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what percent of ppl admitted with ACS with die each year?
What is the continuum of syndromes for ACS?
Which of the ACS syndromes (UA, NSTEMI, STEMI) cause myocardial necrosis?
NSTEMI and STEMI
Does UA result in coronary necrosis?
No, as long as the ischemic event is terminated before necrosis occurs
What type of thrombus is typically responsible for UA and NSTEMI?
What's the shared pathophysiology for ACS (all syndromes?
plaque disruption, platelet aggregation, this causes a coronary thrombus, this then results in an imbalance between cardiac O2 supply and demand
What determines the type of ACS that results?
Degree of coronary occlusion and its associated ischemia
What type of thrombus is typically responsible for STEMI
a thrombus that completely obstructs the coronary artery
How much O2 does the heart require as a minimum to stay alive? How much does it normally receive?
- -1.3 ml O2 / 100 g heart muscle as a minimum
- -it usually receives 8 ml O2 / 100 g
Describe the evolution of an MI
- -acute coronary occlusion with insufficient collateral flow
- -infarction results
- -local vessels dilate and fill with stagnant blood
- -muscle fibers con't to use up O2 and Hgb becomes deoxygenated
- -vessel walls become very permeable and fluid leaks out
- -local edema occurs
- -death of heart muscle
What area of the myocardium is most susceptible to risk due to lack of perfusion?
The subendocardium, these vessels are compressed during systole, and rely on diastole for perfusion
2 pathologic classifications of necrosis
transmural and subendocardial
-what is it?
-how is it caused?
- -extends thru entire thickness of muscle
- -due to prolonged total occlusion of epicardial coronary arteries
-what is it?
-how is it caused?
- -involves innermost layers of myocardium
- -this area is especially susceptible to ischemia (no perfusion during systole), plus it has few collaterals
What area of the heart will die first?
The area supplied by the occluded vessel. Adjacent area may or may not necrose, it depends on if the vessel supplying that area is patent
If O2 supply continues to decrease, and the region of infarction spreads outward, what 5 factors predict the amount of tissue that dies?
- 1) mass of myocardium perfused by the occluded vessel
- 2) magnitude and duration of impaired flow
- 3) O2 demand in the affected area
- 4) collateral flow and how well it perfuses the area
- 5) degree of response of the tissues that might modify the ischemic process
What are the 2 stages of pathologic changes that occur during an MI?
- 1) Early changes- occur at the time of infaction
- 2) Late changes- occur during the period of healing and remodelling
When do the early changes occur?
From start of ischemia to 2-4 days after
When do the late changes occur?
begin 5-7 days after MI and continue for up to 7 weeks
Describe the early changes that occur due to an MI (give an overview)
- -Evolution of infarct at the tissue level
- -Functional impact of O2 deprivation on contractility
- -Within 2-4 days total coagulative necrosis occurs
What occurs on a cellular level during the early changes due to an MI?
- -LA forms due to anaerobic metabolism (no O2)
- -ATP production fails
- -local acidosis
- -lack of ATP causes Na+/K+/ATPase pump to fail, hence more Na+ inside and K+ outside
- -water follows Na+ into the cell, causing edema
- -the increased ECF K+ leads to arrhythmias
- -Ca accumulates inside the cell- contributing to the whole pathway of cell destruction
- -Ca goes into the cell as the cell membrane is not functioning properly
- -cell membrane malfunction causes biomarkers to leak out
- -finally, there's also an acute inflammatory response
How long does it take for irreversible cell injury to occur?
How long does it take for the heart muscle to become edematous due to the early changes?
Overview of the late changes
- -clearing of necrotic myocardium
- -collagen deposition which forms yellow scar tissue it its place
- -ventricular remodelling
Late changes- what occurs on a cellular level?
- -neutrophils go in as part of the inflammatory response, they and macrophages remove dead tissue (yellow softening)
- -necrotic myocardium is cleared and collagen is deposited in its place
- -this leads to thinning of dilation of the infarcted area which makes the ventricular wall weaker
- -this makes the ventricle more susceptible to rupture
- -fibrosis and scarring occur and are complete by 7 weeks post infarct
What functional alterations can occur as a result of an MI?
- -impaired contractility and compliance- causes systolic dysfunction, loss of synchronus contraction of myocardial cells, further reducing CO
- -diastolic dysfunction
- -stunned myocardium
- -ventricular remodelling
types of systolic dysfunction: hypokinesis
localized region of reduced contraction
types of systolic dysfunction: akinesis
segment of the heart not contracting at all
types of systolic dysfunction: dyskinesis
region that bulges out during systole, the normal part of the ventricle moves inward (like it's supposed to), this part goes in the opposite direction
How does an MI affect diastolic dysfunction?
