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Flashcards in Monitoring Deck (111):

What is the definition of intraabdominal hypertension?

sustained or repeated pathologic elevation of IAP of >12 mm Hg


What is abdominal compartment syndrome?

sustained increase in intraabdominal pressure of >20 mm Hg that is associated w/ new organ dysfunction/failure


approximately how many ICU patients (people) have abdominal hypertension?



How many human ICU patients have intraabdominal hypertension severe enough to be classified as having abdominal compartment syndrome?

14% of the patients who have intraabdominal hypertension


What are 4 conditions that are associated with increased risk of intraabdominal hypertension in people?

1. diminished abdominal wall compliance
2. increased intraluminal content
3. increased abdominal content
4. capillary leak syndrome


T/F: in human studies it is determined that a physical exam is a reliable tool to evaluate intraabdominal pressure?



Briefly describe the method for determining intraabdominal pressure

U. bladder method is gold standard
-Urethral catheter placed- tip just inside trigone
-sterile urine collection system hooked up to 2 three way stop cocks
-water manometer attached to upright stopcock port
-35 or 60 ml syringe of 0.9% NaCl attached to distal stopcock
-bladder emptied
-0.5 to 1 ml/kg (max 25 ml/patient) NaCl instilled
-system zeroed to midline, stopcock closed to fluid source, and pressure is read


What is normal intraabdominal pressure in a dog? A cat?

0-5 cm H2O dogs
6-11 cm H2O cats


What are some hemodynamic effects of increased intraabdominal pressure?

Initially increased CVP & RA/pulmonary pressure; then decreased cardiac output; can falsely increase CVP


Name some renal effects of intraabdominal hypertension

decreased GFR and urine output, oliguria/anuria when IAH >25 cm H2O


Name some pulmonary and thoracic effects of IAH

Decreased pulmonary compliance, decreased chest wall compliance, more severe lung injury


What type of ventilator setting is recommended in patients with IAH?

volume controlled


Name CNS effects of IAH

increased intracranial pressure


Name visceral effects of IAH

hDecreased hepatic, portal, intestinal and gastric blood flow; decreased lymphatic drainage, increased intestinal permeability, possible increased bacteremia from gut


Name systemic/hormonal effects of IAH

Increase in ADH, elevated plasma renin activity, increased aldosterone levels, increased epi and norepi, rise in IL1B, IL6, TNFalpha, MODS, thrombotic disease, impairment of wound healing


What is the recommended course of action if your patient has an IAP of 10-20 cm H2O?

ensure normovolemia, pursue underlying cause


What should you do if your patient has an IAP of 20-35 cm H2O?

volume resuscitate if necessary; perform diagnostics to identify cause, consider decompression


Recommendation if patient's IAP is >35 cm H2O?

decompression via paracentesis or surgical explore is strongly recommended; consider managing patient as open abdomen


What percent of the original fluid volume that enters the nephron will be excreted as urine?

Less than 1%


Between what MAP is auto regulation maintained?

Between 80 and 180 mmHg
This means that renal blood flow and therefore GFR is maintained


What is the lowest normal urine output value reported for dogs?

0.27 ml/kg/hr


What is the difference between absolute and relative oliguria?

Absolute oliguria refers to a UOP less than 1 ml/kg/hr in a hydrated, well-perfused patient.

Relative oliguria refers to a UOP between 1 and 2 ml/kg/hr in a patient receiving IV fluids


Name some common conditions that can cause pre-renal oliguria

Severe dehydration, hypovolemia, hemorrhage, cardiac failure, SIRS, sepsis


A urine sodium of less than what value is consistent with the action of aldosterone? (in the absence of diuretic administration or intrinsic renal disease)

Urine Na of less than 20 mEq/L


A urine sodium level of what value supports a diagnosis of syndrome of inappropriate ADH?

Serum hyponatremia with urine Na of more than 40 mEq/L


Name 10 causes of pre-renal polyuria

Increased intake (polydipsia, fluid administration)
Drugs (diuretics, alpha 2 agonists, K agonists, alcohols, glucocorticoids, anticonvulsants)
Hormonal conditions (cushings, addisons, DI, hyperthyroidism, cerebral salt wasting syndrome)
Electrolyte abnormalities (hypokalemia, hypercalcemia)
Osmotic conditions (DM, salt ingestion or administration, glycols)
E. coli endotoxin
Liver disease


what is special about a swan-ganz catheter in comparison to other pulmonary arterial catheters?

it has a sensor 4 cm distal to the tip that allows temp measurement


what type of PAC can measure blood oxygenation?

oximetry thermodilution catheter


what are most thermodilution catheters (besides swan-ganz) made of? why?

polyurethane, it softens at body temperature


how big should the catheter introducer sheath be for a PAC?

