Part 2 Flashcards
anesthesia considerations for pt coming into surgery with pacer
- know what kind of pacer
T/F: AICD can act as a pacer and defibrillator
TRUE
if using a bovie in the OR and pt has a AICD what should you do
place magnet on pts chest to shut off cardioverter - still allows pacer to fx but will not pick up interference from bovie, thus will not give un-needed shock to pt
how do you know if a temporary pacer is capturing
- check pulse
- check a line
- do not assume activity of the pacer on the monitor is generating a pulse
with spontaneous breathing LV filling and SV is reduced during ______________; but with mechanical ventilation LV filling and SV is lower during _______________; (this is 2ndary to increase in intrathoracic pressure)
inspiration; expiration
systolic blood pressure typically fluctuates with spontaneous breathing by about ______________ mmHg
5-10
pulsus paradoxus is when systolic BP fluctuates with breathing by > ___________ mmHg
10
___________________ occurs during controlled mechanical ventilation when arterial pressure rises during inspriation and falls during expiration 2/2 changes in intrathoracic pressure 2/2 PPV
reverse pulsus paradoxus
with pulsus paradoxus (spontaneous breathing) SBP increases during _______________
expriation
with reverse pulsus paradoxus (mechanical ventilation) SBP increases during __________________
inspiration
formula for SVV
(SVmax - SVmin)/ SVmean over a respiratory cycle
SVV > _______% suggests that the pt is fluid responsive as it indicates the SV is sensitive to fluctuations in preload 2/2 respiratory cycle
10
formula for pulse pressure
SV / arterial compliance
causes of increased SVV
- hypovolemia
- tamponade
- constrictive pericarditis
- LV dysfx
- massive PE
- bronchospasm
- dynamic hyperinflation
- pneumothorax
- raised intrathoracic pressure &/or intraabdominal pressure
SVV > 10-13% what should you do?
fluid challenge
SVV < 10% but SV is normal, what should your intervention be
pressors
SVV < 10%, but SV is low, what is your intervention
inodilator
SVV < 10% but SV is high what is your intervention
diuretic
T/F: Swan and CVP monitors have been proven to improve outcomes
FALSE
limitations to arterial based monitoring (flotrac, vigelio)
- pt must be intubated, sedated, paralyzed
- severe arrhythmias (do not get adequate information)
- have to have a pulse rate (IABP, ventricular assist device)
cerebral oximetry is based on ____________ technology
near infared spectroscopy (NIRS)
NIRS should be kept at least ____________% of baseline saturation
70-75
NIRS should be placed ________________ forehead
midline
what is rSO2
regional oxygen saturation; what the NIRS will typically be set to monitor
if doing a “body” NIRS in peds, what type of O2 monitoring will you set the monitor to
regional cerebral tissue oxygen saturation (SctO2)
healthy rSO2 on NIRS
58-82%
intervention threshold for rSO2 number with NIRS monitoring
~20% from baselin
Critical threshold for rSO2 number with NIRS monitoring
~25% from baseline
interventions to improve Cerebral rSO2 (NIRS)
- rule out mechanical cause (head position, cannula position)
- increase supply (O2 delivery): increase CO, BP, DO2, PaCO2, Hgb/Hct
- decrease demand: increase anesthetic, decrease temperature
_________________ is the leading cause of death in the US
coronary artery disease
risk factors for CAD
- obese
- sedentary life style
- smoking
- HTN
- DM
______________ is the most stressful event for the CV system
exercise
during exercise CO can be increased by______________x 2/2 increased HR and contractility
2.5-7
at rest the coronary sinus Po2 is __________
27%
ischemia of the myocardium occurs when __________________ exceeds ______________
O2 demand; supply
formula for O2 content of blood
hgb x 1.34 x SpO2 + (0.003 x PAO2)
what is the normal O2 content of blood
20 mL / 100 mL
what is the primary determinant of O2 content of blood
hgb
coronary perfusion pressure is “autoregulated” btw ____________ - _______ mmHg
50-150
CPP is completely dependent on ___________, if it is outside of the autoregulation pressure (50-150mmHg)
HR
ways to optimize coronary perfusion pressure (CPP)
- normal to high ADBP
2.. Low LVEDP - Low HR
formula for Coronary blood flow
CBF = coronary perfusion pressure (CPP)/Coronary vascular resistance (CVR)
normal Coronary blood flow value?
