1 Flashcards
A-line wave from central to periphery
- steeper upstroke, high systolic peak, later dicrotic notch, more prominent diastolic wave and lower end-diastolic pressure
- overall higher systolic, lower diastolic (increase PP)
a line and pathology
- AS: late systolic peak and small amplitude (tardus and parvus)
- AR: bisferious wave form (beating twice)
- HOCM: spike and dome appearance
- Cardiac tamponade: pulsus paradoxus
CVP wave form
- ACV peaks, XY decents
- A: atrial contraction
- C: isovolumic ventrical contraction
- V: systolic atrial filling
- X: relaXation of atria
- Y: tricuspid opening and early ventricular filling
Measurements from Swan Ganz
- CVP, PAP, temp, PCWP, MVO2, SVR, PVR, CO, CI
Contraindication of PA catheters
- Absolute: LBBB as you can cause complete heart block with placement (induce a RBBB)
- Relative: WPW, Ebsteins anomaly (likely to induce a malignant ventricular tachyarrhythmia
Insertion of PA catheter
1) go 17-20cm then inflate balloon
2) 20-25 cm tip is in RA (1-5 mmHg, mean of 3)
3) 25-30 cm tip is in RV (increase in systolic 15-30 mmHg mean of 25)
4) 35-45 cm tip in is pulmonary artery (diastolic step up to around 12)
5) wedge the balloon (flattens around previous diastolic)
6) deflate balloon and withdraw 1-2 cm
Heart pressures
- RA: 5/1
- RV: 25/5
- PA: 25/10-12
- LA: 10-12/2
- LV: BP
Complications of PA catheters
- ventricular dysrhythmias
- heart block (preexisting LBBB)
- bacteremia/endocarditis
- thrombogenesis
- valve injury
- air emboli
- PA rupture (really rare but 50% mortality)
PA catheter indications
1) Patient: ASA 4 or above (not indicated for low or moderate risk patients
2) Procedure: high risk procedures (heart, lung, kidney, liver or brain)
3) Practice: skilled proceduralist and support staff to not misinterpret date
CO Thermodilution
- fixed amount (10cc) of cold or room temp injected through proximal port and subsequent temperature change detected by thermistor on PA catheter tip
- Plot: X time, Y delta T
- CO = integral of area under the curve
- high CO correlates to small changes
- low CO correlates with large changes
CO thermodilution requirements
- flow of blood, volume and PA temp are constant
- absence of intracardiac shunt
- absence of significant valvular disease
- temperature and volume of solution is acurate
CO themodilution errors
- Over estimate CO: smaller volume or warmer solution
- Under estimate CO: larger volume or colder solution
Mixed venous O2 sats
- samples in the PA (mix of superior/inferior vena cava and coronary sinuses)
- normal 70-75% (25-30% extracted)
- SvO2 = SaO2- (VO2 / Q X 1.34 X Hgb)
- VO2 = oxygen consumption ml/min, Q = CO (L/min)
Arterial O2 content
CaO2 = (1.34 X Hgb X SaO2) + (0.0003 X PaO2)
How much O2 consumption can occur
- 50-60%
- after maximal oxygen extraction occurs it become supply dependent
- anaerobic metabolism, acidosis and multi-organ failure can occur
Decreased SvO2
- insufficient O2 delivery: hypoxia, decreased CO, anemia or abnormal Hgb
- increase O2 consumption: shivering, fever, exercise, pain, hyperthyroid, malignant hyperthermia
increase SvO2
- decrease O2 consumption (commonly in vasodilatory shock)
- L to R shunt
- impaired tissue uptake (CN or CO)
- hypothermia
- sepsis
- increased CO
- sampling error
Non invasive CO measurement
- cardiac cycle changes in thorax and aortic blood volume alters electrical impedance across the chest wall
- changes in electrical conductance are proportional to changes in blood volume and can be used to calculate a SV
Coagulopathies result from which etiologies
1) failure in primary hemostasis (platelet plug formation: requires functioning platelets and endothelial damage)
2) incompetent coagulation cascade
3) excessive fibrinolysis
Tests of primary hemostatis
1) CBC for platelet quantity
2) Bleeding time/ platelet aggregation tests ect.
