Phys And Pathophys - Valve Disorders And Loop Problems

Front 1

a loop problem refers to

Back 1

the graphical relationship between LV volume and LV pressure

Front 2

slope is

Back 2

change in pressure over change in volume

Front 3

the slope of the curve on the pressure volume loop is an indicator of

Back 3

the ventricular elastance or "stiffness"

Front 4

the compliance of the heart as seen on a pressure volume loop is

Back 4

the inverse of the slope of the line at that point

Front 5

the relationship between volume and pressure is

Back 5

not linear - a curve

Front 6

both pressure and volume are indices of

Back 6

preload

Front 7

elastance increases as

Back 7

volume or pressure increases (as the slope of the line increases)

Front 8

beginning of the curve is

Back 8

very compliant - small increase in pressure even though large increase in volume

Front 9

be able to draw the normal pressure volume loop of the left ventricle

Back 9

include ABCD, valve closures, stroke volume,

Front 10

describe the stages of the normal pressure volume loop

Back 10

A - opening of the mitral valve and ventricular filling. B - mitral valve closes and isovolumetric contraction begins as pressure builds to point C - where the aortic valve opens because the pressure in the ventricle is greater than that in the aorta. between C and D the blood is ejected from the ventricle. At D the aortic valve closes and isovolumetric relaxation begins again.

Front 11

what to look at in loop problems

Back 11

LVEDV, LVESV, LVEDP, LVESP, SV

Front 12

the most important indicator of preload is

Back 12

LVEDV

Front 13

when preload is increased, the pressure volume loop

Back 13

volume on bottom shifts right a bit, greater stroke volume overall, valves open and shut at the same point - most of the extra blood is ejected in a healthy heart so have almost the same ESV (slightly more)

Front 14

the indicator of decreased preload is

Back 14

LVEDV

Front 15

when preload is decreased the loop

Back 15

shifts left - less EDV, valves open and close about the same, less stroke volume, almost the same ESV (slightly less)

Front 16

increased afterload causes loop to

Back 16

be taller and narrower - increased pressure to open valve makes it taller, and valve closes sooner making it narrower. LVEDV is the same - same preload but reduced stroke volume

Front 17

LVESV increases and stroke volume decreases due to increased afterload because

Back 17

ventricle can not empty as well because pushing against greater resistance and aortic valve closes early because of increased aortic pressure

Front 18

will a positive inotrope compensate for increased afterload

Back 18

yes - contracting with more force will overcome afterload resistance easier, allowing valves to open earlier, stay open longer, improving stroke volume

Front 19

chronic increases in afterload causes

Back 19

LV hypertrophy - the LV chamber thickens as the body tries to lay down more contractile tissue

Front 20

LV hypertrophy results in a need

Back 20

for more O2

Front 21

how is the PCWP or PCOP affected by increased afterload

Back 21

will increase due to the increased volume and pressure in the LV

Front 22

chronic increased afterload shifts the curve (like in a HTN pt)

Back 22

up and to the right and will worsen if condition is not treated.

Front 23

how does Starling's curves change as afterload increases?

Back 23

slide with layered curves - as afterload increases stroke volume decreases and EDV increases - volume left in the heart keeps increasing

Front 24

EF =

Back 24

(LVEDV - LVESV)/LVEDV

Front 25

decreased afterload makes the curveloop

Back 25

be shorter and fatter - increased stroke volume, lower ESV, almost as high EDV, valves open earlier and stay open longer

Front 26

decreasing afterload affects PCWP by

Back 26

decreasing it because the LV volume and pressure is decrease

Front 27

phenylephrine is a

Back 27

alpha 1 agonist

Front 28

nipride is a

Back 28

NO donar - arteriole vasodilator

Front 29

cardiac valve lesions affect heart function by either

Back 29

causing pressure overload or volume overload

Front 30

valve pathologies that cause pressure overload are

Back 30

mitral and aortic stenosis

Front 31

valve pathologies that cause volume overload are

Back 31

mitral regurg and aortic regurg

Front 32

when choosing anesthetics for a heart condition consider

Back 32

drugs effect on HR, preload, afterload, contractility, heart rhythm

Front 33

valvular heart conditions interfere with

Back 33

the forward movement of blood

Front 34

dirty cases are

Back 34

ENT, urinary, dental

Front 35

preoperative antibiotics and valve conditions

Back 35

in general recommendations are still to give antibiotics preoperatively, although there is much discussion. Ask if patient takes antibiotics prior to dental procedures.