at least 1 size larger than the catheter itself (i.e. a 6-6.5 fr introducer for a 5 fr catheter)


describe the 2 different ports and what they are used to measure in a PAC designed for thermodilution method of cardiac output

proximal port- CVP port; measures RA or CV pressure; used for fluid boluses
distal port-central lumen; measures PA pressure and PCWP; samples mixed venous blood


what is the K constant of the steward-hamilton equiation?

computation constant that is manually entered into computer that adjusts for amt of thermal signal during each measurement, volume of catheter dead space, and specific heat/volume/gravity of the injectate used


briefly describe the technique for CO measurement using a PAC

1.5 ml/kg of saline of known temp injected into proximal port; the thermistor probe on distal end of PAC measures change in blood temp and calculates CO based on AUC of temperature; the bolus should be given as quickly as possible to minimize changes in temperature


what does PCWP estimate?

LV preload (LV end diastolic pressure)


in which patients might PCWP not be accurate as an estimate for LV preload?

pulmonary hypertension, mitral regurgitation, decreased ventricular compliance; patients on PPV


why might RV end diastolic volume be useful as an estimate of volume status?

if patients are on PPV with PEEP or other scenarios in which PCWP may not be accurate for indicating LV end diastolic pressure


what is required of the patient/ECG to measure RVEDV?

catheter must be synced to ECG; R-R interval must be regular


besides PCWP and RA pressure and CO, what other measurements/diagnostics can be made using PAC?

pulmonary angiography, calculate systemic vascular resistance, pulmonary vascular resistance


t/f- a recent meta analysis of PAC monitoring showed no increased morbidity but no benefit?



patients with which type of shock may benefit the most from PAC measurement?

cardiogenic; the other types of shock showed uncertain benefit in 1 study


briefly describe placement of a PAC (without flow directed placement)

clip/prep wide area of skin; place sterile drapes and use sterile gown/gloves/mask/cap; sedation of patient with benzo/opioid; local with lidocaine; skin incision over vessel; placement of introducer sheath into external jugular vein via cutdown or seldinger technique; premeasure to cardiac structures; wrap the neck up; make sure the balloon is good; flush all ports with hep NaCl before placing


describe flow-directed placement of a PAC

attach the distal port of catheter to a calibrated pressure transducer and connection to a monitor; monitor pressure tracing as catheter is introduced into jugular vein; once the catheter is in the RA the balloon can be inflated with ~1.5 ml of air; make sure the balloon is always deflated before withdrawing catheter to prevent valvular damage and knotting of catheter


t/f- the balloon of a PAC should always be deflated after PCWP measurement?

true; to avoid unnecessary obstruction of blood flow


what might be seen on the ECG if the PAC is contacting the RV wall?

ventricular arrhythmias


List the normal systolic/mean pressures for different chambers of PAC placement? For use for flow-directed placement

RA- systolic 4-6 mm Hg, diastolic 0-4 mm Hg, mean 2-5 mm Hg
RV- mean 15-30 mm Hg, diastolic 0-4 mm Hg
PA- diastolic 5-15 mm Hg (no longer has diastolic pressure at 0 b/c pulmonic valve), mean 8-20 mm Hg
PCWP- mean 5-12 mm Hg


what is the max length of PCWP measurement before deflating the balloon?

2 resp cycles or 10-15 seconds


what should you do if you try to fill the air in the ballooon to measure PCWP and you are unable to get the full 1.5 ml into the balloon?

balloon should be deflated and catheter backed out out until PCWP is noted with full inflation of 1.5 ml of air


pros/cons of fluoroscopy for PAC placement?

pros- may increase speed, can quickly identify misplacement
cons-special equipment, generation of radiation


complications of PAC placement?

wire/catheter embolus, carotid artery rupture, cardiac arrhythmias, knotting, cardiac tamponade, tricuspid valve damage, hemothorax, pneumothorax, pulmonary artery rupture


alternatives to PAC placement for cardiac output monitoring?

LiDCO, PulseCO, transesophageal echo, lithium chloride


what is the equation for MAP? MAP= ???



t/f- normal blood pressure does not necessarily mean adequate blood flow?



what other monitoring techniques, besides arterial BP, can be useful into patient blood flow and tissue perfusion?

serial PE, cardiac output, blood lactate, central venous hemoglobin, direct imaging of microcirculation


in which clinical scenarios may ABP be the most useful?

