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N506 Health Assessment > Hemodynamic monitoring > Flashcards

Hemodynamic monitoring Flashcards

0
Q

How can oxygenation, ventilation, circulation, and temperature specifically be monitored?

A

Oxygenation: mental changes, fail safe, spo2, skin, ABGs
Ventilation: EtCO2, pressure alarms, chest rise, work of breathing, auscultation
Circulation: HR, pulse, color, BP, auscultation
Temp: touch, temp probe

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1
Q

What is the purpose of hemodynamic monitoring?

A 
Assess homeostasis and trends
Observe for adverse reactions
Assess therapeutic interventions
Manage anesthetic depth
Evaluate equipment function
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2
Q

What monitors are required to be used by the AANA?

A

EKG (HR and rhythm), BP, precordial stethoscope, pulse ox, oxygen analyzer, EtCO2
Graphic Display of: EKG, BP, HR, Ventilation status, oxygen sats

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3
Q

What are the 5 audible alarms?

A

HR, BP, pulse ox, O2 analyzer, airway pressures

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4
Q

Where are esophageal stethoscopes placed?

A

Only used in intubated patients, placed 28-30 cm into the esophagus

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5
Q

What is monitored in a 3 lead ECG and 5 lead ECG?

A

3 lead: Leads I, II, III, 3 views of the heart (no anterior) you can see inferior, posterior, and lateral
5 lead: Leads I, II, III, aVR, aVL, aVF, V lead, 7 views of the heart, septum and anterior view included
V4-V5 are best for ischemia detection

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6
Q

How should gain and filtering bandwidth/capacity be set on the EKG?

A

Gain should be set to a standard: 1 mV produces 10 mm calibration pulse (this is in order to assess amplitude of ST segment change)
Filtering capacity should be set to “diagnostic mode”, this mode doesn’t filter out any artifact (“monitor mode” may be useful if there is cautery or other continuous vibrations to filter out the artifact)

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7
Q

What are 5 principle indicators of acute ischemia?

A 
ST elevation >1mm
T wave inversion
Q waves
ST depression, flat or downslope of >1mm
Peaked T waves
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8
Q

What leads will you see changes in for inferior (&posterior) wall ischemia (RCA)? Lateral wall ischemia (circumflex of LCA)? Anterior wall ischemia (LCA)? Anterioseptal ischemia (LAD)?

A

Posterior/Inferior: lead II, III, AVF
Lateral wall: lead I, AVL, V5-V6
Anterior wall: lead I, AVL, V1-V4
Anteriorseptal ischemia: lead V1-V4

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9
Q

Systolic vs. Diastolic BP: what is the difference and which is supply/demand?

A

Systolic BP is the peak pressure during systolic ventricular contraction, changes in SBP correlate with changes in myocardial O2 requirements
Diastolic BP is the pressure during diastolic ventricular relaxation, it reflects coronary perfusion pressure
SBP is demand on the heart, DBP is supply of the heart

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10
Q

MAP equation using SBP and DBP

A

MAP = [SBP + 2(DBP)] / 3

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11
Q

How does oscillometry (automated cuff) work in measuring BP?

A

Senses oscillations/fluctuations in cuff pressure while deflating the BP, 1st oscillation is SBP, peak oscillation occurs at MAP, oscillations cease at DBP

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12
Q

What is the proper length and width of a blood pressure cuff?

A

Width 40% of the circumference of the extremity (Think”WD40”)
Bladder length should encircle 80% of the extremity

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13
Q

What causes a false high vs. false low BP?

A

False high: cuff too small, cuff too loose, extremity below heart, arterial stiffness (HTN, PVD)
False low: cuff too large, extremity above heart, poor tissue perfusion, deflating the cuff too quick
Either high/low: improper cuff placement, dysrhythmias, tremors/shivering

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14
Q

Complications of NIBP?

A

Edema, petechiae/bruising, ulnar neuropathy, interference of IV flow, altered timing of IV drug administration, pain, compartment syndrome

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15
Q

What are indications for IABP?