Front 36

mitral stenosis caused by

Back 36

fusion of leaflets by rheumatic fever as a child

Front 37

normal mitral valve area is

Back 37

4-6 cm2

Front 38

in mitral valve area decreases to less than 1 cm2, left atrial pressure is

Back 38

about 25 mmHg

Front 39

a LAP > 25 mmHg will cause

Back 39

pulmonary hypertension

Front 40

mitral stenosis is indicated if

Back 40

the gradient is greater than 10 mmHg across the valve - the bigger the gradient the worse the problem

Front 41

rheumatic fever is a type of

Back 41

streptococcal A infection and valve complications do not materialize for over 20 years

Front 42

mitral stenosis can cause

Back 42

a distension of the atria, afib, afib, and thrombi formation b/c of increased turbulent flow

Front 43

mitral stenosis often detected when

Back 43

woman is pregnant because of increased demand for cardiac output

Front 44

normal pressure gradient between LA and LV is

Back 44

5 mmHg

Front 45

LAP should equal the

Back 45

PAOP which should equal the PADP

Front 46

characteristics of mitral stenosis

Back 46

narrowing mitral valve, increasing LA volume, decreasing LV volume, loss of cardiac output, increase in LA pressure, diastolic filling time remains the same, LA distension causes afib

Front 47

#1 cause of tricuspid regurg is

Back 47

mitral valve stenosis

Front 48

mitral stenosis is staged to help

Back 48

decide who gets valve replacements

Front 49

stage 1 mitral stenosis is characterized by

Back 49

area of 1.5 - 2.5 cm2 with symptoms of dyspnea with moderate exercise

Front 50

stage 2 mitral stenosis is characterized by

Back 50

area of 1 - 1.5 cm2, dyspnea with mild exertion, development of CHF, and new onset a fib

Front 51

stage 3 mitral stenosis is characterized by

Back 51

< 1 cm2 area, dyspnea at rest, tricuspid regurg, CHF, RV dilation

Front 52

describe progression of mitral valve stenosis

Back 52

as mitral valve narrows time to empty LA decreases, LV gets less blood, so CO decreases. Blood backs up into LA and pressure increases causing further back up into pulmonary beds. CHF will ensue and increase RV pressure causing tricuspid regurg.

Front 53

as the mitral valve becomes stenotic the LA pressure

Back 53

is increased but is lost because it's pushing against a fixed lesion

Front 54

symptoms of mitral valve stenosis don't develop until valve has stenosed to

Back 54

1.5 - 2.5 cm2 in area

Front 55

conditions that induce high cardiac output are

Back 55

pregnancy, thyrotoxicosis, anemia, fever - worsens mitral stenosis symptoms

Front 56

mitral stenosis induced afib

Back 56

results in complete loss of atrial kick which worsens CO even more

Front 57

mitral stenosis pressure volume loop looks like

Back 57

same height, narrower, decreased LVEDV and a little decreased LVESV, valves open and close at the same time, decreased stroke volume - looks like decreased preload curve

Front 58

mitral stenosis pressure volume loop is the same as

Back 58

decreased preload curve

Front 59

volume loops are from the view of

Back 59

the left ventricle

Front 60

anesthetic implications for mitral stenosis

Back 60

the faster the more the disaster
keep HR slow, regular rhythm, maintain preload, maintain after load, maintain contractility

Front 61

why do you want a slower heart rate with mitral stenosis

Back 61

because more time in diastole means more time for blood to get through the stenosed valve to allow for greater time filling and better cardiac output

Front 62

why do you want a regular rhythm with mitral stenosis?

Back 62

preserve atrial kick for increased EDV

Front 63

what do you want to maintain in mitral stenosis

Back 63

preload, afterload, contractility

Front 64

what do you avoid in patients with mitral stenosis?

