Cardiac

Front 1

Primary risk factors

Back 1

Htn, smoking, obesity hyperlipedemia, dm

Front 2

why is age itself a risk factor

Back 2

because of impaired nitric oxide production from vessels and vessel constriction, hardening

Front 3

what is conventional ischemia

Back 3

angina, MI, ischemic cardiomyopathy, sudden death)

Front 4

prevention of ischemia is accomplished pharmacologically by

Back 4

Pharmacologic manipulation of oxygen supply & demand through heart rate control & adequate coronary perfusion pressure

Front 5

...are the mainstay treatment for ischemic heart disease

Back 5

bb

Front 6

bb should be reconsidered if there is a fixed defect and poor LV function with an EJ of.. or with ...

Back 6

35% or less or with active congestive heart failure

Front 7

what is the cornerstone of therapyt

Back 7

nitrates

Front 8

why are nitrates so effective

Back 8

dilate coronary arteries, improving coronary blood flow and a decrease in preload

Front 9

nitrates cause Vasorelaxation of .. & large conduit arterial vessels

Back 9

veins

Front 10

Anginal chest pain with normal coronary angiography & lack of extracardiac etiology of the angina is called

Back 10

syndrome x

Front 11

syndrome x occurs in ..% of people with chest pain

Back 11

20%

Front 12

tx for coronary vasospasm

Back 12

nitroglycerin

Front 13

the major defect with syndrome x is

Back 13

coronary vasospasm

Front 14

stunning occurs after and because of

Back 14

bypass due to reperfusion of formerlly ischemic areas

Front 15

parameters to come of bypass

Back 15

1 L flow with 90 sys bp

Front 16

hibernation

Back 16

is impaired myocardial function in the setting of ongoing myocardial dysfunctinal flow

Front 17

pre conditoning

Back 17

when brief periods of ischemia confer protection against upcoming prolonged periods of ishemia and limit infract size

Front 18

Left coronary artery/ left main bifurcates into

Back 18

eft ant descending and circumflex

Front 19

left main disease is disease of

Back 19

the entire left ventricle

Front 20

Left main equivalent presents as

Back 20

-high degree of stenosis of both lad and circumflex

Front 21

the...artery supplies the posterior surface of the left atrium and left venticle.

Back 21

circumflex

Front 22

why do patients have to be on a pump for bypass of the circumflex artery

Back 22

because its posterior

Front 23

....Arise from a single ostium behind the left cusp of the aortic semilunar valve

Back 23

left coronary artery

Front 24

Aka anterior interventricular artery

Back 24

left anterior descending

Front 25

....Delivers blood to portions of the left and right ventricles and much of the interventricular septum

Back 25

left anterior descending

Front 26

... travels down the anterior surface of the interventricular septum toward the apex of the heart

Back 26

left anterior descending

Front 27

...Travels in a groove called the coronary sulcus

Back 27

circumflex artery

Front 28

...supplies blood to the left atrium and lateral wall of the left ventricle

Back 28

circumflex artery

Front 29

often branches to the posterior surfaces of the left atrium and left ventricle

Back 29

circumflex artery

Front 30

collateral arteries are...

Back 30

Connections or anastomoses between two branches of the same coronary artery or connections of branches of the right coronary artery with branches of the left

Front 31

why is a young person with an mi worse of than on an older person

Back 31

because an older person would have developed collateral circulation

Front 32

the right coronary artery originates

Back 32

Originates from an ostium behind the right aortic cusp

Front 33

the...Travels behind the pulmonary artery, and extends around the right heart to the heart’s posterior surface, where it then branches to the atrium and ventricle

Back 33

right coronary artery

Front 34

the..Right marginal: traverses the right ventricle to the apex

Back 34

the right marginal artery

Front 35

the..lies in the posterior interventricular sulcus and supplies smaller branches to both ventricles

Back 35

posterior descending branch

Front 36

when coronaries cant fill, this does not allow enough time for diastole /otherwise called ..or..

