Basic2 Flashcards
Contraindications for CSE
patient refusal, sepsis, hypovolemia, coagulopathy or therapeutic anticoagulation, elevated ICP, infection at site
dose for caudal in infants
CSF volume per percentage of body weight is greater in infants than adults. Need a comparatively larger doses per kg of LA
Caudal in infants
heart rate is preserved better due to poorly developed parasympathetic activity
-infants rely more on diaphragmatic contribution due to more compliant ribs and loss of intercostal muscles with high spinal
epidural test dose
3 ml of lidocaine 1.5% with epinephrine 1:200000
- lidocaine tests for intrathecal placement: detectable sensory block 1-2 minutes with motor 3-4 minutes
- Intravascular: lidocaine will cause dozziness, tinnitus, circumoral paraethesia, metallic tase and blurred vision
- Epinephrine will cause sudden tachycardia (>10bpm) and HTN (>20mm Hg change), some will report palpitations and headache
TNS (transient neurologic syndrome)
possible that pregnancy can decrease incidence
epidural test dose during contractions
need to perform test dose between contractions to not be confused about increases in HR and HTN
- also concern for decreased uterine blood flow with epinephrine
High spinal
1) sudden and profound BP drop :vasodilation from sympathetic nerves
2) hypotension can cause nausea and vomitting
3) Accessory muscles of respiration are blocked decreasing TV
4) cardiac accelerator fibers are block; severe bradycardia
5) diphragm can be blocked
6) if spreads to brain unconciousness is assured
complications of neuraxial
- high spinal or intravascular injection
- infection: from superficial skin to life threatening epidural abscess
- epidural hematoma: pressure applied to spinal cord or nerve root resulting in ischemia and possible irreversible nerve damage
- arachoiditis (rare) due to inappropriate drug causing inflammation: various neurologic deficits such as paraplegia, quadriplegia, hydrocephalus, syringomyelia
post dural puncture headache
- reduction of the buoying effect of CSF on brain, causes traction and stretching of the meninges as the patient assumes the upright position
- improved with recumbency
- tx: fluids, caffeine, NSAIDs, narcotics and or epidural blood patch
Heparin MOA
binds to antithrombin with high affinity and subsequently inactivate thrombin (IIa), factor Xa, and factor IXa
Warfarin MOA
interferes with Vit K dependent clotting factors ( II, VII, IX, X)
Fondaparinux
inhibits factor Xa
Risk factors for awareness
C section, Cardiac surgery, emergent surgery, trauma, RSI, TIVA, difficult intubations, history of substance abuse, ASA 4 or 5, history of awareness
Auditory Evoked Potential Monitor
electrical responses of the brainstem, auditory radiation and auditory cortex to auditory sound stimuli (clicks)
- analyze the AEP wave form (latency and amplitude) to generate an AEP index that correlates to anesthetic concentration and level of consciousness.
Flexible fiberoptic intubation
nasal or oral
- pt selection (psychological preperation), anxiolytic, anti-sialagogue
- numbing
awake nasal intubation requires which additional nerve blocks
greater and lesser palatine and anterior ethmoid nerve
- plus the glossalpharyngeal and superior laryngeal nerve
- afrin or phenylephrine should be used to minimize bleeding risk
absolute indications for one-lung ventilation
- massive bleeding in one lung
- infection in one lung
- bonchopleural/bronchocutaneous fistula
- lung bullae
- alveolar lavage
- minimally invasive cardiothoracic surgery
lung with upper lobe coming of on average 1.5 cm from carina
right
Bronchial BLockers
- ideal if only single lumen is achievable
- more susceptible to displacement
- not optimal lung deflation
- difficult to place
- dislodge
- difficult to suction secretions
Lighted stylet
- blind approach; watcht he pretracheal glow as you advance
- as you advance a localized glow indicated a tracheal intubation vs a diffuse indicate esophageal
- contraindications too much skin to properly see the light (obesity), skin pigmentation issues, airway tumors/infections/trauma/foreign bodies (blind approach)
pediatric ETT size
ID= (age/4)+4
size of ETT
millimeter of internal diameter
cuffed tube
> 6 years old
Evaporative fluid losses
minimal surgery (laproscopic) 0-2 ml/kg
moderate (open chole) 2-4 ml/kg
severe (open bowel) 4-8ml/kg
Corneal abrasions
GA induces lagophthalmos (lid not closing all the way) and inhibits Bells phenomenon (eyeball turns up whilst sleeping- protective measures)
Post op vision loss
Most common after spinal fusion or cardiac surgery or long steep T-burg cases
-male sex, obesity, diabetes, use of wilson fram, EBL >2L, case >4-6 hours, BP 40% lower than baseline for >30 minutes
Ischemic optic nerve neuropathy