Back 64

increasing heart rate - anxiety, shivering, pain, ketamine (or other sympathomimetics), pavulon, atropine, glycopyrrolate
and any abnormal rhythms also - trendelenburg position

Front 65

things to remember in interpretation of mitral stenotic data

Back 65

large A wave on the swan, PAOP will not be equal to the LVEDP

Front 66

why is there an increased A wave on the swan in patients with mitral stenosis

Back 66

the atria are contracting against a fixed valve so you have increased pressure in the atria causing a larger A wave

Front 67

if a patient has mitral stenosis the swan values are

Back 67

pretty much useless

Front 68

the second most common valve disorder is

Back 68

aortic stenosis

Front 69

normal size of the aortic valve is

Back 69

2.5 - 3.5 cm2

Front 70

what is affected by aortic stenosis

Back 70

reduced SV, increased LVESV, increased LVEDP, concentric hypertrophy, and congestive heart failure/pulmonary edema

Front 71

as the patients develop aortic stenosis they experience

Back 71

dyspnea upon exertion that worsens as disease progresses - disease has three stages

Front 72

symptoms are significant in aortic stenosis when valve size is less than

Back 72

1 cm2 - this is when they recommend replacement of valve

Front 73

why is hypertrophy (along with increasing LVEDP and LVESV in aortic stenosis) a problem for oxygen heart supply

Back 73

hypertrophy increases oxygen demand and decreases supply because the extra muscle, volume, and pressure compress the subendocardial coronary blood vessels

Front 74

symptoms of aortic stenosis

Back 74

triad - angina, dyspnea, and syncope

Front 75

you can have angina even without heart disease if you

Back 75

have aortic stenosis

Front 76

aortic stenosis can be detected pre symptoms by

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a mid systolic murmur

Front 77

pt with aortic stenosis have an increased risk of

Back 77

sudden death

Front 78

why does a patient with aortic stenosis experience angina?

Back 78

the cardiac output is decreased through the stenotic valve, pressure in the aortic root is reduced, LVEDP is big and LVESV is increased, therefore CPP is decreased as O2 demand increases due to hypertrophy and dilation of the heart muscle

Front 79

why does syncope occur in a patien with aortic stenosis

Back 79

decreased CO leads to decreased blood flow to the head

Front 80

increasing myocardial thickness is aka

Back 80

concentric hypertrophy - when the muscle replicates in parallel

Front 81

anesthetic goals for a patient with aortic stenosis

Back 81

slow heart rate, maintain preload and rhythm, maintain or slightly increase afterload, maintain contractility

Front 82

what to avoid in patients with aortic stenosis

Back 82

reducing cardiac output, spinal anesthetics, and tachycardia

Front 83

if you must do a regional block on a pt with aortic stenosis then

Back 83

do an epidural not a complete spinal

Front 84

why must you maintain or slightly increase afterload in a patient with aortic stenosis

Back 84

if SVR is greatly reduced, chance of stroke, MI greatly increased because of reduced CO causing decreased coronary and cerebral perfusion pressures

Front 85

type of anesthesia preferred for patients with aortic stenosis

Back 85

general

Front 86

why do you want to avoid tachycardia in a patient with aortic stenosis

Back 86

tachycardia reduces time in systole and you need more time in systole to increase time for unloading of ventricle through the stenotic valve

Front 87

what does the pressure volume loop look like for aortic stenosis

Back 87

narrow, tall, and to the right - high pressure, crappy stroke volume

Front 88

aortic stenosis does what to stroke volume

Back 88

decreases because it is hard to push out against the stenosed valve

Front 89

aortic stenosis does what to ESV

Back 89

increased - because the LV doesn't have as great a stroke volume because it is hard to push out against the stenosed valve so blood is left in the heart

Front 90

aortic stenosis does what to EDV

Back 90

same

Front 91

aortic stenosis does what to EDP

Back 91

same

Front 92

aortic stenosis pressure volume loop looks like the volume loop for

Back 92

increased afterload

Front 93

aortic stenosis is an absolute contraindication for

Back 93

a spinal anesthetic because extreme vasodilation would tank the CO and there would be no Coronary PP (may consider carefully an epidural but probably shouldn't do that either!)

Front 94

coronary perfusion pressure =

Back 94

diastolic blood pressure - LVEDP

Front 95

why do you want a slow heart rate with aortic stenosis

Back 95

gives more time to eject blood

Front 96

why do you want to maintain afterload in a patient with aortic stenosis?