225-250
what influences Coronary vascular resistance (CVR)
- metabolic factors
- ANS
- hormonal
- endothelial factors
- anatomic factors
- blood viscosity
how does ANS influence coronary vascular resistance
- alpha-1 constriction, mainly epicardial arteries
- beta-1 dilation, mainly intramuscular arteries
what metabolic factors influence coronary vascular resistance
- pH
- CO2
- lactate
- O2
- adenosine
what hormones influence coronary vascular resistance
- vasopressin
- angiotensin
- prostacyclin
- TXA
what anatomic factors influence coronary vascular resistance
- capillary recruitment
- collateral artery development.
what increases Coronary vascular resistance
- increased O2
- decreased CO2
- increased pH
- increased alpha-adrenergic tone
- increased cholinergic tone
- increased vasopressin
- increased angiotensni
- increased TXA
what decreases coronary vascular resistance
- decreased O2
- increased CO2
- decreased pH
- lactate
- adenosine
- increased Beta-adrenergic tone
- increased prostacyclin
- increased nitric oxide
- increased endothelium derived hyperpolarizing factor
- increased prostaglandin I2
___________________ vessesl are already maximally dilated; therefore they cannot respond to increase in demand (and are most susceptible to ischemia)
subendocardial
_______________ is the MOST susceptible to ischemia
subendocardium
coronary stenosis ___________ CVR and __________ CBF
increase; decrease
T/F: sequential lesions/plaques in the coronaries are additive
true; LAD + circ occlusion is a left main equivalency
coronary blood flow is reduced with coronary stenosis based on ______________ law
poiseuilles
if you have a 50% decrease in coronary diameter 2/2 stenotic lesion, that area of the heart is now only receiving _______________ of flow
1/16
why do young individuals with an MI have worse outcomes than older individuals with MI
younger individuals have not developed collateral flow
what are the 3 main determinants of myocardial oxygen consumption (MVO2)
- HR
- contractility
- wall stress
formula for myocardial oxygen consumption (MVO2)
MVO2 = CBF - (CaO2 - CvO2)
what is the MOST important determinant of myocardial oxygen demand
HR
doubling the heart rate ___________________ the myocardial oxygen demand
more than doubles
increased contractility causes ______________ myocardial oxygen demand
increased (d/t needing more energy and more O2)
clinical measurement of contractility
- visually during open heart
- briskness of upstroke on arterial waveform tracing
- echocardiogram (*most accurate)
cardiac wall stress is dependent on ________________, ________________, and ________________
afterload; chamber size (preload), and thickness
what law helps explain wall stress
law of laplace: tension(wall stress) = (P x radius)/(2x wall thickness)
MAP = _______________
MVO2
doubling MAP, ________________ myocardial oxygen demand (MVO2)
doubles
clinically to decrease myocardial O2 demand, what do you want to decrease?
SVR
MVO2 is increased by an increase in…
- HR
- preload
- contractility
- afterload
- temperature
- hgb
T/F: ECG is the least sensitive method for monitoring for myocardial ischmeia
TRUE
ST depression = ______________, elevation = _________________
ischemia; infarction
flattening or inversions of T waves indicate __________________
ischemia
ST changes will occur on ECG ____________ after ischemia occurs
1-2 min
what leads are the most sensitive for ischemia monitoring?