3) TEG
Prothrombplastin time (PTT)
- tracks intrinsic coagulation cascade
- extremely sensitive to heparin
Prothrombin time (PT)
- tracks extrinsic pathway
- warfarin
- INR= PT sample/PT normal
Anti-Xa activity test
- tracks the effects of LMWH or unfractionated heparin
Reptilase time
- measures deficiencies in fibrinogen
Hemophilia A/B
- A is deficient in factor VIII: need >30% of factor VIII for minor surgery, 100% for major
- B is deficient in IX
ACT
- normal is generally 80- 120 seconds
- level of 300-400 for CPB
- hypothermia increases ACT in a dose-dependent fashion
Inadequate rise in ACT to therapeutic doses of heparin
- most likely etiology is a deficiency in function AT-III levels
Reaction time (R)
- time in minutes elapsed from the start of test until clot moves the pin enough to produce a 2-mm amplitude on the tracing
- reflects activity of the coagulation cascade (coagulation deficiency)
- if prolonged give FFP
- normal depends on type of clotting factor used
alpha angle
- measure in degrees the speed of clot formation
- 45-55 degrees is normal
- ## decreased angle = low fibrinogen = give cryoprecipitate
Coagulation time (K)
- minutes from end of R to when tracing amplitude reached 20 mm
- depends on type of clotting factor used
- if prolonged = low fibrinogen = give cryoprecipitate
Maximum amplitude (MA)
- point f maximum clot strength in millimeters
- normal is 50-60 mm
- if decreased means there is thrombocytopenia and or platelet dysfunction
- give platelets
Lysis index 30
- percentage reduction in MA after 30 minutes.
- Higher fibrinolytic activity produces a greater Ly30
- normal 7.5-8%
- if elevated = hyperfibrinolysis
- give TXA or amicar
Pacemaker code
1) Paced (A, V or D)
2) Sensed (A,V, or D)
3) Response ( I inhibited, T triggered or D)
4) rate modulation (R)
5) Multisite pacing ( A,V, or D)
OPMR1 receptor
mutation can cause a resistance to morphine
MH
- results from abnormal excitation-contraction coupling in skeletal muscle leading to uncontrolled release of Ca2+ from the sarcoplasmic reticulum
- mutation in RYR1 channel
- triggers volatiles and succinylcholine
- hypercarbia, tachy, masseter spasm, rhabdo, rigidity, hyperthermia
treatment of MH
- stop tiggering agent
- dantrolene 2.5 mg/kg IV
- get access
- a line
- foley for UOP monitoring
- hyperventilate
- monitor for 24 hours
Pseudocholinesterase (PCE) deficiency
- autosomal recessive disorder cause by atypical or absent PCE
- dibucaine number 80% is inhibited in normal, 20-60 in heterozygous and < 30 in homozygous
- avoid pancuronium, metoclopramide, esmolol, chlorpromazine, bambuterol and acetylcholinesterase inhibitors
Prolonged QT syndome
- corrected QT male > 470 millisecond and > 480 millisecond for females
- correct al electrolyte abnormality
Methadone
- long active opioid agonist with some NMDA activity
- do not use in patients with prolonged QT interval
Buprenorphine
- partial mu-opioid agonist
- suboxone is combination with nalaxone preventing ability to inject
- high affinity for mu-receptors, will displace more potent drugs causing difficult with analgesia
Stellate ganglion block
- face, neck, arm and upper arm pain, vascular insufficiency of the arm (extravasation of noxious meds)
- lies anterolateral to the vertebral body just anterior to the transverse process
- inferior to chassaignacs tubercle (transverse process of C6)
- success will cause Horner’s syndrome, nasal congestion/ flushing of the face
- complications include RLN or RLN blocks, phrenic paralysis, pneumothorax, trachea or esophagus puncture, epidural or spinal injections
Celiac plexus block
- pain from upper abdominal viscera, pancreatic cancer
- ganglia located anterior to the aorta near the celiac arterial trunk at T12-L1
- complications include diarrhea, cramping and orthostatic hypotension
- risk for hematoma, IV injection, vascular injury, kidney puncture
Lumbar sympathetic block
- LE pain or vascular insufficiency
- anterolateral to the L2 vertebrae inside a fascial sheath, posteriorly to the psoas muscle
- genitofemoral neuralgia (burning groin pain) is a complication
Cervical plexus block
- cervical plexus is composed of the anterior rami of C1- C4
- CEA, neck dissection, tracheostomy, thyroidectomy,
- superficial and deep needed
Eye blocks
- retrobulbar vs peribulbar
- retrobulbar requires less because its deposited directly in the cone.
