Nurs614 Exam3 Cardiac Anesthesia For Non-Cardiac Surgery

Front 1

How many patients undergo noncardiac surgery each year in the United States?

Back 1

25 million

Front 2

Of the 25m Americans who undergo noncardiac surgeries annually, how many patients have clinical evidence or multiple risk factors for CAD?

Back 2

3 million

Front 3

Of the 25m Americans who undergo noncardiac surgeries annually, how many are > 65 yrs old

Back 3

4 million

Front 4

Of the 25m Americans who undergo noncardiac surgeries annually, how many are at risk for cardiovascular complications?

Back 4

Nearly 1/3 of surgical patients

Front 5

What has contributed to the reduced rate of major cardiac complications r/t surgery

Back 5

Advances in anesthesia, post-op analgesia, and surgical technique.

Front 6

What is the risk of perioperative MI and cardiac death with noncardiac surgery?

Back 6

0.1% & 0.4% respectively
Overall risk remains low.

Front 7

Prevalence of cardiovascular disease increases with age.
How may people does cardiovascular disease kill annually?

Back 7

1 million people (more than all other causes of death combined).

Front 8

Majority of cardiac deaths are related to?

Back 8

CAD

Front 9

Estimated of all elective non-cardiac surgery patients that have CAD or have multiple cardiac risk factors?

Back 9

28%

Front 10

What are the major cause of perioperative morbidity and mortality?

Back 10

Cardiac complications related to the frequent presence of underlying CAD. (1-5% of all surgical patients).

Front 11

½ of perioperative cardiac complications are from?

Back 11

Ischemia or coronary artery plaque rupture with thrombus formation and coronary artery occlusion.

Front 12

How many anesthetics are currently performed each year to persons > 65yrs old?

Back 12

6 million.
Over the next 30 years that number will double to 12 million.

Front 13

During preoperative studies, when is a cardiology consult
recommended?

Back 13

Only when the information obtained will result in a change in.

Front 14

What is the role of the cardiology consult?

Back 14

To communicate the severity and stability of the patients cardiovascular status to help determine if pt is ok for surgery to be done.

Front 15

What is goal of the preop cardiac eval is to improve outcome. What else is the purpose of the preop eval?

Back 15

Goal = Improved Outcome
Detect the presence of CVD
Determine prior and current therapy
Define severity and stability
Equate severity and stability to proposed surgery
Determine if the patient is optimally prepared.

Front 16

The presence of CVD is indicated by?

Back 16

SOB with exertion (like climbing a flight of stairs) or having had a prior MI.

Front 17

Exercise tolerance is one of the most important determinants of?

Back 17

Perioperative risk. An excellent exercise tolerance, even in the presence of angina, suggest that the myocardium can be stressed without becoming dysfunctional.

Front 18

True/false?
Anesthesia within 6 months of an MI is associated with increased risk.

Back 18

False.
Because of recent advances related to thrombolytics, angioplasty, stents, etc., that is no longer true.

Front 19

the AHA/American College of Cardiology Task Force on Perioperative Evaluation of the Cardiac Patient undergoing non-cardiac surgery has advocated that having higher risk is an MI < _____ ____ ago.

Back 19

30 days

Front 20

True/false
Further studies may be required for elective surgery with patients with symptomatic CAD.

Back 20

True

Front 21

Pre-Operative cardiac clinical evaluation should include?

Back 21

History and Physical
Electrocardiogram (EKG)
Type of surgery (high/intermediate/low risk)
Algorithm for every patient
Cardiac Risk Index
Functional Capacity (metabolic equivalents

Front 22

What scales are used to assess the preoperative risk assessment?

Back 22

ASA classification
Goldman classification
ACC/AHA recommendations

Front 23

ASA Physical Status Assessment classifications:

Back 23

Class I: Healthy pt/elective operation
Class II:Pt with mild systemic disease
Class III: Severe systemic disease that limits activity but is not incapacitating
Class IV: Incapacitating systemic disease that is a constant threat to life
Class V: Moribund pt not expected to survive 24hrs with or without operation.

Front 24

ASA Classification Shortcomings?

Back 24

Subjective
Poorly reproducible in certain subsets (Elderly, Obese, Prior MI, Mild systemic diseases)

Front 25

List the areas assessed by the Revised Cardiac Risk Index - Goldman

Back 25

High risk types of surgery
H/o IHD
H/o CHF
H/o cerebrovascular disease
Preop isulin tx
Preop serum creatinine >2.0

Front 26

The RCRI is used to assess?

Back 26

The probability of perioperative cardiac risk.
It is used to direct preoperative cardiovascular testing and guide perioperative management.

Front 27

Surgical Risk Factors - high?

Back 27

Emergency surgeries;
Major vascular;
Peripheral vascular; Prolonged surgeries with major fluid shifts.

Front 28

Surgeries with intermediate surgical risk actors:

Back 28

Carotid Endarterectomy
Head & Neck surgies
Intraperitoneal surgeries Intrathoracic surgies
Orthopedic / Prostate

Front 29

Surgical Risk Factors - Low?

Back 29

Endoscopic
Superficial Procedures Cataract
Breast

Front 30

How are the risk factors identified by the Revised Cardiac Risk Index - Goldman
scored?