anterior; central retinal artery and small branches of ciliary artery
posterior: small branches of ophthalmic and central retinal arteries
- both because of ischemia
- increased venous pressure can cause perfusion of optic nerve
Anterior Ischemic optic neuropathy
- infarcts of the watershed perfusion zones between the small branches of the short posterior ciliary arteries
- cardiac surgery, hemorrhagic hypotension, anemia, head and neck surgery, cardiac arrest, hemodyalisis
Posterior Ischemic Optic Neuropathy
- more common
- Prone posterior spinal fusion cases, steep T burg
- decreased O2 delivery to the posterior portion of the optic nerve between the optic nerve and the point of entry to central retinal artery
- more frequent in healthy ASA 1-2
Cortical blindness
after profound hypotension or circulatory arrest
- infarcts in parietal or occipital lobes
- loss of vision but retention of pupillary reactions to light
Retinal artery Occlusion
- pale edematous retina on exam
- emboli or intranasal alpha adrenergic agonist
- stellate ganglion block can help
Venous Air Embolism
- surgery where operational site is higher than heart ( sitting neuro is the most, but thoracotomy, open vessels, cesarean sections -when uterus is out
- depends on volume of air entrapment and rate of accumulation
- 2-5 ml/kg is lethal dose
- large can cause a gas air-lock causing complete R ventricular outflow obstruction
- PFO can cause cerebral air embolisms
symptoms of VAE
cardiovascular pulmonary and neurologic
Cardiovascularly: tachy, ST changes, CO drops, BP drops
Pulmonary: dyspnea, coughing, lightheadedness, CP, decrease ETCO2, SaO2, PaO2 with hypercarbia
-Neuro: stroke with PFO
Monitoring for VAE
- TEE is most sensative
- Precordial doppler: R or L sternal border at 2-4 intercostal space: normal washing machine turbulence changes to erratic high-pitched swishing, progresses to “mill wheel” murmur
- transcranial doppler if PFO
- PA catheter: insensitive
- End tital Nitrogen: most sensative, 30-90 seconds before ETCO2 changes; not useful if nitrous is being used
- ETCOs: change of 2 mm Hg can indicate
- Vigilance
Management of VAE
-tell surgeon
-flood operation site with saline or wax
- optimize position (left lateral decub or t-burg)
-ACLS
-aspiration from catheter is only 6% effective
-optimize myocardial perfusion
- inotropic support
hyperbaric O2 therapy can be beneficial
Intraarteral injections
- leads to cyanosis, gangerene, loss of limb ect.
- signs of accident arterial are pulsatile flow, blood in the IV tubing palpable pulse proximal, signs of ichemia distal to catheter, worse pain than expected
- worse of benzo, barbs or vasoconstrictors.
- leave catheter in to flush out area/confirmation of arterial injection
- anticoagulate
- elevation, warms, massage
- LA can help reduce vasoconstriction
- stellate ganglion block or regional
- papaverine can induce smooth muscle relaxation
N2O cylinders
- Reads 745 PSI till 80% gone
- roughly 250L left when pressure begins to fall
- full tank hold roughly 1590L of N2O
first stage
allows preferential use of the pipeline oxygen when the higher pressure in this system is sensed. The oxygen cylinder tanks enter at a lower pressure
lowest pka for opioids
alfentanil
infared spectometer
- measures CO2
- Cannot measure O2
- End-tidal CO2 (ETCO2) is measured by infrared spectrophotometry where a wavelength of infrared light is passed through a gas sample and the amount of energy detected is inversely proportional to the gas partial pressure
most effective PONV med for children
Zofran
aprepitant is close but requires long onset time
AV nodal blockade due to stenosis
PDA
drugs that reduce ketamine emergence delerium
Benzodiazepines, propofol, and barbiturates
Cytochrome P450
Cytochrome p450 is a heme protein that utilizes molecular oxygen to oxidize organic compounds
pRBCs over time
acidemia, decreased 2,3 DPG and increase K
Myocyte action potential
4: resting
0: Na in (jump up)
1: K, CL out (dip down)
2: Ca in K out (plateau)
3: K out (drop down)
“nine Koala cause Kookiness” (sodium in k out ca out k out)
sub-ambient pressure alarm
- alarm is triggered when the pressure in the breathing circuit falls below atmospheric pressure by a pre-determined amount (typically below -10 cm H2O)
- Suction in the trachea
- Patient inhalation against an increased resistance in the circuit
- Patient inhalation against a collapsed reservoir bag
- A malfunctioning active closed scavenging system (excessive vacuum or valve dysfunction)
- A blocked inspiratory limb during exhalation
angiotensin II effect on GFR
Angiotensin II causes efferent glomerular arteriolar vasoconstriction which will maintain or increase glomerular filtration rate (GFR) in states of hypovolemia.