A

Elective deliberate hypotension, wide swings in intra-op BP, risk of rapid BP changes, rapid fluid shifts, titrate vasoactive drugs, end organ disease, repeated blood sampling, failure of non-invasive BP measurement

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16
Q

What measures can be taken to improve accuracy when the IABP is hooked up to the transducer?

A

Minimize tube length, limit stop cocks, no air bubbles, mass of fluid is small, use non compliant stiff tubing, calibrate at level of heart, continuous flush 1-3 ml/hr of NS to prevent thrombus formation

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17
Q

Where is the IABP transducer leveled at when the patient is supine? Sitting?

A

Supine: mid axillary line
Sitting: level of ear (circle of willis)

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18
Q

In arterial-line waveforms.. What does the rate of upstroke show? Rate of downstroke? Variations in size with respirations? Dicrotic notch?

A

Rate of upstroke: contractility
Rate of downstroke: SVR (the end of the downstroke is end diastolic pressure)
Exaggerated variations in size with respirations: hypovolemia
Dicrotic notch: closure of aortic valve
(area under the curve is MAP)

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19
Q

What happens to the IABP waveform with distal pulse amplification (when IABP is taken more distal)?

A

SBP peak increases, DBP wave decreases (so pulse pressure widens), MAP not altered
Dicrotic notch becomes less and appears later

20
Q

IABP complications?

A

Nerve damage, hemorrhage, hematoma, infection, thrombosis, air embolus, skin necrosis, loss of digits, vasospasm, arterial aneurysm, retained guide-wire

21
Q

CVC indications?

A

Measuring R heart filing pressures, assess fluid status/blood volume, rapid administration of fluids, administration of vasoactive drugs, removal of air embolus, insertion of transvenous pacing leads, vascular access, sample central venous blood, PA catheters

22
Q

What are possible insertion sites for CVCs?

A

Internal/external jugular veins (careful for carotid), subclavian veins (lower infection rates), femoral veins

23
Q

Where does the tip of the CVC go?

A

Within the SVC just above the junction of the vena cava and the RA, parallel to vessel walls, positioned below the inferior border of the clavicle and above the level of the 3rd rib, the T4/T5 interspace, the carina, or takeoff right main bronchus

24
Q

Contraindications of placing a CVC?

A

R atrial tumor, infection at site, contralateral pneumo for IJ

25
Q

Risks/complications of placing a CVC (usually due to poor technique)?

A

Air/thromboembolism, dysrhythmia, hematoma, carotid puncture, pneumo/hemothorax, vascular damage, cardiac tamponade, infection, guidewire embolism

26
Q

What can cause a high CVP?

A

hypervolemia, PEEP, CHF, tension pneumothorax

27
Q

What is the CVP measuring? At what point is the most accurate reading, inspiration/expiration?

A

RAP, RV preload
1-7 mmHg is normal
Most accurate at end-expiration

28
Q

What are the 5 phasic events of the CVP waveform?

A

3 peaks: a, c, v

2 descends: x, y

29
Q

What does happens during the “a” wave of CVP?

A

The peak of the “a” wave coincides with the “atrial kick” which causes the point of maximal filling of the RV, this value is RVEDP.
The “a” wave is due to contraction of the RA which results in increased pressure in the atrium (since there is no pressure difference between the vena cava and the atrium)

30
Q

Why would someone have a big “a” wave? Why would there be no “a” wave?

A

Giant “a” wave: tricuspid stenosis, pulmonic stenosis, pulmonary hypotension
Loss of “a” wave: A fib

31
Q

What happens during the “c” wave of the CVP?

A

“c” wave is due to RV contraction (tricuspid valve closure) and isovolemic ventricular contraction, results in the tricuspid valve “bulging” back into the atrium
Occurs in early systole, right after QRS

32
Q

What happens during the “x” descent of the CVP?

A

Atrial pressure continues to decline during ventricular contraction due to atrial relaxation
Mid-systolic event
Systolic collapse in atrial pressure

33
Q

What happens during the “v” wave of the CVP?

