Patho Ii, Exam 1- Cumulative

Front 1

What types of congenital heart diseases are acyanotic?

Back 1

atrial septal defect
ventricular septal defect
aortic stenosis
pulmonic stenosis
coarctation of the aorta
patent ductus arteriosus

Front 2

What types of congenital heart diseases are cyanotic?

Back 2

tetralogy of fallot
eisenmenger's syndrome
transposition of the great arteries

Front 3

What are the most and least common types of acyanotic defects?

Back 3

most- ventricular septal defects
least- atrioventricular septal defects

Front 4

What is the most common type of cyanotic defects?

Back 4

tetralogy of fallot

Front 5

What cardiac conditions are associated w the highest risk of adverse outcomes from endocarditis for which prophylaxis for dental procedures is reasonable?

Back 5

1. prosthetic heart valve or prosthetic material used for cardiac valve repair
2. previous infective endocarditis
3. congenital heart diseases

Front 6

What congenital heart diseases indicate prophylaxis for dental procedures?

Back 6

1. unrepaired congenital heart dz, including palliative shunts and conduits
2. completely repaired congenital heart defect w prosthetic material or device, whether placed by surgeon or cath intervention during first 6 mo. afterward
3. repaired congenital heart disease w residual defects at site or adjacent to site of prosthetic patch or prosthetic device (which inhibit endothelialization)
4. cardiac transplantation recipients who develop cardiac valvulopathy

Front 7

Why is abx prophylaxis within 6 mo of repaired congenital heart defects necessary prior to dental procedures?

Back 7

because endothelialization of prosthetic material occurs within 6 mo. of procedure

Front 8

What is preferred SBE prophylaxis in a pt not allergic to PCN?

Back 8

amoxicillin

Front 9

What is preferred SBE prophylaxis in a pt allergic to PCN/ampicillin?

Back 9

cephalexin, clindamycin, azithromycin, clarithromycin

Front 10

What is preferred SBE prophylaxis for a pt not allergic to PCN but unable to take oral meds?

Back 10

IV/IM ampicillin, cefazolin or ceftriaxone

Front 11

What is preferred SBE prophylaxis in pts allergic to PCN/ampicillin and unable to take PO meds?

Back 11

IM/IV cefazolin, ceftriaxone or clindamycin

Front 12

When is SBE prophylaxis given?

Back 12

single dose 30-60 min before procedure

Front 13

______ should not be used in an individual w history of anaphylaxis, angioedema, or urticaria w PCN/ampicillin.

Back 13

cephalosporins

Front 14

Left to right shunt, incr pulm blood flow, pulm HTN, RV hypertrophy, and CHF are all characteristics of...

Back 14

acyanotic congenital heart disease

Front 15

Atrial septal defects are 2-3x more prevalent in

Back 15

females than males

Front 16

This is the communication between L and R atria, and blood enters R atria from L atria, opposite of PFO.

Back 16

atrial septal defect

Front 17

What are the classification factors for small vs large Atrial septal defect?

Back 17

small: < 0.5 cm, small shunt, usually asymptomatic

large: >/= 2 cm, incr pulm blood flow, systolic ejection murmur in 2nd ICS, afib or svt, r axis deviation on EKG, dyspnea on exertion

Front 18

In atrial septal defect, SBE prophylaxis (is/isn't) recommended.

Back 18

is not unless a concommitant valvular abnormality (MVP/MV cleft) is present

Front 19

The anesthesia goals in atrial septal defect are?

Back 19

maintain systemic blood flow to ensure no alteration of IAs

Front 20

In atrial septal defect, IV agents may be..

Back 20

diluted, but this is unlikely

Front 21

What increases the magnitude of shunt in Atrial septal defect pts?

Back 21

drugs that produce prolonged SVR increases -- avoid!

Front 22

What does high Fi02 do in atrial septal defect pts?

Back 22

decr pulm blood flow and incr L to R shunt

volatile agents decr SVR whereas pos pressure ventilation incr PVR
(both beneficial)

Front 23

In atrial septal defect pts, it is crucial to avoid entrance of ____ into circulation.

Back 23

air!

Front 24

Anesthesia Mgmt Bottom line for atrial septal defect pts?

Back 24

1. maintain SVR in normal levels
2. use volatile agents and PosPresVent during surgery
3. avoid high Fio2 - ltd to 50%
4. regional can be considered as long as SVR maintained
5. SBE prophylaxis if in doubt

Front 25

This is the most common congenital cardiac defect?

Back 25

ventricular septal defect

Front 26

Approx 70% of ventricular septal defects are located in

Back 26

membranous portion of intraventricular septum

Front 27

At the lower left sternal border, this auscultation abnormality is heard during moderate to large ventricular septal defect

Back 27

holosystolic murmur

Front 28

ventricular septal defect pts are at risk for developing

Back 28

infective endocarditis

Front 29

Is SBE prophylaxis indicated in ventricular septal defect?

Back 29

yessiree

Front 30

Are inhaled and injected drug pharmacokinetics altered in ventricular septal defect?

Back 30

nope

Front 31

Acute or persistent incr in _____ or decr in ______ should be avoided in ventricular septal defect pts. These chnges can increase the magnitude of left to right shunting, like in ASD.

Back 31

SVR, PVR
these changes are likely w incr Fi02

Front 32

Are pos pressure ventilation and IAs tolerated in ventricular septal defect pts?

Back 32

yep

monitor induction effects on SVR (IAs especially)

Front 33

It is important to avoid (hypo/hyper)volemia in ventricular septal defect pts.

Back 33

hypovolemia

aggressively replace blood loss!

Front 34

____ pts have similar surgical mgmt as ventricular septal defect pts. SBE prophylaxis should _____ be provided.

Back 34

ASD, always

Front 35

This is present when the ductus arteriosus fails to close spontaneously after birth.

Back 35

patent ductus arteriosus

Front 36

Most patent ductus arteriosus pts are asymptomatic, but if the shunt is large, then pt will have...

Back 36

LV hypertrophy

Front 37

Neonates w patent ductus arteriosus are treated with _______ because....

Back 37

indomethacin regimen, can also use ibuprofen

want to inhibit cyclooxygenase - helps facilitate closure and surgery is indicated to repair if conservative tx fails

Front 38

Is SBE prophylaxis necessary in patent ductus arteriosus?

Back 38

yep

Front 39

What do decreases in SVR and positive pressure ventilation do to help in patent ductus arteriosus pts?

Back 39

improve systemic blood flow and increase PVR and decr L to R shunt

Front 40

In patent ductus arteriosus pts, it is crucial to avoid entrance of _____ into the pt.

Back 40

air into IV!

Front 41

Are IAs and PPV well tolerated in patent ductus arteriosus pts?

Back 41

yep

Front 42

Bicuspid aortic valves occur in ____% of the US population, and usually remains asymptomatic until ____.

Back 42

2-3%, adulthood

Front 43

Aortic stenosis is associated with a _____ heart sound audible over the 2nd ICS.

Back 43

systolic murmur

Front 44

What are the EKG and CXR findings in aortic stenosis?

Back 44

ST depression during exercise, LV hypertrophy

Front 45

Aortic stenosis leads to a _____ aortic valve and ____ wall of LV.

Back 45

narrowed, thickened/hypertrophic

Front 46

In aortic stenosis pts, it is crucial to maintain NSR because LV is dependent on...

Back 46

properly timed atrial contractions to ensure optimal LV filling and SV.

Front 47

In aortic stenosis, it is important to avoid prolonged or extreme alterations in what values?

Back 47

HR, SVR, IVFs

Front 48

In aortic stenosis pts, general anesthesia is preferred to regional in order to avoid

Back 48

sympathectomy

carefully titrate IAs to ensure no signifcant drop in BP; may use TIVA/N20/Opiate cocktail

Front 49

Is SBE prophylaxis indicated for aortic stenosis pts?

Back 49

yes!

Front 50

_____ produces obstruction to R ventricle outflow and is identified by a loud systolic ejection murmur at the L 2nd ICS.

Back 50

pulmonic stenosis

Front 51

Side effects of pulmonic stenosis:

Back 51

dyspnea on exertion, peripheral edema, ascites

Front 52

What happens when there is a patent foramen ovale in the presence of pulmonic stenosis?

Back 52

R to L shunting can occur -> cyanosis and clubbing due to bypass of pulm circulation

Front 53

The goal of managing pulmonic stenosis pts under anesthesia is to avoid....

Back 53

RV oxygen demand increase.

Front 54

How do you decrease RV oxygen demand increase for better anesthesia outcomes in pts w pulmonic stenosis?

Back 54

-avoid incr HR and contractility
-pos pressure vent well tolerated (impact of changes in PVR minimized by presence of fixed obstruction in pulm valve)
- aggressively treat decr BP w sympathomimetic drugs (phenylephrine-works quicker)
- aggressively treat dysrhythmias

Front 55

Which is better tolerated in pulmonic stenosis pts, general or regional anesthesia?

Back 55

general

Front 56

This heart defect arises from diaphragm-like ridge that extends into aortic lumen just distal to the left subclavian artery.

Back 56

coarctation of the aorta

Front 57

In pts w coarctation of the aorta, most adults are asymptomatic until the defect is detected during this part of physical exam?

Back 57

systemic HTN is detected in arms w diminished or absent femoral pulses

Front 58

coarctation of the aorta results in what heart sound on auscultation?

Back 58

harsh systolic murmur along L sternal border in back

Front 59

What does Ekg reveal in coarctation of the aorta pts?

Back 59

LV hypertrophy

Front 60

What are the complications of coarctation of the aorta?

Back 60

- HTN
- LV failure
- aortic dissection
- ischemic heart disease
- infective endocarditis
- CVA

Front 61

During surgical resection of coarctation of the aorta, what are important parts of monitoring strategy?

Back 61

-continuous BP monitoring on both upper and lower extrem
-monitor propensity of systemic HTN during cross-clamping of aorta (use nitroprusside infusion prn, assess renal and spinal cord perfusion)
-assess for neuro ischemic injury (SSEP)
-careful I/O, urine output

Front 62

Is SBE prophylaxis indicated in coarctation of the aorta?

Back 62

yes

Front 63

What are anesthesia post op concerns for coarctation of the aorta?

Back 63

watch for paradoxical HTN, use nipride to treat with or without esmolol

Front 64

Which is indicated as better technique for coarctation of the aorta, general or regional anesthesia?

Back 64

general - monitor for systemic hypo/hypertension
opioids for pain control
careful titration of vasodilators during

Front 65

What are the characteristics of cyanotic congenital heart disease?

Back 65

R to L intracardiac shunt,
decr pulm blood flow, arterial hypoxemia, erythrocytosis (HCT >70%, coag defects due to Vit K dependent clotting factors and defective platelet aggregation), brain abcess (due to hypoxic brain, mimics stroke)

Front 66

Most pts w tetralogy of fallot are _____ From birth.

Back 66

cyanotic

Front 67

What heart sounds accompany tetralogy of fallot?

Back 67

ejection murmur along L sternal border

Front 68

What does a SP02 reading demonstrate in tetralogy of fallot?

Back 68

low even when 100% Fi02 admin

Front 69

Is SBE prophylaxis indicated in tetralogy of fallot?

Back 69

YEP

Front 70

What are the characteristics of compensatory erythropoiesis in tetralogy of fallot pts?

Back 70

- hyperviscosity
- risk for CVA/cerebral abcess
- risk for infective endocarditis - SBE proph.

Front 71

____ is a common positioning feature in tetralogy of fallot.

Back 71

squatting!

Front 72

This is the sudden onset of arterial hypoxemia in tetralogy of fallot pts.

Back 72

hypercyanotic attacks

Front 73

What is treatment for hypercyanotic attacks in tetralogy of fallot pts?

Back 73

beta adrenergic antagonists to alleviate spasm to pulm outflow tract (esmolol, propranolol)

Front 74

What are the 4 features of tetralogy of fallot?

Back 74

1. VSD
2. pulm stenosis (many levels of obstruction from RV to lungs)
3. overriding aorta (lies directly over VSD and RV)
4. thickened RV muscle

Front 75

It is important to avoid increased R to L shunting in tetralogy of fallot pts because....

Back 75

increase in shunt results in decrease in pulm blood flow and PaO2.

Front 76

What actions increase R to L shunting magnitude in tetralogy of fallot pts?

Back 76

pulm blood flow is relatively fixed and inversely proportional to SVR (decr SVR, incr PVR, incr myocardial contractility)

Front 77

SVR can be decr in tetralogy of fallot pts by

Back 77

IAs, opioids, histamine release, ganglionic blockade, alpha adrenergic agents

Front 78

Pulm blood flow can be decr in tetralogy of fallot pts by

Back 78

pos pressure ventillation (but risk of hypoxemia outweighs risk of not using PPV), PEEP

Front 79

Preop considerations for tetralogy of fallot pts?

Back 79

- avoid dehydration (oral feedings)
- avoid crying (IM injections, IV starts)
- continue beta adrenergic antagonists until induction
- SBE prophylaxis

Front 80

Induction technique for pts w tetralogy of fallot?

Back 80

-ketamine 3-4 mg/kg IM or 1-2 mg/kg IV (incr SVR and pulm blood flow)
-for intubation, avoid histamine releasing NMB (Atracurium), use pancuronium if ketamine not used
- IA: sevo may lower SVR significantly, halothane preferred bc decr contractility and maintains SVR to greater degree

Front 81

What are maintenance strategies for pts w tetralogy of fallot?