an inferior lead (II, III, or aVF) + V5
_____________% of ischemic events are captured if an inferior lead (II, III, aVF) + V5 are used to monitor
90
Sudden increase in PAP indicates what
decrease in cardiac function
if there is a new onset of prominent V wave on PCWP waveform, this indicates what
papillary muscle dysfunction
____________________ precedes ECG and PAP changes with myocardial ischemia
regional wall motion abnormalitiy (detected with TEE)
gold standard for myocardial ischemia montioring
TEE
_________________ monitoring assess preload, contractility, Reigonal wall motion abnormality, valvular fx, antatomy, and presence of pericardial effusion
TEE
on TEE you see lack of movement of wall, this is called _________________
akinesis
on TEE you see decreased regional wall movement, this is called _______________
hypokinesis
on TEE you see paradoxical movement during systole this is called ____________________
dyskinesis
dyskinesis is typically d/t __________________, and this is an emergency situation
ventricular aneurysm
ideal induction agent for cardiac patients
etomidate
ketamine effects on CV
- increase SVR
- increase preload
- increase contractility
- increase HR
what is the perfect induction agent for a pt with cardiac tamponade
ketamine
__________________ is not an ideal induction agent for pts with cardiac ischemia
ketamine; d/t increased MVO2
propofol CV effects
- decrease BP
2.. Decrease SVR - decrease contractility
BZ effect on CV
minimal HD effects
opioids effect on CV
decrease myocardial demand, without decreasing contractility
CV effects of precedex
hypotension and bradycardia
volatile anesthetics effects on MVO2
- all decrease contracility
- all decrease afterload
- minimal change in preload
- HR increase (esp with des)
- vasodilation of normal coronary vasculature decrease perfusion to ischemic areas
which anesthetic gas is a very poor choice for pts in RV failure or pts with pulmonary HTN
nitrous oxide
effects of nitrous oxide on MVO2
decreases contractility and increases PVR
___________ HR, _______________ contractility, ________________ SVR, ______________Preload, & _____________ SNS stimulation
decrease; minimal effect, decrease, decrease, decrease
succinylcholine effect on MVO2
bradycardia especially with repeated doses
pancuronium effect on MVO2
increases HR by 20%
how can you attenuate the increased HR (and thus increased MVO2) with pancuronium administration
high dose narcotics
vecuronium and rocuronium effect on MVO2
minimal CV effect (thus minimal MVO2 effect)
cisatracurium effect on MVO2
no CV effect (thus no MVO2 effect)
what muscle relaxants are the best choice for cardiac cases
vec, roc, or nimbex
treatments for CAD (surgical)
- angioplasty
- stents
- CABG
what is “fast track” cardiac anesthesia
- driven by desire to reduce cost
- accomplished by better drug selection/dose, new surgical techniques, warmer bypass temps
- early extubation and hemostatic control = essential
anesthetic approach for myocardial revascularization procedures
- fast track anesthesia
- ERAS cardiac
- off bypass revascularization
- MIDCAB, port access, redo CABG
which heart failure is more common (systolic or diastolic)?
systolic
systolic HF is more common in _____________________, where diastolic HF is more common in ________________
middle aged men (2/2 CAD); elderly women (2/2 obesity, htn, DM postmenopause)
T/F: heart failure is primarily a disease of the elderly
TRUE
T/F: HF spends more healthcare dollars than any other dz
TRUE
most common cause of RV failure?