Back 30

One point assigned per risk factor:
IHD
CHF
CV disease
High-risk surgery
DM requiring insulin
Pre-op creatinine >2.0 mg/dl

Next, determine the cardiac complication rate according to the Risk Class below:
Class I zero 0.4%
Class II one 0.9%
Class III two 6.6%
Class IV three +11%

E.g., a person with no risk factor is a CLass I with a cardiac complication rate of 0.4%

Front 31

The ACC and AHA Task Force have provided a framework to assess cardiac risk for noncardiac surgery. Why were these guidelines established?

Back 31

To optimize treatment strategies and preoperative testing for the benefit of the noncardiac patient

Front 32

According to the American College of Cardiology and AHA Predictors of increased risk in the CAD pt, AMI is defined as?

Back 32

Less than 7 days ago

Front 33

According to the AHA Predictors of increased risk in the CAD pt, recent MI as defined as?

Back 33

7 days to 30 days ago

Front 34

Patient Risk Factors - major:

Back 34

Recent MI
Severe or Unstable Angina Decompensated CHF
Significant Dysrhythmias

Front 35

Patient Risk Factors - intermediate:

Back 35

Mild Angina/Old MI/ Compensated CHF/Diabetes

Front 36

Patient Risk Factors - monor:

Back 36

Advanced Age / Abnormal EKG / Rhythm other than Sinus / Uncontrolled Hypertension

Front 37

List the types of monitoring used in surgery for the pt with cardiac risk

Back 37

NIBPe
ECG
Computerized ST Trending
Echo (TEE)
Aline
CVP
PAP
Mixed Venous Oxygen Saturation

Front 38

Compare NIBP to intra-arterial BP monitoring

Back 38

Intra-arterial DBP may be as much as 10 mm Hg higher that of the NIBP.

Front 39

Advantages of NIBP monitoring?

Back 39

Easy, automatic & reliable

Front 40

Disadvantage of NIBP?

Back 40

Incomplete deflation from rapid measurements --> inadequate venous drainage --> venous stasis –-> limb swelling –-> nerve damage.

Front 41

What % of the time does the 12 lead ECG detect ischemia compared to just the monitoring lead II

Back 41

60 to 85% of the time

Front 42

If using a 3 lead configuration, how can you can do a modified V5?

Back 42

By placing the R arm lead on the R shoulder & the L arm in the V5 position and the LL in the usual position.

Front 43

Which lead is best for arrhythmia and which is best for ischemia detection?

Back 43

Lead II & V5 respectively

Front 44

How does the monitor analyze ST segments?

Back 44

By using PR interval as a baseline and providing a visual and numerical value. 2 mm change may indicate ischemia.

Front 45

What type of echo is best in the OR?

Back 45

TEE.
Transthoracic approach gets in the way of surgery and doesn’t provide the best view.

Front 46

True/false?
The TEE can be done by the a/provider when the pt is in the OR

Back 46

False.
It must be done by a skilled clinician.

Front 47

How does the TEE compare to the ECG for detecting abnormalities?

Back 47

TEE can detect ischemia(segmental wall motion abnormalities) quicker than ECG ST changes.

Front 48

Pressure wave forms of the Aline offer information useful information.
Narrow waveforn =

Back 48

Constricted arterial vasculature (hypovolemia or perhaps vasoconstrictor therapy)

Front 49

Pressure wave forms of the Aline offer information useful information.
Eg, wide waveforms =

Back 49

Myocardial depression (for whatever reason - anesthetic agents, b-blockers)

Front 50

Arteries commonly used for Alines?

Back 50

Radial / femoral / axillary / dorsalis pedis.

Front 51

The CVP is an accurate measurement of fluid status only when ?

Back 51

Left Ventricular function is normal

Front 52

Normal MEAN venous pressure is?

Back 52

Between 5 and 10 mm Hg.

Front 53

PAC provides information related to?

Back 53

Pulmonary circulation and LV function

Front 54

Causes of elevated SVO2?

Back 54

Increased O2 delivery (increased FiO2/Hb)
decreased O2 utilization(anesthesia, sepsis, hypothermia).

Front 55

Causes of decreased SVO2?

Back 55

Decreased delivery (decreased Hb – Decreased CO – Hypoxemia)
Increased O2 Utilization(hyperthermia – shivering – Thyroid Storm)

Front 56

Five Questions to ask yourself in your preop evaluation:

Back 56

What are the medical issues for this pt?
Is the pt optimally treated?
If not, what needs to be done to optimize the pt?
How long will it take?
Is this an emergency or elective surgery?

Front 57

Types of cardiac testing:

Back 57

12L ECG
CXR
Exercise Stress Test
Ambulatory EKG monitoring
Echocardiography
Myocardial Perfusion Imaging
Dobutamine Stress Test
Cardiac Catheterization

Front 58

What is the 12 Lead ECG used to detect & when should it be done relative to the time of surgery?

Back 58

It detects areas of ischemia and is also used as a baseline to compare intraop ECGS.
It should be done no earlier that 24 hours preop.

Front 59

What are CXRs used for?

Back 59

To detect increase in heart size.
Increase cardiac size by 50% of width of thorax = ventricular dysfunction

Front 60

Increased pulmonary vascular markings =

Back 60

Elevated pulmonary venous pressure from LV dysfunction.

Front 61

Exercise Stress Test determines?

Back 61

Functional capacity and prognostic stratification. IE, is there need for more tests? Is surgery/procedure a high risk pt.?

Front 62

Over what period of time is an ambulatory EKG done & what is it used for?