- -Diastole relies on ATP to relax
- -also affects ventricular compliance
- -after a period of prolonged ischemia, the heart tissue will demonstrate prolonged systolic dysfunction
- -even though blood flow is restored, the heart is stunned and will not pump properly
- -over a period of days to weeks it recovers its pumping ability
- -initially it may appear that there's an infarct, but as long as it's only stunned, and not necrotic, systolic function will return
- -the volatiles can mimic this
- -brief periods of ischemia make the heart more resistant to subsequent episodes of ischemia
- -so if this pt sustain an MI, there will be a lower mortality rate as opposed to someone who never had any angina
- -MOA not really understood
- -after an MI there are changes in the geometry of the ventricle
- -these changes affect LT prognosis and functioning
- -area of the infarct can expand, leading to increased wall stress
- -there can also be dilation of the non-infarcted areas that are now working harder (subj to increased wall stress)
How can we modify ventricular remodelling?
- 1) reperfusion therapy (limit size and expansion of infarct)
- 2) drugs (ACEI and ARBs), attenuate remodeling and decrease ST and LT post infarct mortality
In what 3 ways can UA present?
- 1) crescendo- pt had chronic stable angina, now it's at rest, not just with exertion
- 2) increase in freq, duration, and intensity of episodes
- 3) new onset
T or F, unless treated, the pt with UA will continue onto NSTEMI and STEMI?
LA accumulation in the heart may be the mediator for the chest pain and can radiate because ?
It's at dermatome level C7-T4
What percent of pts experience a silent MI?
How do the symptoms of MI compare with UA?
- -more severe and lasts longer
- -may radiate more widely
- -symptoms crescendo fast
- -feeling of doom
- -pain not relieved by rest or by NTG
- -SNS effects (diaphoresis, tachycardia, clammy skin)
- -dyspnea and pulmonary congestion (due to LV dysfunction)
- systolic dysfunction, volume overload, LV failure
- "sloshing in"
- atrial contraction into noncompliant LV
- "a stiff wall"
Differential dx: aortic dissection
- -tearing or ripping pain that migrates over time to chest or back
- -asymmetric arm BPs
- -widened mediastinum on CXR
Diagnosis of UA
- -symptoms and transient EKG abnormalities
- -biomarkers are not yet elevated at this time
Diagnosis of NSTEMI
- -persistant EKG changes
- -biomarkers positive
Diagnosis of STEMI
-ST elevation and positive biomarkers
What biomarkers are most helpful?
CK-MB and tropI or tropT
- -protein found in muscle cells that helps actin and myosin come together
- -3 subunits found in both cardiac and skeletal muscle
- -cardiac forms are structurally unique (trop I and T)
Does a normal person have detectable levels of trop I or T?
No, so this is specific to cardiac injury
In what other cardiac issues could an elevated trop I or T be detected?
- -cardiac strain
- -PE (due to RV strain)
troponin onset, peak, and duration
- onset: 3-4 hours after onset chest discomfort
- peak: 18-36 hours
- duration: up to 12-14 days
What's the preferred biomarker for necrosis?
Where is CK located? CK-MB?
- -CK: skeletal muscle, heart, and other organs
- -CK-MB: mostly the heart, but also tongue, prostate, gut, diaphragm, and 1-3% is in the skeletal muscle
CK to CK-MB ratio?
- >2.5 is indicative of an MI
- if less its likely from another source
CK-MB onset, peak, and duration
- Onset: 3-8 hours
- Peak: 24 hours
- Duration: 48-72 hours
T or F, the sequence of rise and fall of CK-MB is specific to the myocardium only?
ischemia EKG changes
transient T wave inversion due to altered repolarization of ischemic cells
injury EKG changes
ST segment deviates from baseline
subendocardial injury EKG changes
transmural injury EKG changes
infarction (necrosis) EKG changes
rank the following in terms of severity: infarction, ischemia, injury
- least severe: ischemia
- infarction: most severe
When is a Q wave significant?
- when they are at least:
- -1/3 the height of the QRS
- -1 mm wide (1 small square on the EKG paper)
Will a standard EKG capture ischemia that only occurs with activity?
No, hence the benefit of getting a stress test
T or F, an NSTEMI has transient ST depressions or T wave inversion?