LV failure
causes of systolic HF
- CAD
- Dilated CM
- chronic pressure overload (AS, HTN)
- chronic volume overload (valve insuff, high output failure)
sx of systolic HF
- decreased EF
- ventricular dysrhythmias are common (risk of sudden death)
- S3 heart sound
s/sx of diastolic HF
- normal EF, but sx of failure
- S4 heart sound
- increased LVEDP (classic sign)
hallmark sign of systolic HF
decreased EF
classic sign of diastolic HF
increased LVEDP
which HF is age dependent? increased incidence in 50+; > 50% in those > 70 years of age
diastolic
______________ HF is an inability to pump; where ______________ HF is an inability to fill
systolic; diastolic
causes of diastolic HF
- ischemic heart disease
- chronic HTN
- progressive aortic stenosis
- age
T/F: diastolic HF may coexist with Systolic HF
TRUE
inotropes effect on PV loops
shift loop left
1. increase SV
2. decrease ESV
diuretics and vasodilators effect on PV loops
decrease LVEDP
vasopressors effect on the PV loop
*shift loop up
increases SBP
_________________ = acute or worsening imbalance of myocardial oxygen supply to demand
acute coronary syndrome
most common cause of ACS
focal disruption of atheromatous plaque –> partial/complete occlusion of coronary
3 categories of ACS
- STEMI
- NSTEMI
- Unstable angina
ST segment depression/nonspecific ECG changes with elevated cardiac biomarkers = _______________
NSTEMI
ST depression/nonspecific ECG changes with normal cardiac biomarkers = __________________
unstable angina
________________ occurs when coronary blood flow decreases abruptly
STEMI
5 common pathophysiologic process that causes NSTEMI
- rupture/erosion of coronary plaque that leads to non-occlusive thrombosis
- dynamic obstruction d/t VC
- worsening coronary luminal narrowing due to progressive atherosclerosis, instent restenosis, or narrowing of CABG
- inflammation
- myocardial ischemia due to demand increase
Basic set up for CABG
- std monitors + ABP/PAP/CVP, cerebral oximetry, BIS, TEE
- emergency meds: inotrope (epi), vasopressor (neo), vasodilator (cardene)
- routine induction meds: etomidate, paralytic, narcotics, heparin
- at least 2 units blood ready
- temporary pacer checked, and battery is working
- infusions are set up and ready
what is the purpose of giving versed and fentanyl prior to CABG
decrease unwanted SNS response 2/2 anxiety
pt coming in for CABG who should you caution premedication of versed and fentanyl with ?
CHF, low CO, and pulmonary HTN pts
pre-bypass goals
- keep pt at baseline
- do not start correcting numbers until surgical correction has been made
- do no harm
periods of increased stimulation (pre-bypass CABG)
- incision
- sternotomy & retraction
- sympathetic nerve dissection (at LIMA)
- pericardiotomy
- aortic cannulation
inadequate anesthesia during times of increased stimulation with CABG (prebypass) can result in…
increased circulating catecholamines –>
1. HTN
2. dyrhythmias
3. tachycardia
4. ischemia
5. HF
pre-bypass CABG, periods of decreased stimulation (“slump”)
- preincision
- peripheral graft harvest (from leg)
- IMA dissection
- venous cannulation
periods of decreased stimulation (“slump”) with prebypass CABG - what are the risks?
- Hotn
- bradycardia
- dysrhythmias
- ischemia
what is teh most stimulating part of the induction period for CABG pt?
laryngoscopy
what is your first line tx for hypotension for the pt on pump
neosynephrine (not fluids, need to avoid hemodilution)
autologous blood removal for CABG
taking 1 unit of blood prior induction via gravity.
risks with autologous blood removal
- Hotn 2/2 hovolemia
- decreased O2 carrying capacity (will be reflected through mixed venous sat)
- infection
autologous blood is stored in a bag with _________________ (similarly to banked blood)
citrate phosphate dextrose solution
relative c/i to autologous blood removal
- left main dz
- LV dysfx (cannot handle hovol with losing 1 unit blood
- anemia with hgb < 12
- emergent surgery
when would you expect there to be a high risk of major structure accidently being cut during CABG?
redo sternotomy 2/2 adhesions and scar tissue
if a major structure is accidently cut during CABG (specifically with sternotomy) what do you do
- put on bypass immediately
- have blood products checked and ready for administration
prolonged sternotomy dissection for CABG increases the risk of _______________ redo surgery
dysrhythmias
what are the vessels that could be used for coronary bypass
- LIMA/RIMA
- saphenous vein
- radial artery
endoscopic vein harvest for CABG is typically done if which vein is used
saphenous
what is the preferred agent for anticoagulation with CPB
unfractionized heparin
initial dose of unfractionized heparin for anticoagulation prior to CPB
300 units/kg
retrograde autologous priming
draining blood out of pt through aortic cannula to prime CPB circuit
what is the most common arterial access site for aortic cannulation
distal ascending aorta
before aortic cannulation, ACT must be greater than ___________
400 s
if the distal ascending aorta is not an arterial access option for aortic cannulation, what are the other arterial access sites that can be used?