Back 36

systolic compression or diastolic dysfunction

Front 37

modulating factors

Back 37

oxygen, hydrogen, nitric oxide, prostoglandin, co2, osmolarity

Front 38

increased metabolism and o2 demand decreases..and causes a release of

Back 38

myocardial o2 and modulating factors

Front 39

oxygen demand is most increased with

Back 39

increased contractility

Front 40

rate pressure product

Back 40

higher rate times the pressure-more demand

Front 41

semilunar valves

Back 41

pulmonic and aortic

Front 42

blood leaves the right ventricle through the

Back 42

pulmonic valve

Front 43

decreased diastolic and end aortic pressure caused a..shift in oxygen delivery

Back 43

left

Front 44

..cause a left shift in oxygen delivery

Back 44

decreased oxygen delivery, anemia, hypoxemia, decreased hr, dec end diastolic, decreased aortic pressure.

Front 45

..are The heart valve openings are guarded by flaps of tissue called leaflets or cusps that are attached to the papillary muscle by the chordae tindineae

Back 45

chordae tendenea

Front 46

....are They are extensions of the myocardium that pull the cusps together and downward at the onset of ventricular contraction, thus preventing their backward expulsion into the atria

Back 46

papillary muscles

Front 47

..are Located between the right atria and ventricle

Back 47

tricuspid

Front 48

..has the largest diameter of any of the valves

Back 48

tricuspid

Front 49

..located between left atria/ventricle

Back 49

mitral

Front 50

atrioventricular valves

Back 50

mitral/tricuspid

Front 51

blood leaves the left ventricle throug the

Back 51

aortic valve

Front 52

When ventricles relax, xxxx fills the cusps, closing them and preventing backflow

Back 52

blood

Front 53

.... IS THE SINGLE MOST COMMON CONGENITAL HEART LESION

Back 53

congenital valve disease

Front 54

..most common cardiac valve lesion

Back 54

aortic stenosis

Front 55

aortic stenosis is considered severe if

Back 55

the pressure in the left ventricle exceeds 50 mmhg and the valve area is less than .8 cm h20

Front 56

aortic stenosis patients depend on their

Back 56

atrial kick

Front 57

key to managment of aortic stenosis

Back 57

avoid hypotension and increased afterload/depend on atrial kick so maintain sr

Front 58

hypetrophic cardiomyopathy is

Back 58

ventricular hypertrophy w no obvious cause.

Front 59

hypertrophic cardiomyopathy is an..disease and occurs in

Back 59

autosomal dominant and occurs in 1 of 500 people

Front 60

..most common cause of scd in peds

Back 60

hypertrophic cardiomyopathy

Front 61

in hypertrophic cardiomyopathy there is a..to flow

Back 61

systemic obstruction to flow

Front 62

key anes managment of hypertophic cardiomyopathy

Back 62

Maintain as euvolemic, normal to increased hr. sinus rhythm is critical. And avoid a decrease in afterload. Maintain hd stability. Hypertensive even more trouble puming, hypotension/decreased afteroald ( poor coronary filling and need more flow because they have a large left ventricle)

Front 63

causes of primary av leaflet disease are

Back 63

Most common causes: rheumatic fever, infective endocarditis, loss of comissural support with cusp collapse, congenital bicuspid AV

Front 64

causes of aortic root disease

Back 64

Degenerative diseases of aorta (Marfans), cystic medial necrosis, dissection, rare conditions

Front 65

managment of aortic regurgiation is to ensure

Back 65

fast flow forward( Avoid bradycardia, augment forward flow. Enough volume and afterload reduction. Inotropic augmentation

Front 66

mitral stenosis is usually caused by

Back 66

rheumatism

Front 67

severe mitral stenosis parameters

Back 67

less than 1 cm, normal is 4

Front 68

managment of mitral stenosi

Back 68

Imp left ventricular filling, require an atrial kick and need to stay in SR> and maintain euvolemia