Back 62

Over a 24 hour period.
It is useful for diagnosis of dysrhythmias and myocardial ischemia.

Front 63

Preoperative ischemia is predictive of?

Back 63

Adverse postoperative outcomes.

Front 64

The Echocardiogragm is helpful in identifying

Back 64

The type, location, severity and physiologic significance of valvular and pericardial disease – as well as ischemia, cardiomyopathies and ventricular function. (TEE is better than transthoracic).

Front 65

Myocardial Perfusion Imaging (pharmacologic stress imaging) is used to?

Back 65

Predict the physiologic response to surgery and anesthesia in patients who are unable to exercise. A vasodilator is administered to cause maximal dilatation of the coronary arteries. Vessels with “fixed” stenosis will not dilate.

Front 66

Dobutamine Stress Echocardiography is used in?

Back 66

Patients unable to exercise. Dobutamine is administered and echo.
Dobutamine increases HR & BP similar to the effect of exercise.
The rise in HR increases the oxygen demand of the heart and helps to determine if the heart muscle is getting enough blood and oxygen.

Front 67

What is the gold standard for diagnosis of cardiac pathology?

Back 67

Cardiac Catheterization

Front 68

What is stroke volume dependent on?

Back 68

Inotropic state of the myocardium
Preload or end diastolic myocardial fiber length
Afterload or resistance to ejection

Front 69

What is preload?

Back 69

It is the volume of venous return that dictates CO via the Frank-Starling Curve

Front 70

How can preload be increased?

Back 70

Via fluid boluses or by increasing venous tone

Front 71

Small change in afterload is capable of producing?

Back 71

Large shifts into central circulation as capacitance vessels contain 60-80% of the total blood volume

Front 72

What is afterload?

Back 72

A measure of impedance to ventricular ejection (resistance is measured as MAP).
It is the only factor in the CO equation that when increased will cause a drop in CO.

Front 73

______ dictates CO in a healthy heart vs _______ dictates CO in an aging or failing heart

Back 73

Preload
Afterload

Front 74

What becomes the dominant factor in determining CO when inotropy of the heart is impaired?

Back 74

Afterload

Front 75

What prophylaxis is used in:
Bacterial Endocarditis
Turbulent Blood Flow
Prosthesis

Back 75

Antibiotics

Front 76

What prophylaxis is used in thromboembolism?

Back 76

Anticoagulation

Front 77

What causes essential (primary )HTN?

Back 77

Cause Unknown

Front 78

What % or HTN is d/t essential HTN?

Back 78

95% of all cases
(20% of adults in USA have it)

Front 79

True/false?
Essential HTN can be effectively tx'd

Back 79

True

Front 80

What causes secondary HTN?

Back 80

It is r/t an identifiable underlying cause

Front 81

What % of those with HTN have secondary HTN?

Back 81

5% of all cases (2.9m Americans).
It is often r/t renal,
endocrine, anatomic disorders
& obesity

Front 82

Optimal BP is?

Back 82

<120/<80

Front 83

Normal BP is?

Back 83

<130/<85

Front 84

What is high-normal BP

Back 84

130-139/85-89

Front 85

Stage 1 HTN is?

Back 85

140-159/90-99

Front 86

Stage 2 HTN is?

Back 86

160-179/100-109

Front 87

Stage 3 HTN

Back 87

SBP = 180 or greater
DBP = 110 or greater

Front 88

General Guidelines for HTN

Back 88

Continue Medications;
Determine adequacy of control;
Review Pharmacology of current drugs;
End-organ Damage?
Auto-regulation curve Right Shifts ;
HTN Patients tend to be Hypovolemic;

Front 89

Many antihypertensive drugs have anesthetic implications. Eg, if a pt is on a b/blocker, what does it tell us?

Back 89

We do not want an increase in HR with surgical stimulation nor do we want volume depletion.

Front 90

Many antihypertensive drugs have anesthetic implications example. If a pt is on an ACE inhibitors, what does it tell us?

Back 90

Pts on ACE inhibitors may experience an anesthetic induced hypotension due to decreased SNS vasoconstrictive response.

Front 91

For the pt on antihypertensive tx getting a diuretic, BOLO for:

Back 91

Hypokalemia & volume depletion.

Front 92

What induction agents are best for pts with cardiac impairments

Back 92

Any induction agent is okay except probably Ketamine b/c it exaggerates existing HTN.
(vasodilation and decreased intravascular volume).

Front 93

DVL (direct view laryngoscopy) may produce?

Back 93

Exaggerated increases in BP. Keep attempt short and smooth! Blunt this response to prevent increased HR & ischemia

Front 94

What is atherosclerosis?

Back 94

Accumulation of plaques deposits on the inner surface of arteries. Plaque deposit is progressive.
Plaques get larger and more numerous.
Plaques consist of lipid, protein, and immune cells.
As plaques develop, they calcify and become atherosclerosis.

Front 95

The most common cause of myocardial ischemia is?

Back 95

Atherosclerosis of epicardial coronary arteries

Front 96

Factors affecting global oxygen supply

Back 96

Blood O2 carrying capacity
CO
SVR
Coronary resistance

Front 97

Factors affecting oxygen demand?

Back 97

Major determinants of MVO2
(systolic work - HR, BP/afterload, duration of systole);
ventricular wall tension (LaPlace)
contractility;
myocardial mass.