femoral artery
what is the number one complication from aortic cannulation (CABG)
embolic phenomena 2/2 air or atherosclerotic plaque dislodgement
aortic cannulation complications (CABG)
- emboli
- Hotn
- dysrhythmias
- aortic dissection with cannula misplacement
- bleeding
- air entrainment from around cannula with systemic embolization
CPB venous cannulation
- incision into right atrium –> cannula placed into atrium and down into IVC
- accompanied by significant dysrythias and hypotension
bicaval venous cannulation (CPB)
SVC cannula added through RA (in addition to the IVC cannula)
alternative venous cannulation site from RA –> IVC
femoral vein
complications with CPB venous cannulation
- Hotn
- Bleeding (if RA or SVC/IVC torn)
- dysrhythmias
- air entrainment
what is cardioplegia
Cold K+ solution that stops the heart before a CABG procedure
aortic root vent on the cardioplegia (anterograde) line
used for de-airing the heart at end of CPB
blood pressure goals when cannulating your cardioplegia lines
SBP 90-100 (same as aortic cannulation)
what is the basic sequence of CPB (starting with going on by pass)
- go on bypass
- cool pt (32-36)
- Ao cross clamp
- cardioplegia infused either anterograde or retrograde to arrest the heart
- operation: SVG placed on most severely dz’d coronary first; IMA constructed last
- rewarming when final distal anatamosis is begun
- Ao unclamped
- pacing wires placed
- come off bypass
anterograde cardioplegia is achieved by administering the solution into the ________________
aortic root (btwn Ao valve and XC)
why is the time btwn cross clamping of Ao and administration of cardioplegia kept to a minimum?
to prevent any warm ischemia
cardioplegia is a solution high in __________, which arrests the heart in _______________
potassium; diastole
retrograde cardioplegia is administered through the _______________
coronary sinus
hypothermia for CPB will ____________ anesthetic requirements
decrease
what monitoring should be used to monitor depth of anesthesia during CPB?
- HD cues
- check pt for pupil dilation and/or sweating (*sign of awareness)
- monitor BIS
what is the best drug for induction with heart failure
etomidate
what is the most common genetic CV disease
hypertrophic cardiomyopathy
hypertrophic cardiomyopathy is a _______________ genetic d/o
autosomal dominant
hypertrophic cardiomyopathy is aka
idiopathic hypertrophic subaortic stenosis (IHSS)
_____________ is LV hypertrophy in the absence of any other cardiac dz
hypertrophic cardiomyopathy
pathophysiology of hypertrophic cardiomyopathy
myocardial hypertrophy –> dynamic LVOT obstruction –> systolic anterior movement of the mitral valve –> diastolic dysfunction
s/sx of hypertrophic cardiomyopathy
wide range: asymptomatic - sudden death
- angina
- fatigue
- syncope
- tachydysrythmias
- HF
- murmur present with gallop
sudden death 2/2 hypertrophic cardiomyopathy is most common in thosed aged _____________
10-30
with hypertrophic cardiomyopathy, _____________ will relieve the sx, but _____________ aggravates them
lying down; valsalva
Dx of hypertrophic cardiomyopathy
- ECG
- echo
- histology via endomyocardial biopsy
what is the most common and best way to dx hypertrophic cardiomyopathy? what is the only way to definitively dx hypertrophic cardiomyopathy
echo; histological endomyocardial biopsy (reserved for pts where dx cannot be established otherwise)
Tx goals with hypertrophic cardiomyopathy
- improve diastolic filling
- reduce LVOT obstruction
- decrease myocardial ischemia
what are the three most common responses to pericardial injury
- acute pericarditis
- pericardial effusions
- constrictive pericarditis
tamponade presents with….
fluid under pressure
acute pericarditis is most commonly caused by ___________
viral infection
what is acute pericarditis that presents 2 weeks - months after a myocardial event ?
dresslers syndrome
dresslers syndrome is often _____________
autoimmune
what is acute benign pericarditis
acute pericarditis in the absence of pericardial effusion
T/F: acute benign pericarditis alters cardiac function
FALSE
Dx of acute pericarditis
- based on sx (chest pain, friction rub, EKG changes)
- low grade fever with ST
- friction rub
- EKG changes in 90% of people
EKG changes with acute pericarditis? this is caused by what?