F, it has persistent ST depressions or T wave inversions
UA has transient ST depressions and or T wave inversions
Describe the evolution of EKG changes of a STEMI
- Acute- ST elevation
- Hours- ST elevation, Q wave begins to develop, decreased R wave height
- Days 1-2- Q wave deeper, T wave inversion
- Days later- ST normalizes, T wave inversion
- Weeks later- Q wave persists, T and ST normalize
- Q and ST elevation in:
- -V1, V2, V3, V4
- Q and ST elevation in:
- -L circ
- -1 and AVL
- Q and ST elevation in:
- -RCA (in most individuals this supplies the PDA)
- -II, III, AVF
- Large R wave and ST depression (reciprocal changes) in leads:
- -V1, V2, V3
- -possible Q V6
- -RCA (85% of the population), 8% circ, the rest are codominant
anteroseptal vs anterolateral EKG changes
- anteroseptal = V1 and V2
- anterolateral = V3 and V4
If you have a posterior infarct, what else might you suspect and why?
-Inferior infarct as RCA usually supplies inferior and posterior parts of the heart
What is the overall goal in treatment of an MI?
restore O2 supply and demand
With a STEMI, what's the major treatment?
- -Immediate reperfusion therapy
- -Either pharm or mechanical
- -NSTEMI pts do not respond to this in the same way
UA and NSTEMI acute treatment
anti-ischemia and anti-thrombotic treatment to prevent further growth of thrombus
beta blockers, nitrates, calcium channel blockers
- anti-platelets- ASA, plavix, GP 2b3a inhibitors
- anticoagulants- LMWH, heparin
GP 2b3a inhibitors
- -usually reserved for high risk patients as they are potent anti-platelet agents
- -helpful to decrease incidence of acute coronary event when undergoing PCI
adjunctive treatment for ACS management
statins and ACEI
invasive approach for ACS
-what is it
- -STEMI, UA or NSTEMI with high TIMI score, refractory angina, VEA, shock
- -PCI or fibrinolytic therapy within 24 hours
conservative approach for ACS
-what is it
- -low risk UA or NSTEMI (TIMI score)
- -medical treatment
- -angiography only if ischemic episodes recur or if stress test shows substantial inducible areas of ischemia
-what is it?
-what score is significant?
- -used to assess individual risk of death or ischemia in pts presenting with ACS
- -Thrombolysis in MI= TIMI
- ->= 3 early invasive approach is recommended
TIMI score variables
- 1) age >= 65
- 2) >= 3 CAD risk factors
- 3) known stenosis of >= 50% by prior angiography
- 4) current ST segment deviations
- 5) 2+ anginal episodes in last 24 hours
- 6) use of ASA in past 7 days (implies rx to effect of ASA)
- 7) elevated troponin or CK-MB
Goal HR with beta blockers
- -for STEMIs only
- -accelerates lysis of thrombus
- -drugs used are TPA, RPA, streptokinase
Within what time frame does revascularization need to occur in a pt presenting with MI
within 90 mins
How do newer fibrinolytic drugs (tpa and rpa) differ from the older drugs (streptokinase)?
- -Newer drugs preferentially bind to fibrin that's in a formed thrombus
- -less risk of systemic bleeding
How successful is fibrinolytic therapy in restoring circulation?
-restores circulation in 75-80% of pts
How do we know reperfusion was successful?
- -Resolution of symptoms
- -ST segment returns to baseline
- -Earlier than usual biomarker peaking
T or F, reperfusion arrhythmias are worrisome ?
F, they are common during the acute reperfusion period
How effective is PCI?
-Effective in over 90% of pts
Which is preferred, fibrinolytic therapy or PCI?
PCI, greater survival and less incidence of reinfarction
- -it can be performed by experienced provider within 90 mins of hospital arrival or > 3 hours since symptom onset
- -fibrinolysis contraindicated
- -cardiogenic shock
- -rescue for pt with no response from fibrinolysis
ACEI are an adjunctive therapy for ACS- what benefits do they have and in what pts?
- -limit ventricular remodelling, decrease HF incidence and recurrent ischemia and death
- -additive benefit when combined with ASA and BB
- -useful in high risk pts
What are potential complications of UA and in what percent of pts do they occur?
- -death (5-10%)
- -progression to infarction (10-20%)
What percent of pts experience recurrent ischemia? What's the treatment?
- -Urgent cath and cardiology consult
What are the complications from STEMI due to?
- mechanical, electrical, and inflammatory abnormalities associated with tissue necrosis
- -early changes are from necrosis itself
- -late changes are from healing and inflammation of necrotic tissue
Is recurrent ischemia and post angina infarction reduced in pts who've had anti-thrombotic treatment?