Propofol guidelines
- bacterial protection for 12 hours after opening (most recommend 6-8 hours, truelearn 12)
- dont mix it with other drugs
Desflurane effects
Desflurane primarily decreases arterial pressure by decreasing afterload. Desflurane increases heart rate, particularly when the concentration is quickly increased, and also causes dose-dependent depression of myocardial function. Cardiac output is maintained and there is no significant effect on left ventricular diastolic function.
LEast stable factor in FFP
VIII and V
- VIII interacts with vWF
Post operative cognitive delay
advancing age, lower educational level, and a history of previous cerebral vascular accident with no residual impairment.
Vapor pressure
- pressure exerted by the vapor when in equilibrium with the solid/liquid
- desflurane > isoflurane > sevoflurane
- Vol = FGF * Pvap / (Pbar - Pvap)
amount of fibrinogen in cry
Cryoprecipitate contains approximately 200 mg/unit of fibrinogen
Lorazepam premedication
Lorazepam premedication does not significantly improve patient satisfaction and can prolong extubation time, particularly in shorter cases
myocardial ischemia
- st elevation is transmural
- ST depression is subendocardial
K sparing diuretics
“The K+ STAys,” for Spironolactone, Triamterene, and Amiloride.
Anticholinergic syndrome
hyperthermia, tachycardia, blurry visions, dry skin, urinary retention
Cholinergic poisoning
Diarrhea, Urination, Miosis, Bradycardia, Bronchospasm, emesis, lacrimation, lethargy, salivation
Bronchospasma pathophysiology
noxious stimuli ->afferent sensory fibers in vagus->neurons in nucleus of the solitary tract->efferent fibers through vagus->bronchial smooth muscles-> released Ach bind to M3 muscarinic receptor->increased C GMP->bronchial smooth muscle contraction
Pharmacological causes of bronchospasm
desflurane B blockers NSAIDS cholinesterase inhibitors (neostrigmine) histamine releasing drugs (atracurium, mivacurium, sodium thiopental, morphine)
Signs of bronchospasm
rapid increase in peak airway pressures
decreased exhaled TV
shark finnig capnograph
Auto peep can occur
Bronchospasm management
increase O2 to 100%
increase anesthetic depth ( sevo and iso can bronchodilate
manual ventilate for tactile knowledge
B2 adrenergic agonists (albuterol)
magnesium can be beneficial for asthmatics
Epinephrine 10 mcg IV
Hypersensativity reactions
1) anaphylactic IgE mediated: anaphylaxis, allergic rhinitis, asthma
2) classic compliment system, IgG and IgM; ABO incompatability, HIT
3) immunce complxes of antigens and antibodies; serum sickness
4) delayed hypersensitivity, proliferaation of cytotixic T lymphocytes; GVH, tuberculin immunity
Anaphylaxis
-cross linking of IgE causes basophils and mast cell degranulation
-release of inflammatory markers; prostaglandins, leukotrienes, histamine and typtase
Signs: hypotnesion, tachy, bronchospasm, edema, hypoxia, rash
Causes of anaphylaxis
- # 1 NDNMB (though evidence of suggamdex is rising)
- B lactam antibiotics (PNC, cephalosporins)
Management of anaphylaxis
- discontinue drug
- 100% O2
- Volume expansion
- Epinephrine 5-10 mcgs (alpha causes vasoconstriction, B bronchodilation, stabalizes mast cells)
- admit to ICU for 24 hours
Laryngospasm
More common in kids and ENT surgery
- muscles are the lateral cricoarytenoids, the thyrorytenoids and cricothyroid
- causes by stimulus on oropharync; tube, secretions, blood
Treatment of laryngospasm
- 100% O2 with CPAP or PEEP
- jaw thrust
- larsons manuever
- deepen anethesia or sux (0.5-2 mg/kg)
Risk factors for aspiration
abdominal /GI surgery, strokes (swallowing dysfunction), diabetes, bowel obstruction, prego, old, GETA
Bad outcomes for aspiration
volume of 0.4 ml/kg and a pH less than 2.5
H2 agonists