- ST segment elevation, PR segment depression, & T wave inversion
- caused by inflammation of the superficial myocardium
Primary tx for acute pericarditis
asprin or NSAIDs
tx for acute pericarditis
- Asprin or Nsaids
- codeine
- colchincine
- steroid
why are steroids typically not a first line tx with acute pericarditis
once the steroids are stopped –> pericarditis relapse; only used when other therapies do not work
pericarditis presents in _____% of pts after cardiac surgery
10-40
pericarditis is most common in ____________ patients after cardiac surgery
pediatric
pericardial space normally contains _________cc of fluid
25-50
causes of pericardial effusion
- infection
- MI (dresslers syndrome)
- trauma or cardiotomy (cardiac surgery)
- metastatic dz
- drugs
- mediastinal radiation
- systemic Dz (lupus, RA)
with pericardial effusion as pericardial pressure increases ________ increases; –> atrial and ventricular filling being restricted –> SV becoming FIXED, thus CO becoming _____________ dependent
RAP; rate (HR)
a large pericardial effusion can compress structures –> what sx
- anorexia & dysphagia (esphogeal compression)
- dyspnea, cough, hoarseness (tracheal & lung compression)
up to ___________L can be accomodated in the pericardial sac with chronic effusion, but with acute increases of ________mL –> tamponade
2; 40-50
s/sx of tamponade
- kussmauls sign (JVD w/ inspiration)
- pulsus paradoxus
- becks triad (distended neck veins, muffled heart sounds, Hotn)
changes with cardiac numbers with tamponade
- CVP > RAP
- tachycardia (CO becomes HR dependent)
- good ctx, poor preload
- eventual equilibration of pressures
causes of cardiac tamponade
- trauma/iatrogenic injury
- infection
- neoplastic dz, uremia, connective tissue d/o
- acute MI
- postop bleeding
- Ao dissection
Tx of tamponade
- pericardiocentesis (at bedside)
- drainage of fluid through subxiphoid or mini thorocotomy incision (OR)
anesthetic management goals with cardiac tamponade
- FAST (tachycardia)
- TIGHT (vasocontriction)
- FULL (volume)
what is the drug of choice for cardiac tamponade anesthetic management?
ketamine
cardiac stimulant, keeps pt spontaneously breathing
what drug is avoided with cardiac tamponade
BETA blockers
*any drugs that depress that myocardium
anesthetic management of cardiac tamponade
- ketamine for induction
- avoid BB
- arterial BP prior to induction
- correct metabolic acidosis from low CO state
- if have to use GA –> fast RR and low TV until relieved
- be prepared for post HTN
what is “concretio cordis”
constrictive pericarditis
causes of constrictive pericarditis
- idiopathic (most common)
- previous cardiac surgery
- radiation therapy
- Tb
_____________ is characterized by a fibrous scarring and adhesions that obliterate the pericardial space –> “rigid shell” around the heart
constrictive pericarditis
S/Sx of constrictive pericarditis
- progressive dyspnea and fatigue (dec CO)
- increased CVP
- JVD, edema, ascites
- afib (25%)
- SV maintained
- Square root sign on RVP tracing
- kussmauls and pulsus paradoxus
how do you dx constrictive pericarditis
TEE, CT, or MRI
what is the difference btwn tamponade and constrictive pericarditis with ventricular filling
with constrictive pericarditis the restriction to ventricular filling only occurs during the last 2/3 fo diastole, and SV is maintained
with ________________ you will see a “square root sign” on the RVP tracing
constrictive pericarditis
anesthetic management with constrictive pericarditis
- maintain HR, volume, and ctx
- use ketamine and pancuronium
- note that arrhythmias, hotn, and bleeding is common
with blunt injuries to the chest, which part of the heart is most likely to be injured
RV
with pericardial traumas, they will do a ______________ incision for quick access to the thoracic cavity
clamshell
what is commotio cordis
- syndrome caused by blunt trauma to the heart –> ventricular dysrhythmias and death if untx
- the mechanical “thud” –> R on T
a kid playing baseball gets hit in the chest with baseball, and immediately drops requiring CPR, what has occured?