-patients in shock with hypotension or CV collapse
-patients on vasopressors
-titration of medications for afterload reduction in patients with CHF
-patients receiving meds for severe hypertension
-patients on ventilator
-patients with high anesthetic risk


advantages of noninvasive/indirect BP monitoring?

inexpensive, less technically challenging, don't require arterial catheterization


what is the major limitation to noninvasive BP monitoring?

less accurate in dogs and cats, whether awake or anesthetized; espec true in hypotensive/hypothermic or small patients


which factors can affect accuracy of noninvasive BP ?

cuff size, technique, operator error


pro/con to oscillometric BP monitoring?

pro- provides more information (systolic, diastolic and MAP)
con- less reliable in cats and small dogs compared to doppler or invasive methods


benefits of invasive BP monitoring?

-"hands off", allowing tech to spend more time doing other things
-beat to beat monitoring
-less stress to patient, less patient handling
-arterial cath allows for easy ABG sampling


risks of invasive BP monitoring?

technically challenging to place arterial cath, expensive equipment necessary, errors can occur


complications assoc with arterial catheterization?

hematoma, bleeding, infection, arterial thrombosis, tissue ischemia, hemorrhage if transducer disconnected


t/f- dorsal pedal artery is more accurate than femoral or coccygeal for invasive BP monitoring?

false- they are all similar


briefly describe the procedure for arterial catheterization

aseptically prepare area
+/- 2% lidocaine over artery
palpate artery and advance catheter
use only small movements, as lumen is smaller than vein
secure catheter with tape and protective wrap
label it ART LINE


briefly describe set-up of pressure transducer and monitoring system

pressure transducer attached via line to pressurized 500 ml or 1L bag of 0.9% NaCl (contains heparin 1-2 U/ml)
inflate pressure bag to 250-300 mm Hg
flush heparinized NaCl through system to prime tubing, make sure no air bubbles present
at other end of transducer, noncompliant tubing will be attached that is attached to art line
zero the transducer; set to level of right atrium if CVP desired; set to level of catheter if peripheral pressures desired
open tubing to patient and waveform should appear


In a spontaneously breathing patient, what changes in CVP will you see with respiration?

CVP will decrease during inspiration

CVP will increase during expiration


In what phase of respiration should the CVP reading be taken?

End-expiration if the patient is breathing normally.

If pronounced abdominal effort, measurement should be taken at the beginning of the expiratory phase


Describe how to take an intermittent CVP measurement

1. Connect the three-way stopcock to the manometer, to the saline-filled syringe, and to the fluid tubing.
2. Orient the three-way stopcock valve so that it is closed to the manometer and open to the tubing and fluid-filled syringe.
Then, prime (fill) the stopcock and fluid tubing with 0.9% NaCl from the syringe. Connect the fluid tubing to the central
venous catheter. If a multilumen catheter is being used, connect the tubing to the central lumen.
3. Orient the stopcock valve so that it is closed to the patient’s central venous catheter and open between the manometer
and the fluid-filled syringe. Using the 20-mL syringe, fill the manometer with 0.9% NaCl to a level that is approximately
10–20 cm H2O greater than the patient’s expected CVP. Do not allow the manometer to overflow while filling.
4. Locate the 0 cm H2O mark and position the manometer so that it is level with the zero reference
point (the patient’s right atrium).
5. Close the stopcock valve toward the syringe, which will open a fluid column between the manometer and the patient.
6. When the measurements have been completed, turn the stopcock off to the manometer and disconnect the pressure tubing from the central venous catheter.


What tasks should be performed to maintain a continuous CVP system?

• Flush q4h
• Re-zero transducer at least q12h
• Change flush solution and tubing q48h
• Ensure there are no air bubbles in the fluid line at anytime.
• Periodically inspect and reinflate the pressure bag to300 mm Hg as necessary, and verify the heparinized saline
bag is not empty.


True or false:
Right atrial pressure is a major determinant of right ventricular end-diastolic pressure



When are right atrial and right ventricular pressures equal?

When the tricuspid valve is open and pressures have equilibrated at the end of ventricular diastole


How is right ventricular end-diastolic pressure related to preload?

65%Right ventricular end-diastolic pressure is in turn related to right ventricular end-diastolic volume, which determines end-diastolic myocardial wall stretch, or preload.


What percent of the systemic blood volume is contained within the venous system?



True or False:
In the presence of normal cardiac function, patients with a low CVP are more likely to respond to volume than patients with a normal or high CVP



If a patient with a CVP of greater than 10 mmHg responds well to a fluid bolus, what might be causing the elevated CVP?

Elevated intra-thoracic pressure
Elevated intra-abdominal pressure


If a patient has a rising CVP with worsening tissue perfusion, what might be occurring?

Declining cardiac function


What are the possible causes of a flat line CVP waveform?

Occlusion of the catheter, stopcock, or fluid line

Small patient

Air bubble of leak in the system


What are the possible causes of a lack of CVP on the monitor?

Monitor settings are incorrect

Transducer not zeroed

Transducer cable is broken


What are the possible causes of a higher than expected CVP reading?