bind to histamine receptors on the gastric parietal basal cells that produce gastric production
-ranitidine and famotidine
PPI
- block H+/K+ ATPase on the acidic luminal side of the gastric parietal cells
- -prazole
Antacids
only decreasae current acid in stomach
- use nonparticulate materials
Cricoid pressure
44N
Interscalene Block
- Brachial plexus at the level of roots/trunks
- shoulder and upper arm procedures
- side effects; stellate ganglion, phrenic nerve, recurrent laryngeal nerve, peumothorax
- Horner syndrome with stellate ganlgion ( ptosis myosis and anhidrosis
Supracavicular nerve block
- brachial plexus at level of trunks
- elbow, wrist and hand surgery
- highest incidence of pneumothorax
- can get stellate ganglion, phrenic and RLN
Infraclavicular nerve block
- brachial plexus at level of cords
- wrist and hand
Sciatic nerve block location
-7 cm superior to the popliteal crease and midpoint between the biceps femoris tendon laterally and the semitendinosus and semimembranosus muscles medially
Ankle blocks covers which nerves
deep peroneal (first web space)
superficial peroneal (dorsum of foot)
posterior tibial (calcaneus and plantar surface)
sural (cutaneous sensation to lateral ankle and foot and 5th digit)
saphenous (anteromedial of leg and medial of foot)
TAP block
- betweel the internal obliques and transversus abdominis muscles
- blocks T8-L1 nerves
Risks for PNA post op
intubation >48 hours >65 years old prolonged surgery trauma or emergency surgery intraoperative transfusion
Causes for hypotension post op
- inadequate volume recesitation
- EBL or ongoing loss
- Myocardia ischemia (especially if patient has stents and held antiplatelet)
- residual anesthetics
- decreased SVR; sepsis, spinal cord injury, histamine release from anaphylacsis, epidural/spinal
HTN post op
pain
- increased CO2
- held home meds
- urinary retintion/bladder distension
- if intubated; irritation of tube
differential for cardiac arrest
Hypoxia hypovolemia hyperkalemia hypokalemia H ions (acidosis) hypoglycemia toxins (anesthetic or anaphylaxis) tension pneumo thrombus tamponade QT prolongation Pulm hypertension
Zofran MOA
5-HT3 antagonist
anti emesis > anti nausea
Droperidol
is a butyrophenone
- .625-1.25 mg IV ppx for PONV
- black box warning for cardiovascular events (though at low doses seems fine)
CBF
mostly due to autoregulation (MAP 50-150)
- above or below autoregulation is mainly from CPP (normal 80-100)
- CO2 is directly proportional
- PaO2 < 50 causes large increase in CBF
- CMRO2 is directly proportional
- Temperature (5-7% per centigrade) directly proportional
Cerebral PErfusion PRessure
CPP= Map - ICP or CVP or cVP (cerebral venous pressure) [which ever is greatest) -80-100 mm Hg is normal < 50 has EEG slowing 25-40 has flat EEG <25 irreversible brain damage
CBF effects by anesthetics
IV agents: generally decrease CBF; exception of ketamine
Opioids; no effect or decrease
Benzos: reduce CBF
Volatiles increase CBF at >1 MAC; Halo>enflurane > des= iso>sevo
Nitrous; increases
Cerebrospinal Fluid
- produced in lateral cerebral ventricles by the choroid plexus; 20 ml/h
- Flow from lateral ventricle to 3rd ventricle through the intraventricular foramina, to 4th ventricle via the cerebral aqueduct, from fourth ventricle to subarachnoid space to surround brain and spinal cord
Medication affecting CSF
decrease CSF production: carbonic anhydrase inhibitors (acetazolamide), furosemide and thiopental
increase CSF: des, halothane and ketamine
Cerebral protection
hypothermia, glycemic control, hemodilution (decreases viscosity to improve O2 delivery), MAP control
Dorsal column
- control fine touch, vibration, proprioception and pressure
- sensory in the Meissner corpuscles, Pacinian corpuscles, muscle stretch receptors and Golgi tendon organs.