commotio cordis
Tx of commotio cordis
- rapid defibrillation with AED
Tx of constrictive pericarditis
surgical “stripping”
how do you tx mild sx (with sx of HF) of hypertrophic cardiomyopathy
- beta blockers
- CCB
- diuretic
preoperative anesthetic management of hypertrophic cardiomyopathy
- minimize LVOT obstruction by decreasing contractility and increasing afterload and preload
- cardiac eval, ECg, echo, continue meds, turn off ICP apply pads
- anxiolytics to blunt SNS
intraoperative anesthetic management of hypertrophic cardiomyopathy
SLOW-TIGHT-FULL
1. blunt SNS to DL (consider BB)
2. ABP and TEE
3. use NEOSYNEPHRINE (avoid Beta Agonist)
4. NO vasodilators
5. maintain NSR, treat SVT quickly
what vent settings are appropriate for pt with hypertrophic cardiomyopathy
- avoid PPV (avoid PEEP)
- small Tv, increase Rate
postop anesthetic management of hypertrophic cardiomyopathy
- avoid all SNS stimulation (pain, shivering, anxiety, hypoxia, hypercarbia)
- maintain euvolemia with prompt tx of Hotn
MOST heparin resistance can be managed by _________________
giving more heparin
if pt is unresponsive to heparin: requires > 600 units/kg and/or cannot get ACT > 450 what should you do
give ATIII, FFP or plasma
heparin resides physiologically in ____________, but is commerically derived from __________________
mast cells; bovine lung or porcine intestine
heparin is ____________ charged at physiologic pH
negatively
MOA of heparin
binds to ATIII and potentiates its action 10x; inhibits thrombin, Xa, IXa, XIa, and XIIa
inhibition of thrombin requires stimultaneous binding of heparin to __________ & __________
thrombin and ATIII
s/e heparin
- bolus will decrease SVR
- anaphylaxis
- bleeding
- HIT
what is a normal ACT value
110-140 s
goal of ACT for bypass (range)
400-480 (>450 great!) s
ACT is prolonged by
hypothermia and hemodilution
_______________ is a cation that binds with anionic heparin –> neutralization and elimination of anticoauglation activity
protamine
_________ mg of protamine neutralizes 1 mg (100 units) of heparin
1
post protamine ACT should return to ____________ above pts baseline
<10%
s/e of protamine
- Hotn with rapid administration (<3 min)
- anaphylaxis
- pulmonary vasoconstriction –> RV failure
- antihemostatic effects
protamine is c/i in what pts
- those with allergy to vertebrate fish
- those with allergy to NPH
what do you want your blood pressure to be prior to administering protamine? if it < SBP goal, how should you intervene
SBP 90-120; fluid
what are the antifibrinolytic agents used with cardiac surgery
amicar and TXA
MOA of amicar and TXA
lysine analogues that bind to the lysine binding site of plasminogen –> reversible complex with plasmin inhibiting fibrinolysis
which antifibrinolytic agent is 5-10 x more potent w/ higher affinity for plasminogen ? (TXA or amicar)
TXA
evaluation of hemostasis post CPB
- ACT to assess heparin neutralization
- TEG maximal amplitude for plt fux
- PT, aPTT, TEG-R, TEG-K to assess coagulation
- TEG-lysis index, fibrin degradation products, D-dimer to assess fibrinolysis
s/sx of aortic stenosis
Triad:
1. angina
2. syncope
3. dyspnea on exertion
murmur with aortic stenosis will be heard in _____________
systole
once the triad of sx present with aortic stenosis life expectancy is __________
<5 years
changes with pressure volume loop with aortic stenosis
- elevated peak SBP
- decreased SV
- LVEDP increased