Back 81

- N20 and ketamine to preserve SVR, (N20 may incr PVR but offset by positive effect on SVR)
-N20 disadvantage is reduction of Fi02 w/ its use
- pancuronium is preferred NMB
- controlled ventillation preferred

Front 82

This congenital heart defect occurs w L to R intracardiac shunt reversed through an ASD or VSD when the blood flow through the pulm bed equals or exceeds SVR.

Back 82

eisenmenger's syndrome

Front 83

This congenital heart defect manifests w cyanosis and decr exercise tolerance w/ palpitations. Also characterized by afib or flutter, visual disturbance, headache, dizzy, paresthesias.

Back 83

eisenmenger's syndrome

Front 84

This congenital heart defect is associated w an incr risk of CVA, brain abcess, pulm infarction, incr blood viscosity from erythrocytosis, and RV hypertrophy.

Back 84

eisenmenger's syndrome

Front 85

______ is characterized by a reversal of a L to R shunt into a R to L shunt caused by incr PVR to a level equal or exceeding SVR.

Back 85

eisenmenger's syndrome

Front 86

In eisenmenger's syndrome, it is important to maintain preop levels of ____ and recognize that sudden incr in R to L shunt will occur if a sudden drop in ____ occurs.

Back 86

SVR, SVR

Front 87

What gtt is commonly used to maintain SVR in eisenmenger's syndrome pts?

Back 87

phenylephrine gtt

Front 88

It is important to avoid hypovolemia and paradoxical embolization in eisenmenger's syndrome, and _________may be indicated if HCT > 65%.

Back 88

prophylactic phlebotomy

Front 89

Laparoscopic procedures are routinely contraindicated in eisenmenger's syndrome pts because

Back 89

insufflations of peritoneal cavity w CO2 may precipitate acidosis, hypotension and dysrhythmias.

Front 90

Which anesthesia technique is preferred in eisenmenger's syndrome?

Back 90

general preferred over regional, early tracheal intubation desirable

Front 91

If you have to give an eisenmenger's syndrome pt an epidural, it is best to use a local anesthetic solution that doesn't contain _______ because....

Back 91

epinephrine,

can exaggerate decr in SVR (catecholamine release)

Front 92

______ entails a failure of the truncus arteriosus to spiral, resulting in the aorta arising from the anterior portion of the RV and the pulm artery arising from the LV. There is complete separation of the _____ and ____ circulations.

Back 92

transposition of the great arteries,
pulmonary and systemic circ.

Front 93

Survival is only possible in transposition of the great arteries if...

Back 93

there i sa communication between the 2 circulations in the form of a VSD, ASD, or PDA.

Front 94

______ at birth are often present w transposition of the great arteries.

Back 94

cyanosis, tachypnea, CHF

Front 95

CHF in transposition of the great arteries pts results from

Back 95

LV failure due to volume overload created by L to R shunt created for survival.

Front 96

What is the required treatment for transposition of the great arteries?

Back 96

surgical correction

Front 97

During repair of transposition of the great arteries, infusion of _____ is necessary to maintain patency of ductus arteriosus.

Back 97

prostaglandin E

Front 98

Admin of O2 in transposition of the great arteries helps to decrease _____.

Back 98

PVR.

Front 99

____ and ____ are drugs of choice to treat the CHF associated with transposition of the great arteries.

Back 99

diuretics and digoxin

Front 100

It is crucial that the anesthetist take into account the separation of ______ in caring for pts w transposition of the great arteries.

Back 100

pulm and systemic circulations

Front 101

How are drug doses titrated for pts w transposition of the great arteries?

Back 101

decr doses because of minimal dilution to heart and brain

Front 102

How are IAs affected by transposition of the great arteries?

Back 102

may be delayed, only small amt of inhaled drug reaches circulation

Front 103

What are the induction and maintenance techniques in transposition of the great arteries?

Back 103

- ketamine 1-2 mg/kg IV w NMB for intubation
- maint w ketamine 0.25-0.5 mg/kg/hr w opioids and benzos
- avoid dehydration (careful I/O)
- limited use of N20 due to high need for Fi02 concentration

Front 104

For pts with prosthetic heart valves, they may have to discontinue ____ prior to surgery, and carry a greater risk of ___ and ____.

Back 104

anticoagulation, thromboembolism and bacterial endocarditis

Front 105

In ______, which is commonly caused by rheumatic heart disease, the ____ is not affected.

Back 105

mitral stenosis, LV not affected

Front 106

In mitral stenosis, _____ growing on valves makes them immobile/fixed, leading to poor ____ because there is only a pinhole for the L atria to flow into the LV. This results in _____ enlargement.

Back 106

calcium, poor opening, L atrial enlargement

Front 107

In mitral stenosis, there is a mechanical obstruction to ____ filling. This leads to incr ____ volume and pressure, with a subsequent pressure overload of the R ventricle. Mitral stenosis may then progress to _____.

Back 107

LV filling, incr L atrial vol and pres., pulmonary edema

Front 108

Mitral stenosis is treated with diuretics because ...

Back 108

excess volume can end up in pulmonary circulation

Front 109

Mitral stenosis requires good control of afib because...

Back 109

you need a good atrial kick to prevent congestion

Front 110

It is important to control _____ and provide _____ in mitral stenosis.

Back 110

control HR, provide anticoagulation

Front 111

The goal HR in valvular disease is

Back 111

70

Front 112

What are the anesthetic techniques for pts w mitral stenosis?

Back 112

- avoid ketamine (tachycardia, heart filling occurs at expense of diastole, less filling when tachy)
- maintain HR control
- avoid vol overload (tberg can cause pulm edema)
- avoid incr pulm vascular resistance (hypercarbia and hypoxia)

Front 113

Hypercarbia and hypoxia both cause this vascular change in the lungs

Back 113

pulmonary vasoconstriction

Front 114

Mitral regurgiation is (more/less) amenable to surgery than mitral stenosis.

Back 114

less

Front 115

The _____ support leaflets from opening inappropriately.

Back 115

chordae

Front 116

Mitral regurg is a ____ valvular disease with ruptured ______, caused by....

Back 116

ischemic, ruptured chordae

caused by endocarditis, cardiomyopathy, rheumatic illness

Front 117

Mitral regurgitation leads to ______ stroke volume and C.O.

Back 117

decreased

Front 118

Mitral regurgitation is associated with ____ overload of the LV.

Back 118

volume overload

Front 119

What effect does mitral regurgitation have on the L atrium?

Back 119

L atrial enlargement and afib -- dilation interrupts conductivity

Front 120

When L atrial enlargement can no longer compensate for mitral regurgitation, _____ ensues.

Back 120

pulmonary edema

Front 121

The regurgitant fraction in mitral regurg is affected by...

Back 121

heart rate and pressure gradient across mitral valve.
>0.6 is considered significant regurg

Front 122

What are the diagnostic criteria for mitral regurgitation?

Back 122

- holosystolic apical murmur radiating to axilla
- LVH and cardiomegaly on CXR
- echocardiogram

Front 123

What are the anesthesia strategies indicated for mitral regurgitation?

Back 123

- prevent bradycardia
- prevent incr SVR
- minimize myocardial depr
maintenance of fluid volume is importantt for maintaining LV volume and CO

Front 124

This is the most common type of valvular disease, affecting ___ % of the population.

Back 124

mitral valve prolapse, 1-2.5%

Front 125

What are the auscultatory sounds of mitral valve prolapse?

Back 125

midsystolic click, late systolic murmur

Front 126

What diseases are associated with mitral valve prolapse?

Back 126

- marfan's syndrome
- SLE
- thyrotoxicosis
- rheumatic carditis

Front 127

Mitral valve prolapse is usually benign, but could cause...

Back 127

- embolism
- dysrhythmia
-death

Front 128

Do mitral valve prolapse pts require abx prophylaxis?

Back 128

- if regurg present

Front 129

What is the management of mitral valve prolapse

Back 129

-same as for mitral regurg
-prevent brady, prevent increases in SVR, min myocardial depression, maintain IVF)

Front 130

____ is a calcification of aortic leaflets during aging, or the presence of a bicuspid aortic valve.

Back 130

aortic stenosis

Front 131

In aortic stenosis, obstruction of LV output leads to ______.

Back 131

LV pressure overload (pinhole opening at aortic valve between LV and aorta)

Front 132

In aortic stenosis, the LV tries to compensate with...

Back 132

concentric LV hypertrophy (hypertrophy will result with any fixed mechanical obstruction)

Front 133

What are the classic symtpoms of aortic stenosis?

Back 133

angina, syncope, dyspnea on exertion

Front 134

What are the diagnostic criteria for severe aortic stenosis?

Back 134

- transvalvular gradient 50 mmHg
- peak pressure gradient 80 mmHg
- aortic valve area less than 0.8 cm^2

Front 135

In managing aortic stenosis during anesthesia, there exists a high risk of major perioperative ____ complications. Therefore, it is important to maintain _____ because _____ is very important to function.

Back 135

cardiac complications, maintain sinus rhythm, atrial kick is very important

Front 136

What is the ideal HR for aortic stenosis pts during anesthesia?

Back 136

70! avoid brady/tachycardia
-avoid hypotension

Front 137

Why is it crucial to avoid hypotension in aortic stenosis pts?

Back 137

hypertrophied hearts are harder to perfuse, loss of preload leads to decr CO

Front 138

If you need to restore BP and contractility during a case in a pt w aortic stenosis, it is important not to use...

Back 138

ephedrine or phenylephrine! use epinephrine instead to restore BP and incr contractility, because you need a kick and a squeeze

Front 139

In aortic stenosis it is important to avoid hypovolemia so that you can maintain adequate ____.

Back 139

preload

Front 140

___ is the failure of the aortic valve leaflet's coaptation (closing) due to primary valve disease.

Back 140

aortic regurgitation

Front 141

What are the causes of aortic regurgitation?

Back 141

- endocarditis
- rheumatic fever
- bicuspid aortic valve

Front 142

Aortic regurgitation may result from abnormalities of the aortic root, as in the following conditions....

Back 142

idiopathic, HTN, syphilis, connective tissue disorder, ankylosing spondylitis

Front 143

Aortic regurg leads to a decr in CO due to

Back 143

flow back into the LV during diastole

Front 144

Aortic regurg leads to ___ and ___ overload of the LV.

Back 144

pressure and volume

Front 145

The regurgitant fraction in aortic regurgitation is affected by ...

Back 145

HR and pressure gradient across the aortic valve

Front 146

Over time, aortic regurg causes the ____ to fail and ____ develops.

Back 146

LV fails, Pulm edema

Front 147

In acute aortic regurg, ____ and ___ may occur quickly.

Back 147

coronary ischemia, CHF

Front 148

What are the 2 primary mgmt techniques for pt with aortic regurg?

Back 148

- vasodilator therapy
- valve replacement

Front 149

What are the anesthesia strategies for a pt with aortic regurg?

Back 149

- maintain forward stroke volume
- keep HR above 80
- avoid incr in SVR
- minimze myocardial depr
*FAST, FORWARD AND FULL*

Front 150

What are the causes of tricuspid regurg?

Back 150

- annular dilation due to RV enlargement or pulm HTN
- endocarditis
- rheumatic heart disease

Front 151

What are the anesthesia strategies for a pt in tricuspid regurg?

Back 151

- maintain preload
- beware of R to L shunting across PFO, high R atrial pressures lead to shunting to L heart without traveling first through lungs -- leads to hypoxia

Front 152

___ complications are the leading cause of perioperative morbidity and mortality.

Back 152

cardiac

Front 153

___ surgery pts have higher incidence of CAD and have more significant risk of perioperative MI than any other surgical category of pts.

Back 153

Vascular surgery pts

Front 154

What are the 2 main vascular diseases of the thoracic and abdominal aorta?

Back 154

- aneurysm
- dissection

Front 155

This is the dilation of all 3 layers of an artery, with a 50% incr in diameter from normal.

Back 155

thoracic or abdominal aneurysm

Front 156

This is when blood enters the media layer in the aorta, creating a false lumen and dropping BP when abdomen is open.

Back 156

dissection

abdomen is keeping dissection tamponaded, when opened it can explode and pt can bleed (possibly to death!)

Front 157

Aortic aneurysms can be classified by 3 different morphologies:

Back 157

1. fusiform: vascular out-pouching shaped like spindle
2. saccular: resembles a small sac
3. dissecting: dissects longitudinally

Front 158

What are the 3 debakey type classifications of thoracoabdominal aortic aneurysms?

Back 158

type 1: intimal tear originates in the ascending aorta and dissection involves the aorta, arch and some thoracic aorta
type 2: dissection confined to ascending aorta
type 3: dissection confined to descending aorta but may extend to abdominal region and iliac arteries

Front 159

What are the 2 types of Stanford classifications for aneurysms of the thoracoabdominal aorta?

Back 159

type a: includes all cases that involve ascending aorta with or without involving the arch or descending aorta
type b: includes all others in which ascending aorta is not involved

Front 160

For pts undergoing surgery for a thoracic aneurysm, the principle causes of morbidity and mortality include ____, ____, ____ and ____. Therefore, assessment of these functions is needed preop.