Front 69

the severity of calcification of mtiral stenosis correlates with

Back 69

Severity of calcification correlates with the transvalvular pressure gradient

Front 70

pathophysiology of mitral regurgitation

Back 70

Acute vs chronic vs mixed
Acute: LA has not undergone adaptive changes that allow for compensation
Acute pulmonary edema- due to high hydrostatic pressure
chronic-left atrium is dilated

Front 71

number one cause of acute pulmonary edema is

Back 71

high hydrostatic pressure

Front 72

with mitral regurgitation the is ejection into both the

Back 72

aorta and left atrium

Front 73

perioperative evaluation of mitral regurgiation

Back 73

Assessment of ventricular function
LVEF not good index since LV ejects both into the aorta & LA
Must measure non-ejection indices of function (LV ESP/LVESV relationships)

Front 74

indicators for pa lines

Back 74

ej less than 40, left main coronary artery dis, right ven ischemia and pulmonary hypertension

Front 75

last minute checks before induction

Back 75

Reassessment of the patient’s overall cardiopulmonary and airway status
Integrity of the breathing circuit and suction
Availability of blood for transfusion
Proximity of a surgeon or fellow
Immediate availability of emergency cardiac drugs

Front 76

..will offset the bradycardia associated with fentanyl

Back 76

pancuronium

Front 77

avoidance of nitrous oxide with bypass is related to

Back 77

air bubbles

Front 78

2 mg/kg of propofol can drop the MAP

Back 78

20-40%

Front 79

induction dose of thiopental is

Back 79

2-4 mg/kg

Front 80

fast track cardiac anesthesia

Back 80

Extubation within 8 hours
No increase in ischemia or respiratory morbidity or mortality
Lower dose narcotics – Fentanyl limited to 10-15 mcg/kg
Volatile anesthetics/ Propofol infusion supplements

Front 81

og tube placement during bypass occurs

Back 81

before inscision, place and decompress and then place TEE proble, place NG prior to ICU

Front 82

first incision for a cabg is in the

Back 82

saphenous vein

Front 83

during bypass it is important the lungs are down prior to the

Back 83

sternal split

Front 84

the paddles on the defibirlillator should be changed after

Back 84

the chest is cracked open

Front 85

setting on the defibrillator after the chest is open

Back 85

10 J to a max of 20J

Front 86

the patient has to be heperanized before

Back 86

arterial cannulation

Front 87

normal act

Back 87

105-167

Front 88

before heperanization you have to

Back 88

check ont he act with the perfusionist

Front 89

heparin is always given through a

Back 89

central line and aspirate to make sure you are getting blood back

Front 90

act is drawn

Back 90

3 minutes after heparin in a 3 cc plain syringe

Front 91

dont draw up the protamine untill

Back 91

the perfusionist tells you at the end of the case

Front 92

venous cannula goes into the

Back 92

ivc/svc

Front 93

BP parameters when cannulating the aorta

Back 93

90, higher pressure may result in a dissection

Front 94

prebypass checklist

Back 94

infusions-turned off
anticoagulation-adequate?
cannulation-proper and patent
anesthesia-adequate?
monitoring-in place and checked?
pupils-inspected?

Front 95

bypass pulmonary pressure should be

Back 95

less than 15 mm hg

Front 96

bypass arterial blood pressure should intiatlly be

Back 96

30-60 mmhg

Front 97

bypass cvp should be

Back 97

less that 5

Front 98

ventilation should be stopped when

Back 98

aoritc ejection by the hear ceases

Front 99

when going on bypass and the blood is drained by the cannula, the blood pressure..

Back 99

always drops

Front 100

..of the face can result from a misplaced venous cathter

Back 100

edema

Front 101

if the mean pressure at bypass is very low then..if its high then..