Back 96

because if SVR drops then there is a decreased pressure in the aorta and not enough pressure for the perfusion of the heart overtop the increased pressure in the heart at the LVEDP

Front 97

in a patient with aortic stenosis, pressure in the left ventricle is

Back 97

high

Front 98

in a patient with aortic stenosis the left ventricle will

Back 98

hypertrophy

Front 99

mitral regurg facts

Back 99

usually due to rheumatic fever, almost always associated with mitral stenosis, LA enlarges due to backflow during systole, large V wave in PAOP wave form

Front 100

in a patient with mitral regurg the v wave on the swan will

Back 100

be large - the bigger the v wave the worse the regurg

Front 101

usual causes of mitral regurg are

Back 101

rheumatic fever, mitral stenosis, or papillary muscle dysfunction following an MI or rupture of a chordae tendinae due to infective endocarditis

Front 102

placement of a PA or Swan cathether

Back 102

placed through the subclavian or jugular veins, fed through the RA, RV, into the pulmonary artery. proximal port in the RA, distal port in the PA

Front 103

wedging or a PAOP pressure is

Back 103

when we inflate a balloon on the end of the PA catheter, occluding a branch of the pulmonary artery. the catheter should then be able to measure the pressure ahead of it (since the pressure behind it is occluded).

Front 104

in the absence of mitral valve dysfunction or pulmonary hypertension then the PAOP pressure should equal

Back 104

the LA pressure which should be equal to the LVEDP

Front 105

describe the waveforms as the PA cath is floated through the heart

Back 105

RA - small up and down, the RV has large up and down waveform with each beat, and the PA has a smaller, tight waveform with a nice dicrotic notch. A wedged waveform has minimal waves

Front 106

describe the PAOP waveform

Back 106

a two peaked wave - peak a and peak v

Front 107

peak a on the paop waveform correlates with

Back 107

atrial contraction

Front 108

peak v on the paop waveform correlates with

Back 108

ventricular contraction

Front 109

goals of anesthesia in a patient with mitral regurg

Back 109

maintain or increase heart rate, decrease SVR, maintain or improve contractility, maintain volume, regular rhythm, Full, Fast, and Forward

Front 110

Full, Fast, and Forward means

Back 110

maintain volume, maintain or improve contractility and decrease afterload, and keep the heart rate going

Front 111

why do you want to avoid bradycardia in a patient with mitral regurg

Back 111

increases amount of regurg and less gets circulated to the body (more gets shunted back into the atria) - the longer in systole the worse the regurg

Front 112

describe the mitral regurg volume loop

Back 112

looks like an egg laying on its side (draw an M in it) - no good isovolumetric contraction or relaxation, huge stroke volume (but much of the volume is going back into the atria), can't see when the AV valve opens or close

Front 113

acute causes of aortic regurgitation are

Back 113

endocarditis, trauma, dissection of a thoracic aneurysm

Front 114

chronic causes of aortic regurgitation are

Back 114

rheumatic fever, prolonged hypertension

Front 115

aortic regurgitation causes

Back 115

reduced forward blood flow, LV overload, and decreased CO

Front 116

management of aortic regurg is the same as management of

Back 116

mitral regurg - Full, Fast, and Forward

Front 117

management of aortig regurg guidelines are

Back 117

maintain or increase HR and preload, RSR, avoid increasing afterload.

Front 118

increasing afterload in a patient with aortic regurgitation will result in

Back 118

decreased CO because more blood will flow back into ventricle rather than out the aorta

Front 119

the pressure volume look for aortic regurg looks like

Back 119

a lopsided egg that's top is laying to the right - draw and A on the left side of the loop - no isovolumetric contraction, huge stroke volume because blood is kind of flowing in and out of the ventricle all the time

Front 120

LV remodeling occurs either

Back 120

in parallel or in series

Front 121

parallel replication is aka

Back 121

concentric hypertrophy

Front 122

concentric hypertrophy occurs with

Back 122

pressure overload

Front 123

replication in series is aka

Back 123

eccentric hypertrophy

Front 124

eccentric hypertrophy occurs with

Back 124

volume overload

Front 125

most hearts have what type of remodeling

Back 125

new research shows there is usually a combination or eccentric and concentric hypertrophy

Front 126

what positions should you avoid in mitral valve prolapse

Back 126

sitting position

Front 127

mitral valve prolapse is aka

Back 127

click-murmur syndrome or Barlow syndrome

Front 128

mitral valve prolapse is characterized by

Back 128

an abnormality of the support structure that permits prolapse of the valve into the LA during contraction of the LV.