Back 160

MI, resp failure, renal failure, CVA

Front 161

Before correcting the actual aneurysm, some pts with CAD require what other procedure?

Back 161

pre op percutaneous coronary intervention w CABG

Front 162

Thoracic aneurysm pts may require medications to manipulate what two values?

Back 162

preload and afterload

Front 163

In order to assess for resp failure with thoracic aneurysm repair, what inquiries should be made?

Back 163

- PFTs
- smoking hx
- use of bronchodilator treatment

Front 164

Preop renal dysfunction is the most important indicator of _____ in thoracic aneurysm cases.

Back 164

post op renal problems

Front 165

What strategies may be employed intraop to prevent post op renal dysfunction?

Back 165

adequate hydration, normotension, avoidance of nephrotoxic drugs (gentamycin, meperidine)

Front 166

Before thoracic aneurysm surgery, what imaging test is useful to ensure adequate brain perfusion?

Back 166

duplex imaging of carotid arteries (often a bruit present)

Front 167

Most common symptoms of abdominal aortic aneurysm?

Back 167

back pain

Front 168

S/S of rupture of descending thoracic aorta

Back 168

- persisting overriding chest pain
- hypotension
- L hemothorax
- ischemia of legs, abdominal viscera or spinal cord
- renal failure

Front 169

Surgical treatment of distal (Further from myocardium) aortic dissection is associated with ___% mortality.

Back 169

29%

Front 170

All pts with acute dissection of ____ are candidates for surgery, this is more emergent that dissection of ____ Aorta.

Back 170

ascending more emergent than descending

Front 171

What is unique about a repair of type A dissection involving the aortic arch?

Back 171

requires cardio-pulmonary bypass, profound hypothermia and circulatory arrest (30-40 min at body temp of 15-18 deg C)

Front 172

Indication for surgery on a descending thoracic aortic aneurysm involves

Back 172

dissection > 5-6 cm

type b repair if pts have s/s of impending rupture

Front 173

What are the mortality rates of a Type A TA dissection if treated medically vs surgically?

Back 173

med- 56%
surg- 27%

long term survival in surg tx is 90-96%, only 69-89% if med tx.

Front 174

Medical treatment of a TA dissection type A involves...

Back 174

a-line monitoring, drugs to control BP and LV contractility (beta blockers and nitroprusside)

Front 175

This is the ischemic damage to the spinal cord that can result from cross-clamping of thoracic aorta.

Back 175

anterior spinal artery syndrome

Front 176

Cross-clamping of the thoracic aorta is associated with severe ____ and ____ disturbances in all organ systems.

Back 176

hemodynamic and homeostatic

Front 177

What are the pharmacologic interventions to offset the effects of cross-clamping the TA?

Back 177

nitroprusside, NTG

also volume replacement concerns during clamping

related to effects of drugs on arterial/venous capacitance

Front 178

Unclamping the TA is associated with substantial decr in ____. Sometimes ____ is given right before unclamping.

Back 178

SVR, Calcium

Front 179

What causes declamping hypotension after unclamping TA?

Back 179

- central hypovolemia from repooling of blood in tissues below clamp level
- hypoxia-mediated vasodilation causing incr vascular capacitance in tissues below level of clamp
- accumulation of vasoactive and myocardial depressant metabolites in those tissues
- CO2 release and incr O2 consumption (correct metabolic acidosis!)

Front 180

CO2 and thromboxane are powerful _____.

Back 180

vasodilators

Front 181

Why is the R arm best for A-line measurement in thoracic aneurysm anesthesia?

Back 181

thoracic cross-clamping is just distal to L subclavian artery and L carotid -- can occlude measurement in L arm (This is a standard of care)

It is also important to monitor above R radial and below L femoral to assess for cerebral, renal and spinal cord perfusion

Front 182

SSEP (Somatosensory evoked potentials) are not indicated for assessing neuro function in thoracic aneurysm repairs because...

Back 182

requires lighter anesthesia, which is not indicated in this type of case, not reliable and difficult to perform

Front 183

To assess cardiac function during a thoracic aneurysm case, ____ is more useful than _____ because it is less invasive and more reliable.

Back 183

TEE better than PA cath

Front 184

What type of catheter is indicated in thoracic aneurysm cases?

Back 184

cordis - can measure cvp, allows placement for post op swan placement PRN

Front 185

This is considered the "poor man's swan"

Back 185

foley catheter

Front 186

The diuretics given prior to cross-clamping in thoracic aneurysm cases are:

Back 186

mannitol (improves renal cortical blood flow and GFR) and furosemide

Front 187

____ causes the same catecholamine response as doing a sternal split with a saw.

Back 187

laryngoscopy

Front 188

What are the induction and maintenance techniques for anesthesia during thoracic aneurysm repair?

Back 188

- induction and intubation must minimze impact on SVR
- etomidate best to avoid hypotension (as w propofol)
- LTA (squirt down throat) or lidocaine injection to blunt laryngoscopy
- vasodilators and beta blockers to blunt laryngoscopy
- maintain MAP 70-80 mmHg
- double lumen tube to collapse L lung and facilitate surgical exposure
- general anesthesia w opioids (volatile agents, fentanyl, sufentanil -- avoid morphine due to possible hypotension w histamine release)
- NMBs chosen based on renal clearance (avoid gallamine, pancuronium due to high renal excretion and effects on myocardium -- use vec or roc)

Front 189

What are the post op management techniques for thoracic aneurysms?

Back 189

- thoracic epidural cath for post op analgesia- routine if not heparinized
- monitor for sensory and motor deficits in low extrem -- can have delayed paraplegia (12hr-21 days) - q1h neuro exam
- monitor renal fcn
- careful titration of vasoactive substances and neuraxial anesthesia
- local anesthetic use can produce sensory and motor deficits -- can delay recognition of anterior spinal artery syndrome (opioids preferred to LAs)

Front 190

What are the hemodynamic responses to aortic cross clamping?

Back 190

- severe homeostatic disturubances to all organs
- incr in BP and SVR with no significant change in HR, but a drop in CO
- HTN attributed to incr afterload and bc blood volume is redistributed from collapse of venous vasculature distal to cross clamp --> results in incr preload also
- changes in ventricular function and wall motion
- offset these changes w drugs (nitroprusside for afterload, NTG for preload, continuous fluid adjustments)

Front 191

What are the hemodynamic responses to aortic cross clamp removal?

Back 191

- significant hypotension -- treat w crystalloid w balanced salt in solution (LR, NS, 1/2 NS)
- colloids (albumin, PRBC vs whole blood)
- titrate to adequate urine output
- suspect unrecognized bleeding if hypotension persists a few min after cross clamp removed
- echo useful to check if adequate volume replacement has been done/determine cardiac fcn

Front 192

Describe the rollercoaster effect seen in clamping and unclamping of thoracic aorta?

Back 192

initially BP drops due to CO2 accumulation, then rises due to catecholamine release -- may lead to myocardial ischemia or death!

Front 193

CV system mgmt throughout thoracic aneurysm repair (preop, intraop, postop)

Back 193

preop: assess aneurysm extent, cardiac eval per guidelines, beta blockade, statins
intraop: adquate IV access and invasive monitoring, BP control to prevent rupture, manage HD changes of clamp/unclamp, possible bypass
post op: BP controll to ensure SCPP, monitor for s/s of myocardial dysfunction

Front 194

What are the pulmonary anesthesia considerations for thoracic aneurysm repair?

Back 194

preop- smoking cessation 4-6 wk, assess tracheobronch. involvement, discuss possible trach
intraop: DLT placement - possible single ung ventilation, cpap, peep, bronchodilators
postop: airway edema (keep intubated), RLN injury possible, potential for pulm edema, TRALI, ARDS

Front 195

What are the renal anesthesia considerations for thoracic aneurysm repair?

Back 195

preop: assess preexisting renal dysfunction, discuss possible post op renal failure
intraop: renal protection w hypothermia, distal aortic perfusion, cold crystalloid perfusate
postop: monitor for s/s of failure, HD possible

Front 196

What are the CNS anesthesia considerations for thoracic aneurysm repair?

Back 196

preop: assess baseline neuro status and document deficits, discuss potential for paralysis, baseline SSEPs and MEPs
intraop: neuroprotection strategies (permissive hypothermia, LHB, CSF drainage, epidural cooling, reimplantation of intercostal arteries), SSEP/MEP monitoring
postop: assess neuro status, maintain Spinal cord perfusion pressure

Front 197

What are the hematology anesthesia considerations for thoracic aneurysm repair?

Back 197

preop: assess coag status and use of anticoag/antiplatelet drugs, discuss likelihood of blood tx, type and cross
intraop: systemic heparinization (LHB), antifibrinolytic therapy, potential for massive transfusion, promtamine considerations
postop: coag monitoring, ensure normal coags before removing CSF cath

Front 198

What is the antidote to heparin?

Back 198

protamine

used in cardiopulmonary bypass surgery to neutralize the anti-clotting effects of heparin as well as to increase pulmonary artery pressure and decrease peripheral blood pressure, myocardial oxygen consumption, cardiac output, and heart rate

Front 199

When using endovascular approach to repairing thoracic aortic aneurysm, what type of anesthesia is indicated?

Back 199

GETA with TEE, less invasive so lower analgesic requirements

Front 200

What are the primary goals of anesthesia strategy for endovascular approach to thoracic aneurysm repair?

Back 200

- avoid tachycardia and HTN
- preserve cardiac, spinal, splanchnic blood flow
- maintain intravasc. vol, O2, temp
-maintain CSF drains, goal mean pressure 100 mmHg

Front 201

What is the best induction agent for "Sick" hearts?

Back 201

etomidate

Front 202

How are AAAs usually detected?

Back 202

asymptomatic, pulsatile abdominal masses, usually <5 cm

Front 203

In a AAA rupture emergency, the pt goes into severe ______ shock and requires _____. There is no time for an adequate work up, so just ask this one question: ____.

Back 203

hypovolemic shock, volume resuscitation, does the pt have allergies??

Front 204

What is the classic AAA triad of symptoms?

Back 204

- hypotension
- back pain
- pulsatile abd mass

Front 205

If a pt with AAA repair has COPD, they should have a preop ____ test because....

Back 205

PFT -- severe reductions in vital capacity and FEV1 with abnormal renal function may mitigate against AAA resection

Front 206

If a AAA repair pt has ischemic heart disease, it is important to eval. cardiac function with...

Back 206

exercise or pharm. stress test with or without echo or radionucleotide imaging

Front 207

Describe the concerns regarding clamping above the renal vessels during a AAA repair.

Back 207

if above, will not perfuse kidneys during clamping-- time the clamping and try to keep < 60 min to avoid renal impairment. When unclamped, immediately treat acidosis, give volume/colloids/pressors), should start making urine by the end of the case, may take a few hrs if in renal shock -- use heparin to prevent clot formation associated w clamped vessels

Front 208

What kind of monitoring is necessary during anesthesia for AAA repair?

Back 208

foley, PA cath, TEE with CVP cordis, intraop echo useful to eval cardiac response to aortic cross clamp, a-line

Front 209

What are the maintenance techniques for anesthesia during AAA repair?

Back 209

- no single agent ideal
- combo of volatile agents, opioids, w/ or w/o N20
- vasopressors or vasodilators to maintain MAP 70-80 mmHg
- combined general w epidural anesthesia (but may not be indicated depending on anticoag use)

Front 210

What are the post-op considerations for AAA repair?

Back 210

- at risk for developing CV, pulm, and renal dysfunction
- assmt of graft patency and lower extrem blood flow
- overzealous intraop hydration or post op hypothermia may exacerbate HTN post op -- treat immed. by eliminating specific cause (pain) or giving antihypertensive meds
- ensure adeq. pain control

Front 211

Surgery is usually indicated when the diameter of the aorta reaches ___ cm.

Back 211

5 cm

Front 212

What are the 4 parts of the aorta?

Back 212

ascending, arch, thoracic, abdominal (stops at belly button)

Front 213

Pts often refuse open AAA repair, making ____ AAA repair a common alternative when possible.

Back 213

endovascular repair

cant use this on everyone bc some people don't do well -- not as good blood flow as in open AAA repair (still a new technique, hasn't been perfected)

Front 214

What does the preop work up consist of for Endovascular AAA repair?

Back 214

Echo, EKG, carotid ultrasound, PFTs, CBC, Coags, cardio consult

start beta blockers pre op

Front 215

What are the anesthesia options for endovascular AAA repair?

Back 215

- regional: length of procedure dictates choice (if >3 hr, combined spinal epidural technique better choice), contraindicated in LMWH
- GETA: when using LMWH
-MAC
- spinal is best technique for AAA repair w endovasc technique - better morbidity and mortality statistics

Front 216

This is the chronic impairment of blood flow most often due to atherosclerosis whereas arterial embolism is most likely responsible for occlusion -- results in compromised blood flow to the extrem.

Back 216

peripheral vascular disease

Front 217

Risk factors for PVD include:

Back 217

anything that causes peripheral neuropathies!
- ischemic heart disease
- DM
- HTN
- smoking
- hyperlipidemia

Front 218

The principle symptoms of PVD

Back 218

intermittent claudication, rest pain

Front 219

This occurs when the metabolic demands of exercising skeletal muscle exceed the available O2 supply

Back 219

intermittent claudication

Front 220

This occurs when the arterial blood supply does not meet even the minimal nutritional requirements for the affected limb.