Back 101

low-dissection at site of cannula, hight not enough narcotic, give perfusionist fentanyl

Front 102

..vessels are rewarmed first

Back 102

distal

Front 103

stunned myocardium may be

Back 103

paced

Front 104

..mg protamine test dose

Back 104

10 mg

Front 105

factors that may weaning from bypass difficult

Back 105

Factors that may make weaning from CPB difficult ---- fibrillation, potassium or acid/base disturbance, need for pacing, need for inotropic support, optimal preload

Front 106

termination of bypass

Back 106

Rewarm
Remove air if necessary
Optimize metabolic condition
Factors that may make weaning from CPB difficult ---- fibrillation, potassium or acid/base disturbance, need for pacing, need for inotropic support, optimal preload

Front 107

it is most important to ensure ventilation to ....lung

Back 107

left lower

Front 108

differential diagnosis after LV failure

Back 108

Ischemia – graft failure, air in graft, kinking of graft
Inadequate coronary blood flow – incomplete revasc (inoperable vessels), inadequate coronary perfusion pressure, emboli, spasm, increased demand
Valve failure
Gas Exchange problems – hypoxemia, atelectasis , “pump lung”
Preload – inadequate or excessive
Reperfusion injury

Front 109

Epinephrine increases SVR, ...doesnot

Back 109

milaranone

Front 110

normal SVR is

Back 110

1400 dynes/sec/70 meters sq

Front 111

..... may be more appropriate if SVR is increased

Back 111

Dobutamine or Milronone

Front 112

..... may be appropriate if HR is normal and SVR is low or normal

Back 112

Epinephrine or Dopamine

Front 113

post bypass LV failure treatement

Back 113

Inotropic drug support – first line agent often Epi or Milrinone, but varies by institution
Epinephrine or Dopamine may be appropriate if HR is normal and SVR is low or normal
Dobutamine or Milronone may be more appropriate if SVR is increased
Low-dose Epi or Milronone may be appropriate if HR is elevated

Front 114

patients at risk for RV failure

Back 114

pulm hypertension, mitral valve disease, RV infarct or ischemia, RV outflow obstruction, tricuspid regurg

Front 115

treatment for RV failure

Back 115

Treatment – NTG if systemic BP permits
optimize preload
preserve coronary perfusion pressure
inotropic support – Milronone, Dobutamine, Isoproterenol

Front 116

complication of pt transfer

Back 116

aComplications of Transfer: extubation, coronary or air embolism from dislodgement, invasive line removal, IABP line disruption, pacemaker wire disconnect, corneal injury, loss of vasoactive infusions, venodilation and hypotension

Front 117

advantages of minimally invasive cardiac surgery

Back 117

avoidance of bypass
less risk of stroke or neuro defecits
shorter hospital and iCU stay
cost saving
decreased transfusion requirements

Front 118

disadvantages of minimally invasive cardiac surgery

Back 118

technically more demanding
multivessel disease is contraindicated
may not be a reprouducible technique
hemodynamic instability and arrythmias
unsafe in unstable patients

Front 119

unknowns about cardiac minimally invasive surgery

Back 119

operative risk
appropriate patient selection
adquacy of overall revascularization
cost considerations

Front 120

pressure overload produces....and and increase in...

Back 120

pressure overload produces concentric ventricular hypertophy with an increase in ventricular wall thickness with a cardiac chamber of normal size

Front 121

volume overload leads to.....with ...wall thickness and

Back 121

volume overload lead to eccentric hypertrophy with normal wall thickness and dilatd cardiac chamber

Front 122

as is classified as

Back 122

vulvular, subvalvular, supravalvular obstruction of the LV outflow tract

Front 123

in AS there is ..hyperophy in response to increased...pressure and wall tension necessary to maintain forward flow

Back 123

concentric hypertophy ( thickened ventricular wall with normal chamber size) in response to the increased intraventricular systolic pressure and wall tension necessary to maintain forward flow.