- complications” retrobulbar hematoma, globe perforation. optic nerve damage. intra-arterial or intra optic nerve sheath (direct to brain), and oculocardiac reflex
Airway block
- need glossopharyngeal, superior laryngeal and recurrent laryngeal (trigeminal if nasal intubation)
Supplemental blocks for labor
- paracervical- 1st stage
- pudendal - 2nd stage
Psysiologic effects of HBOT
1) increased barometric pressure (contraction of gas)
2) increased partial pressure of O2
3) Increased partial pressure of nitrogen (more potent)
4) high pressure nervous syndrome (15-20 ATA: tremor, ataxia, nausea and vomiting
5) Pressure reversal of anesthesia (not seen in elevations of HBOT)
HBOT
- carbon monoxide poisoning
- Gas embolism/ decompression sickness
- infections
- arterial oxygenation
- O2 transport in severe anemia
Carbon Monoxide poisoning
- nausea, vomiting, headache, dizziness, myocardial ischemia, AMS and absence of cyanosis
Oxygen toxicity
- directly related to the Po2 of inspired gas
- lungs, eyes and CNS at risk
- lungs” chest pain, cough or throat irritation, rarely reduced vital capacity and ARDS
- CNS: nausea, numbness and twitching, rarely seizures
Aveolar gas equation
PaO2= FiO2 *(Patm-PH2O)- Co2/RQ
Adaptation to high altitude
- Initially increased RR and CO
- overtimes: increase 2,3DPG, increased erythropoesis, renal compensation for the alkalosis of hypocarbia
Altitude sicknesses:
- Acute mountain Sickness (AMS)
: headaches, nausea, anorexia. sleep disturbances and peripheral edema
- decrease altitude, rest, hydration, analgesic, acetazolamide, dexamethasone and O2 therapy
Altitude sickness:
- High- altitude pulmonary edema (HAPE)
- form of right heart failures caused by exaggerated hypoxemic pulmonary vasoconstriction and high CO2
- dyspnea, tachypnea, CP, rales, tachycardia, dry cough, pink frothy sputum
- rapid descent, supplemental O2, PEEP or BiPap
- nidedipine, NO, hydralazine, phentolamine, sildenafil
ALtitude sinckness
- high altitude cerebral edema (HACE)
- increased cerebral blood flow and alterations in the blood-brain barrier permeability due to severe hypoxemia
- gross CNS dysfunction
- immediate rapid decent, O2 therapy, dexmethasone, and diuretics
Cerebral metabolism
- 3.5mlO2/100g of brain
- 60% of cerebral metabolism is linked to neuronal depolarization = can decrease CMRO2 by 60% with anesthetics
- gray matter consumes twice as much O2 as white
glucose consumption of brain
5mg/100g brain/min
temperature and CMRO2
decrease in temperature decreases CMRO2 by 6%
EEG waves
Delta <4 Hz
Theta 4-8
Alpha 8-13
Beta > 13
Somatosensory Evoked Potentials
- via peripheral nerve, up posterior columns of the spinal cord to dorsal column nuclei at the cervical medullary junction, then medial lemniscus to thalamus onto sensory cortex
Motor evoked potentials
- monitor the ventral spinal cord
Phenytoin
- decreases excitatory glutamate release due to inhibition of sodium channels.