- travel up the fasiculus gracilis ( below T6) or fasciculus cuneatus (C2-T6) to nucleus gracilis or nucleus cuneatus.
- terminate at the ventral posterior lateral nucleus of the thalamus
Spinothalamic tract (anterolateral system)
- pain and temperature
- travel up then decussate in the anterior white commissure
- somatotopically arranged- lateral from lower and medial from upper
- travel to VPL of the thalamus through the posterior limb of the internal capsules and corona radiate and terminate in the postcentral gyrus.
Upper motor nerve injury
spastic paralysis and hyperactive DTR, + Babinski
Lower motor nerve injury
flaccid paralysis, diminished or absent DTR, muscle atrophy, fasciculations
lateral corticospinal tract
-rapid and skin voluntary movement of distal muscles of the upper and lower extremities.
Sensory Evoked potentials
- electrodes placed near peripheral nerves- measure the potential and latency in the scalp at the sensory cortex.
- measure the integrity of the dorsal columns
Motor evoked potentials
- from transcranial stimulation (or directly on the spinal cord) to peripheral nerves , spinal column or muscle.
- measure integrity of the ventral column and motor pathways
Agents that effect potentials
- Volatiles decrease (MAC of .5-.75 is ideal)
- Nitrous oxide further interfere
- IV except for etomidate and ketamine
- IV when given as infusions have negligible effects
- paralytics for MEPS
nicotonic post synaptic receptor
- five subunits- 2 alpha, beta, gamma and delta
- Ach binds both alpha
- allow Na and Ca influx and some K efflux
Extra junctional receptors
- an epsilon replaces the delta sub-unit
- up-regulated which causes the hyperkalemic response with sux
Myasthenia Gravis
autoimmune disorder that produces antibody against the ACh receptor
- muscle weakness
- resistant to depolarizing and sensitive to non depolarizing
Lambert-Eaton
autoimmune disorder in which antibodies attack the Ca2+ channel located on the presynpatic membrane
- proximal muscle weakness
- Lambs are sensitive (both depolarizing and non depolarizing)
Nociception
neural occurrences of encoding and processing noxious stimuli
- transduction
- transmission
- modulation
- perception
Sympathetic Nervous system fibers
preganaglionic fibers are short, postganglionic are long
Alpha receptors
- adrenoreceptors
- Alpha 1: in peripheral vasculature = vasoconstriction
- Alpha 2: presynaptic and act via G protein subgroup Gi, inhibiting adenylate cyclase= reduced cAMP and calcium levels. down regulation of SNS
Beta receptors
- Adrenoreceptors
- Beta 1: cardiac which causes increase HR and positive inotropy
- Beta 2: relaxation of bronchial and uterine smooth muscle, vasodilation and some positive inotropy and chronotropy
Parasympathetic nervous system
pregnaglionic fibers are long, postganglionic fibers are short
Muscarinic acetylcholine receptors
M1; gastric parietal cells M2; heart ( bradycardia) M3; contracts smooth muscle in the gut M4; epi release from the adrenal medulla M5 CNS effect that is poorly understood
ARDS
ARDS is an acute process where the immune system causes leak of fluid from the pulmonary capillaries and interstitium into the alveoli and resultant pulmonary edema.
- causes shunting
- increasing FiO2; does not improve PaO2
Lithium
prolongs succinylcholine and non-depolarizing relaxants such as rocuronium and vecuronium.
-Lithium may decrease anesthetic requirements (lower MAC) because it blocks brainstem release of norepinephrine, epinephrine, and dopamine.
Suggamadex dosing
2 mg/kg (actual body weight): 2 twitches
4 mg/kg; 2 post tet
16 mg/kg: immediate
Shunt:
portion of the lungs that is perfused but not ventilated while dead space is the opposite (portion of the lungs that is ventilated but not perfused)
with caudal last structure the need transverses until you are in the epidural space
Sacrococcygeal ligament
Hepatic blood flow
changes in portal venous flow will result in compensatory changes by the hepatic artery
Epidural morphine vs clonidine
longer duration of anesthesia for clonidine
Acute normovolemic hemodilution
decreased blood viscosity, decreased peripheral vascular resistance, increased cardiac output, and increased regional blood flow.