Front 98

According to Poiseulle, resistant is dependent on?

Back 98

Radius and length

Front 99

According to Poiseulle, -doubling the radius result in?

Back 99

A 16-fold increase

Front 100

According to Poiseulle, - decreasing the radius by half result in?

Back 100

A decrease to 1/16th of the original

Front 101

General Guidelines for the IHD

Back 101

Preload – keep normal to slightly decreased to decrease wall tension & LVEDP;
Afterload – Maintain (HTN is better than hypotension);
Contractility – slightly depressed only if LV is normal;
Rate – slow (to decrease O2 consumption);
Rhythm – sinus (for max efficiency and efficient use of oxygen delivery);
MVO2 – monitor and treat supply/demand issues aggressively.

Front 102

Premedication for the pt with IHD includes anxiolytic because?

Back 102

Pt may be nervous & this could lead to a hyperdynamic response --> increase BP & HR --> increased MVO2 (myocardiac O2 demand).
Tailor anxiolytics to patient needs.

Front 103

Why is Etomidate a good choice of induction agents in the pt with IHD?

Back 103

Etomidate reduced MVO2 by 50% and increases coronary sinus artery saturation by 20 to 30%.

Front 104

Many methods work to reduce autonomic response in the IHD pt, like giving high dose narcotics. What should you BOLO for?

Back 104

Hypotension and tachycardia.

Front 105

Aortic Stenosis results in?

Back 105

Obstruction to ejection of blood into the aorta;
Chronic obstruction to Left ventricular ejection;
Left ventricular emptying is impaired because of high outflow resistance caused by a reduction in the valve orifice area when it opens.

Front 106

What is the over all effect of concentric hypertrophy?

Back 106

Decreased diastolic compliance and increased oxygen demand.
In the concentric hypertrophy, the chamber size is unchanged but the muscle mass is increased.
We need to fixed the SV!

Front 107

What type of remodeling is involved in eccentric hypertrophy?

Back 107

The chamber size and muscle size is increased --> increase in ventricle compliance.
There is no major change in oxygen supply or demand.

Front 108

Causes of Aortic Stenosis?

Back 108

Most often - Degenerative Bicuspid Valve;
Secondary to Degeneration of Tricuspid Valve ( > 65 yrs);
Secondary to Rheumatic Heart Disease of Tricuspid Valve.

Front 109

In the pt with aortic stenosis, what causes increased oxygen demand ?

Back 109

Increased LV Wall Stress
Increased Myocardial Mass (Concentric);
Increased Pressure Work;
Increased LV Ejection Time.

Front 110

In the pt with aortic stenosis, what causes decreased oxygen supply ?

Back 110

Decreased Diastolic Time
Inadequate Coronary Artery Proliferation
Increased Transmural Pressure
Increased LVEDP

Front 111

When does the coronaries of the LV get perfused?

Back 111

Diastolic time perfuses coronaries of the LV.

Front 112

What causes increased transmural pressure?

Back 112

Inadequate coronary artery proliferation in the face of increased muscle mass
prevents blood flow to subendocaridal tissue.

Front 113

For the pt with aortic stenosis,where should we keep the pt's HR & why?

Back 113

Maintain HR to 60 -80 bpm to control oxygen utilization and prevent myocardial ischemia.
Avoid bradycardia b/c it causes a decrease in CO because SV is fixed.
Tachycardia causes decrease time for LV filling and ejection which --> decreased SV --> decreased coronary perfusion and increased O2 demand.

Front 114

For the pt with aortic stenosis,what is our ECG rhythm goal & why?

Back 114

Maintain sinus rhythm. The atrial kick is required to ensure an optimal LV end-diastolic volume because it could account for 30 to 40% of Left ventricle filling. Treat junctional or bradycardia with atropine. Tachycardia treated with beta blockers and SVTs are cardioverted. Lidocaine treats dysrhythmias.

Front 115

For the pt with aortic stenosis,what is our preload goal?

Back 115

Maintain or increase preload to provide adequate filling and CO.

Front 116

For the pt with aortic stenosis,what is our afterload goal?

Back 116

Maintain or increase to keep coronary perfusion pressure stable. Avoid sudden increases or decreases in SVR. Increased afterload is required to FILL Coronaries during diastole. A decrease in afterload will decrease coronary perfusion.

Front 117

For the pt with aortic stenosis,what is our contractility goal?

Back 117

Maintain (this is usually not a problem however).
In the case of persistent hypotension, use an inotrope.

Front 118

For the pt with aortic stenosis,what is our MVO2 goal?

Back 118

Avoid Tachycardia/Hypotension.
Ischemia is an ever present risk.

Front 119

Why do we premedicate with prophylactic antibiotics in the pt with aortic stenosis?

Back 119

To prevent Endocarditis.

Front 120

Why do we premedicate with anxiolytic in the pt with aortic stenosis?

Back 120

To avoid catecholamine surge related to anxiety. BOLO for increased HR and or myocardial depression.

Front 121

What induction agenst should be used in the pt with aortic stenosis?

Back 121

Anything is okay as long as you don’t decrease CO or cause increase HR.

Front 122

Guidelines for maintenance of anesthesia in the pt with aortic stenosis?

Back 122

NO, VAs or opioids are ok. Use low dose VAs to prevent myocardial contractility depression. (High dose opioids and low dose VAs work well).

Front 123

What is our guideline(s) for BP management in the pt with aortic stenosis?

