Myocardial Injury Flashcards
Venous drainage of the heart occurs through
coronary sinus - RA btwn IVC and tricuspid valve
Major epicardial vessels
RCA
LCA - divides into the LAD and circumflex
LAD divides into the diagonal branches
Circumflex divides into the obtuse marginal arteries
Ischemia occurs when . . .
Supply/demand of oxygen to the heart is not balanced
Nerves from the heart
T1-T5
What % of atherosclerosis in CA causes pain
when 70% of vessel is occluded
Vulnerable plaques characteristics
- lipid cores with thin fibrous cap
- Have reduced smooth muscle cells
- increased macrophage activity
Chronic stable angina
Predictable chest pain
Lasts 2 or more hours
Unstable angina
At rest
New onset
Increasing severity or frequency
Etiology of CAD
endothelia damage with cholesterol deposition
LDL formation
Macrophage infiltration - Foam cells causing ROS, causing cellular damage
Revascularization
CABG when:
- Severe left main
- 3 vessel disease
- Diabetic with 2 or 3 vessel disease
ACS
Acute worsening or destabilizing angina
Usually from plaque break off
STEMI or NSTEMI
Atherosclerosis
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
Treatment of ACS
O2
Pain medication - morphine
sublingual NTG
Aspirin
Unfractionated heparin if pt going to PCI
BB unless the pt is hemodynamically unstable or has HB
Treatment for STEMI
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
NSTEMI
Oxygen Pain medication BB CCB can be used NTG ASA Clopidogrel *No thrombolytic therapy bc risk of hemorrhage outweighs the benefit
Most common arrhythmia after MI
Ventricular
Other complications after MI
20% have afib/flutter
15% Pericarditis
Signs of pericarditis
Friction rub when pt sits up and leans forward
Pain is pleuritic
Dressler syndrome
Pericarditis that develops weeks to months after MI
Mitral valve regurg after MI
from ischemia to papillary muscles
most commonly after inferior MI
Results in pulmonary edema and cardiogenic shock
Cardiogenic shock
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
Ventricular Septal Rupture
After anterior wall MI
Holosystolic murmur
Treat with surgery
Myocardial rupture
1% of pts
Death via tamponade
RV infarct
Inferior wall MI
Hypotension, increased jugular venous pressure, clear lungs
*Do not give NTG and diuretics (reduce preload)
*Do give fluids and inotropic support
Anterior wall and apex infarct
result in thrombus formation
AMI biomarkers
Earliest is Myoglobin CK
Best is Troponin
MI correlates with
Cortisol levels - early morning being highest risk because catecholamines peak 1 hr after waking
BB block this rhythm
Ischemia of the myocardial wall causes immediate loss of
contractility - hypokinesis
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)
Viable myocardium attempts to compensate via
increased contractility (hypokinesis)
4-12 hours post MI
coagulation necrosis - cells swell, organelles breakdown and proteins denature
18 hours post MI
neutrophils move in to begin breaking down cells
3 days post MI
granulation tissue appears on the edges of the infarct
macrophages and fibroblasts form scar tissue and new capillaries
4-7 days post MI
tissue is very soft
increased risk for rupture and aneurysm formation
3 months post MI
infarct heals and leaves behind a fibrous, noncontracting region of thein wall myocardium
Ventricular remodeling continues
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.
What is the most common cause of post op MI?
oxygen demand ischemia
1st 4 days
Most perioperative MIs are what type?
NSTEMI with subendocardial injury
Lack chest pain
Nonspecific ECG changes
CA perfusion pressure
Diastolic - LVEDP
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
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
How does anti-platelet therapy increase bleeding risk?
1.5 x greater risk
Adding clopidogrel increases this by 50% more
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
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
Alpha 2 agonists
reduce sympathetic outflow
Statins
Should be continued
Blood sugar control
below 180 mg/dL
Hyperventilation causes
CA vasoconstriction
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
Intra-op events that cause increased oxygen requirements
SNS stimulation Tachycardia HTN Increased myocardial contractility Increased afterload Increased preload
What drugs help block SNS stimulation during laryngoscopy?
Esmolol Fentanyl Remifentanil Precedex Masking with volatile agent Opioid induction for pts with EF < 45%
Muscle relaxants and CAD
Choose those that limit HR and BP effects
Roc, Vec, Cisatracurium
Atracurium
causes histamine release
Succ
increases Oxygen demand
tachycardia
Pancuronium
causes tachycardia from ganglion blockade
Ischemia manifests as what in PAC?
increase in PAWP
Most sensitive measure of ischemia
Echo - RWMA first sign
If pt manifests signs of ischemia:
- Turn to 100% O2
- Optimize o2 demand and supply (i.e. treat tachycardia, cool if have fever, avoid hypercarbia, etc)
- NTG can be given if hemodynamically stable bc acts immediately to reduce preload and wall tension through venodilation
- BB can blunt SNS response
- Correct hypotension to improve CA perfusion