- EDPVR increased
- ESV increased
intraop management of aortic stenosis
SLOW-TIGHT-FULL
1. adequate preload (volume)
2. lower HR (50-70): gives longer diastole and adequate systolic ejection
3. keep SVR high with neosynephrine (alpha agonist)
anesthetic management of Aortic stenosis
- light premed to avoid drop in SVR
- A line
- if ischemia develops use NTG cautiously
- PCWP may overestimate preload d/t noncompliant LV
- TEE
pts with aortic stenosis are ___________ dependent
preload
primary cause of mitral stenosis
rheumatic heart disease (2/2 scarring and fibrosis)
s/sx of mitral stenosis
- first associated with exercise/high CO
- progressive decline with repeated epsiodes of fatigue, chest pain, palpatations, SOB, paroxysmal nocturnal dyspnea, pulmonary edema, hemoptysis
- hoarseness
- diastolic murmur (at apex)
- broad notched p wave on ECG = p mitrale
- afib in 1/3 of pts
severe mitral valve stenosis valve area
< 1 - 1.5
smallest mitral valve area compatible with life
0.3-0.4 cm
changes to pressure volume loop with mitral stenosis
- EDV and ESV decreased
- SV decreased
- LVEDP decreased
HD management of mitral stenosis
SLOW, TIGHT, FULL
1. preload dependent for forward flow across valve - ensure adequate volume, but be careful LAP already increased
2. slower HR bc blood flows across MV at diastole
3. SVR and PVR will be increased - try to keep them there
anesthetic management of pt with mitral stenosis
- light premed to avoid decrease in preload or oversedation
- avoid ketamine
- short acting BB (esmolol) to tx tachycardia
- PA catheter
- TEE
- slow muscle relaxant reversal to avoid tachycardia with anticholinergic administration
indication for TAVR
aortic valve replacement for…
1. high risk or inoperable 2/2 age and comorbidities
2. want to avoid sternotomy
3. want to avoid going on pump
what are the different approaches for a TAVR
- retrograde (percutaneous via femoral artery)
- anterograde (aka transapical, through the apex)
- transaortic approach (through Ao root)
what is the preferred approach for a TAVR
retrograde (percutaneous through the femoral artery)
complications of TAVR
- stroke
- cognitive dysfunction
- Ao dissection
- bleeding
- mediastinal hematoma
- femoral/Iliac artery injury
- valve size mismatch
- conduction system issues
- perivalvular leaks
why do we pace with TAVR
rapid pacing at 180 bpm keeps the aortic valve open
use of BB with heart failure
- decrease SNS stimulation –> decreased circulating catecholamines
- increases EF
- decreases remodelling
use of natriuretic peptides for HF
- diuresis
- natriueresis
- vasodilation
- antiinflammatory
- inhibits SNS and RAAS
use of RAAS medications for HF
- prevents cardiac remodelling
2.. prevents vasoconstriction –> no increase in cardiac filling, no decrease in CO - prevents sodium and water retention (no increase in cardiac filling pressures
management of diastolic HF
- if have SHF –> prevent!
- caution use of diuretics
- maintain normal sinus rhythm and HR control
- correct preciptiating factors
surgical mangement of heart failure
- PTCA or CABG
- cardiac resynchronization therapy
- AICD
- cardioMEMS - implanted PAP monitor
- VAD bridge therapy
- total artifical heart
- transplant
anesthesia considerations with heart failure
- optimize pt condition
- cardiac resynchronization therapy
- AICD
- cardioMEMS - implanted PAP monitor
- VAD bridge therapy
- total artifical heart
- transplant