A

Reflects venous return against a closed tricuspid valve (which encompasses a portion of RV systole)
Occurs during filling of the atrium, in late systole with the tricuspid still closed after the T-wave on EKG
A large “v” wave will occur with regurgitation

34
Q

What happens during the “y” descent of the CVP?

A

After ventricular relaxation, the tricuspid valve opens due to the venous pressure and blood flows from the atrium into the ventricle
The y descent is the fall in atrial pressure following the opening of the tricuspid valve
“diastolic collapse in atrial pressure”

35
Q

What does the PA catheter assess?

A

Left side of the heart! Intracardiac pressures (CVP, PAP, PCWP), LV filling pressures, LV function, CO, mixed venous oxygen sats, PVR and SVR
Also, there are pacing options with a PA catheter

36
Q

Size of Central line vs. PA cath?

A

Central line: 7 french, 20 cm length

PA cath: 7/9 french, 110 cm marked at 10 cm intervals, 4 lumens

37
Q

What is going on at all four lumens of the PA catheter?

A

Distal port: PAP
Second port: 30 cm more proximal CVP
Third: lumen balloon
Fourth: wires for temp thermistor

38
Q

PAP monitoring indications?

A

LV dysfunction, valvular disease, pulmonary hypertension, CAD, ARDS, respiratory failure, shock/sepsis, ARF, surgery (cardiac, aortic, OB)

39
Q

PA catheter complications?

A

*Arrhythmias (V-fib, RBBB, complete heart block), catheter knotting, balloon rupture, thromboembolism, air embolism, pneumothorax, pulmonary infarction, *PA rupture, infection (endocarditis), damage to cardiac structures (valves)

40
Q

What is the pressure reading when the PA catheter is in the RA, RV, PA, PAWP?

A

RA wave from 3-6 (CVP)
RV wave from 0 to 25 (looks like Vtach)
PA wave from 10-25
PAWP wave from 8-12 (looks like CVP wave, shows LVEDP)

41
Q

What is the distance from the R IJ to these structures… Vena cava and RA junction? RA? RV? PA? Wedge?

A 
Vena cava and RA junction: 15 cm
RA: 15-25 cm
RV 25-35 cm
PA 35-45 cm
Wedge: 40-50 cm
42
Q

What happens during the “a” wave of the PAP?

A

Contraction of the L atrium

It is normally a small deflection unless there is resistance into the LV as in mitral stenosis

43
Q

What happens during the “c” wave of the PAP?

A

The “c” wave is due to rapid rise in the LV pressure in early systole, causing the mitral valve to bulge backward into the LA, so that atrial pressure increases momentarily

44
Q

What happens in the “v” waveform in the PAP?

A

The “v” wave is produced when blood enters the LA during late systole
Prominent “v” wave reflects mitral insufficiency causing large amounts of blood to reflux into the LA during systole

45
Q

What are factors that can distort CVP and PAOP waveforms? Specifically- Loss of “a” waves, giant “a” waves, large “v” waves

A

Loss of “a” waves: a fib, ventricular pacing
Giant “a”waves: junctional rhythms, complete HB, mitral stenosis, diastolic dysfunction, myocardial ischemia, ventricular hypertrophy
Large “v” waves: mitral regurgitation, acute increase in intravascular volume

46
Q

What 7 cardiac parameters are viewed in a transesophageal echocardiography?

A

Ventricular wall characteristics and motion/thickness, valve structure and function, estimation of end-diastolic and end-systolic pressures and volumes, CO, blood flow characteristics, intracardiac air, intracardiac masses

47
Q

What are uses for Transesophageal echocardiography?

A

Unusual causes of acute hypotension, pericardial tamponade, pulmonary embolism, aortic dissection, myocardial ischemia, valvular dysfunction

48
Q

Complications of Transesophageal Echocardiography? (most complications in awake patients)

A

Esophageal trauma
Dysrhythmias
Hoarseness
Dysphagia

N506 Health Assessment (7 decks)

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