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What are the 5 clinical predictors for perioperative cardiac events?
1. Hx of IHD
2. Hx of Cerebrovascular Disease
3. Hx of compensated HF
4. DM
5. Renal Insufficiency (creatine >2)
How may clinical risk factors have to be present to consider further preoperative testing?
3
When is the only time you will order further testing?
If it will alter your anesthetic plan
What are the 4 active cardiac conditions that if present will require further pre-op testing and DOS?
1. Unstable Coronary Syndrome
2. New or uncompensated HF
3. Significant arrythmias
4. Severe AS/MS
What is the purpose of using the Cardiac Risk Stratification for Noncardiac Surgical Procedures?
Should be used in conjunction with number of clinical risk factors present when patient's functional capacity is unknown, MET<4, or MET>4 with symptoms
What are the rankings of surgeries in the cardiac risk stratification?
Vascular Surgeries (>5% risk): aortic and other major vascular surgies, peripheral vascular surgery

Intermediate (1-5%):Intraperitoneal and intrathoracic surgery, carotid endarerectomy, head and neck surgery, orthopedic surgery, prostate surgery

Low (<1%): endoscopic proc, superficial pro, cataract sx, breast sx, ambulatory sx
What is the order of steps to follow when determining need for further testing in patient's undergoing non-cardiac sx?
1. Emergency Sx-> proceed
2. Active cardiac conditions-> delay/further testing needed
3. Low risk surgery->proceed
4. Functional capacity-> MET>4 p symptoms, proceed
5. Clinical risk factors-> less than 3 proceed to sx
When is perioperative HR control with beta-blockade appropriate?
1. all patients who are on pre-op beta-blockers, regardless of type of surgery
2. patients with hx of CAD or at least one clinical risk factor with MET>4
3. Patients with 1 or 2 clinical risk factors, in either vascular or intermediate
4.Patients with 3 or more clinical risk factors, in either vascular or intermediate
In what patient populations is beta-blockade not appropriate?
1. Patients having low risk sx who were not on them pre-op
2. Patients with MET >4 with no CAD or clinical risk factors
3. Patients with unknown FC, MET <4, or MET >4 with symptoms who have no clinical risk factors and are not on them at home
What are the 3 categories of cardiovascular pathology?
1. Obstruction of blood flow
2. Regurgitation of Blood flow
3. Shunting of blood flow
Give examples of the 3 categories of cardiovascular pathology
1. OBF: Valvular Stenosis, CAD
2. RBF: AR, MR
3. SBF: ASD, VSD, PFO,PDA, AVM
Cardiovascular pathology produces changes in what 3 cardiac functions?
1. Filling
2. Ejection
2. Cardiopulmonary perfusion
What are the 3 methods that usually identify regurgitation of flow?
1. Auscultation (most common)
2. Echo
3. Pulmonary vascular changes
What are the 2 most common causes of reduced ejection fraction?
1. Ischemia
2. Infarction
What is the cause of decreased oxygen supply to the myocardium in AS with decreased SV
AS causes left ventricular hypertophy to compensate for an increase in impedance of flow. As the ventricle increases in size the coronary arteries are compressed by the hypertrophic muscle mass. The coronary arteries require a higher diastolic aortic pressure to perfuse blood through the narrower coronary arteries.

When the SVR drops there is a drop in the diastolic aortic pressure, therefore there is not a significant pressure to compensate for the narrowing of coronary arteries and that leads to a decrease in perfusion.
The goal of anesthetic management of reguritation is?
Fast, forward, full.
1. Higher HR to decrease diastolic filling time, decreases regurgitation
2. Low SVR to facilitate movement of fluids out of heart chamber, decreases the aortic/ventricular gradient
3. Adequate preload to maintain forward flow. prevents increase SVR r/t hypovolemia
What is the goal of HR control in regurgitation vs. stenosis?
Regurtitation- higher HR tolerated to decrease diastole and filling times

Stenosis- slower HR, 60-70bmp, to increase diastole and increase filling time.
In what valvular diseases is the use of myocardial depressants appropriate and beneficial?
AS

Decreases the amount of O2 consumption.
What valvular diseases require advoidance of myocardial depressants?
AI, MS, MR

AI- must maintain contractility so that blood is pushed out of LV

MS- chronic underfilling of LV causes depressed contractility

MR- increased contractility of LV increases ejected volume, and decreases regurgitant volume
Why is normal SR beneficial in patients with AS and MS?
There is a block of blood flow. Left ventricle is dependent on atrial kick for ventricle filling. Results in adequate CO.
What does angina with ST segment depression indicate? (2 things)
1. Elevation of CKMB/Troponin -> NSTEMI