Back 123

Prompt replacement of blood loss and liberal administration of fluids intraop. DON”T GET BEHIND!
Hypotension can be treated with very small doses of phenylephrine.

Front 124

In the pt with aortic stenosis, what are the guidelines for regional anesthesia

Back 124

Avoid spinal or epidural anesthesia b/c peripheral SNS blockade could rapidly decrease SVR causing a decreased venous return to the heart and decreased coronary artery perfusion.

Front 125

What is the result of mitral stenosis?

Back 125

Mechanical obstruction to left ventricular diastolic filling secondary to progressive decreases in the orifice of the Mitral valve.
(Left Atrial Outflow Obstruction).

Front 126

What causes mitral stenosis?

Back 126

Rheumatoid disease (99.8% of cases);
Congenital mitral stenosis;
Ineffective endocarditis;
Carcinoid syndrome;
Fabray's disease;
Hurler's syndrome;
Left atrial myxoma;
Whipple's disease.

Front 127

Mitral Stenosis Symptoms?

Back 127

Fatigue
Cough
SOB
Left sided failure
Palpitation
Afib
Systemic embolism
Pulmonary infection
Hemoptysis
R/sided failure (Hepatic Congestion & Edema);
Worsened by conditions that increase CO (exertion,fever, anemia, tachycardia, pregnancy).

Front 128

What is the HR guidelines for the pt with mitral stenosis?

Back 128

70 -80
Keep HR slow to allow for diastolic filling of LV;
Avoid tachycardia (it can cause pulmonary edema & decreased CO) and RVR during AFib.

Front 129

What is the ECG rhythm guidelines for the pt with mitral stenosis?

Back 129

Sinus Rhythm.
Atrial kick contributes 30% of LV stroke volume.
If AFib begins, control ventricular rate with digitalis.

Front 130

What is the preload guidelines for the pt with mitral stenosis?

Back 130

Maintain volume or keep slightly increased to help with LV filling however, excess preload may cause pulmonary edema.
Basically a balancing act between too much fluid (pulmonary edema) and not enough fluid (decreased CO).

Front 131

Guidelines for afterload mngmnt in mitral stenosis?

Back 131

SVR should be maintained; Avoid decreases in SVR as decreased SVR --> tachycardia (an attempt maintain BP since SV is fixed;
Avoid increases in PVR.

Front 132

What are the guidelines for contractility management in the pt with mitral stenosis?

Back 132

Maintain contactility to provide adequate CO. A decrease in CO could lead to Pulmonary Edema.

Front 133

WHEN DOES RV CORONARY PERFUSION OCCURS?

Back 133

IN SYSTOLE.
If you increase RV size and wall tension etc. you decrease perfusion.

Front 134

True/false
Most pts with MVS will have a valvuloplasty prior to a concardiac surgery.

Back 134

True
It is a Cath Lab procedure that takes about 2hrs.
It has a HIGH success rate.

Front 135

What premedications are indicated for the pt with mitral stenosis?

Back 135

Antibiotics to avoid endocarditis.
Small doses of anxiolytics – small doses because these patients may be at risk for the ventilatory depressant effects of anxiolytic.

Front 136

Mitral Stenosis Anesthetic Management - monitors?

Back 136

ECG with computerized ST segment analysis,
Pulse oximeter,
A-line,
PAC (or TEE may be better)

Front 137

Mitral Stenosis Anesthetic Management - induction agents?

Back 137

Anything except Ketamine; Avoid tachycardia -
b/blockers for quick response (digitalis 0.25 to 0.5 mg slow IVP for more sustained control).

Front 138

Mitral Stenosis Anesthetic Management - maintenance anesthetics?

Back 138

Anything but keep in mind to avoid changes in HR and SVR and PVR.
Perhaps nitrous oxide should be avoided due to nitrous oxide induced pulmonary vasoconstriction causing an increase in pulmonary pressures and right atrial pressure.
Use lots of opioids!
Keep patients deep enough to control autonomic responses.

Front 139

Mitral Stenosis Anesthetic Management - fluid management goals?

Back 139

Increases in intravascular volume could may cause CHF – pulmonary edema – atrial fibrillation.
Fluid management is a balancing act.

Front 140

Mitral Stenosis Anesthetic Management - giudelines for BP management goals?

Back 140

Maintain SVR.
TX decrease in SVR with sympathomimetics - use small doses!
Phenylephrine may be better than ephedrine (beta agonist = increased HR although epinephrine or ephedrine may be okay in small doses as the beta 1 off sets the increase in SVR to maintain CO.
If systemic HTN occurs intraop, use of Nitroprusside will reduce SVR.
These patients do not tolerate volume overload very well.
Avoid HEAD DOWN positioning as the pulmonary blood volume is already increased.

Front 141

Mitral Stenosis Anesthetic Management - postop guidelines?

Back 141

These pts are at risk for developing pulmonary edema and R sided failure.
Pain, hypoventilation (respiratory acidosis) and hypoxemia could increase HR and PVR.
Continue all monitoring and pay particular attention to pain control.

Front 142

Mitral Stenosis Anesthetic Management - guidelines for regional anesthesia?

Back 142

Spinal anesthesia is not preferred due to sudden decrease in SVR.
Epidural may be okay due to slower onset.

Front 143

Pts with MVS can become apneic from 1-2mg of Midazolam. Why?