Front 129

mitral valve prolapse is best heard

Back 129

at the apex

Front 130

MVP is associated with

Back 130

Marfan's syndrome, pectus excavatum, and kyphoscoliosis

Front 131

what arrythmias are associated with MVP

Back 131

PVC's are most common sometimes leading to vtach, sometimes some SVT

Front 132

best option for treatment of arrhythmia in MVP is

Back 132

beta blockers - sometime lidocaine is used but usually doesn't terminate PVC's so beta blockers is a better option

Front 133

MVP worsens with

Back 133

reduced preload (sitting position, drugs, vasodilators) increased contractility (anxiety, increased sympathetic system activity)

Front 134

SVR in MVP should be

Back 134

maintained

Front 135

MVP should avoid

Back 135

anticholinergics because produce tachycardia

Front 136

MVP should get

Back 136

antibiotics prior to dirty procedures

Front 137

anesthetic goals for MVP

Back 137

increase or maintain preload, decrease contractility, maintain SVR

Front 138

causes of CHF are

Back 138

cardiac valve abnormalities, impaired myocardial contractility due to ischemic heart disease or cardiomyopathy, hypertension, pulmonary hypertension (right sided heart failure)

Front 139

hallmarks of CHF are

Back 139

decreased cardiac output, increased LVEDP, peripheral vasoconstriction, metabolic acidosis, LV failure with associated pulmonary edema, RV failure with associated systemic venous hypertension and peripheral edema

Front 140

does LVF lead to RVF or RVF lead to LVF?

Back 140

left ventricular failure will often lead to right ventricular failure, but RVF doesn't normally lead to LVF.

Front 141

describe compensatory mechanism for CHF

Back 141

a reduction in CO (whether due to increased SVR or decreased contractility r/t MI) leads to increased metabolic acidosis, decreased RBF activated RAAS leading to fluid and sodium retention and vasoconstriction, release epi and norepi increases contractility and heart rate which compensates for a while - really in a vicious cycle because the body compensates but doesn't know the heart is the problem

Front 142

RAAS stands for

Back 142

renin-angiotenstin- aldosterone system

Front 143

EF is reduced in CHF due to

Back 143

reduced myocardial contractility, increased afterload, asynchronous left ventricular contraction

Front 144

why are bi-V's used

Back 144

to help move blood forward in synchrony

Front 145

CHF Classifications

Back 145

I, II, III, IV

Front 146

class I CHF

Back 146

pt with cardiac disease but no limitations with ordinary physical activity

Front 147

Class II CHF

Back 147

pt with cardiac disease causing slight limitations on ordinary physical activity

Front 148

Class III Cardiac Disease

Back 148

pt with cardiac disease causing significant limitations on ordinary physical activity (i.e. symptoms with activities of daily living - showering grocery shopping, vacuuming)

Front 149

Class IV cardiac

Back 149

Patients with cardiac disease causing symptoms at rest

Front 150

because the ventricles remodel they are

Back 150

prone to arrhythmias because they are overstretched and asymmetric

Front 151

at what point is EF indicative of LV failure

Back 151

less than 40%

Front 152

severe CHF is associated with a CO of

Back 152

less that 2.5 L/min

Front 153

what is best lead to determine arrhythmias

Back 153

lead II (any sort of atrial changes)

Front 154

hemodynamic changes in CHF

Back 154

LVEDP is increased, and should reflect the pulmonary end diastolic pressure and the LAP (as long as there is no mitral valve disease.)

Front 155

p wave changes associated with CHF

Back 155

prolonged p wave or biphasic p wave in lead II (bunny ears)

Front 156

dobutamine is a

Back 156

nonspecific beta agonist (beta 1 increase heart rate a little bit and beta 2 cause vasodilation)

Front 157

ABG's in CHF are useful because may detect

Back 157

metabolic acidosis

Front 158

symptoms of left sided heart failure (CHF) is

Back 158

insomnia, confusion, muscle wasting, fatigue at rest, dyspnea, pillow orthopnea, paroxysmal nocturnal dyspnea

Front 159

paroxysmal nocturnal dyspnea occurs because

Back 159

heart rate slows down when sleeping so cardiac output decreases and patient becomes more symptomatic

