Monitors – Chemistry – Flashcards
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| Normal values for cardiac output, cardiac index, and pulmonary artery pressures. |
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| CO:4-7L/min CI: 2.5-4L/min/m2 of BSA PAP: 30s/10d with mean <20 |
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| What is normal CVP,right ventricle pressure,PAW? |
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| CVP: 0-5 RVP: 30/5 PAW/PAOP: <20 |
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| Name normal left atrial, left ventricle, and aortic pressures? |
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| LAP: <12m LVP: 140/12 Aorta: S<140, D<90, M: 70-90 |
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| Name equation for MAP |
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| (systolic-diastolic)/3 + diastolic |
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| Normal ICP values |
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| Normally 7-18 cm water, measured in lumbar area In lateral recumbent 13 cm water If sitting 37-55 cm water |
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| Law of La Place |
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| 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) |
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| Describe BP variance with respiration |
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| Inhalation causes a decrease intrathoracic pressure that aids venour return. Exhalation does the opposite. |
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| Describe BP variance under mechanical ventilation. |
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| PPV= increased intrathoracic pressure, decreased venous return, especiallly during inspiration. Decreased art. line amplitude under PPV= pt is dry. |
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| SVR equation |
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| SVR=[(MAP-CVP)x80]/CO nomal is 1500-1900 dynes/sec/cm-5 As resistance increases, flow (perfusion) decreases |
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| Increased SVR |
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| 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 |
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| Decreased CO |
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| Caused primarily by decreased venous return in a variety of conditions |
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| Causes of increased CO |
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| Septic shock (early), nipride, increased metabolism, etc. Will have a higher mv02 |
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| Hemodynamic trends in septic shock |
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| decreased PCW, MAP, SVR. Increased CI. |
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| Hemodynamic trends in cardiogenic shock. |
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| Decreased MAP, CI. Increased PCW and SVR |
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| Hemodynamic trends in hemhorragic shock |
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| Decreased MAP, CI, PCW. Increased SVR. |
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| Modified Allen's Test |
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| Shows Ulnar nerve patency. To be done before art line insertion |
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| List circumstances in which PWP may not equal LVEDP |
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| Stiff and noncompliant LV, mitral valve disease, LA hypertrophy or pulmonary disease (normal PWP with elevated LAP) |
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| List circumstances in which CVP will not reflect accurate LVEDP |
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| pulmonic and tricuspid valve problems. RAP is influenced by volume, venous tone, increased PVR |
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| CVP reflects... |
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| RAP, RVEDV, preload, |
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| RAP reflects... |
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| cardiac function, venous return to the heart. |
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| 4 determinants of cardiac function |
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| preload, afterload, HR, contractility |
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| Name components of CVP waveform |
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| 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. |
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| Pathologic CVP waveforms |
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| 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 |
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| Contraindications to SWAN |
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| relative: WPW, Ebstein's malformations, L BBB, left fascicular block |
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| Instances where PCWP overestimates LVEDP |
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| chronic mitral stenosis, PEEP, LA myxoma, pulmonary HTN |
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| Instances where PAWP underestimates LVEDP |
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| Things that increase LV pressure: stiff LV, LVED>25 mm Hg, Aortic Insufficiency |
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| Relationship between PCWP and PAEDV |
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| In absence of PVR, difference is 1-4 mm Hg |
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| Determinents of preload |
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| 1. atrial pressure (venous pressure and return) 2. HR 3. ventricular distensibility (compliance) |
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| Depolarizing neuromuscular blockers |
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| Succ. Ach receptor agonist. Metabolized by pseudocholinesterase |
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| Nondepolarizing neuromuscular blockers |
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| 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. |
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| TOF |
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| 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% |
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| Phase I Block |
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| 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. |
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| Phase II BLock |
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| The occurrence of fade, a gradual lessening of evoked response, is characteristic of nondepolarizing blockade. This is a phase II block. |
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| Tetanic Stimulation |
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| 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. |
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| Post-Tetanic Count |
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| 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. |
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| Double Burst Stimulation |
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| 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). |
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| Extubation parameter and associated NIFs |
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| Parameter Negative Inspiratory Pressure (cm H2O) Control -90 Head lift 5 sec -53 Effective swallow -43 Patent airway with jaw lift -39 |
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| Evoked Potentials |
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| 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 |
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| Somatosensory Evoked Potentials (SSEP) |
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| 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 |
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| BIS monitor |
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| (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. |
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| BIS Scale |
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| 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 |
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| Sudden increase in BIS |
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| Increased stimulation Decreased anesthetic level Vaporizer malfunction Movement Bair Hugger interference |
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| Sudden decrease in BIS |
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| Decrease in surgical stimulation Hypothermia Lead placement |