Front 124

In as Ventricular relaxation ..., causing..dysfunction

Back 124

ventricular relaxation decreases causing dyastolic dysfunction

Front 125

Elevated LV end diastolic feature is a hallmark of..stensosis

Back 125

aortic

Front 126

normal atrial contraction accounts for..% of atrial filling

Back 126

20%

Front 127

atrial contraction accounts for..% of ventricular filling in AS

Back 127

40

Front 128

In developing counries, ...is the most common cause of AS

Back 128

rheumatoid arth

Front 129

In Us/europe as is mostly caused by

Back 129

calcification of the native trileaflet or a congential bicuspid valve

Front 130

what is a pressure volume loop

Back 130

plots LV pressure against volume through one complete cardiac cycle

Front 131

pathophysiology of mitral stenosis

Back 131

left atrium experiences pressure overload, with lv underload due to obstruction for forward flow from the atrium. elevated atrial pressure is transmitted to the pulmonary cicuit and lead to pulmonary hypertension and right heart failure. Overdistended atrium is suceptible to afib.

Front 132

anesthetic managment of mitral stenosis

Back 132

intravascular volume must be adequate to maintain flow across the stenotic valve. slower heart rate allows more time for blood to flow across the valve, increasing ventricular filling. sinus should be maintained because atrial contraction contributes about 30% of stroke volume. increases in pulmonary vascular resistance may exacerbate right ventricular failure; thus hypoxemia, hypercarbia, acidosis should be avoided

Front 133

..agents given perioperatively may make mitral stenosis worse by increasing pulmonary vascular resistance

Back 133

respiratory depressants/sedatives

Front 134

hemodynamic goals in AS

Back 134

maintain intravascular volume, contractility, peripheral vascular resistance, sinus rythm while avoiding extremes in heart rate.

Front 135

hemodynamic goals in MS include

Back 135

maintain intravascular volume, afterload and sinus rythm and a slower heart rate. avoid increase in PVR. sedatives carefully

Front 136

lead V is most usefull for

Back 136

detecting ischemia

Front 137

lead II is most useful for

Back 137

right coronary artery destribution and most useful for monitoring P waves and cardiac rythm

Front 138

Pulmonary artery occlusion pressure otherwise called...pressure gives an estimation of

Back 138

pulmonary artery occlusion pressure otherwise called wedge pressure gives an estimation of left ventricular end diastolic pressure

Front 139

major component of the cardiopulmonary bypass circuit

Back 139

venous line ( siphons central venous blood from the pt into a reservoir) oxygenated blood w c02 removed then is returned to the patients arterial circulation. pressue to perfuse the arterial circulation is provided by a roller head or a centrfugal pump; resulting in a non pulsitile arterial flow,. roller head pumps for cardioplegia adminisration ventricular vent to drain the heart during surgery and a pump sucker to remove blood from the surgical field. In addition, the circuit contains filters for air and blood microemboli. heat exchanger to produce hypothermia on bypass and warm the patient before seperating from the CPB. venous reservoir must never be allowed to empty on CPB because of emobli risk

Front 140

adverse effects of hypothermia are

Back 140

platelet dysfunction, reduction in serum ionized calcium concentration caused by enhanced citrate activity, impaired coagulation, arrythmias, increased risk of infection, decreased oxygen unloading, potentiation of neuromuscular blockade, impaired cardiac contractility

Front 141

systemic oxygen demand decreases..% for every degree of temp drop

Back 141

9

Front 142

main concern for CPB

Back 142

prevention of myocardial injury and cns system injury along with renal and hepatic protection

Front 143

common cannulation sites for bypass

Back 143

venous blood is obtained through cannulation of the right atrium using a two stage cannula that drains both the superior and inferior vena cava. alternatively for open heart procedures bicaval cannulation is used with direct, seperate cannulation of the superior and inferior vena cavae. arterial blood is returned to the ascending aorta proximal to innominate artery. Femoral arterly may also be used as a cannulation site. axillary cannulation ( performed before the actual sternotomy)

Front 144

arterial blood is returned to the

Back 144

ascendin aorta proximal to the innominate artery

Front 145

drawbacks to cannulation of the femoral artery are

Back 145

ischemia of leg distal to cannulation site, inadequate venous drainage, possible inadequate systemic perfusion secondary to a small inflow cannula, and difficulty in cannula placement because of artherosclerotic plaques.