Back 220

rest pain

Front 221

The most reliable physical finding of PVD is....other findings include.....

Back 221

absent pulses

other findings include auscultating bruits over abdomen, pelvis or inguinal area coupled w decr pulse in affected limb; subcutaneous atrophy, hair loss, coolness, pallor, cyanosis, dependent rubor

Front 222

Main diagnostic test for PVD

Back 222

-doppler ultrasound
-ankle-brachial index (Ratio of SBP in ankle compared to brachial, ratio of < 0.9 indicative of disease, measures presence and severity)

Front 223

MOST FREQUENT symptom of PVD

Back 223

intermittent claudication

Front 224

What are the medical vs surgical treatment strategies for PVD?

Back 224

- medical: indicated if disease not debilitating, no ischemic rest pain apparent, or if not impending loss of limb apparent; exercise programs, treatment and modification risk factors for atherosclerosis
- surgical: depends on location and severity, aortofemoral bypass (AFB) most typically performed, operative risks similar to those described for AAA (pulm, cardio, renal)

Front 225

AFB requires a huge incision, disrupting a lot of _____. It is often performed under _____ Anesthesia, decreasing the chance of ____ events.

Back 225

valves, regional, thromboembolic

Front 226

What makes a surgical candidate suitable for introp beta blockade?

Back 226

- all pts undergoing vascular surgery with or without evidence of preop ischemia and with or without high or intermittent risk factors (smoking, hx of CVA/cardiac disease)
- pts on long term beta blockers
- pts having vascular surgery

Front 227

What pts may not tolerate regional anesthesia for AFB surgery?

Back 227

copd, orthopnea and dementia pts

Front 228

What are the considerations for use of epidural/spinal anesthesia for AFB surgery?

Back 228

improves blood flow through graft, place epidural at least 1 hr prior to intraop heparinization - useful for pain control (intrathecal opioids)

Front 229

What are the considerations for use of general anesthesia during AFB surgery?

Back 229

better suited for long procedures, TEE useful, volatile agents w or w/o N20, in conjunction w opioids, combo w regional

Front 230

What are the post op strategies for AFB surgery?

Back 230

- epidural/intrathecal opioids (produces analgesia without cardioresp. depression)
- use of LAs
- precedex gtt
- BP monitoring
- monitor for fluid and lyte derangements
- monitor for subclavian steal syndrome (occlusion of subclavian or innominate artery proximal to origin of vertebral artery may result in reversal of blood flow through the ipsilateral vertebral artery, absent/diminished blood flow in ipsilateral arm --> 20 mmHg lower in ipsilateral arm, bruit over subclavian)

Front 231

This is the occlusion of the subclavian or innominate artery proximal to the origin of the vertebral artery - may result in reversal of flow through ipsilateral vertebral artery into distal subclavian artery

Back 231

subclavian steal syndrome

Front 232

This is a rare vascular disorder involving inflammation of the blood vessels usually facilitated through an immune response.

Back 232

Takaysu's Arteritis

Front 233

What are the anesthesia techniques indicated for pts with Takaysu's Arteritis?

Back 233

- consider multi organ involvement and med regimen
- general anesthesia chosen over regional secondary to often pts on anticoag. therapy an dhave significant musculoskeletal changes making lumbar placement impossible

Front 234

What are the CNS effects of Takaysu's arteritis?

Back 234

vertigo, visual disturbance, syncope, seizures, cerebral ischemia or infarction

Front 235

What are the CV effects of Takaysu's arteritis?

Back 235

multiple occlusions of peripheral arteries, ischemic heart disease, cardiac valve dysfunction, cardiac conduction defects

Front 236

What are the respiratory effects of Takaysu's arteritis?

Back 236

pulm HTN, VQ mismatch

Front 237

What are the renal and musculoskeletal effects of Takaysu's arteritis?

Back 237

- renal: renal artery stenosis
- MS: ankylosing spondylosis, Rheumatoid arthritis

Front 238

This is the episodic vasospastic ischemia of the digits, responsive to stress and cold, and more common in women.

Back 238

Raynaud's Phenomenon

Front 239

What are the anesthesia considerations of raynaud's?

Back 239

- incr ambient temp of room (also w sickle cell pts)
- avoid sympathetic response to induction/intubation/surgery
- a-line not usually indicated
- regional anesthesia acceptable --> do not include epi as part of admixture!

Front 240

Why is surgery not typically performed in severe carotid disease that remains asymptomatic, especially in men?

Back 240

greatly incr risk of stroke

Front 241

What are the preop considerations for carotid endarterectomy?

Back 241

- neuro exam
- assess for response to changes in head position to cerebral fcn (can see compression of the artery, esp w hyperextension, avoid severe rotations and hyperextension of neck)
- presence of comorbidities (CV, ischemia, HTN, renal, pulm, establish normal BP range to ensure perfusion)

Front 242

The two primary goals of anesthesia during carotid endarterectomy are:

Back 242

- maintenance of hemodynamic stability and prompt emergence

maintain VS, normocarbia, pain/stress responses, invasive monitoring

Front 243

What is the technique for regional during carotid endarterectomy?

Back 243

cervical plexus block allows for neuro assmt during surgery, need to have a motivated pt

Front 244

What are the considerations for using general anesthesia during carotid endarterectomy?

Back 244

- use of volatile agents/N20/opioids, need to be able to wake pts for assmt
- monitoring for cerebral ischemia, hypoperfusion and cerebral emboli using EEG or SEP (Can be difficult during case)
- stump of carotid artery pressure monitoring (poor indicator of adequacy of cerebral perfusion, but still used as a guide by many surgeons)

Front 245

What are the post op considerations for carotid endarterectomy?

Back 245

- monitor for airway (patency), cardiac and neuro complications, EKG if suspect
- neuro fcn tests by surgeon and anesthesia provider
- maintain normal BP (HTN common, use nitroprusside and NTG intraop and into post op period indicated)
- carotid denervation may lead to respiratory compromise and predispose pts to aspiration

Front 246

What is the leading cause of post op morbidity/mortality in PVD surgeries?

Back 246

DVT and subsequent PE

Front 247

What factors predispose pts to thromboembolism (DVT) formation?

Back 247

- venous stasis
- recent surgery
- lack of ambulation
- trauma
- pregnancy
- low CO (CHF, MI)
- CVA
- abnormality of venous wall (varicose veins)
- drug-induced irritation of vessels
- hypercoag. state
- estrogen therapy (birth control)
- cancer
- deficiencies of endogenous anticoagulants (antithrombin 3, protein C, protein S)
- stress response to surgery
- inflammatory bowel disease
- hx of prior thromboemb.
- morbid obesity
- advanced age

Front 248

What are the diagnostic tests to assess for thromboembolism?

Back 248

- contrast venography
- compression ultrasonography of proximal veins
- impedence plethysmography

Front 249

____ anesthesia can substantially decrease risk of DVTs in vascular surgery.

Back 249

regional
ortho hip and TKR surgeries reduced 20-40% w concommitant use of epidural/spinal anesthesia

causes vasodilation and post op analgesia

Front 250

Regional is contraindicated when pts are on what drug?

Back 250

low molecular weight heparin! (LMWH)

Front 251

Systemic HTN is categorized by a BP reading of greater than ___ on 2 occasions. Only ___% of americans are adequately treated for their HTN.

Back 251

140/90, 30%

Front 252

HTN is more common in _____ and is a major risk factor for...

Back 252

afroamericans,

CAD, CHF, CVA, ESRD

Front 253

Greater than 95% of cases of HTN are ______, occurring with familial incidence.

Back 253

essential HTN

Front 254

In essential HTN, there is an incr _____ activity, and an overproduction of _____.

Back 254

SNS activity,
overprod. of Na-retaining hormones and vasoconstrictors, renin

Front 255

Essential HTN pts often have deficiencies of endogenous ______ such as ____.

Back 255

vasodilators, NO

Front 256

____ and ____ are often seen comorbidities in essential HTN pts.

Back 256

DM and obesity

Front 257

The final common pathway of essential HTN is _______ Retention, leading to .....

Back 257

salt and water retention,
incr vol and BP

Front 258

Essential HTN can also be caused by _____ abuse and obstructive ______.

Back 258

etoh and tobacco abuse, OSA

Front 259

Metabolic syndrome is comprise of...

Back 259

HTN, insulin resistance, dyslipidemia, obesity

Front 260

What are the long term effects of poor BP control?

Back 260

CAD, CHF, CVA, PVD, ESRD

Front 261

Less than 5% of cases are considered secondary HTN, and the usual cause is...

Back 261

renal artery stenosis

Front 262

Other possible causes of secondary HTN besides renal artery stenosis include...

Back 262

hyperaldosteronism, pheochromocytoma, cushing's syndrome, pregnancy-induced HTN,, aortic coarctation, aging-associated

Front 263

Treatment of HTN includes ____ modification

Back 263

lifestyle mod.,

Front 264

____ are the first line of drug therapy in HTN

Back 264

thiazide diuretics

Front 265

HTN crisis is classified as a BP greater than ____, and is better tolerated in pts with ____.

Back 265

>180/120,
chronic HTN

Front 266

Hypertensive emergency can lead to target organ damage, including...

Back 266

- encephalopathy
- pulm edema
- angina
- aortic dissection
- in pregs, DBP over 109 is an emergency

Front 267

When treating HTN crises, you should avoid _____ drops in BP, and lower BP by ___% in the first hour.

Back 267

precipitous, 20%

Front 268

This condition has no target organ damage in HTN, but the pt may experience headache, epistaxis or anxiety, and is treatable in some cases with oral meds.

Back 268

HTN urgency

Front 269

In HTN crisis, how is encephalopathy treated?

Back 269

nitroprusside (Very potent, narrow margin of safety), nicardipine, fenoldopam, labetalol

Front 270

In HTN crisis, how is cardiac ischemia treated?

Back 270

NTG (venodilator, dilates coronary arteries)

Front 271

In HTN crisis, how is pulm edema treated?

Back 271

nitroprusside, NTG, fenoldopam

Front 272

In HTN crisis, how is renal insufficiency treated?

Back 272

fenoldopam, nicardipine

Front 273

In HTN crisis, how is preeclampsia treated?

Back 273

methyldopa (direct acting vasodilator), hydralazine, mag sulfate, labetalol, nicardipine

Front 274

In HTN crisis, how are pheochromocytoma pts treated?

Back 274

phentolamine, phenoxybenzamine, propranolol

Front 275

In HTN crisis, how are cocaine ingestion pts treated?

Back 275

NTG, nitropruside, phentolamine

Front 276

What are anesthesia strategies for pts with HTN?

Back 276

- control BP prior to surgery
- no evidence that complications incr w DBP up to 110 mmHg
- "White Coat syndrome"- exaggerated BP response to laryngoscopy or periop myocardial ischemia
- HTN pts presumed to have CAD until proven otherwise

Front 277

Hypotension after induction is more common in pts taking what kind of drugs?

Back 277

- ace inhibitors or ARBs

risk of hypotension reduced if meds discontinued day prior to OR

Front 278

______ is the essential action of hypovolemia.

Back 278

hemodynamic instability

Front 279

Preop eval of HTN pts should include

Back 279

- determine adequacy of pre op BP control
- review meds
- eval for evidence of end organ damage
- continue BP meds periop.

Front 280

Induction and maintenance techniques for HTN pts include...

Back 280

- anticipate exaggerated response
- quick laryngoscopy
- balanced anesthetic technique
- monitor leads 2 and 5 for myocardial ischemia

Front 281

Post op mgmt of HTN pts should anticipate ____ and continue _____. It is important to monitor for ____ function.

Back 281

HTN, continue BP meds, monitor end-organ fcn

Front 282

If meds that affect ANS (B blockers and Clonidine) are abruptly discontinued, then _____ can occur. However _____ meds are not assoc w rebound HTN.

Back 282

rebound HTN, ace inhibitors

Front 283

What are the 3 BP control systems?

Back 283

SNS, vasopressin system, RAAS

Front 284

After induction of anesthesia, pts on ace inhibitors rely on their ____ system. ____ is key to maintaining BP.

Back 284

vasopressin system, intravascular volume

Front 285

Why is it a good idea to discontinue ACE inhibitors 24-48 hrs prior to OR?

Back 285

less intraop hypotension, risk of loss of BP control

Front 286

What is normal PA pressure?

Back 286

18-25/6-10 mmHg

Front 287

What is normal PA MAP?

Back 287

12-16 mmHg

Front 288

In primary pulmonary HTN, PA mean pressure is >

Back 288

25 mmHg

Front 289

Idiopathic primary pulm artery HTN occurs in ___ Cases per million, and it has ____ inheritance in 10% of cases.

Back 289

1-2, autosomal dominant

Front 290

What are the s/s of primary PA HTN?

Back 290

dyspnea, fatigue, low CO, abdominal distension (Due to RV failure, ascites), "like aortic stenosis of the RV"

Front 291

How is primary PA HTN diagnosed?

Back 291

- pulm catheterization
- vasodilator test (prostacyclin)
- echocardiography

Front 292

In primary PA HTN, there is increased RV Wall stress, leading to ___ and ___, with decreased RV ____.