Elevated intra-thoracic or intra-abdominal pressure

Catheter is clamped or occluded

Transducer below the right atrium

Defective transducer


What are the possible causes of a lower than expected CVP reading?

Transducer is above the right atrium

Defective transducer


What are the possible causes of a "noisy" CVP waveform?

Patient movement


Catheter tip within the heart



What are the possible causes of a sudden change in CVP?

Hemodynamic instability

Transducer position relative to zero reference point has changed


complications associated with under-resuscitation during shock?

organ dysfunction, prolonged O2 deprivation


complications assoc with over-resuscitation during shock?

abdominal compartment syndrome, pulmonary edema, dilutional coagulopathy, exacerbation of cerebral edema, ARDS


research has shown microcirculatory hypoperfusion in what % of severely injured human patients despite normalization of traditional perfusion parameters (HR, MAP, UOP)



untreated compensatory shock and occult shock are assoc with what in critically ill humans?

MODS, increased morbidity/mortality


list the theoretical pathogeneses for occult hypoperfusion related MODS

direct damage from ischemia, reperfusion injury, overwhelming SIRS, compensatory anti-inflammatory response syndrome (CARS), irreversible cellular dysfunction; ischemia activates endothelial adhesion molecules, platelet activating factor, coagulation system (causes breakdown of glycocalyx and increased vascular permeability)


Why/how can hypoxia lead to cell swelling, apoptosis or necrosis?

it interferes with ATP dependent processes such as active electrolyte pumping; causes cessation of cellular metabolilsm


what is the result of increased leukocyte adhesion to endothelium and release of cytokines and ROS in response to overwhelming inflammation

increased chemotaxis, endothelial damage, vascular permeability


what % of the total circulating volume do the venous capacitance vessels make up

75% normally


how is the venous system adversely affected during SIRS

can became less able to constrict in response to sympathetic signalling


what is the appropriate physiologic response to shock (re: the sympathetic nervous system)

first, B adrenergic stimulation enhances CO, oxygen delivery, chronotropy, inotropy
then alpha receptors cause vasoconstriction which shunts blood to vital organs


besides regional hypoxia, what other adverse effects can damage the microcirculation?

TNFalpha, endothelial swelling, alterations in NO, interstitial edema, increased RBC aggregation/adhesiveness, increased blood viscocity, activated platelets causing capillary obstruction


list SIRS diseases that can affect microcirculation

polytrauma, necrotizing pancreatiis, hemorrhagic shock, heat stroke, IMHA, ITP, MUE, HGE, neoplasia, ARDS, hepatic lipidosis


list diseases that can cause severe sepsis and affect microcirculation

peritonitis, pyothorax, pneumonia, pyometra, urosepsis, GI translocation, parvo, endocarditis, hepatic abscess


list diseases that cause ischemia-reperfusion injury which affects the microcirculation

GDV, aortic thrombus, PTE, reexpansion pulmonary injury, post CPR


list causes of anaphylaxis, which can affect microcirculation

bee envenomation, antivenin, drug rxn, transfusion rxn, insects, vaccine rxn


what is the "no reflow" phenomenon

nonfunctional microcirculatory bed despite resuscitation efforts


list upstream hemodynamic parameters



list downstream hemodynamic parameters

UOP, blood lactate, lactate clearance, BD, VO2, O2ER, NIRS, O2/CO2 tissue monitoring


is downstream or upstream more sensitive for detecting underlying physiologic disturbances?



in what types of conditions is lactate produced

under anaerobic conditions when pyruvate isn't used for oxidative phosphorylation


what enzyme converts pyruvate-->lactate

lactate dehydrogenase


t/f- lactate dehydrogenase is present in all tissues except brain?

false; all tissues


why does lactate result in acidosis?

lactate production results in hydrogen ion production from ATP hydrolysis and reduction of NAD->NADH


in what type of cell is pyruvate normally converted to lactate?



what 3 organs receive lactate in order to be oxidized, transaminated or converted back to pyruvate?

heart, kidneys, liver


what might help differentiate type A from type B hyperlactatemia

lactate to pyruvate ratio


mechanism of hyperlactatemia in states of increased glycolysis?

glycolysis occurs faster than pyruvate oxidation-->excessive pyruvate-->more lactate


what things stimulate glycolysis?

dextrose infusion, alkalosis, sepsis, endogenous or exogenous catecholamines


possible pathophys of hyperlactatemia in sepsis?

decreased DO2, microcirculatory shunting, exotoxin mediated impairment of pyruvate dehydrogenase, mitochond dysfunction, hypermetabolism from inflammation, hepatic dysfunction


in what way may increased lactate may be adaptive/protective? in what organs specifically?

heart/brain- may preserve glucose for energy production in O2 poor tissues