Back 143

No one is really sure as to why.
These pts are extremely sensitive to benzos and narcotics.

Front 144

What is Aortic Regurgitation (AKA “Aortic Insufficiency”)?

Back 144

Decrease in forward LV stroke volume because of regurgitation of part of the ejected stroke volume from the aorta back into the LV.

Front 145

If AI is accompanied by MVR (as is often the case), why do we need to be cautious with even small doses of phenylephrine?

Back 145

It can cause fulminant pulmonary edema.
A BETTER CHOICE MAY BE 2-4 MCG OF EPINEPHRINE.

Front 146

Etiology of Aortic Regurgitation?

Back 146

Any conditions resulting in incompetent aortic leaflets;
Congenital Bicuspid valve;
Aortopathy (Cystic medial necrosis, Collagen disorders like Marfan’s, Ehler-Danlos,
Osteogenesis imperfecta,
Pseudoxanthoma elasticum);
Rheumatic heart disease;
Dilated aorta (e.g. hypertension..);
Degenerative Connective tissue disorders
(ankylosing spondylitis, rheumatoid arthritis, Reiter’s syndrome,
Syphilis which --> chronic aortitis,
Acute AI (aortic dissection, infective endocarditis & trauma).

Front 147

General Guidelines for Aortic Regurgitation - HR?

Back 147

Try to keep patient at the HR they showed up with…….
Increase HR --> increased CO;
Tachycardia --> decreased diastole time & decreased
regurgitant fraction;
HR goal is around 90 bpm - this leads to good forward flow without ischemia to myocardium;
Sudden decreases in HR will increase regurgitant volume.

Front 148

General Guidelines for Aortic Regurgitation - rhythm?

Back 148

Try to maintain sinus rhythm but rhythm is not as important as rate.

Front 149

General Guidelines for Aortic Regurgitation - preload?

Back 149

Increase preload to maximize forward CO and maintain BP.

Front 150

General Guidelines for Aortic Regurgitation - afterload?

Back 150

Decrease afterload to favor forward CO.
Increases in afterload will worsen AI.

Front 151

General Guidelines for Aortic Regurgitation - contractility?

Back 151

Maintain contractility

Front 152

Anesthetic Management
Aortic Regurgitation - premedication?

Back 152

Light premeds are okay but don’t over do it.
A little anxiety has a positive effect.
Increased HR is good Hypertension is bad.
Give Antibiotics.

Front 153

Anesthetic Management
Aortic Regurgitation -monitoring?

Back 153

Pt asymptomatic --> probably don’t require invasive monitoring.
Pt symptomatic --> A-line & pulse oximeter;
ECG with computerized ST segment analysis – these patients are prone to ischemia due to LV hypertrophy which increases O2 demand b/c of large muscle mass;
TEE or PAC to guide fluid replacement and BOLO for myocardial depression.

Front 154

Anesthetic Management
Aortic Regurgitation -induction?

Back 154

Just about anything works well, keeping in mind to preserve preload & decrease afterload.
Keep HR around 90 bpm. Ketamine amy increases HR but may increase SVR (bad).

Front 155

Anesthetic Management
Aortic Regurgitation -maintenance?

Back 155

Avoid sudden decreases in HR,
Sudden increased in SVR; Minimize drug-induced myocardial depression;
Bradycardia --> LV volume overload;
Increase SVR can --> LVF;
Use dopamine to increase contractility;
Use nitroprusside to decrease SVR;
If severe LVF, use opioids only;
If no severe LVF, opioid/IAs are ok.
Prompt replacement of any blood loss.

Front 156

Anesthetic Management
Aortic Regurgitation -postop?

Back 156

Maintain monitors – control pain;
continue with the AI management strategies.

Front 157

Anesthetic Management
Aortic Regurgitation - regional?

Back 157

The uncontrolled nature of the decreased SVR that accompanies spinal / epidural make it a poor choice for these patients.

Front 158

What is Mitral Regurgitation?

Back 158

Decrease in forward left ventricular stroke volume due to the fact that part of the stroke volume is regurgitated through the incompetent mitral valve back into the left atrium.

Front 159

Cause of mitral valve regurgitation?

Back 159

Thickening of valve leaflets d/t rheumatoid disease;
Rupture of the chordae (posterior leaflet more frequently affected b/c of trauma or Marfan's);
Papillary muscle rupture or dysfunction (AMI);
LV enlargement --> dilation of mitral annulus;
LV aneurysm --> valvular dysfunction (AMI).

Front 160

Mitral Regurgitation - Symptoms?

Back 160

Similar to MS
Dyspnea, Orthopnea
Fatigue
Pulmonary HTN, right sided failure
Hemoptysis
Systemic embolization in A Fib

Front 161

General Guidelines for
Mitral Regurgitation - HR?

Back 161

Bradycardia --> increases LV volume --> increase in regurgitant --> decreased CO.

Front 162

General Guidelines for
Mitral Regurgitation - Rhythm?

Back 162

Atrial contribution to LV preload is not as important in MR as with MS.
Many of these patients are in chronic AFib. which is okay – just keep ventricular rate up.

Front 163

General Guidelines for
Mitral Regurgitation - preload?

Back 163

LV preload is maintained or slightly increased with one stipulation – IN SOME PATIENTS INCREASE IN LV PRELOAD DILATES THE L/ATRIUM AND VENTRICLE THUS DILATING THE MITRAL VALVE ANNULUS AND INCREASING MR.
Answer: give a fluid challenge & see what happens.
In some patients a preload reduction may reduce regurgitant flow.
Check CO after fluid challenge.