Back 292

hypertrophy, dilatation, stroke volume

Front 293

In primary PA HTN, annular dilatation of the ____ valve leads to regurg, and pulmonary insufficiency from ____ dilation.

Back 293

tricuspid, pulmonary artery

Front 294

Right to left shunting through a patent ____ occurs because tricuspid regurg increases _____ pressures, shunting blood across heart without first oxygenating it.

Back 294

foramen ovale, R atrial pressures

Front 295

Why does hypoxemia occur as a result of PA HTN?

Back 295

fixed cardiac output leads to inr O2 extraction w exertion, incr VQ mismatch

Front 296

The baseline hypoxemia that occurs with PA HTN is made even worse during episodes of hypoxia and hypercarbia, because...

Back 296

these both cause vasoconstriction, making RV performance worse

Front 297

What are the treatment strategies for primary PA HTN?

Back 297

- O2
- anticoagulation (due to risk of mural thrombi formation in RV)
- diuretics
- Ca channel blockers
- Phosphodiesterase inhibitors (sildenafil, rivashio)
- inhaled NO (dilates pulm vasculature)
- prostacyclins
- endothelin receptor antagonists (Bosentan)

Front 298

What are the anesthesia considerations for a pt with primary PA HTN?

Back 298

- incr risk of periop morbidity and mortality due to RV failure, dysrhythmia, and embolism
- avoid hypoxia, acidosis, hypercarbia!!
- maintain intravasc. volume
- maintain sinus rhythm (avoid bradycardia)
- avoid negative inotropes (propofol can cause acute RV failure - use etomidate instead!)
- avoid hypotension and optimize preload
- use controlled ventillation to avoid hyperCO2 (spontaneous modes blunt hypercarbic response to stimulate blowing off CO2)
- PEEP incr pulm vascular resistance (use 5)

Front 299

For treatment of HTN _______ are used in patients with CHF?

Back 299

ACE inhibitors

Front 300

For treatment of HTN _______ are added in patients with CAD

Back 300

beta blockers

Front 301

For treatment of HTN _______ are added in patients with CHF, DM, Renal disease

Back 301

angiotensin receptors blockers (ARBs)

Front 302

For treatment of HTN _______ are useful in patients with post MI and CHF

Back 302

aldosterone agonists

Front 303

For treatment of HTN _______ are used in patients with CAD and DM

Back 303

calcium channel blockers

Front 304

This is the inability of the heart to fill or eject blood at a rate adequate to meet tissue requirements.

Back 304

heart failure

Front 305

____ is the most common medicare discharge diagnosis.

Back 305

heart failure

Front 306

Symptoms of heart failure

Back 306

SOB, swelling BLE, chronic lack of energy, difficulty sleeping due to breathing problems, swollen/tender abdomen, loss of appetite, cough w frothy sputum, inc nocturnal urination, confusion/memory impairment

Front 307

What are the etiologic causes of HF?

Back 307

impaired myocardial contractility
valve abnormalities
systemic HTN
pericardial disease
pulm HTN (cor pulmonale)

Front 308

What is the most common cause of RV failure?

Back 308

LV failure

Front 309

Pts w systolic heart failure exhibit _____ Disease, dilated ______, and ____ and ____ chronic overload.

Back 309

CAD, dilated cardiomyopathy, chronic pressure and volume overload

Front 310

What cause chronic pressure overload in systolic heart failure?

Back 310

aortic stenosis, HTN

Front 311

What causes chronic volume overload in systolic heart failure?

Back 311

aortic and mitral insufficiency (leaking/regurg), high output failure

Front 312

Patients w diastolic HF may have normal _____ function.

Back 312

systolic

Front 313

What are the causes of diastolic heart failure?

Back 313

ischemia, aortic stenosis, HTN, anything that makes heart muscle hypertrophy

Front 314

Describe stage 1 of diastolic HF.

Back 314

abnormal relaxation (LVEDP incr) with normal left atrial pressure

Front 315

Describe stages 2-4 of diastolic heart failure.

Back 315

abnormal relaxation with high left atrial pressure and LVEDP

Front 316

Diastolic heart failure is more common in

Back 316

women

Front 317

Chronic heart failure is seen in pts with _______ cardiac disease. They exhibit ____ congestion, _____ BP, and the process is well tolerated because ______.

Back 317

long-standing,
venous congestion,
well-maintained BP,
bc it occurs gradually

Front 318

Acute heart failure is seen in pts with the following conditions:

Back 318

MI, valve rupture, HTN crisis

Front 319

Pts w acute heart failure have _____ edema, ____ BP, and a more ______ presentation.

Back 319

no edema, hypotension, catastrophic presentation

Front 320

CAD, cardiomyopathy, HTN, valvular disease, and pericardial disease are all causes of _______ output heart failure.

Back 320

low output

Front 321

Anemia, pregnancy, AV fistula, hyperthyroidism, Beri Beri, and Paget's disease are all causes of _____ output heart failure.

Back 321

high output

av fistula- some blood that normally goes through lungs will take shortcut through fistula and too much may take shortcut

Front 322

Starlings Law of the heart describes the relationship between ____ and _____.

Back 322

EDV and cardiac output

Front 323

In a normal person, the relationship between LVED volume and stroke volume is very _____.

Back 323

linear

Front 324

In a normal heart, increased preload leads to ____ CO.

Back 324

increased

Front 325

In pts w heart failure, the starling curve has a more _____ pattern. Increased preload does not improve ______. In fact, it may make things worse and decrease CO.

Back 325

flat curve, stroke volume

Front 326

Will pts in cardiogenic shock or severe heart failure respond to volume challenge?

Back 326

NOPE

Front 327

According to the NYHA, there are 4 classes of heart failure...

Back 327

1. no symptoms w ordinary activity
2. symptoms w ordinary exertion
3. symptoms w less than ordinary exertion
4. symptoms at rest

Front 328

Describe the cocktail of drugs available for medical mgmt of heart failure.

Back 328

ace inhibitors, ARBs, aldosterone antagonists, B blockers, diuretics, digitalis (positive inotrope), vasodilators (Decr afterload), statins

Front 329

When medical management of heart failure is unsuccessful, the next step is...

Back 329

surgery

OHTX (orthotopic heart transplant)
Ventricular assist device
Cardiac resynchronization (to improve electrical conduction)
ICD (implanted cardiac defibrillator)

Front 330

When an LVAD is functioning normaly, the aortic valve does not need to ______.

Back 330

close

Front 331

How is acute heart failure managed?

Back 331

- diuretics and vasodilators
- inotropic support
- Ca sensitizers (levosemindan)
- B-type natriuretic peptide (Natrecor)
- Nitric oxide synthase inhibitors
- intra-aortic balloon pump

Front 332

Milrinone works by preventing the breakdown of ___.

Back 332

cAMP

Front 333

When chronically giving pts meds to improve contractility, they usually die from...

Back 333

side effects

Front 334

An IABP rapidly shuttles helium gas in and out of the balloon, which is located in the ______. The balloon is inflated at the onset of cardiac _____ and deflated at the onset of _____ to improve coronary perfusion

Back 334

descending aorta, inflated during diastole, deflated during systole

Front 335

During systole, an IABP deflates rapidly to cause a sudden decr in ______ to augment LV ejection.

Back 335

afterload

Front 336

IABPs are synced to _____ to set them up, and BP increases when the balloon is _____.

Back 336

EKG, inflated

Front 337

You cannot use _____ in a bradycardic pt with a denervated transplanted heart. Instead you must use ____.

Back 337

no atropine,
use epi instead (beta adrenergic agonists)

Front 338

What are the effects of general anesthesia on heart failure pts?

Back 338

- narcotics decr sympathetic stim/tone
- positive pressure ventilation and PEEP aid LV ejection and decr afterload
- on a vent, lungs squeeze heart to aid LV ejection

Front 339

What are the effects of regional anesthesia in heart failure pts?

Back 339

decr systemic vascular resistance (afterload) may incr CO

Front 340

The transplanted heart is ______, and is _____ dependent.

Back 340

denervated, preload dependent

Front 341

The heart is a ____ chamber within a _____ Chamber.

Back 341

pressurized within pressurized!

Front 342

LV pressure - intrathoracic pressure =

Back 342

LV transmural pressure

Front 343

Positive swings in intrathoracic pressure result in

Back 343

a decrease in LV transmural pressure -- easier for heart to eject

Front 344

Negative swings in intrathoracic pressure result in

Back 344

an increase in LV transmural pressure -- harder for heart to eject

Front 345

Cardiomyopathies are a heterogeneous group of diseases of the myocardium associated with ____ and/or _____ dysfunction that usually (but not invariably) exhibit inappropriate ______ hypertrophy or dilation du to a variety of causes that are frequently genetic.

Back 345

mechanical and/or electrical dysfunction, ventricular

Front 346

_______ either are confined to the heart or are part of generalized systemic disorder, often leading to cardiovascular death or progressive heart failure- related disability.

Back 346

Cardiomyopathies

Front 347

What is the difference between primary and secondary cardiomyopathy?

Back 347

primary- confined to heart muscle
secondary- part of multiorgan disease

Front 348

What are the types of primary cardiomyopathy?

Back 348

- genetic
- mixed
- acquired

Front 349

What are the types of secondary cardiomyopathy?

Back 349

- infiltrative (amyloidosis)
- storage
- toxic
- inflammatory processes
- endomyocardial
- endocrine
- neuromuscular
- autoimmune

Front 350

Hypertrophic cardiomyopathy is a ________ trait, involving hypertrophy of ____ and _____.

Back 350

autosomal dominant trait,
hypertrophy of septum and anterolateral LV free wall

Front 351

Describe the dynamic LV outflow obstruction of hypertrophic cardiomyopathy.

Back 351

the harder the heart works, the worse the flow, because the valve gets sucked into the ventricle and valve leaks - common in athletes

Front 352

Hypertrophic cardiomyopathy results in ____ movement of the mitral valve during systole.

Back 352

anterior

Front 353

Mitral regurg, diastolic dysfunction, myocardial ischemia, and dysrhythmias are all symptomatic of what type of cardiomyopathy?

Back 353

hypertrophic

Front 354

Describe systolic anterior motion (SAM).

Back 354

blood leaks back through mitral valve (mitral regurg), mitral valve presses against septum causing obstruction to blood flow ---> leads to SAM

The LV outflow tract becomes very narrow, close to the anterior leaflet of the mitral valve. Due to the bernoulli principle, with high velocity through narrow area --> causes leaflet to be sucked into LV outflow tract, leads to mitral regurg and sudden decr in CO because blood isn't leaving the heart

Front 355

What factors may increase left ventricular outflow tract obstruction?

Back 355

-incr contractility (B agonist, digitalis)
-decr preload
-decr afterload

Front 356

What factors may decrease left ventricular outflow tract obstruction?

Back 356

-decreased contractility (B blockers, anesthetics, ca channel blockers)
-incr preload
-incr afterload

best to keep heart optimally filled w afterload normal or high

Front 357

Hypertrophic cardiomyopathy is usually ______, but patients may have angina relieved by _____.

Back 357

asymptomatic, lying down

Front 358

In some circumstances, hypertrophic cardiomyopathy may present as sudden ____.

Back 358

death

Front 359

In patients with hypertrophic cardiomyopathy, the murmur of MR may be increased by ______ because it causes a drop in preload and venous return.

Back 359

valsalva

Front 360

What are the medical and surgical treatment options of hypertrophic cardiomyopathy?

Back 360

- medical: beta blockers, Ca channel blockers
- surgical: septalplasty to make larger LV outflow tract

Front 361

What are the anesthesia management goals of hypertrophic cardiomyopathy?

Back 361

- minimize LV outflow tract obstruction
- avoid sympathetic stimulation, hypotension and hypovolemia
- maintain sinus rhythm

Front 362

What effects do anesthetics have on contractility?

Back 362

- depr contractility by decr Ca entry into cells
- halothane (like inhaled beta blocker, potent negative inotrope) and enflurane have most negative inotropic effects
- N20 and ketamine - minimal effects
- local anesthetics, esp bupivicaine/ropivicaine/tetracaine cause myocardial depr

Front 363

Primary dilated cardiomyopathy is also referred to as

Back 363

idiopathic cardiomyopathy

Front 364

The etiology of dilated cardiomyopathy may be ____ or ____.

Back 364

genetic, infectious

Front 365

Secondary types of dilated cardiomyopathy have similar _____ to primary types.

Back 365

clinical appearance

Front 366

Symptoms of dilated cardiomyopathy

Back 366

heart failure, dysrhythmia, embolization, low CO, stasis, mural thrombi, high CVA risk

Front 367

Peripartum cardiomyopathy carries a risk of ____ % mortality within 3 mo of delivery, and occurs in 1 out of every ____ Births.

Back 367

25-50%, 3000-4000

Front 368

Risk factors for peripartum cardiomyopathy

Back 368

obesity
multiparity
advanced maternal age
preeclampsia
afroamerican

Front 369

What are the possible etiologies of peripartum cardiomyopathy?

Back 369

viral, autoimmune, maladaptive response to hemodynamic effects of pregnancy

Front 370

Peripartum cardiomyopathy is an enlargement of the ___ Due to _______.

Back 370

left ventricle due to dilated cardiomyopathy

Front 371

What are the 3 types of secondary cardiomyopathies with restrictive physiology?