- does not increase O2 delivery
Temperature receptors
Cold: sends impulses on A delta nerve fibers
Hot: sends impulses on C nerve fibers
Regional anesthesia temperature
- epidural/spinal blocks afferent fibers from preventing cold input into the hypothalamus
- thermoregulation of body improperly judges skin temperature in blocked areas to be abnormally elevated
Carotid bodies
- sensory chemoreceptors that detect changes to O2 tension, CO2 tension, pH and temperature
- mainly use PaO2
Aortic bodies
- sensory chemoreceptors and barorecptors
- scattered in the aortic arch and its branches
- changes in PaO2, PaCo2, pH
LaPlace Law
Alveolar pressure = 2 X Surface tension/ Radius of alveoli
Alveolar ventilation
Va= (tidal volume- dead space) X RR Va= Vco2/PAco2
West lung zones
Zone 1: ALveolar pressure > pulm artery pressure > pulm venous pressure
Zone 2: PAP>AP>PVP
Zone 3: PAP>PVP>AP
-both ventalation and perfusion improves from apex (zone1) down
Cells in alveolar
Type one: 95% and make the surface
Type 2: make surfactant
macrophages
Fick’s law
Volume of gas diffused = area/thickness X diffusion constant X delta P
Ficks prinicple
oxygen consumption (Vo2)= Q X (aO2-VO2)
Oxygen content
CaO2= 1.34 Hgb X SaO2/100 (%bound) + 0.0003 PaO2
Hyperoxia
Toxicity develops from the excessive production of oxygen free radicals; superoxide anion, hydroxyl radicals and singlet oxygen species
- high O2 predisposes patients to mucous plugging and atelectasis
Carbon Dioxide transport
1) 70% as bicarb
2) 23% bound to hemoglobin and plasma proteins
3) 7% dissolved in plasma
isohydric transport
transport of CO2 as bicarbonate
- in RBC
-CO2 + H2O H2CO3 (carbonic acid) Hco3- (bicarb)+ H+
H ion is buffered by histidine and bicard undergoes chloride shift (hamburger shift)to exchange for chloride
Haldane effect
- O2 travels down pressure gradient in lungs
- O2 binds to hemoglobin causes a conformation change from T (tense) to R (relaxed) state that promotes release of CO2
- In R state H ions are released which combine with bicarb and go back to CO2 for release
Central chemoreceptors
mainly responsive to changes in PCo2, pH and acid/base parameters
Peripheral Chemoreceptors
mainly responsive to decreases in arterial Po2, increases in PCo2 and H+, and decreases in perfusion pressure
Hering Breuer reflex
increased stretch and pulmonary transmural pressure gradient in a sustained inflation leads to apnea
Increase ciliary activity in the respiratory system
high dose ketamine and fentanyl
Innervation of the larynx
RLN: all intrinsic muscles of the larynx except the crycothyroid muscle
SLN: sensory innovation to the base of the tongue, epiglottis aryepiglottic folds, and the artynoids. Motor innervation to cricothyroid muscle.
Bronchodilation facts
- Mediated by Beta 2. Stimultation increases the formation of cAMP by activating adenylate cyclase
- cAMP bronchodilates, cGMP bronchoconstricts; this balance is what dictates relaxation or constriction
Bronchodilators
1) sympathomimetics- B1 and B2; epinephrine, isoproterenol, isoetharine (cautious due to cardiac influences)
2) B2 selective: albuterol, terbutaline and metaproterenol
3) Phosphodiesterase inhibitors; inhibit cAMP breakdown; aminophyline and theophylline
4) Steroids; anti-inflammatory and membrane stabilizing; beclomethasone, triamcinolone, fluticasone and budesonide
5) Parasympatholytic drugs; antimuscarinic and block cGMP; atropine and ipratropium
6) volatiles; decrease smooth muscle contratility
JVP pulse wave
A wave, x decent, C wave, V wave, Y decent
- atrial contraction
- atrial relaxation
- ventrical contration, bulding of tricuspid
- passive artial filling
- tricuspid valve opens and atria empties
Stroke volume
SV= EDV-ESV
SVR
SVR= (Map-CVP)/CO
Ejection fractions
EF= SV/EDV
SA node manipulations
- Parasympathetic: large release of Ach, cell sbecome more permeable to potassium and become hyperpolarized; more negative membrane and reduces slope of phase 4
- Sympathetic; beta 1 adrenergic receptors cause a decrease in potassium permeability but increase in sodium and calcium; increased slope of phase 4 and reduce extent of re-polarization
Calcium induced calcium release
Long lasting (L-type) CA2+ channels located in t-tubule membranes are the main portals for CA2+ entry into the cell, which triggers the secondary release of Ca2+ from sarcoplasmic reticulum
excitation-contraction coupling
process by which mechanical shortening is transduced from an electrical signal ; triggers the release of calcium
Sympathetic nerve innervation of heart
R sympathetic nerve fibers predominantly innervate the SA and left mainly innervate the AV nodes and ventricles
Parasympathetic innervation of the heart
right and left vagal nerves both provide bilateral innervation of the SA and VA node
Factors that increase LVEDV and CO thus shifting starling curve up and to the left