2. Normal CKMB/Troponin -> UA
What is more common STEMI or UA/NSTEMI?
UA/NSTEMI
When is measurement of ventricular function a more accurate indicator of longterm prognosis?
2-3 months after MI
What is the likely cause of plaque rupture?
Inflammatory cells in atherosclerotic plaques that cause inflammation leading to rupture of plaque and formation of thrombus that occludes the coronary artery
Are plaques that are large enough to cause flow-restrictionin the CA more prone to cause a STEMI?
No, these plaques are less likely to rupture and more likely to cause the development of collateral ciriculation, but still cause angina pectoris
Criteria for the diagnosis of an acute MI?
2 of 3 criteria:
1. Chest pain
2. Serial ECG changes that are indicate an MI
3. Inc and Dec of serum cardiac enzymes.
S & S of an acute MI? 7
Typical:
1. Anxiety
2. Pale
3. diaphoretic

4. ST
5. HOTN
6. Rales
7. Murmur
What is the likely cause of a murmur associated with an MI?
Papillary muscle rupture of the mitral valve, causing MR
What is the progression of Troponin levels in an AMI?
1. Initial increase within 4 hours after myocardial injury

2. Elevated for 7 to 10 days
When is an echo useful for diagnosis of an AMI? Signs of AMI?
1. Pt with LBBB or abnormal ECG without ST elevation

2. Regional wall motion abnormalities
Initial treatment of an AMI?
1. Evaluate hemodynamic stability, 12 lead, and O2 therapy

2. IV morphine and/or sublingual nitro
3. ASA
What does morphine and/or nitroglycerin do to benefit patient during AMI?
Decrease catecholamine release which would cause increase in myocardial O2 requirements
What does ASA or plavix do for an AMI?
decreases further thrombus formation
WHat is the primary goal of management of a STEMI?
Reestablish blood flow to the obstructed coronary artery ASAP.
Should all patients with an AMI receive reperfusion therapy?
NO!

Not indicated in patients that do not have ECG changes indicating STEMI or BBB, ie UA/NSTEMI
When should reperfusion therapy be initiated if indicated?
Streptokinase, TPA, or tenecteplase should be initiated within 30 to 60 minutes of hospital arrivals
Risks of reperfusion therapy? At risk populations?
1. Intracranial hemorrhage
2. Most likely in elderly (>75yo) and pt w/ uncontrolled hypertension

When should coronary angioplasty be performed?
WIthin 90 minutes arrival to hospital and within 12 hours of symptom onset
When is PTCA the modality of choice for reperfusion of coronary arterys caused by STEMI
1. Contraindication to thrombolytic therapy
2. severe HF
3. Pulmonary edema
What patients are canididates for emergent CABG?
1. Angioplasty reveals coronary anatomy that precludes PCI

2. Patient with failed angioplasty
3. Pt with evidence of infarction-related VSD or MR
4. Pt with STEMI who develops cardiogenic shock, LBBB, or Posterior MI within 36 hours of an AMI
Who should Beta blockers be given to after AMI?
All patients should receive IV Beta blockers ASAP after AMI if not contraindicated
How do Beta blockers benefit patient after AMI?
Decrease infarct size by:
1. Decreasing HR
2. Decreasing BP
3. Decreasing Myocardial contractility
What patients should recieve an ACE I or ACE II inhibitor after AMI?
All large AWMI with evidence of LV failure, EF< 40%, or Diabetes
When should prophylactic lidocaine or other antidysrhytmics not be given post STEMI?
In the absence of ventricular dysrhythmics
When is the coronary blood flow differences found between STEMI and UA/NSTEMI?
STEMI- coronary blood flow decreases abruptly, caused by rupture of plaque that causes platelet aggregation and formation of a thrombus

UA/STEMI- reduction in myocardial oxygen supply caused by vasoconstriction related to inflammation
What is the progression of patho of UA/NSTEMI?
Rupture or erosion of atherosclerotic coronary plaque-> thrombus, inflammation and vasoconstriction
3 classic signs of UA/NSTEMI?
1. Angina at rest (lasts 20 mins)
2. Chronic angina that becomes more frequent and more easily provoked
3. New-onset angina that is severe, prolonged, and disabling
Treatment of UA/NSTEMI?
Goal is to decrease myocardial O2 demand:
1. Bed rest
2. O2 therapy
3. Analgesia
4. B-blocker
What patients with UA/NSTEMI are canididates for early invasive evaluation? 8 things
1. Recurrent ischemia or angina at rest.
2. HF
3. Hemodynamic instability
4. Sustainted VT
5. PCI within 6 months
6. previous CABG
7. Inc Trop
8. Angina at low-level activity
When is VF most likely to occur post AMI?
- first 4 hours after AMI
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