Back 371

1. myocardial infiltration: causes severe diastolic dysfunction, very stiff, can't relax
2. amyloidosis: classic example
3. infiltrative diseases: hemochromatosis, sarcoidosis, carcinoid

Front 372

The symptoms of secondary cardiomyopathies with restrictive physiology include ____ and ____.

Back 372

heart failure, afib

Front 373

An echocardiogram of a pt w secondary restrictive cardiomyopathy reveals

Back 373

normal systolic function, severe diastolic function

Front 374

With pts in secondary restrictive cardiomyopathy, it is important to maintain ____ and _____.

Back 374

sinus rhythm, preload

Front 375

The diastolic function of less compliant hearts exhibits ______ end diastolic pressure and volume.

Back 375

higher than normal

Front 376

The diastolic function of more compliant hearts exhibits ____ end diastolic pressure and volume.

Back 376

lower than normal

Front 377

_____ dilatation is seen in diseases that induce pulmonary HTN, which include...

Back 377

RV dilatation,

COPD, OSA, restrictive lung disease

Front 378

The other name for cor pulmonale is

Back 378

pulmonary HTN

incr BP and resistance in lungs leading to R sided Heart failure

Front 379

OSA is characterized by ____ Retention, _____ vasoconstriction, and the heart having to pump against elevated pulm artery pressures, leading to ____ failure.

Back 379

CO2 retention, Pulm vasoconstriction, R heart failure

Front 380

_____ is essential to improving prognosis of cor pulmonale.

Back 380

O2 therapy

Front 381

Spontaneous depolarization is initiated in the ______ cells of the ____ node and as the electrical impulse moves along the conduction system, a wave of depolarization is propagated throughout the heart.

Back 381

pacemaker cells, SA node

Front 382

The ____ node is the primary site of impulse conduction, and it discharges at a rate of ____ beats/min.

Back 382

SA, 60-100 bpm

Front 383

The _____ node is located in the septal wall of the R atrium. Like the SA node, it is innervated by both _____ and _____ nerves.

Back 383

AV node,
sympathetic and parasympathetic

Front 384

The AV node slows conduction velocity off the impulse allowing time for ______.

Back 384

atrial contraction

Front 385

Atrial kick contributes to ___% of CO.

Back 385

20-30%

Front 386

The _______ is a relatively thin bundle of fibers down the right ventricle that doesnt branch until the right ventricular apex. Late branching makes it more vulnerable to ____.

Back 386

Right bundle branch (RBB),
vulnerable to interruption!

Front 387

The ____ divides into 2 fasciles, the L anterior and posterior fasciles.

Back 387

Left bundle branch (LBB)

Front 388

The _____ bundle branch is worse to block than the ___ bundle branch, and the former is more indicative of serious cardiac damage.

Back 388

left more serious than right BB

Front 389

The RBB and LBB distal branches interlace into a network of _____.

Back 389

purkinje fibers

Front 390

____ bundle branch block occurs more often, and ____ bundle branch block is more serious.

Back 390

Right often, Left serious

Front 391

Cardiac dysrhythmias are classified according to ______ and _____.

Back 391

heart rate and site of abnormality

Front 392

What 3 things lead to cardiac dysrhythmia?

Back 392

- incr automaticity in normal conduction tissue or in an ectopic focus
- reentry of electrical potentials through abnormal pathways
- triggering of abnormal cardiac potentials due to afterdepolarizations

Front 393

The fastest pacemaker is the

Back 393

SA node

Front 394

___ changes when the slope of phase 4 depolarization shifts or the resting potential changes.

Back 394

automaticity

Front 395

____ can have abrupt onset and require 2 pathways which conduct at different velocities through accessory tracts that bypass AV node to stimulate SA. The often result in _____.

Back 395

reentry pathways, SVT

Front 396

Triggering by _______ is the oscillation in membrane potential that occurs during or after depolarization, usually triggered by slow HR.

Back 396

triggering by afterdepolarizations

Front 397

Afterdepolarization is treated by

Back 397

incr HR w atropine or glycopyrrolate.

Front 398

_____ is caused by an accelleration through the SA node, HR between 100-160 bpm.

Back 398

sinus tachy

Front 399

This is the most common dysrhythmia associated with acute MI (30-40% incidence).

Back 399

sinus tachy

Front 400

How do i treat sinus tachy?

Back 400

1. correct underlying cause (hypovolemia, hypoxia, fever, infection, pain, MH)
2. supplemental O2
3. avoid vagolytic drugs (pancuronium, atropine, glycopyrrolate)
4. beta blockade (if pt is not hypovolemic, bronchospastic (hx of asthma), or has impaired cardiac fcn)

Front 401

_____ arise from ectopic foci in the atria. It is most commonly seen in pts w chronic lung disease, ischemic heart disease and digitalis toxicity.

Back 401

premature atrial beats

Front 402

_____ is the second most common dysrhythmia assoc w acute MI.

Back 402

premature atrial beats

Front 403

How are premature atrial beats managed?

Back 403

avoid excessive sympathetic stimulation,
can be suppressed w beta blockade or Ca channel blockers

Front 404

______ is any tachydysrhythmia initiated by tissue at or above the SA node, with avg HR of 160-180 bpm.

Back 404

SVT

Front 405

S/S of SVT

Back 405

lightheaded, dizzy, fatigue, chest discomfort, dyspnea, syncope (15%)

Front 406

How is SVT managed?

Back 406

1. avoid factors that provoke SVT:incr sympathetic tone, electrolyte imbalances, acid-base disturbances (GI)
2. if stable, vagal maneuver
3. if unstable, AV node blockade: adenosine (can cause temp cardiac standstill), Ca channel blockers, beta blockers

Front 407

_____ occurs when atrial contraction rate is between 250-350 bpm, and is usually associated with structural heart disease.

Back 407

atrial flutter

Front 408

Most atrial flutter pts present with ___ AV conduction, which means a ventricular rate of ______.

Back 408

2:1 AV conduction,
150 bpm

Front 409

Atrial flutter is treated with....

Back 409

1. cardioversion (50 j)
2. if present before induction of elective cases, cancel and treat by cardio
3. if occurs during anesthesia, treat based on hemodynamic stability (cardiovert w 50 j, pharm mgmt based on comorbidities: adenosine, amiodarone, diltiazem, verapamil)

Front 410

_____ is characterized by no uniform depolarization or contraction of atria.

Back 410

atrial fibrillation

Front 411

Rhematic heart disease, hx of rheumatic fever, HTN, COPD, ASD all predispose pts to what dysrhythmia?

Back 411

atrial fibrillation

Front 412

What is the most effective treatment for afib?

Back 412

elective cardioversion

digoxin useful to control ventricular rate but ineffective in converting afib

Front 413

How is afib managed pre op?

Back 413

postpone surgery if present prior to elective surgery in new onset pts

Front 414

How is a chronic afib pt managed intraop?

Back 414

1. maintain on antidysrhythmic drugs (amiodarone most frequently prescribed and works during phase 3; propfenone prolongs phase 0; ibutilide prolongs phase 3; sotalol prolongs phase 3)
2. monitor preop labs (electrolytes, esp Ca, K, Mg; coag profile -- pts on oral anticoag meds w afib, often coumadin, monitor for adverse events from anticoag discontinuance)

Front 415

_____ is the dysrhythmia that occurs when ventricles contract without accompanying atrial contraction.

Back 415

PVCs

Front 416

In ______, volume of blood ejected is smaller than normal, and there is a compensatory pause longer than normal.

Back 416

PVCs

Front 417

If PVCs are isolated, then in most people they are ____.

Back 417

benign

Front 418

When PVCs are ____, they are more concerning.

Back 418

multifocal instead of unifocal.

3 PVCs together constitute vtach, 3 in a minute suggest impending vtach event

bigemminy vs trigemminy

Front 419

How are PVCs managed?

Back 419

1. treat for > 6 PVC/min and repetitive or if multifocal
2. treat underlying cause (acidosis, electrolyte disturbance, prodysrhythmic drugs, mechanical stimulation from intracardiac caths)
3. beta blockers, lidocaine, amiodarone

Front 420

Why are lidocaine gtts beneficial during open abdomen cases?

Back 420

decr ileus 15-20 %

Front 421

This dysrhythmia is present when 3+ PVCs occur at a calculated HR of > 120 bpm.

Back 421

vtach

Front 422

How is vtach managed?

Back 422

1. during anesthesia, immediate investigation required into possible causes before it becomes sustained
2. conventional antidysrhythmics: lidocaine bolus 2 mg/kg, infusion post op

Front 423

_____ is irregular ventricular rhythm incompatible with life.

Back 423

Vfib

Front 424

This is the only effective method to convert vfib

Back 424

electrical defib within 3-5 min,
also give epi 1 mg IV or vasopressin 40 u IV to improve response to defib

Front 425

What is the anesthetic mgmt of a vfib pt?

Back 425

initiate CPR, ACLS protocol!

Front 426

This dysrhythmia begins in early adulthood, and is characterized by paroxysmal palpitations with/without syncope, dizzy, dyspnea, and angina.

Back 426

wolf-parkinson-white syndrome (WPW syndrome)

Front 427

This is the most common tachydysrhythmia assocated with WPW syndrome.

Back 427

AV nodal re-entry tachycardia (AVNRT) - usually triggered by a PAC or PVC

Front 428

In AV nodal reentry tachycardia, ventricular preexcitation causes an earlier than normal....

Back 428

deflection of QRS called a delta wave -- trigged by PAC or PVC

Front 429

How is AV nodal reentry tachycardia classified?

Back 429

either orthodromic (narrow QRS bc cardiac impulses conducted from atrium through normal AV node-HIS purkinje system and return to atrium through accessory pathways), more common 90-95%) or antidromic (wide QRS)

Front 430

What is the anesthesia mgmt technique for WPW syndrome pts?

Back 430

1. Pts w known WPW syndrome presenting for sx should continue to receive antidysrhythmic drugs (procainamide)
2. avoid any event w incr SNS activity (due to pain/anxiety/hypovolemia) OR drug (Digoxin) that could enhance anterograde conduction of cardiac impulses through an accessory pathway
3. electrical cardioversion is used in presence of instability

Front 431

What are the 2 types of prolonged QT syndrome?

Back 431

congenital and acquired

Front 432

What is the hallmark sign of long QT syndrome?

Back 432

syncope

-- could become sudden death syndrome!

Front 433

How is long QT syndrome treated?

Back 433

correct electrolyte abnormalities, particularly Mg and K

Front 434

What causes acquired long QT syndrome?

Back 434

abx, antidysrhythmics, antidepressants, antiemetics (ondansetron, droperidol), diet pills (metabolife)

Front 435

If a pt has history or fam hx of WPW syndrome, it is important to get a pre op ___.

Back 435

EKG

Front 436

What IAs have been shown to prolong QT?

Back 436

isoflurane and sevoflurane
(desflurane inconclusive)

Front 437

Best choice for WPW anesthetic?

Back 437

TIVA

Front 438

In WPW pts, it is important to avoid abrupt increases in ______.

Back 438

sympathetic activity
ex: pain, hypovolemia

Front 439

Intraop mgmt of WPW pts should ensure adequate ______ Balance, consideration of giving ____ prior to induction and laryngoscopy, and its important to have ______ available.

Back 439

electrolyte balance, beta blocker prior to induction, defibrillator available

Front 440

____ is characterized by HR < 60 due to decr in normal discharge of SA node.

Back 440

sinus brady

Front 441

Is treatment of sinus brady required while pt is asymptomatic?

Back 441

nope

Front 442

To treat symptomatic sinus brady, give....(med and dose)

Back 442

0.5 mg IV atropine q 3-5 min to max dose of 3 mg

Front 443

This is inappropriate sinus brady associated w degenerative changes in the SA node.

Back 443

sick sinus syndrome (SSS)

Front 444

Sinus brady can be associated w _____ and _____ anesthesia.

Back 444

spinal and epidural

Front 445

What is the anesthetic mgmt during sinus brady under spinal/epidural anesthesia?

Back 445

1. assess level of block- if T5 or above, can knock out cardiac accelerators
2. probably from sympathectomy that decr venous return thereby initiating vagal response
3. treat w vagolytic medications, glycopyrrolate then atropine

Front 446

During anesthesia, sinus brady pts should be monitored for...

Back 446

worsening of symptoms.

Front 447

When symptoms present intraop on sinus brady pts, anesthesia mgmt entails

Back 447

1. atropine- crosses BBB and causes visual disturbances, vasodilation, dry, crazy, disinhibition
2. glycopyrrolate
3. when severe, immediate transcutaneous pacing

Front 448

What are the drugs that can be given down the ETT?

Back 448

LANE
lido, atropine, nitro, epi

Front 449

What is the waveform like for junctional rhythm?

Back 449

HR 40-60, regular rhythm, P wave inverted, absent or after QRS

Front 450

______ is due to activity of a cardiac pacemaker in the tissues surrounding the AV node, with an intrinsic HR of 40-60.

Back 450

junctional rhythm

Front 451

Transient junctional rhythms require ______

Back 451

no treatment

Front 452

Junctional rhythms under anesthesia are not infrequent during

Back 452

general anesthesia with halogenated agents

Front 453

The loss of _______ in junctional rhythms may be detrimental to some populations.

Back 453

atrial kick

Front 454

Junctional rhythms are treated with _______ for hemodynamically significant rhythms.