1) volume expansion
2) avoiding increases in the intrathoracic pressure or pericardial pressure
3) augmenting venous tone and venous return to the heart
Normal cardiac index
CI = CO/BSA
2.5-4.2 L/min/m^2
Systolic effects on pressure-volume loop
positive inotropy = up and left
negative inotropy = down and right
Diastolic effects on pressure-volume loop
diastolic failure = downward shift
compliant ventricle= shifts loop up and left
Right coronary artery
supplies O2 to RA, RV, inferior portion of LV, AV and SA nodes
Left coronary artery
supplies the LA, interventricular septum and the anterolateral walls of the left ventricle
- branches include the left coronary artery (LCA) and LAD
Coronary perfusion pressure
CPP= ADP (aortic diastolic pressure) - LVEDP
– LV perfuses during diastole
- RV perfuses through systole and diastole
CPP increased with ADP, decreases with higher LVEDP, increases in HR
MAP
MAP = (2 DBP + SBP)/3 MAP= (CO X SVR) + CVP
Resistance calculations
In series= sum of all resistances
in parallel= sum of the reciprocals of individual resistances
Carotis SInus
baroreceptors
- Afferent impulses travel within Hering’s nerve (glossopharyngeal)
- travel to nucleus solitarius
Aortic arch baroreceptors
travel through the aortic nerve (vagus)
- travel to nucleus solitarius
Nucleus Solitarius
receive impulses from baroreceptors from IX and X
- send inhibitory signals to preganglionic sympathetic neurons in the spinal cord to decrease sympathetic nerve outflow to peripheral blood flow
- increase in parasympathetic response through Vagus nerve
- Overall; decrease in cardiac contractility, HR, SVR
Anesthetics vs baroreceptors
dose dependent attenuation of baroreceptor activity
V/Q of the west lung zones
1) V/Q > 1
2) V/Q = 1
3) V/Q < 1
Hormones controling RBF
1) ADH; released from the posterior pituitary in response to hypernatremia or hypovoemia causing H2O retention. Also shifts blood flow from cortex to (ischemic prone) medulla
2) Atrial natriuretic peptide; increases GFR via afferent arteriole dilation
3) Nitric Oxide; dilates renal vessels and increases perfusion
4) renal prostaglandins; cause dilation of renal arterioles
Starling equation
Fluid movement = filtration constant X (capillay hydrostatic pressure- interstitial hydrostatic pressure) - reflection constant X (capillary oncotic pressure - interstitial oncotic pressure)
Renal diuresis
- pressure natriureses; increased renal perfusion resultsin increases excretion of sodium and water
- Osmotic diuresis; osmotically active solutes (glucose and mannitol) in renal tubules causes increased oncotic pressure and water excretion
Renal control of blood volume
1) Angiotensin II; efferent arteriolar constriction (raising renal perfusion and GFR), stimulated ADH release
2) ADH increases sodium reabsroption in proximal tubule, stimulates aldosterone release
3) Aldosterone; enhances absorption of sodium and water from DCT/collecting duct
- ADH and aldosterone shift RBF to medulla
Release of ADH
angiotensin II stimulation, hypernatremia, increased osmolarity, arterial baroreceptors and atrial stretch receptors
Indications for digitalsi
1) Ventricular rate control of chronic a fib or flutter
2) treatment of narrow complex paroxysmal supraventricular tachycardia
3) treatment of congestive heart failure
Digitalis MOA
binds to and inhibits the sodium potassium adenosine triphosphate pump leading to an increased cystolic sodium concentration
- this gradient disallows sodium calcium transporter to remove calcium thereby increasing calcium concentration
- At pacemaker cells digitalis increases the absolute refractory period and decreases action potential conduction- negative chronotropy
Digitalis toxicty
- hypoxemia renal insufficiency, hypothyroidism hypoglycemia, hypomagnesiumia, and hypercalcemia
- pathognomonic dysrhythmia; paroxysmal atrial tachycardia with 2:1 AV block
- can cause severe hyperkalemia
Treatment of digitalis toxicity
- preferred antidysrhythmic drug is phenytoin, can use lidocaine
- digifab
Epinephrine
Beta 1, alpha 1 and alpha 2
- Low doses ( <0.04mcg/kg/min): B>A; positive inotropy and vasodilation
- medium ( 0.04-.12) B=A with vasoconstriction beating vasodilation
- High (>0.12) A>B, potent vasoconstrictor
Norepinephrine
Alpha 1 and Beta 1
0.02-0.25 mcg/kg/min
Alpha effect increases with dose
Dopamine
low doses (0.5-3 mcg/kg/min) D1 and D2; increase renal and mesenteric blood flow through vasodilation
moderate (3-5) beta 1
high (5-20) alpha 1
Dobutamine
B1 > Alpha=Beta2
Isoproterenol
nonselevtive beta agonist
- increases stroke volume through beta 1
- Vasodilation through beta 2
- can cause myocardial ischemia
Phosphodiesterase inhibitors
- increase inotropy and lusitropy
- increase Ca2+ intracellular due to blocking of phosphodiesterases breaking down cAMP.