No, but it is reduced in pts who've had stent or angioplasty as part of early intervention
What are the possible issues that come from tissue necrosis?
- -VSD, ventricular rupture, papillary muscle ischemia
- -above can lead to CHF or tamponade
- -MI complication
- -hypotension SBP< 90
- -severe decrease in CO
- -poorly perfused peripheral tissues
- -occurs when >40% of LV mass is infarcted
- -cardiogenic shock
How is cardiogenic shock self perpetuating?
hypotension leads to decreased coronary perfusion, this makes ischemia worse, decreased SV will increase LV size, and this increases myocardial O2 demand
What percent of pts experience cardiogenic shock post-MI?
What's the mortality rate?
- -10% post MI
- -mortality rate is 70%
- -early revascularization
- -balloon pump
What vessel supplies the SA and AV nodes in most pts?
What vessel supplies the bundle of His in most patients?
What vessel supplies the right and left bundle branches?
- L- LAD and PDA
- R- LAD and RCA
What processes are responsible for arrhythmias seen with acute MI?
- -anatomic interruption to conduction system
- -accumulation of toxic waste products (acidosis)
- -abnormal ion concentration inside and outside the cell due to leaky membranes
- -ANS stim can cause SB due to increased vagal tone
- -arrhythmogenic drugs like dopamine
Are arrhythmias more likely to be fatal when they occur pre-hospital or in the hospital?
- -Pre-hospital, major source of pre-hospital mortality
- -Once is hospital they are recognized and treated
Most common arrhythmias seen with acute MI
- -VF (largely responsible for sudden cardiac death in acute MI)
- -conduction block
Which is associated with a higher mortality rate- VF that occurs during the reperfusion period (1st 48 hours) or after?
- -VF that occurs after the initial 48 hours is worse
- -It's usually associated with severe LV dysfunction
Why does ST need to be treated quickly?
It increases myocardial O2 demand
What factors can contribute to ST in an acute MI?
- -chronotropic drugs (dopamine)
What % of pts with an inferior infarct will have a RV infarct?
- -RCA perfuses both areas
papillary muscle rupture complications
- -mechanical complication of an MI
- -acute and severe MR which can be fatal
- -partial rupture can lead to pulmonary edema or HF
ventricular wall rupture
- -mechanical complication of an MI
- -a tear in the necrotic myocardium can lead to ventricular wall rupture
- -can occur in 1st 2 weeks
- -uncommon and poor survival rates
- -fatal as rupture causes ventricle to bleed into pericardium and causes tamponade
- -partial rupture can lead a to a pseudo aneurysm (cardiac time bomb)
mechanical complications of an MI
- -ventricular wall rupture
- -papillary muscle rupture
- -ventricular aneurysm
- -ventricular septum rupture
- -late complication that occurs in weeks to months
- -ventricle wall is weakened by phagocytosis of necrotic tissue
- -local bulge and dyskinesis results
- -can lead to embolism, HF, or arrhythmias
- -MI complication
- -inflammation that occurs in area of infarct can spread to adjacent pericardium
- -s/sx: sharp pain, friction rub, fever, usually responds to ASA and NSAIDS
- -MI complication, can occur in the weeks following an MI
- -uncommon form of pericarditis
- -thought to be an immune process, not totally clear
- -responds to NSAIDS
- -MI complication
- -due to LV not pumping properly, leading to stasis of blood
- -often occurs if area of infarct is LV apex or with a true aneurysm
Causes of death from ACS
- -decreased CO
- -damming of blood in venous system
- -infarct rupture
How are the actual area of infarct and the surrounding area affected by infarct?
- -looks like a bullseye
- -Area of infarct (center)- muscle cells die within 1-3 hours due to total loss of blood supply
- -area surrounding it is non functional (first ring), there's a failure of contraction and impulse conduction
- - (second ring) going further out, there's an area that's contracting only weakly due to mild ischemia
Will the non functional area (area surrounding the dead cells) recover usually?
- -depends on collateral, with good collaterals, most of it can recover
- -some may die due to prolonged ischemia
- -after a few days to 3 weeks it either dies or recovers
T or F, the non functional area (surrounding the dead fibers) hypertrophy to compensate for the fibrous tissue that has now taken the place of the dead cells
Why is rest important to recovery?
- -Minimizes O2 demand and helps to restore balance between O2 supply and demand
- -minimizes coronary steal
- -can occur during MI recovery when the heart is stressed (exercise)
- -the normal vessels respond to stress by vasodilating and "stealing" blood from the ischemic areas of the heart
- -hence rest is so important in recovery
Does the heart retain its pumping ability post MI?
