Normal values for cardiac output, cardiac index, and pulmonary artery pressures.
CI: 2.5-4L/min/m2 of BSA
PAP: 30s/10d with mean <20
What is normal CVP,right ventricle pressure,PAW?
CVP: 0-5
RVP: 30/5
Name normal left atrial, left ventricle, and aortic pressures?
LAP: <12m
LVP: 140/12
Aorta: S<140, D<90, M: 70-90
Name equation for MAP
(systolic-diastolic)/3 + diastolic
Normal ICP values
Normally 7-18 cm water, measured in lumbar area
In lateral recumbent 13 cm water
If sitting 37-55 cm water
Law of La Place
sphere: P=2t/r
cylinder:P(2RL) = T(2L) or T = PR
• Where
o P = pressure at outlet
o T = tension of wall
o R = radius of wall
• Note
o If the wall is stationary, the outward and inward forces
across it are equal.
o Cross-sectional area: A = 2RL
o Distending force (outward pressure times area):
PA = P(2RL)
o Restraining pressure acting inward (tension times
length): T(2L)
Describe BP variance with respiration
Inhalation causes a decrease intrathoracic pressure that aids venour return. Exhalation does the opposite.
Describe BP variance under mechanical ventilation.
PPV= increased intrathoracic pressure, decreased venous return, especiallly during inspiration. Decreased art. line amplitude under PPV= pt is dry.
SVR equation
nomal is 1500-1900 dynes/sec/cm-5
As resistance increases, flow (perfusion) decreases
Increased SVR
Adaptive in low volume states
Maladaptive post MI where it decreases tissue perfusion and increases cardiac afterload
Also seen during SNS response, increased catecholamine release
Decreased CO
Caused primarily by decreased venous return in a variety of conditions
Causes of increased CO
Septic shock (early), nipride, increased metabolism, etc. Will have a higher mv02
Hemodynamic trends in septic shock
decreased PCW, MAP, SVR. Increased CI.
Hemodynamic trends in cardiogenic shock.
Decreased MAP, CI. Increased PCW and SVR
Hemodynamic trends in hemhorragic shock
Decreased MAP, CI, PCW. Increased SVR.
Modified Allen’s Test
Shows Ulnar nerve patency. To be done before art line insertion
List circumstances in which PWP may not equal LVEDP
Stiff and noncompliant LV, mitral valve disease, LA hypertrophy or pulmonary disease (normal PWP with elevated LAP)
List circumstances in which CVP will not reflect accurate LVEDP
pulmonic and tricuspid valve problems. RAP is influenced by volume, venous tone, increased PVR
CVP reflects…
RAP, RVEDV, preload,
RAP reflects…
cardiac function, venous return to the heart.
4 determinants of cardiac function
preload, afterload, HR, contractility
Name components of CVP waveform
a wave:right atrial contraction, p wave
c wave: tricuspid valve bulge during early RV contraction. QRS
x descent: downward movement of RV during contraction. Before T wave
v wave:RA full and tricuspid is bulging. As T wave is ending
y descent: Tricuspid open, RV diastole, before p wave.
Pathologic CVP waveforms
Afib: no A waves
AV dissociation: Cannon A waves. Increased in size
Tricuspid regurg: looks like artline waveform. c wave and x descent replaced by regurg wave. False high mean, look at pressures between regurg waves
Tamponade: all pressures elevated, y descent small or gone
Contraindications to SWAN
relative: WPW, Ebstein’s malformations, L BBB, left fascicular block
Instances where PCWP overestimates LVEDP
chronic mitral stenosis, PEEP, LA myxoma, pulmonary HTN
Instances where PAWP underestimates LVEDP
Things that increase LV pressure: stiff LV, LVED>25 mm Hg, Aortic Insufficiency
Relationship between PCWP and PAEDV
In absence of PVR, difference is 1-4 mm Hg
Determinents of preload
1. atrial pressure (venous pressure and return)
2. HR
3. ventricular distensibility (compliance)
Depolarizing neuromuscular blockers
Succ. Ach receptor agonist. Metabolized by pseudocholinesterase
Nondepolarizing neuromuscular blockers
Ach competative antagonists. No depolarization.Reversal of their blockade depends on redistribution, gradual metabolism, excretion, or administration
of specific reversal agents (cholinesterase inhibitors) that inhibit acetylcholinesterase enzyme activity.
Train of four is four supramaximal stimuli every 0.5 sec (2 Hz).
T4 is lost at 80% receptor occupancy, T3 at 85%, T2 at 90%, T1 at 95%
Phase I Block
A phase I block (depolarizing blockade-Succinylcholine) does NOT exhibit fade during train of four. If enough Succinylcholine is
given, however, you can witness a phase 2 blockade. This usually occurs with repeated dosing and succinylcholine infusions.
Phase II BLock
The occurrence of fade, a gradual lessening of evoked response, is
characteristic of nondepolarizing blockade. This is a phase II block.
Tetanic Stimulation
Characterized by:
o Fade and post-tetanic facilitation (NDMR and phase II depolarizing block) or
o Diminished height from control without fade or PTF (depolarizing block).
• Disadvantages: It is painful and may produce lasting antagonism of block during recovery. It may also hasten onset by
increasing blood flow to the limb.
Post-Tetanic Count
Post-tetanic count (PTC) – Apply tetanus at 50 Hz x 5 sec, wait 3 sec, then begin single twitch at 1 Hz.
• Number of PTCs correlates inversely with time to recovery of a deep block.
Double Burst Stimulation
This is a mode consisting of two short bursts of 50 Hz tetanic stimulation separated by 750 msec.
• The aim is to allow tactile detection of small amounts of residual blockade under clinical conditions (more sensitive than TOF in
detecting residual paralysis).
Extubation parameter and associated NIFs
Parameter Negative Inspiratory Pressure (cm H2O)
Control -90
Head lift 5 sec -53
Effective swallow -43
Patent airway with jaw lift -39
Evoked Potentials
Can be sensory, motor, visual or auditory
Signals are produced as a nervous system response to stimuli, and altered signals can indicate dysfunction
Latency – time between the stimulus and potential
Amplitude – intensity or height of stimulus
Somatosensory Evoked Potentials (SSEP)
Monitor the integrity of the sensory spinal cord (dorsal columns)
Can warn against spinal cord ischemia (posterior spinal arteries)
Technology is square-wave signals with sensory input, transfer to sensory (posterior) cord, then to the
thalamus and eventually the sensorimotor cortex
Volatile anesthetics decrease amplitude and increase latency of SSEPs. Use about 0.5 MAC of a volatile
agent and no greater than 50-60% N20
BIS monitor
(Bispectral) monitor is used to measure depth of anesthesia.
• Data measured by EEG (electroencephalography) are taken through a number of steps to calculate a single number that
correlates with depth of anesthesia and hypnosis.
• BIS monitoring may reduce patient awareness and resource utilization in terms of drugs. It may also help facilitate a faster wakeup
time. Many of the initial studies were observational in nature and not randomized, prospective trials.
BIS Scale
100 – awake
90-70 light/moderate sedation
70-60 deep sedation (low probability of recall)
60-40 general anesthesia
40-10 deep hypnotic state
10-0 flat EEG
Sudden increase in BIS
Increased stimulation
Decreased anesthetic level
Vaporizer malfunction
Bair Hugger interference
Sudden decrease in BIS
Decrease in surgical stimulation
Lead placement

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