis

A

Inflammatory disorder
Vulnerable plaques break off, collagen is exposed, then platelets aggregate over to the site
Thromboxane A2 causes vasoconstriction
GP2b3a on platelets is activated
Clotting cascade is activated to form fibrin to stabilize the clot
Vasoconstriction, spasm

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13
Q

Treatment of ACS

A

O2
Pain medication - morphine
sublingual NTG
Aspirin
Unfractionated heparin if pt going to PCI
BB unless the pt is hemodynamically unstable or has HB

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14
Q

Treatment for STEMI

A 
Reperfusion therapy
Thrombolytics w/in 30-60 min of hospital arrival/12 hrs of symptom onset
PCI - door to balloon within 90 minutes
IV heparin for 48 hrs after thrombolytic therapy
BB to decrease infarct size
ACEI
Glycemic control
Statins
*no CCB bc decrease contractility
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15
Q

NSTEMI

A 
Oxygen
Pain medication
BB
CCB can be used
NTG
ASA
Clopidogrel
*No thrombolytic therapy bc risk of hemorrhage outweighs the benefit
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16
Q

Most common arrhythmia after MI

A

Ventricular

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17
Q

Other complications after MI

A

20% have afib/flutter

15% Pericarditis

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18
Q

Signs of pericarditis

A

Friction rub when pt sits up and leans forward

Pain is pleuritic

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19
Q

Dressler syndrome

A

Pericarditis that develops weeks to months after MI

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20
Q

Mitral valve regurg after MI

A

from ischemia to papillary muscles
most commonly after inferior MI
Results in pulmonary edema and cardiogenic shock

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21
Q

Cardiogenic shock

A

CO doesn’t maintain appropriate perfusion to organs

Inotropes and pressure support - If BP is appropriate NTG can be added to reduce preload and afterload

Reduce afterload
Improve CA perfusion
*IABP

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22
Q

Ventricular Septal Rupture

A

After anterior wall MI
Holosystolic murmur
Treat with surgery

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23
Q

Myocardial rupture

A

1% of pts

Death via tamponade

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24
Q

RV infarct

A

Inferior wall MI
Hypotension, increased jugular venous pressure, clear lungs
*Do not give NTG and diuretics (reduce preload)
*Do give fluids and inotropic support

25
Q

Anterior wall and apex infarct

A

result in thrombus formation

26
Q

AMI biomarkers

A

Earliest is Myoglobin CK

Best is Troponin

27
Q

MI correlates with

A

Cortisol levels - early morning being highest risk because catecholamines peak 1 hr after waking

BB block this rhythm

28
Q

Ischemia of the myocardial wall causes immediate loss of

A

contractility - hypokinesis

29
Q

Necrosis path

A

first onsets to the sub-endocardial regions bc most vulnerable (w/in 20 minutes)

Then over 2-6 hours spans myocardial wall

The edges of the necrotic area demonstrate stunning (reversible damage)

30
Q

Viable myocardium attempts to compensate via

A

increased contractility (hypokinesis)

31
Q

4-12 hours post MI

A

coagulation necrosis - cells swell, organelles breakdown and proteins denature

32
Q

18 hours post MI

A

neutrophils move in to begin breaking down cells

33
Q

3 days post MI

A

granulation tissue appears on the edges of the infarct

macrophages and fibroblasts form scar tissue and new capillaries

34
Q

4-7 days post MI

A

tissue is very soft

increased risk for rupture and aneurysm formation

35
Q

3 months post MI

A

infarct heals and leaves behind a fibrous, noncontracting region of thein wall myocardium

Ventricular remodeling continues

36
Q

Autoregulation and ischemia

A

pts with CAD have a partial or complete loss of the ability to auto regulate and pressure is flow dependent

Sub endocardium is the most vulnerable to ischemia bc pressure dependent whereas the epicardial region has autoregulation

Normal CA perfusion pressure is able to autoregulate btwn 60-140 mmHg.

37
Q

What is the most common cause of post op MI?

A

oxygen demand ischemia

1st 4 days

38
Q

Most perioperative MIs are what type?

A

NSTEMI with subendocardial injury
Lack chest pain
Nonspecific ECG changes

39
Q

CA perfusion pressure

A

Diastolic - LVEDP

40
Q

Coronary steal

A

blood flow redirected from ischemic tissue to healthy tissue that has a higher metabolic demand

Ischemic tissue is max dilated so if we dilate other tissues, blood is shunted away from the ischemic tissue

41
Q

After PCI, how long is CA vulnerable?

A

2-3 weeks

Early stent thrombus w/24 hours due to CA dissection or improper stent expansion

Late stenosis (30 days - 1yr) due to stent malposition or neointimal growth

42
Q

How does anti-platelet therapy increase bleeding risk?

A

1.5 x greater risk

Adding clopidogrel increases this by 50% more

43
Q

When does risk of bleeding outweigh continuing anti-platelet therapy?

A

Spinal cord decompressions, neuro, aortic aneurysm, proctectomy

Or for pts who take ASA to prevent MI but do not have stents

44
Q

BB

A 
reduce O2 consumption
improve CA flow
improve supply/demand ratio
stabilize myocardial membranes
inhibit platelet aggregation
Suppression of perioperative tachycardia
*continue day of surgery
45
Q

Alpha 2 agonists

A

reduce sympathetic outflow

46
Q

Statins

A

Should be continued

47
Q

Blood sugar control

A

below 180 mg/dL

48
Q

Hyperventilation causes

A

CA vasoconstriction

49
Q

Intra-op events that cause decreased O2 delivery

A 
Decreased CA blood flow
tachycardia
hypotension
hypocapnia
CA spasm
Anemia
Arterial hypoxemia
Shift of oxyhemoglobin curve to the left
50
Q

Intra-op events that cause increased oxygen requirements

A 
SNS stimulation
Tachycardia
HTN
Increased myocardial contractility
Increased afterload
Increased preload
51
Q

What drugs help block SNS stimulation during laryngoscopy?

A 
Esmolol
Fentanyl
Remifentanil
Precedex
Masking with volatile agent 
Opioid induction for pts with EF < 45%
52
Q

Muscle relaxants and CAD

A

Choose those that limit HR and BP effects

Roc, Vec, Cisatracurium

53
Q

Atracurium

A

causes histamine release

54
Q

Succ

A

increases Oxygen demand

tachycardia

55
Q

Pancuronium

A

causes tachycardia from ganglion blockade

56
Q

Ischemia manifests as what in PAC?

A

increase in PAWP

57
Q

Most sensitive measure of ischemia

A

Echo - RWMA first sign

58
Q

If pt manifests signs of ischemia:

A
  1. Turn to 100% O2
  2. Optimize o2 demand and supply (i.e. treat tachycardia, cool if have fever, avoid hypercarbia, etc)
  3. NTG can be given if hemodynamically stable bc acts immediately to reduce preload and wall tension through venodilation
  4. BB can blunt SNS response
  5. Correct hypotension to improve CA perfusion

6902 test 2 (8 decks)

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