Front 164

General Guidelines for
Mitral Regurgitation - afterload?

Back 164

An increase in afterload --> increase MR --> decreased CO.
For this reason a reduction in afterload is desired.

Front 165

General Guidelines for
Mitral Regurgitation - contractility?

Back 165

SV is dependent on maximal function of the hypertrophied LV.
Avoid anything that depresses myocardial contractility.

Front 166

General Guidelines for
Mitral Regurgitation - contractility?

Back 166

MVO2 is usually not an issue unless MR coexists with IHD.

Front 167

Anesthesia Management
Mitral Regurgitation - premedications?

Back 167

Use judiciously because over sedation can lead to hypercapnia and increase in PVR.
A little anxiety to produce increased HR is not a bad thing
Give antibiotics.

Front 168

Anesthesia Management
Mitral Regurgitation - monitors?

Back 168

ECG with ST analysis, pulse ox, A-line and TEE or PAC.
NOTE: regurgitation of blood into the LA produces a V wave on tracings of the PAOP;
Changes in V wave amplitude can assist in estimating the magnitude of MR.

Front 169

Anesthesia Management
Mitral Regurgitation - induction?

Back 169

Anything can be used but avoid agents that may cause a
decrease in HR, increase in SVR or myocardial depression.

Front 170

Anesthesia Management
Mitral Regurgitation - maintenance?

Back 170

With severe LV dysfunction opioid anesthetic is the choice.
Normally – VA/opioids work well.
VA tend to reduce SVR, increase HR and in small doses have minimal myocardial depressant effects. Myocardial depression should be treated with an Inotropic agent to increase contractility, increase forward flow and decreases regurgitation due to constriction of the mitral annulus.

Front 171

Anesthesia Management
Mitral Regurgitation - regional?

Back 171

Regional is not ideal due to uncontrolled reduction in SVR

Front 172

What is Mitral Valve Prolapse?

Back 172

Billowing of the posterior mitral leaflet into the left atrium during systole.
It called billowing if it is >3mm above annlus.

Front 173

What is the most common valvular heart disease?

Back 173

Mitral Valve Prolapse.
In 5 to 10% US population;
There ia a genetic Predisposition;
Predominantly benign condition;
Severe MV prolapse will lead to MV regurgitation;

Highest among young women, who are tall, thin & who have small breasts.
Seems to be a relationship between connective tissue disorders and MVP;
Most patients are asymptomatic.

Front 174

Symptoms of Mitral Valve Prolapse?

Back 174

Fatigue
Palpitations
Chest Pain
Arrhythmias
Diagnosed by echocardiograph findings

Front 175

What are the symptoms in MVP d/t?

Back 175

Autonomic dysfunction which leads to increased catecholamine concentrations which leads to abnormal amounts of vasoconstriction which leads to papillary muscle ischemia.
Arrhythmias are nonspecific.

Front 176

Complications of Mitral Valve Prolapse?

Back 176

MVRegurg
Endocarditis
Ruptured Chordae Tendineae
TIA / CVA
Nonspecific cardiac dysrhythmias;
VT;
AVB;
ST segment / T wave changes;
Sudden Death (rare).

Front 177

General Guidelines for
symptomatic patients Mitral Valve Prolapse - HR?

Back 177

Slow for diastolic filling

Front 178

What are the treatment guidelines for nonsypmotmatic patients with MVP?

Back 178

They don’t require anything special.

Front 179

General Guidelines for
symptomatic patients Mitral Valve Prolapse - afterload?

Back 179

Slightly increased to reduce LV emptying thus reducing prolapse.

Front 180

General Guidelines for
symptomatic patients Mitral Valve Prolapse - contractility?

Back 180

Slightly decreased to reduce prolapse.
Increased contractility could exaggerate prolapse --> acute MR.

Front 181

General Guidelines for
symptomatic patients Mitral Valve Prolapse - anesthetic management ?

Back 181

Based on specific patient condition.
Most patients are asymptomatic and don’t require anything special. Those that are symptomatic treat similar to Mitral Stenosis anesthetic management.

Front 182

What are the different types of Hypertrophic Obstructive Cardiomyopathy (HOCM)?

Back 182

Idiopathic Hypertrophic Sub-aortic Stenosis (IHSS);
Asymmetric Septal Hypertrophy (ASH);
Muscular Sub-aortic Stenosis (MSS);
Hypertrophic Cardiomyopathy (WHO).

Front 183

What is the pathophysiology of Hypertrophic Obstructive Cardiomyopathy (HOCM)?

Back 183

Dynamic left ventricular 0utflow tract obstruction;
Mitral regurgitation;
Diastolic dysfunction;
Myocardial ischemia;
Cardiac arrhythmias.

Front 184

With dynamic LV outflow obstruction, the severity of obstruction increases with?

Back 184

Any maneuver that increases the force of contraction (like inotropes);
Any maneuver that decreases filling of the ventricle (like exercise, volume depletion);
Sudden assumption of upright posture, tachycardia, valsalva maneuver).

Front 185

What is diastolic dysfunction?

Back 185

LV DBP is elevated;
Ventricles become relatively "stiff," & thus it difficult to fill the in between heart beats.
The early diastolic filling phase (when most of the filling occurs under normal conditions) is prolonged and diminished and most of the filling occurs late in ventricular diastole, during the atrial systole.

