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6902 test 2 > Myocardial Injury > Flashcards

Myocardial Injury Flashcards

(58 cards)

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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

Study These Flashcards
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
Anterior wall and apex infarct
result in thrombus formation
26
AMI biomarkers
Earliest is Myoglobin CK | Best is Troponin
27
MI correlates with
Cortisol levels - early morning being highest risk because catecholamines peak 1 hr after waking BB block this rhythm
28
Ischemia of the myocardial wall causes immediate loss of
contractility - hypokinesis
29
Necrosis path
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
Viable myocardium attempts to compensate via
increased contractility (hypokinesis)
31
4-12 hours post MI
coagulation necrosis - cells swell, organelles breakdown and proteins denature
32
18 hours post MI
neutrophils move in to begin breaking down cells
33
3 days post MI
granulation tissue appears on the edges of the infarct | macrophages and fibroblasts form scar tissue and new capillaries
34
4-7 days post MI
tissue is very soft | increased risk for rupture and aneurysm formation
35
3 months post MI
infarct heals and leaves behind a fibrous, noncontracting region of thein wall myocardium Ventricular remodeling continues
36
Autoregulation and ischemia
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
What is the most common cause of post op MI?
oxygen demand ischemia | 1st 4 days
38
Most perioperative MIs are what type?
NSTEMI with subendocardial injury Lack chest pain Nonspecific ECG changes
39
CA perfusion pressure
Diastolic - LVEDP
40
Coronary steal
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
After PCI, how long is CA vulnerable?
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
How does anti-platelet therapy increase bleeding risk?
1.5 x greater risk Adding clopidogrel increases this by 50% more
43
When does risk of bleeding outweigh continuing anti-platelet therapy?
Spinal cord decompressions, neuro, aortic aneurysm, proctectomy Or for pts who take ASA to prevent MI but do not have stents
44
BB
``` 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
Alpha 2 agonists
reduce sympathetic outflow
46
Statins
Should be continued
47
Blood sugar control
below 180 mg/dL
48
Hyperventilation causes
CA vasoconstriction
49
Intra-op events that cause decreased O2 delivery
``` Decreased CA blood flow tachycardia hypotension hypocapnia CA spasm Anemia Arterial hypoxemia Shift of oxyhemoglobin curve to the left ```
50
Intra-op events that cause increased oxygen requirements
``` SNS stimulation Tachycardia HTN Increased myocardial contractility Increased afterload Increased preload ```
51
What drugs help block SNS stimulation during laryngoscopy?
``` Esmolol Fentanyl Remifentanil Precedex Masking with volatile agent Opioid induction for pts with EF < 45% ```
52
Muscle relaxants and CAD
Choose those that limit HR and BP effects | Roc, Vec, Cisatracurium
53
Atracurium
causes histamine release
54
Succ
increases Oxygen demand | tachycardia
55
Pancuronium
causes tachycardia from ganglion blockade
56
Ischemia manifests as what in PAC?
increase in PAWP
57
Most sensitive measure of ischemia
Echo - RWMA first sign
58
If pt manifests signs of ischemia:
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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