Front 160

symtoms of CHF are due to

Back 160

decreased cardiac output

Front 161

pulmonary edema as a result of CHF will present as

Back 161

increased BP and HR, rales and maybe wheezes, PCOP increases, S3 gallop

Front 162

treatment of pulmonary edema is

Back 162

head up position, oxygen, morphine, ABG's and intubation if necessary, lasix, dopamine, dobutamine,

Front 163

why "head up" for pt with pulmonary edema

Back 163

increases oxygen resevoir - functional residual capacity

Front 164

why morphine for pt with pulmonary edema

Back 164

improve coronary perfusion by coronary vasodilation

Front 165

why dopamine for pt with pulmonary edema

Back 165

improve renal blood flow

Front 166

why dobutamine for pt with pulmonary edema

Back 166

reduced SVR (other vasodilators too if necessary)

Front 167

babies and fat people have

Back 167

decreased oxygen resevoir

Front 168

things to consider with a pt with CHF

Back 168

delay elective procedure until health is optimized, ketamine or etomidate are ideal, may not need fluid loading before regional, know that opiods and nitrous will cause cardiac depression, as will benzos and opiods, remember inhalation agents are negative inotropes, keep supportive drugs handy

Front 169

induction drugs for CHF

Back 169

ketamine (increased HR, but also vasoconstrictive)
etomidate is usually chosen because keeps hemodynamics the same

Front 170

drug choices for CHF

Back 170

decreased amount of inhalation anesthetics and increase the opiods

Front 171

most important thing to remember is

Back 171

prepare for disaster (then you won't have one - or if you do the damage will be minimized)

Front 172

why regional anesthesia for CHF

Back 172

will reduce SVR and improve CO
pt can communicate if having difficulty breathing for them (hard to tell what's normal for them otherwise)

Front 173

if have to give fluid to a person with CHF (ex. for spinal anesthesia)

Back 173

give it slowly! tolerate gradual fluid loads better

Front 174

pericardial disease presents as

Back 174

pt complaining of chest pain that is worse with inspiration and diffuse ST segment elevation,may hear a friction rub that is worse with expiration and tachycardia

Front 175

chronic pericarditis occurs with

Back 175

chemotherapy patients b/c drugs are toxic to cardiac tissue and cancer patients lose lots of proteins

Front 176

usual treatment for pericarditis

Back 176

steroids and analgesics

Front 177

pericardial effusions are

Back 177

the accumulation of fluid in the pericardial space

Front 178

a slowly accumulating pericardial effusion can accommodate up to

Back 178

a liter or 1500 ml

Front 179

a fast accumulation of pericardial fluid can cause tamponade at a volume of

Back 179

100 or 200 ml

Front 180

constrictive pericarditis is

Back 180

fibrous scarring and adhesion of the pericardial layers causing a rigid shell around the heart which impedes diastolic filling and decreases stroke volume

Front 181

constrictive pericarditis occurs with

Back 181

chronic renal failure, radiation therapy, rheumatoid arthritis, and cardiac surgeries

Front 182

cardiac tamponade occurs when

Back 182

an accumulation of fluid in the pericardial sac impairs diastolic filling, decreases the stroke volume, and causes hypotension

Front 183

cardiac tamponade is diagnosed by

Back 183

echo - can not tell on xray until over 250 ml of fluid accumulates - so useless in acute situations where 100 ml can cause problems

Front 184

signs and symptoms of cardiac tamponade ar

Back 184

increased CVP, decreasing PAP
SNS activation (tachycardia, vasoconstriction), decreased voltage on EKG (dampened waveforms), pulsus paradoxus, hypotension

Front 185

Beck's triad is

Back 185

hypotension, distant heart sounds, distended neck veins

Front 186

Becks triad is used to diagnose

Back 186

cardiac tamponade

Front 187

equalizing between CVP and PAP is indicative of

Back 187

cardiac tamponade

Front 188

pavulon is

Back 188

a long acting NDMR

Front 189

cardiac tamponade anesthetic goals (general concept behind)

Back 189

do not knock out SNS - that's the only thing keeping that heart beating at this point

Front 190

ideal induction drug for pericardial tamponade is

Back 190

ketamine

Front 191

cardiac tamponade anesthetic thought to keep in mind

Back 191

local vs general, support SNS, no vigorous positive pressure maneuvers, benzos, nitrous, fentanyl, pavulon, ketamine, supportive drugs like epi, and good monitoring devices