No, but it does maintain resting CO. The ability to respond to stress is affected.
-when do they usually occur
- -24-48 hours post-op
- -tachycardia and ST depression precede
surgical factors that can contribute to peri-op MI
- -creates decreased O2 supply and increased O2 demand
- -surgery sets up an inflammatory response which creates a hypercoagulable state
- -blood loss (decreased O2 carrying capacity)
- -surgical stress leads to increase HR and increased O2 demand
- -post-op shivering
How can we assess cardiac reserve capacity pre-op
- -by asking about functional status
- -if a person have limited exercise tolerance and no lung disease that's a good predictor of poor reserve
Post MI how long is surgery delayed for (at a minimum)
How long is surgery delayed for after a BM stent? A drug eluding stent?
- BM 6 wks
- DES 12 mos (to allow completion of anti-plt therapy and endothelialization)
T or F, a pt with vascular dz has increased risk of MI
What are the 6 predictors of cardiac risk for pts undergoing non-cardiac surgery (Lee revised cardiac index)?
- 1) high risk surgery (AAA, peripheral vascular, major abd, or thoracotomy)
- 2) ischemic heart disease (history of MI, Q waves)
- 3) CHF
- 4) Cerebrobasc dz
- 5) IDDM
- 6) Creatinine > 2
What possible cardiac risks does the Lee revised cardiac index refer to?
- 3rd degree HB
- pulm edema
What factors are not risk factors according to the Lee revised cardiac index?
- -critical AS
- -prior CABG
- -BB use
- -advanced age
- -abnormal cardiac rhythms
- -pre-op ST or T wave changes
pre-anesthesia risk assessment of pt with ischemic HD: pt needs emergency surgery
optimize medical treatment
pre-anesthesia risk assessment of pt with ischemic heart disease: pt has unstable CAD (major risk factors) or change in cardiac condition
pre-op major clinical risk factors (algorithm)
- -unstable coronary syndrome
- -decompensated HF
- -signif arrhythmias
- -severe valvular dz
these pts might need to have surgery delayed for further eval
pre-op intermediate clinical risk factors (algorithm)
- -stable angina
- -previous MI by history or Q waves
- -h/o HF or compensated HF
- -renal insufficiency
-these pts have increased risk for peri-op complications
pre-op minor clinical risk factors (algorithm)
- -L BBB
- -non specific ST / T wave changes
- -h/o CVA
-not proven to be independent risk factors
what's considered high risk surgery? What's the risk of a cardiac event?
- -emergency or major surgery
- -aortic and other major vascular
- -long surgery with significant blood and fluid loss
what's considered intermediate risk surgery? What's the risk of a cardiac event?
- -head and neck surgery
- -intraperitoneal surgery
- -thoracic surgery
- -risk < 5%
what's considered low risk surgery? What's the risk of a cardiac event?
- -<1% risk
Per AHA guidelines if 2 out of 3 of which risk factors are present means the pt needs further cardiac work-up?
- -high risk surgery
- -low exercise tolerance
- -moderate clinical risk factors
What qualities to the alpha 2 agonists have that can help to decrease peri-operative injury?
-sedation and anxiolytic properties
Where would be typically place the EKG leads and what leads would we monitor and why?
- lead II (RA)- good to detecting arrythmias
- V- V5 area to monitor LV
Is increased HR or BP more likely to cause intra-op ischemia?
- -Increased HR, esp if >110 bpm
- -Increases O2 demand and reduces supply (shortened diastolic filling time- subendocardial vessels)
What's considering maintenance of stable HD?
- -BP within 20% of normal
What percent of pts have myocardial ischemia (detected by thallium scan) during intubation?
- most occur without HD changes
What induction drug should we avoid with ACS
What NMB agents are ok to use with ACS
- -succ or NDMR are ok
- -prolly want to avoid panc
How can we attenuate the response to laryngoscopy?
- -IV lido, 1.5 mg/kg 90 seconds before
- -fentanyl (slows the HR)
L BBB vs R BBB
L BBB- impulse goes to right side first, then left; R R' in V5 or V6
R BBB- impulse goes to left side first; R R' in V1 or V2
- -non simultaneous ventricular depolarization
- -widened QRS
Can you detect infarct with EKG with a pt with a LBBB?
- -large R wave in V1 and V2 (should be small)
- -right axis deviation
- -large S wave in V1
- -large R wave in V5 and V6
- -common from AS or HTN
extreme right axis deviation