Front 146

basic anest techniques for cardiopulmnary bypass

Back 146

fast tracking- decreased time to extubation and faster arrival in ICU.

Front 147

why are nmba specifically usefull for bypass

Back 147

decrease movement/shivering and myocardial oxygen demand

Front 148

two types of oxygenators

Back 148

bubble oxygenators work by bubbling oxygen through the blood and then defoaming the blood to minimize air mircoemboli. membrane oxygenators have a lower risk of microemboli , using a semipermeable membrane that allows diffusion of oxygen and co2.

Front 149

what is pump prime

Back 149

priming solution of crystalloid, colloid, blood to fill the CPB circuit. when bypass is initiated , the circuit must contain fluid to perfuse the circulation until the patients own blood can circulate through the pump. priming volumes are 800- 2l.

Front 150

what is the hemodynamic response to initiating bypass

Back 150

acute hemodilution of the patients circulating blood volume mixing with the prime volume can cause an acute reduction in mean arterial pressure and hemoglobin concetration

Front 151

how is the adeuacy of anticoagulation measured before and during bypass

Back 151

act is measured 3-4 minutes after heparin administration and every 30 min on CPB.

Front 152

ACT longer than..sec is considered acceptable

Back 152

400

Front 153

...is a measure of anticoagulant activity

Back 153

ACT

Front 154

what must be ascertained before placing a patient on cardiopulmonary bypass

Back 154

adequate arterial flow of oxygenated blood with acceptable pressure
sufficient venous return to the pump
act of atleast 400 sec
appropriate placement of retrograde cardioplegia cannula
arterial line monitor of mean blood pressure
core temp monitoring
adequate depth of anes

Front 155

why is a left vent used

Back 155

left ventriular distension during bypass can be caused by aortic regurgitation or blood flow through the bronchial and thesbian veins. the resultant increase in myocardial wall tension can lead to myocaridal ischemia by precluding adequate subendocarial carioplegia disribution and elevating myocardial oxygen demands. a left ventricular vent, placed through the right superior pulmonary vein, decompresses the left side of the heart and returns theis blood to the CPB

Front 156

what are the characteristics of cardioplegia

Back 156

cardioplegia is a hyperkalemic solution containing varoius metabolic energy substrates. perfused through the coronary vasculature, cardioplegia induces diastolic electromechanical dissociation. myocardial oxygen and energy requirements are reduced to those of cellular maintenance. cardioplegia is perfused either antegrade via the arotic root coronary ostia or retrograde through the right atrial coronary sinus.

Front 157

how is the myocardium protected during cardiopulmonary bypass

Back 157

cellular integrity must be maintained to ensure cardiac performance after CPB. a critical factor to prevent cellular damage is intraoperative myocardial protection. preservation of the balance between myocardial oxygen consumption and delivery is essential, an the following are key elements in achieving this. adequate cardioplegia, hypothermia 12-15c. topical cooling of the heart with icy saline flush. left ventricular venting to prevent distention. insulating pad on the posterior cardiac surface to prevent warming from mediastinal blood flow. minimizing bronchial vessel collateral flow ( which rewarms the arrested heart)

Front 158

what is the function of the aortic cross clamp

Back 158

clamping occurs accross the proximal aorta and isolates the heart and coronary circulation. arterial bypass inflow enters the aorta distall to the clamp. cardioplegiais infused between the clamp and aortic valve, thus entering the coronary circulation. this isolation of the heart from the systemic circulation allows for prolonged cardioplegia activity, diastolic arrest of the heart and profound myocardial cooling