Back 454

0.5 mg IV atropine

Front 455

_____ rhythm is characterized by PR interval > 0.20 sec, normal QRS, and regular rhythm.

Back 455

1st deg AVB

Front 456

First deg AVB can be found in pts without

Back 456

heart disease

Front 457

First deg AVB may be caused by

Back 457

incr vagal tone, digitalis toxicity, inferior wall MI, and myocarditis

Front 458

What are the anesthesia techniques in first deg AVB?

Back 458

1. avoid incr vagal tone
2. assess digoxin levels
3. careful use of spinal/epidural anesthesia (Start lower)

Front 459

What are the 2 types of 2nd deg AVB?

Back 459

1. mobitz type 1 (wenckebach): progressive prolongation of PRI until beat is dropped
2. mobitz type 2: no progressive prolongation, more indicative of serious cardiac conduction problem

Front 460

What is the anesthetic mgmt of 2nd degree AVB?

Back 460

Type 1- therapeutic decisions depend on ventricular HR
Type 2- higher incidence of developing VFIB or 3rd deg AVB, so cardiac pacemaker is mandatory

Front 461

This dysrhythmia is characterized by a complete interruption of AV conduction, signaled by syncope or vertigo.

Back 461

3rd degree AVB

Front 462

What is the treatment for 3rd degree AVB?

Back 462

transcutaneous or transvenous pacing must be in place prior to induction; isoproterenol may be needed to maint acceptable HR, caution w antidysrhythmics (may suppress ectopic pacemakers that are responsible for maint HR)

Front 463

This is the conduction disturbances that occur at various levels of the HIS-Purkinje system.

Back 463

Bundle branch blocks (BBBs)

Front 464

In pts without structural heart disease, which bundle branch block is more common?

Back 464

Right more common

Front 465

In RBBB, the waveform entails...

Back 465

1. identical P wave before each QRS
2. possibly prolonged PRI
3. widened QRS complex and rSR in V1 and V2 leads

Front 466

How is RBBB managed in anesthesia?

Back 466

1. avoid hypotension, hypoxemia, alterations in electrolytes (disturbances can result in 3rd deg AVB)
2. can use general or regional
3. prophylactic cardiac pacer not required, but continuous EKG monitoring is!

Front 467

In LBBB, the waveform entails...

Back 467

1. identical P wave before each QRS
2. possibly prolonged PRI
3. wide QRS w RR' in V5

Front 468

LBBB is often a marker for ....

Back 468

serious heart disease, HTN, CAD, aortic valve disease, cardiomyopathy

Front 469

How is LBBB managed under anesthesia?

Back 469

avoid hypotension, hypoxemia, alterations in electrolytes (disturbances can result in 3rd deg AVB)
2. can use general or regional
3. same as RBBB, special attn should be made for insertion of intracardiac cath bc can induce RBBB.

Front 470

_____ is a temporizing measure in which you place chest and back electrodes over areas of lesser skeletal muscle mass and low density constant currents are delivered.

Back 470

transcutaneous cardiac pacing

Front 471

This is the most common indication of permanent implanted cardiac pacemakers.

Back 471

sick sinus syndrome

Front 472

This is the only long term treatment for symptomatic bradycardia, and offers different pacing modes.

Back 472

permanently implanted cardiac pacemakers

Front 473

What is the 5 letter genetic code used to describe various characteristics of cardiac pacemakers?

Back 473

1st letter: denotes cardiac chamber being paced (a atrial, v ventricular, d dual chamber)
2nd letter: denotes cardiac chamber that detects the electrical signals (A,V,D)
3rd letter: indicates response to the sensed signals (i inhibition, T triggering, D dual inhibition and triggering)
4th letter: R denotes activation of rate response features
5th letter: denotes chamber(s) in which multisite pacing is delivered

Front 474

What are the most common pacing modes?

Back 474

AAI, VVI, DDD

Front 475

In ____ pacing, the atrial output is inhibited if an intrinsic atrial signal is sensed, and, if no ventricular activity is sensed by the end of the programmed AV interval, ventricular output is activated. If intrinsic ventricular activity is sensed then the ventricular activity is inhibited.

Back 475

DDD pacing

Front 476

Dual chamber pacemakers maintain synchrony between...

Back 476

atria and ventricles

Front 477

____ pacing minimizes the incidence of "pacemaker syndrome."

Back 477

DDD pacing

Front 478

This syndrome is a constellation of symptoms that includes weakness, orthopnea, paroxysmal nocturnal dyspnea, hypotension, and pulmonary edema.

Back 478

pacemaker syndrome

Front 479

This type of pacing involves sensing in both the atria and the ventricle but only a response to a sensed event is inhibited. It is useful in pts w frequent atrial tachydysrhythmias.

Back 479

DDI pacing

Front 480

Most cardiac pacers can be converted to an _______ by placing an external magnet over the pulse generator. Conversion may be considered prior to _____ in some pts.

Back 480

asynchronous mode, surgery

Front 481

This type of pacer is considered for pts who do not have an appropriate response to exercise.

Back 481

rate adaptive pacers

Front 482

This type of pacer uses sensors to detect physical or physiologic indices of exercise and mimics the rate response of NSR. Indices include body mvmt, minute ventilation, QT interval, and SV.

Back 482

rate adaptive pacers

Front 483

The single most important factor for survival from cardiac arrest from vfib is

Back 483

time between arrest and defibrillation

Front 484

____ respond to a dysrhythmia by delivering an internal shock within 15 sec of dysrhythmia, and may be single or dual chamber.

Back 484

ICD (implanted cardioverter defibrillator)

Front 485

Pre op eval for pts with cardiac devices should include:

Back 485

1. determine reason for pacer/ICD and its current fcn
2. coordinate plan w cardio MD
3. ICDs often switched off prior to sx
4. pacemakers usually allowed to continue functioning intraop

Front 486

Pre-op pacemaker interventions:

Back 486

1. assess function by eval before, during and after sx
2. cxr to determine positioning of electrodes
3. change to asynchronous mode because we use bovie in OR, could cause pacer damage or confuse signals it receives

Front 487

DO NOT place bovie grounding pads on...

Back 487

the chest!!!

Front 488

What are the intraop considerations for pacemaker pts?

Back 488

1. monitor EKG to confirm proper fcn of pulse generator
2. ensure proper equipment and meds available for ACLS and a magnet
3. intracardiac caths do not disturb epicardial electrodes fcn but may become entangled or dislodge transvenous electrodes
4. ensure proper shielding of generators from bovie (grounding eletrode placed as far away from generator as possible)
5. avoid hyperventilation to ensure normokalemia (succ use w caution)

Front 489

Myocardial cells are high in ____ and low in ___ and ___.

Back 489

high-K
low- Na, Ca

Front 490

Pacemaker cells are located in the

Back 490

SA node

Front 491

Slow ____ influx opens calcium channels

Back 491

sodium

Front 492

Slow ____ ion channels account for the heart's refractory period.

Back 492

calcium

Front 493

In cardiac action potential, phase 0 represents

Back 493

upstroke/ rising phase

Front 494

In cardiac action potential, phase 1 represents

Back 494

early rapid repolarization

Front 495

Phase 0 upstroke occurs due to

Back 495

rapid influx of sodium into cell

Front 496

In cardiac action potential, phase 2 represents

Back 496

plateau - slow influx of Ca causes K outflow

Front 497

In cardiac action potential, phase 3 represents

Back 497

final repolarization - moving back toward equilibrium

Front 498

In cardiac action potential, phase 4 represents

Back 498

resting potential diastolic repolarization

Front 499

What is the primary difference between cardiac and skeletal muscle?

Back 499

no calcium-mediated plateau phase in skeletal muscle

intercalated disks fire faster and carry action potential faster

Front 500

____ fibers arise from segments _____ of the spinal cord to stimulate the AV node and myocardium.

Back 500

sympathetic, T2-T4

Front 501

The ____ nerve provides parasympathetic control to the heart by depression of the ____.

Back 501

vagus, AV node

Front 502

The right sided nerves affect the ____ node, and the left sided nerves affect the ____ node.

Back 502

SA, AV

Front 503

Halothane, enflurane and isoflurane all depress automaticity of

Back 503

the SA node,
minimal effects on AV node

Front 504

Administration of anticholinergics frequently results in

Back 504

junctional tachycardia

Front 505

Activation of alpha 1 and beta receptors potentiates ______ and causes _____.

Back 505

catecholamines, dysrhythmias

Front 506

Depressing calcium channels has _____ effects.

Back 506

antiarrhythmic

Front 507

Local anesthetics affect sodium channels. At low levels they are _______, and at high levels they cause ______.

Back 507

therapeutic (lidocaine),
deperession of SA node and dysrhythmia or CV collapse

Front 508

In excitation-contraction coupling, everything start with a ____ receptor stimulation. This causes a chain of events in which ___ is the energy source that the cells run on (From Ca and ATP). _____ breaks down cAMP and Ca is sequestered in the ______ when not in use.

Back 508

beta receptor, cAMP,
phosphodiesterase, sarcoplasmic reticulum

Front 509

Thin filaments are _______ and thick filaments are ______.

Back 509

actin, myosin

Front 510

Describe the 4 steps of the contractility cycle of muscle

Back 510

1. myosin cross bridge attaches to actin myofilament
2. working stroke - myosin head pivots and bends as it pulls on the actin filament, sliding it toward the M line
3. as new ATP attaches to the myosin head, the cross bridge detaches
4. as ATP is split into ADP and Pi via ATP hydrolysis, cocking of the mysoin head occurs

Front 511

_____ is the most notorious local anesthetic for cardiac toxicity, and is treated with intralipid 10 cc/kg bolus.

Back 511

bupivicaine

Front 512

What effects do anesthetics have on contractility?

Back 512

-depress contractility by decr Ca entry into cells
-halothane and enflurane have most negative inotropic effects
-N20 and ketamine have minimal effects
- locals, esp bupivicaine, ropivicaine and tetracaine cause myocardial depression by inhibitng Ca transport

Front 513

LVEDP should be ____ mmHg

Back 513

10-15

Front 514

The AV valve closes at the end of

Back 514

diastole

Front 515

Diastolic pressures are much higher (60-80 mmHg) in the

Back 515

periphery

Front 516

CVP waveform reflects

Back 516

atrial pressures

Front 517

A wave of CVP

Back 517

Atria contracts

Front 518

C wave of CVP

Back 518

early ventricular contraction, and bulging of tricuspid into R atrium during isovolumetric systole

Front 519

What does the v wave on CVP represent?

Back 519

atrial venous filling against a closed tricuspid

Front 520

What does x descent on CVP represent?

Back 520

atrium relaxaes and tricuspid valve moves downward

Front 521

What does y descent on CVP represent?

Back 521

filling of ventricle after tricuspid valve opening

Front 522

Systole represents ventricular _____ and diastole represents ventricular ______. Both are energy dependent and active processes

Back 522

ejection, filling

Front 523

What is the main determinant of CO in normal hearts?

Back 523

venous return (preload)

Front 524

SV x HR =

Back 524

CO
normal=5-5.5 L

Front 525

CO / BSA =

Back 525

CI
normal=2.6-4.2
CI relates peformance of heart to the size of the individual

Front 526

A sudden drop in BP (getting out of bed) results in ______ and therefore decreased stroke volume. However, heart rate increases due to _____ activity, and normal CO is maintained.

Back 526

low venous return,
sympathetic activity

Front 527

Is CI a reliable indicator?

Back 527

no, has a wide normal range, depends on HR, decreases are much more meaningful during exercise, usually signifies gross impairment

Front 528

What is a better measure of cardiac performance than CI?

Back 528

mixed venous O2 sat

Front 529

SVO2 (mixed venous O2 sat) reflects ______.

Back 529

oxygen extraction

Front 530

What are the 4 values derrived from SV02 monitoring?

Back 530

CO, O2 sat, O2 carrying capacity of Hgb, and O2 consumption

Front 531

What are the 5 determinants of stroke volume?

Back 531

1. preload/venous return
2. afterload
3. contractility
4. wall motion abnormalities
5. valvular dysfunction

Front 532

This law of the heart represents the relationship between EDV and CO.

Back 532

Starling's law of the heart

Front 533

What effect does an incr in preload have on SV?

Back 533

if preload incr, so does SV!

Front 534

If a pt has heart failure, their heart is weak, enlarged and doesn't perform well. Therefore, as volume is added...

Back 534

stroke volume decreases because pumping capacity is overwhelmed

Front 535

What is the main factor in ventricular filling?

Back 535

diastolic time

Front 536

Increases in HR occur at the expense of

Back 536

diastolic filling

Front 537

Atrial kick accounts for ____ % of ventricular filling

Back 537

30+

Front 538

If the ventricles are less compliant, this means they will be

Back 538

difficult to fill, stiff

Front 539

What are the 2 causes of diastolic dysfunction?

Back 539

problems w active relaxation (Contributes to stiffness) and increased passive stiffness

Front 540

Hypertrophy, ischemia, and asynchrony of the ventricles cause problems with

Back 540

active relaxation

Front 541

Hypertrophy, fibrosis, pericardial disease (restrictive, prevents heart from expanding) or external compression (From fluid in cavity) cause problems with

Back 541

increased passive stiffness

Front 542

During hypertrophy, an enlarged septum may eventually lead to

Back 542

LV obstruction! uh oh!

