# Monitors

 Normal values for cardiac output, cardiac index, and pulmonary artery pressures.
 CO:4-7L/minCI: 2.5-4L/min/m2 of BSAPAP: 30s/10d with mean <20
 What is normal CVP,right ventricle pressure,PAW?
 CVP: 0-5RVP: 30/5PAW/PAOP: <20
 Name normal left atrial, left ventricle, and aortic pressures?
 LAP: <12mLVP: 140/12Aorta: 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 areaIn lateral recumbent 13 cm waterIf sitting 37-55 cm water
 Law of La Place
 sphere: P=2t/rcylinder:P(2RL) = T(2L) or T = PR• Whereo P = pressure at outleto T = tension of wallo R = radius of wall• Noteo If the wall is stationary, the outward and inward forcesacross it are equal.o Cross-sectional area: A = 2RLo Distending force (outward pressure times area):PA = P(2RL)o Restraining pressure acting inward (tension timeslength): 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
 SVR=[(MAP-CVP)x80]/COnomal is 1500-1900 dynes/sec/cm-5As resistance increases, flow (perfusion) decreases
 Increased SVR
 Adaptive in low volume statesMaladaptive post MI where it decreases tissue perfusion and increases cardiac afterloadAlso 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 reflects…
 4 determinants of cardiac function
 Name components of CVP waveform
 a wave:right atrial contraction, p wavec wave: tricuspid valve bulge during early RV contraction. QRSx descent: downward movement of RV during contraction. Before T wavev wave:RA full and tricuspid is bulging. As T wave is endingy descent: Tricuspid open, RV diastole, before p wave.
 Pathologic CVP waveforms
 Afib: no A wavesAV dissociation: Cannon A waves. Increased in sizeTricuspid regurg: looks like artline waveform. c wave and x descent replaced by regurg wave. False high mean, look at pressures between regurg wavesTamponade: 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
 1. atrial pressure (venous pressure and return)2. HR3. 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 administrationof specific reversal agents (cholinesterase inhibitors) that inhibit acetylcholinesterase enzyme activity.
 TOF
 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 isgiven, 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, ischaracteristic 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) oro 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 byincreasing 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 indetecting residual paralysis).
 Extubation parameter and associated NIFs
 Parameter Negative Inspiratory Pressure (cm H2O)Control -90Head lift 5 sec -53Effective swallow -43Patent airway with jaw lift -39
 Evoked Potentials
 Can be sensory, motor, visual or auditorySignals are produced as a nervous system response to stimuli, and altered signals can indicate dysfunctionLatency – time between the stimulus and potentialAmplitude – 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 thethalamus and eventually the sensorimotor cortexVolatile anesthetics decrease amplitude and increase latency of SSEPs. Use about 0.5 MAC of a volatileagent 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 thatcorrelates 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 wakeuptime. Many of the initial studies were observational in nature and not randomized, prospective trials.
 BIS Scale
 100 – awake90-70 light/moderate sedation70-60 deep sedation (low probability of recall)60-40 general anesthesia40-10 deep hypnotic state10-0 flat EEG
 Sudden increase in BIS
 Increased stimulationDecreased anesthetic levelVaporizer malfunctionMovementBair Hugger interference
 Sudden decrease in BIS