Front 159

physiologic respose to bypass

Back 159

stress hormones increase
complement activation, initiation of coagulation cascade, platelet activation. initiation of systemic inflammatory response
platelet dysfunction associated with cpb may contribute to post cpb bleeding
hemodilution associated with onset of cpb decreases the serum concentrations of most drugs but decreased hepatic and renal perfusion during cpb will eventually increase the serum concentration of drugs administered by cont infusion

Front 160

appropriate heck list for dc bypass

Back 160

check acid base balance, adequate rewarming to 37C. zero all transducers, adequate heart rr (may need pacing) , reexamine EKG for rhythm and ischemia, evaluate TEE, remove intracardiac, intra aortic air if the aorta or cardiac chambers were opened. initiate ventilation of lungs

Front 161

how is the heparin effect reversed

Back 161

protamine is positively charged protein molecule, binds the negatively charged heparin and this complex is removed from the circulation by the reticuloendothelial system.

Front 162

give..mg protamine per..units heparin

Back 162

1 mg protamine per 100 units of heparin

Front 163

potential complications of protamine admnistration

Back 163

systemic hypotension because of histamine release or true anaphylaxis along with catastrophic pulmonary hypertension due to anaphylactoid thromboxane release. risk factors include preexisting pulmonary hypertnesion, diabetics with NPH insulin preperations, bolus protamine administration and central administation of protamine.

Front 164

why is cardiac pacing frequently useful after bypass

Back 164

impaired cardiac conduction and myocrdial wall motion is suboptimal. sequential cardiac pacing at rate of 80-100 beat/min can sig improve cardiac outcome

Front 165

vasoplegia

Back 165

reduced vascular resistance

Front 166

what are some therapies for the patient with impaired cardiac performance after bypas

Back 166

reduced vascular resistance treated with vasopressors. conractillity problems with the heart may be treated with inotropic agents or a aortic balloon pump. right heart dysfunction and/or pulmonary hypertension may be treated with nitric oxide or vasodilator therapy.

Front 167

review the cns complications for cardiopulmonary bypass

Back 167

1-3% risk of new neuro events, defined as stroke ( including vision loss), tia, coma. 3% incidence of deterioration of intellectual function, memory defects or seizures. cerebral microemboli, in particular platelet microemboli are beleived to be a mor contributing factor

Front 168

what maybe done to decrease the incidence of neuro complications with bypass

Back 168

risk factor id before surgery. optimization of carotoid stenosis preop. sig arthersclerosis is an idependent risk factor for stroke-therefore off pump surgica strategy is of more benefit. perioprative asa therapy. meticulous attention placed intraoperatively to decrease cerebral oxygen requirements through hypothermia. tight glucose control.

Front 169

bradayrrythmias may aris from

Back 169

either SA node dysfunction or abnormal AV conduction or the cardiac impulse. reversible abnormalities due to abnormal vagal tone, electrolyte abnormalities, drug toxicity, hypothermia, myocardial ischemia.

Front 170

if the reservoir is allowed to empty in the CPB machine...

Back 170

air can enter the main pump and cause an emboli

Front 171

,,,,increase pulmonary vascular resistance

Back 171

acidosis, hypercapnia, hypoxia, enhanced sympathetic tone, high mean airway pressure

Front 172

..is usually effective in lowering pVR

Back 172

hyperventilation w 100% fio2

Front 173

patiens with left to right shunting benefit from

Back 173

systemic vasodilation and increased PVR

Front 174

period of greatest hemodynamic instability during bypass

Back 174

after release of aortic cross clamp

Front 175

anes dose requirements are..related to ventricular function

Back 175

inversely

Front 176

most patients with heparin resistance have

Back 176

antithrombin III deficiency

Front 177

heparin dose

Back 177

300-400 u/kg

Front 178

systemic vasodilation worsens..shunting

Back 178

right to left

Front 179

induction of patients with cardiac tempnade may precipitate

Back 179

severe hypotension and cardiac arrest.