Front 543

This term is defined by systolic wall tension or arterial impedance to ejection

Back 543

afterload

Front 544

LaPlace's Law

Back 544

stress = pressure in heart x radius / 2xthickness (h)

S = P x R / 2h

Front 545

Ohms Law

Back 545

SVR = 80 x (MAP - CVP)/CO

Front 546

80 x (pulm art pressure - L atrial pressure) / CO =

Back 546

Pulm Vasc Resistance

Front 547

Pulmonary vascular resistance refers to the afterload of

Back 547

the R ventricle

Front 548

Anesthetics are vasodilators and typically _____ Afterload.

Back 548

decrease

Front 549

CO is ____ related to afterload.

Back 549

inversely

Front 550

The failing heart is very _____ sensitive.

Back 550

afterload

Front 551

The ____ ventricle is thin walled and is more sensitive to changes in afterload than the _____ ventricle.

Back 551

right, left

Front 552

You don't wanna give phenylephrine to patients in

Back 552

heart failure -- buckle under incr afterload

Front 553

Bad hearts thrive with pharmacologic ______.

Back 553

afterload reduction

Front 554

Contractility is dynamic. It is increased by _______ And decreased by ________.

Back 554

incr: SNS, meds, hormones
decr: anoxia, acidosis, ischemia

Front 555

RVEF may be measured by _____, but afterload will affect its readings.

Back 555

PA catheter

Front 556

EF =

Back 556

(EDV-ESV)/ EDV
normal EF= 55-75%

Front 557

EF does not reflect contractility, it is ______ dependent.

Back 557

load (preload/afterload)

Front 558

In the left ventricular pressure-volume loop, end diastole occurs with _____ and end systole occurs with ______.

Back 558

isovolumetric contraction, aortic valve closure

Front 559

Ischemic heart disease is present in ____ % of pts undergoing sx.

Back 559

30%

Front 560

Risk factors for ischemic heart disease include

Back 560

male gender, incr age, high chol, HTN, smoking, sedentary, genetics

Front 561

Angina pectoris occurs when

Back 561

myocardial O2 demands exceed supply

Front 562

Describe angina pectoris

Back 562

chest, jaw, left arm pain/pressure/heaviness;
dyspnea-like

Front 563

What are non-cardiac causes of angina?

Back 563

GI problems, costochondritis, esophogeal spasm

Front 564

How is ischemia diagnosed?

Back 564

standard EKG and exercise EKG; nuclear stress imaging, stress echocardiography, coronary angiography

Front 565

What are the limitations of angiography?

Back 565

cannot predict stability of plaques

Front 566

Unstable angina nad MI are most commonly due to plaque rupture in what vessels

Back 566

<50% stenosis

Front 567

Most frequent cause of intraop MI?

Back 567

plaque rupture

Front 568

How do you treat ischemic heart disease?

Back 568

- lifestyle modification
- meds (antiplatelet drugs, beta blockers, Ca channel blockers, nitrates, ace inhibitors, statins)
- revascularization w CABG or percutaneous intervention (Stents)

Front 569

This is a hypercoagulable state that occurs with STEMI, NSTEMI or UA

Back 569

acute coronary syndrome

build up of RBCs and platelets

Front 570

Diagnosis of an MI requires 2 out of these 3 criteria:

Back 570

1. chest pain
2. serial EKG changes
3. incr and decr of serum cardiac enzymes

Front 571

Treatments for MI:

Back 571

reperfusion therapy (clot busting w tPa, stenting), angioplasty (balloon introduced stents), CABG

Front 572

Complications of acute MI

Back 572

1. dysrhythmia (vfib, vtach, afib, bradyarrhythmias, heart block)
2. pericarditis
3. mitral regurg
4. Ventricular septal defect
5. CHF/cardiogenic shock
6. myocardial rupture

Front 573

RV MI is rare because

Back 573

RV has better O2 supply/demand ratio, and receives coronary blood flow in systole and diastole

Front 574

What is the clinical triad for RV MI?

Back 574

hypotension, incr JVP, clear lung fields

Front 575

How does treatment differ for RV MI?

Back 575

vasodilators and diuretics may worsen situation, 3rd degree block common, inotrope may be needed

Front 576

Pulmonary edema occurs with ____ heart problems.

Back 576

L sided

Front 577

Periop MI is more likely in ____ surgeries (5-15% prevalence).

Back 577

high risk vascular and emergency surgeries

urgent hip sx 5-7% risk, elective hip sx < 3%

Front 578

Perioperative MIs are more frequently _____ type, and may be heralded by nagging ____ and ____. Plaque rupture is caused by _____ mediators.

Back 578

NSTEMI, Tachycardia, ST depression, inflammatory

Front 579

Catecholamines, hormones, changes in blood viscosity, cortisol levels, and tissue plasminogen activators can all cause _____ states.

Back 579

hypercoagulable

Front 580

The highest risk of ischemia, infarction and death occurs after acute ____ days and recent ____ days MI.

Back 580

1-7 acute, 18-30 recent

Front 581

Several interventions can be made based on a preop cardiac evaluation, which include:

Back 581

- forego surgery
- modification of surgical procedure
- delay case for treatment of unstable symptoms
- medical therapy w beta blockers, statins, alpha 2s
- modification of post op monitoring - send to ICU
- change location of care (Surgicenter vs hospital)
- coronary revascularization

Front 582

High surgery-specific cardiac risk is considered cardiac risk greater than ___%. It includes the following surgery types.

Back 582

5%,
emergent major operation, aortic or other major vascular surgery, peripheral vascular surgery, prolonged surgery w large fluid shifts and/or blood loss

Front 583

Intermediate surgical risk (less than 5%) include these procedures:

Back 583

head and neck, intraperitoneal/intrathoracic, orthopedic, prostate

Front 584

Low surgical risk of cardiac events (<1%) occurs w these procedures

Back 584

endoscopic procedures, superficial procedures, cataract sx, breast sx

Front 585

Major clinical predictors of incr cardiac risk:

Back 585

- unstable or severe angina
- recent MI 7-30 days
- decompensated CHF
- symptomatic dysrhythmias or high grade AV block
- severe valvular disease

Front 586

Moderate clinical predictors of incr cardiac risk:

Back 586

-mild angina
-prior MI by hx of EKG
-compensated CHF
-DM
-renal insufficiency

Front 587

Minor clinical predictors of incr cardiac risk:

Back 587

-advanced age
-abnormal EKG (LVH, LBBB, ST-T changes)
-dysrhythmia
-low functional capacity
-hx of CVA
-uncontrolled HTN

Front 588

Functional capacity is excellent with a score of > 7 METs, which includes

Back 588

- carry 24 lbs up to 8 steps
- carry 80 lb object
- outdoor work
- recreation (Ski/jog)

Front 589

A functional capacity score of moderate (4-7 METs) indicates these signs:

Back 589

- have sex without stopping
- walk 4 mph on level ground
- light outdoor work
- light recreation (dance, skating)

Front 590

A poor functional capacity (<4 METs) indicates these signs:

Back 590

- shower/dress without stopping
- lighit housework
- walk 2.5 mph on level ground
- recreation (golf, bowling)

Front 591

What pts require pre op non-invasive cardio testing?

Back 591

2 of the following: high risk sx, low exercise tolerance, moderate clinical risk factors

pts w low functional capacity

Front 592

Which pts don't require non invasive pre op cardio testing?

Back 592

pts w/ stable, medically optimized CAD or good exercise tolerance may proceed (even w/ high or intermediate risk surgery and moderate clinical risk factors)

Front 593

The risk of MI after having PCI or stenting is not decreased until...

Back 593

complete endothelialization occurs and dual antiplatelet therapy completed

bare metal stent 3 mo.
drug eluting stent 12 mo.

Front 594

What is the implications of prior CABG on OR candidates?

Back 594

cabg within 5 yrs and no change in medical condition is considered safe for OR

Front 595

What is the risk of casual use of beta blockers? (They aren't indicated for everybody!)

Back 595

increased risk of stroke and death when used casually

Front 596

When are beta blockers indicated for perioperative pharmacologic mgmt?

Back 596

vascular, high and intermediate risk sx.
pts already on beta blockers
pts w multiple moderate clinical risk factors
pts w major clinical risk factors or ischemia on preop testing

Front 597

Alpha agonists are helpful in pts with CV risk factors because...

Back 597

analgesic, sedative and sympatholytic effects may help decr cardiac events (like dex)

Front 598

How are statins helpful in pts w CV risk factors?

Back 598

anti-inflammatory effects help stabilize coronary plaques

Front 599

What are 2 other drugs (Besides alpha agonists, beta blockers and statins) that are helpful in CV risk pre op candidates?

Back 599

insulin and aspirin

Front 600

Fact or fiction??
IV nitroglycerin prevents myocardial ischemia during surgery

Back 600

Fiction!
no documented advantages, may adversely affect loading conditions and complicate fluid mgmt

Front 601

What are some important strategies for intraoperative mgmt of CV risk pts?

Back 601

-prevent myocardial ischemia by optimizing myocardial O2 supply and demand
-monitor for ischemia and treat effectively

Front 602

The 2 primary causes of ischemia are

Back 602

decr O2 delivery,
incr O2 requirements

Front 603

What causes decr O2 delivery?

Back 603

decr coronary blood flow
tachycardia
hypotension
hypocapnia
coronary spasm- prinzmetal angina
anemia
hypoxia

Front 604

What causes incr O2 requirements?

Back 604

SNS stimulation
tachycardia
HTN (incr wall stress)
incr myocardial contractility
incr preload
incr afterload

Front 605

This is the single most important determinant of myocardial demand

Back 605

HEART RATE

Front 606

Tachycardia is an increase in HR at the expense of...

Back 606

diastole

Front 607

The LV is perfused during

Back 607

diastole

Front 608

The _____ is most sensitive to ischemia during systole.

Back 608

endocardium

Front 609

What are the induction considerations for CV patients?

Back 609

-avoid meds that incr HR and BP (ketamine)
-blunt sympathetic response to tracheal intubation w local anesthetics, beta lockers, and swift technique

Front 610

What are the maintenance considerations for CV pts?

Back 610

maintain stable hemodynamics by balancing control of SNS while avoiding hypotension

Front 611

What considerations should be made for CV pts in choosing muscle relaxants?

Back 611

avoid meds that incr HR and BP (pancuronium) or cause histamine release and hypotension (atracurium, morphine)

Front 612

What considerations should be made for continuous regional analgesia in CV pts?

Back 612

-intensive post op analgesia may decr incidence of perioperative cardiac complications
-important to avoid intraop hypotension

Front 613

Fact or fiction??

IAs are bad for the heart?

Back 613

FICTION!
they actually protect the heart from ischemia and provide anesthetic preconditioning

Front 614

What considerations should be made for continuous regional analgesia in CV pts?

Back 614

intensive post op analgesia may decr incidence of perioperative cardiac complications, important to avoid intraop hypotension

Front 615

Fact or fiction??
Sedation is the safest form of anesthesia in CV pts?

Back 615

fiction!
acceptable technique for minor procedures, but incomplete local anesthesia and analgesia increase stress response!

Front 616

Fact or fiction??
Local anesthesia has the lowest risk in CV pts?

Back 616

Fiction!
acceptable for a wide variety of minor procedures, but
incomplete local anesthesia and analgesia incr stress response and may induce ischemia!

Front 617

What are the benefits/drawbacks of 12 lead EKG?

Back 617

inexpensive and sensitive, but impractical in the OR --
use immediately post op and days 1&2 post op

Front 618

What are the benefits of automated ST analysis?

Back 618

highly sensitive, diagnoses up to 95% of ischemia episodes with simultaneous monitoring of leads 2 and 5

Front 619

What are the benefits/drawbacks of PA catheters?

Back 619

unreliable measure of ischemia, indicated in high risk pts undergoing sx w large fluid shifts, not shown to alter outcomes

Front 620

What are the benefits/drawbacks of TEE?

Back 620

sensitive measure of ischemia, even before EKG changes occur, costly, extensive training needed, misses ischemic events during induction

Front 621

What are the main goals of treating intraoperative myocardial ischemia?

Back 621

TREAT THE UNDERLYING CAUSE!
- tachycardia: rate control w beta blockers
- hypertension: vasodilator w nitroglycerine
- hypotension: vasoconstrictor (phenylephrine, ephedrine, epi)


be careful w inotropes and fluids to avoid driving myocardial O2 demand even higher

Front 622

What are post op mgmt techniques in pts at risk for myocardial ischemia?

Back 622

post op shivering dramatically increases myocardial O2 demand; continue beta blockers post op, plan for smooth emergence and intubation, post op pain and bleeding may lead to disaster!

Front 623

Pts undergoing cardiac transplant may present with _____ support.

Back 623

inotropic, vasodilator, and mechanical circulatory support

Front 624

Pts undergoing cardiac transplantation require intensive intraoperative monitoring and _____ therapy is often used after separation from CPB.

Back 624

inotropic

Front 625

The failing heart is dependent on circulating....

Back 625

catecholamines

Front 626

Abrupt decreases in sympathetic outflow may cause acute ______.

Back 626

decompensation

Front 627

Becoming unconscious during anesthesia causes ______ catecholamines.

Back 627

decreased