- also cause vasodilation systemically
Class 1 antiarrythmics
1A: block fast Na and intermediate K; prolong QRS and QT intervals; quinidine, procainamide, dispyramide
1B: fast Na; deccrease QT; lidocainem tocainaide, mexilitine
1C: Na channel , decrease QRS; flecainide, propafone
Class 2 antiarrythmics
Beta blockers
- decrease HR, increase PR
- propranolol, esmolol, metoprolol
Class 3 antiarrythmics
- K channel blockers
- increase QT interval
- amiodarone, sotalol, ibutilide, dronedarone
Class 4 antiarrhythmics
L-type Ca channel blockers
- decrease HR, increase PR interval
- verapamil, diltiazem
Calcium Channel Blockers- vasodilators
NIcardipine, Clevidipine,
- Verapamil - significant negative inotropic and chronotropic effects
- Diltiazem
Nitroglycerin
- relaxes venous > arterial
- Can cause methemoglobinemia
Sodium Nitroprusside
- peripheral vasodilation
- Cyanide poisoning can occur; treatment is sodium thiosulfate, sodium nitrate, or hydroxycobalamin
Hydralazine
direct-acting arterial vasodilator (5-20 mg IV)
-can cause reflex tachycardia
RAAS
- Renin released from the macula densa cells stimulate the JG cells to release renin based off low flow
- Renin cleaves angiotensinogen to angiotensin 1
- Ace converts Angiotensin 1 to 2
- Angiotensin 2 stimulates aldosterone release
Angiotensin II
- smooth muscle contraction
- enhances peripheral sympathetic nervous system
- increases Na reabsorption and H2O retention
- stimulates ADH
- stimulates thirst centers
- stimulates cardiac and vascular hypertrophy and remodeling
- stimulates aldosterone synthesis
ACEi
- april
- used for HTN
- side effects: cough, hyperkalemia, angioedema, teratogenic risk, acute kidney failure
ARBs
- sartan
- Highly selective for AT1 over AT2
- for patients who cant tolerate ACEi
RAAS antagonitist vasoplegia
- variable incidence of severe hypotension during the initial 30 minutes after induction of anesthesia
- more resistant to alpha adrenergic agonists due to chronic AT1 receptor blockade
- use norepi, restores BP and maintains CO (we use vassopressin here; does maintain CO as well)
Vasoplegia
- vasodilatory shock state when vascular tone is profoundly decreased and unresponsive to traditional sympathomimetics drugs
- cardiac surgeries just separated from CPB, septic shock, hemorrhagic shock, post-reperfusion liver transplant recipients, post pheo resections, post induction with ACEi or ARBs
Vasopressin
- ADH
- V2: promotes water reabsorption in the kidneys
- V1: vasoconstriction within the arteriole of the skin, splanchnic, renal and coronary circulatory beds
Methylene Blue
- mainly for urinary tract integrity, or mastectomies for lymphatic system tracing
- treatment of methemogloinemia
- competes directly with nitric oxide in the vascular endothelial cell for enzyme guanylate cyclase (binds to heme moity)
- Block the cascade leading to smooth muscle relaxation: vasoconstriction
- Can precipitate acute hemolytic anemia with G6PD deficiency
- contraindicated in renal insufficiency