Front 186

True/false?
Myocardial ischemia
occurs in the absence significant stenosis of epicardial coronary arteries.

Back 186

True
(Coronary angiogram would be “clean”)

Front 187

The mechanisms of myocardia ischemia include?

Back 187

Supply/demand mismatch due to increased muscle mass;
Increased wall tension due to impaired relaxation during diastole'
Abnormal intramyocardial arteries.

Front 188

PSVT arrhythmias -->?

Back 188

Shorter diastolic filling time;
Patients have palpitations,
SOB;
Pts may experience syncope.

Front 189

Non-sustained ventricular tachycardia occurs during ambulatory monitoring in what % of pts?

Back 189

25%

Front 190

What % of pts with PSVT develop Afib?

Back 190

15-20%.
It is poorly tolerated b/c there is not enough filling time for diastolic filling and patients loose the “atrial kick”.

Front 191

In Afib, the pt loses the atrial kick which results in?

Back 191

Lost of about 30% of preload & decreased diastolic filling time.

Front 192

General Guidelines for HOCM - preload?

Back 192

Preload – Full
Treat aggressively if hypotensive – phenylephrine.

Front 193

General Guidelines for HOCM -afterload?

Back 193

Afterload – slightly increased to lessen degree of obstruction

Front 194

General Guidelines for HOCM -rhythm?

Back 194

Rhythm – sinus is crucial;
Atrial kick needed to maintain preload;
May need atrial pacing (transesophageal or PAC).

Front 195

General Guidelines for HOCM - MVO2

Back 195

MVO2 – Do not increase myocardial oxygen demand

Front 196

HOCM Anesthetic Management - premedication?

Back 196

Premedicate pts to avoid autonomic reactions that worsen obstruction.
IF MR present use antibiotics

Front 197

HOCM Anesthetic Management - monitors?

Back 197

ALine
PAC may be beneficial
ECG with computerized ST analysis

Front 198

HOCM Anesthetic Management - PP vent. & PEEP?

Back 198

Both could decrease venous return to r/heart.
Make sure pt is not hypovolemic.
Decreases in SRV can be treated with small doses of phenylephrine.

Front 199

HOCM Anesthetic Management -induction?

Back 199

Anything but Ketamine is probably okay.

Front 200

HOCM Anesthetic Management - maintenance

Back 200

Inhalational agents will depress myocardium (good thing) but BOLO for decrease in SVR.
Perhaps low dose inhalational agents with lots of narcotics.
Avoid Pancuronium (increase HR) - anything else okay.
BOLO during reversal of nondepolarizing agents – Tachycardia.

Front 201

HOCM Anesthetic Management - postoperative?

Back 201

Avoid hypovolemia, tachycardia, systemic vasodilation and increased contractility.

Front 202

Atrial fibrillation is poorly tolerated.
Should you use inotropes in pts with AFib?

Back 202

No.
Although Afib should be treated immediately, avoid
inotropes, tx hypotension with fluids & phenylephrine.
Hypovolemia and vasodilatation should be avoided at all costs.

Front 203

----% of heart transplant recipients return to OR with in ---- years.

Back 203

30% / 2

Front 204

What are the major issues that heart transplant pts return to the OR with?

Back 204

Ortho issues d/t chronic steroid use;
Infection issues d/t being immunocompromised;
Cholecystitis – high incidence of unknown cause.

Front 205

In transplant pts, there is autonomic denervation b/c?

Back 205

Aorta and main pulmonary artery are transected

Front 206

Heart transplant pts are preload dependent. Explain.

Back 206

Denervated heart responds to demands of increased HR by increasing SV not HR.
(In the normally innervated heart, immediate increase in CO are met with increased HR with little change in SV).

Front 207

In the transplanted heart, HR will increase with some delay probably due to?

Back 207

The time it takes to secrete adrenal catecholamines.

Front 208

How do indirect acting drugs like atropine, pancuronium & neostigmine affect the HR of the transplanted heart?

Back 208

Generally speaking (with some exceptions) drugs that act indirectly will not effect HR.

Front 209

How do direct acting drugs like isoproterenol affect the HR & contractility

Back 209

Increase HR and contractility.
(Propranolol will have the opposite effect. NE has more of a chronotropic effect than you would expect).

Front 210

AICD delivers ------ joules

Back 210

25

Front 211

How does an AICD work?

Back 211

It is a sensing device that senses VTach and VFib and delivers a shock.

Front 212

In the preop eval for the pt with an AICD, what should you ask the pt?

Back 212

How many shocks over past couple of days were delivered. This is an indication of what to expect intraoperatively.

Front 213

What is the preferred anesthetic technique to use for transplant pt?

Back 213

No particular anesthetic techniques is clearly right or wrong.

Front 214

AICD should be turned off OFF before ESWL. How is this done?

Back 214

It depends on the make of the device but normally:
Apply external def. pads before turning off AICD;
Place magnet over device for about 30 sec, listen with stethoscope until beeps turn to solid tone (AICD is off).

Front 215

For the pt with a pacer/AICD that was turned prior to ESWL, how do reactivate it?

Back 215

Place magnet over device and listen for beeps that indicate device returned to normal function.

Front 216

What is the six inch rule regarding AICDs?

Back 216

No use of electrocautery within 6 inches of device or leads.