- fosphenytoin is given (IV) to prevent significant hypotension and severe dysrhythmias
Carbamazepine
- trigeminal neuralgia, seizures
- binds Na channel in inactive state
- secondarily modulates calcium channels
Gabapentin and pregabalin
- GABA analogs with antiepileptic action on calcium channels
- Ethosuxamide
absence seizures
GABA modulation for seizures
- phenobarbital, valproic acid, clonazapam
Levetiracetam
- blocks sodium channels and modulates intracellular synaptic vesicle release
SSRI
- prevent the uptake of serotonin for neuronal clefts
- citalopram, escitalopram, fluoxetine, sertraline
- serotonin syndrome
Serotonin Syndrome
- use of concomitant medications possessing serotonergic effects
- antidepressants
- valproate, ondansetron, metoclopramide, sumatriptan, dextromethorphan, drug abuse, lithium, st johns wort
TCA
- amitrptylinem clomipramine, doxepin,
SNRIs
-venlafaxine, duloxetine, milnacipran
MOAs
deprenyl, phenelzine, selegiline, tranylcypromine
Metoclopramide
- dopamine receptor antagonist
- worsening extra pyramidal symptoms in parkinsonian patients; can treat with diphenhydramine
laudanosine
-metabolic of atracurium that has seizure provoking potential
Autonomic dysreflexia
- frequent above T6 however is possible until T12
- exaggerated autonomic response to pain below the level of the spinal cord injury
- hyperhydrosis, severe headaches, vasodilation above the level
Tetanus
- anaerobic, gram negative bacillus Clostridium tetani
- bacteria releases tetanolysin and tetanospasmin (which enters peripheral nerves and travels intra-axonally/retrograde to CNS)
- binds to presynaptic inhibitory nerves and block the release of inhibitory neurotransmiters by degrading synaptobrevin
- dysphagias, neck stiffness, jaw stiffness
Tetanus treatment
- human tetanus immunoglobulin
- immunixation
- antibiotics (metronidazole IV or penicillin G)
- surgical debridement to eliminate source may be needed
Laplace’s law
P=2T/r
pressure equals two times the tension/radius
Aneurysm
- peak incidence at ages 40-60
- male to female 2:3
- most in circle of willis at anterior communicating artery
SAH
- worst headache of life
- nausea, emesis, photophobia
- can include meningism
Hunt and Hess classification of SAH
1) asymptomatic, mild headache, slight nuchal rigidity
2) moderate/severe headache, nuchal rigidity, cranial nerve palsy
3) drowsiness/confusion, mild focal neurological impairments
4) stupor, hemiparesis
5) coma, decerebrate posturing
Vasospasm (SAH)
- peak incidence at 7 days
- nimodipine, calcium channel blocker
- Triple H: hypertension, hemodilution hypervolemia
- SBP 160-200 for clipped, 120-150 without clipping
Wada test
- anesthetic is injected into either left or right carotid and tests what side speech and memory occurs in the brain
Diabetes Insipidus
- decreased ADH after pituitary surgery
- polyuria (>2 cc/kg/hr), hypovolemia and hypernatremia
- increased serum osmolality >295 mOsm/kg
- decreased urine osmolality <300 mOsm/kg
Resistance
R= 8viscositylength/Pi R^4
West lung zones
1) PA (alveolar)> Pa (arterial) < Pv (venous) {top}
2) Pa > PA > Pv
3) Pa> Pv > Pa
Dead space calulation
Vd/Vt = (PaCO2 X PeCO2)/ PaCO2
Test prior to lobectomy
15/30/40 rule
1) Vo2 max
2) ppoFEV1
3) ppo DLCO
VO2 max (lobectomy)
1) > 15 ml/kg/min
- can approximate with ability to climb 5 flights of stairs or >2000ft in 6 minute walk test
2) < 10 mg/kg/hr is predictive of poor outcome
ppoFEV1
= preoperative FEV1 * (19- segments to be removed/19)
RU: 3 , RM: 2 RL: 5
LE: 3, Lingula:2, LL 4
- <30% predictive of poor outcome (>40% good outcome)
ppoDLCO
ppoDLCO = preoperative DLCO x (1 – %functional lung tissue removed/100)
- single strongest predictor of complications and mortality after lung resection
- < 40% is correlated with increased cardiopulmonary complications
