Hemodynamic normals + waveforms PPT (2/30)

CVP and its fxn (2)

Central venous pressure: 0-6mmHg

1. Determines volume status + RV fxn

2. Correlates w/ RV end diastolic pressure

What to remember about wedges?

WEDGE = LEFT!!

Problems with wedge pressure only happens with the LH.

RVP and its fxn (1)

right ventricular pressure: 20-30 / 0-5mmHg

Determines RV volume + fxn

PAP and its fxn (2)

pulmonary artery pressure: 20-30 / 6-15mHg

Determines pulmonary vascular state of resistance + RV fxn

What happens in pulmonary hypertension? Two examples of what can cause it?

When PAP values increased.

1. insufficient RV → blood backs up into pulmonary space

2. LH is not pumping blood out, which could have blood backup into the lungs.

PAWP and its fxn (2)

pulmonary artery wedge pressure: 4-12mmHg

1. Determines LV fxn

2. Correlates w/ LV end diastolic pressure, being the moment right before it squeezes (systole)

normal SV value, what it measures, and what a decreased SV means?

stroke volume: 60-130mL/beat

1. amount of blood ejected during systole

2. Decreased SV = ventricular dysfxn

CO and its fxn (2)

Cardiac output: 4-8L/min

1. describes BF through tissue

2. Reflects adequacy of overall cardiac fxn

SVI and CI normal values and its fxn (1)

Stroke volume index: 30-50mL/beat/m2
Cardiac index: 2.5-5L/min/m2

These are values that are normalized to pt’s BSA.

PVR

pulmonary vascular resistance: 110-250dynes/sec/cm5

1. State of resistance in pulmonary vasculature (just like Raw)

What does dynes/sec/cm5 refer to

Units takes in account for all the different diameters of vasculature.

SVR and its fxn (1)

systemic vascular resistance: 900-1400dynes/sec/cm5

1. state of resistance in systemic vasculature (refers back to long vs short straw: distance affects resistance. Ex. includes blood from aorta → big toe = more resistance; whereas, aorta → fingers has less resistance).

SvO2 and its fxn (2)

mixed venous O2 saturation: 60-75%

1. Index of O2 status measuring relationship b/w O2 delivery + demand, being the leftover O2 that remains in the blood

2. reflects CV tissue perfusion

Arterial pressure waveform normal

Clear upstroke on left + a dicrotic notch (due to aortic valve closure) on the downstroke.

Arterial pressure waveforms in regards to variability

Normal breathing shouldn’t cause any visible variability in the waveform; however, if it is seen w/ spontaneous breathing, cardiac tamponade may be present.

Normal arterial pressures and what is considered hyper/otensive?

Normal = 120/80mmHg, increased w/ age

hypertension = 160/90, occurring w/ vasoconstriction, increase

Hypotension = 90/60, occurring w/ hypovolemia, cardiac failure and vasodilation (shock)

Normal and low MAP values

normal = 80 - 100mmHg, representing average pressure pushing blood through systemic system

Low = <60mmHg, leading to compromised vital organ fxn (decreased BF to organs)

Should CVP waveform change during spontaneous inspiration? What causes it to increased? When does it decrease naturally?

Yes! CVP normally demonstrates pressure changes induced by spont inspiration. If changes are not seen, waveform is inaccurate, as the CVP should DECREASE (inhalation = - pressure = decreased CVP) and increase w/ mech ventilation breaths (+ pressure ventilation = increased CVP).

What does CVP reflect?

Reflects balance b/w ability of RV to pump blood out of RA and RV + amount of venous return.

What can cause CVP to decrease? (2)

Increased RH pumping and decreased venous return will DECREASE CVP

1. vasodilation

2. hypovolemia

What can cause CVP to increase? (5)

RHF + increased venous return will INCREASE CVP.

1. volume overload (accidental IV left open)

2. pulmonary hypertension

3. cor pulmonale

4. tricuspid or pulmonary valvular stenosis (stiff)

5. pulmonary embolism

PA systolic pressures normals and what causes it to elevate and decrease?

Normal = 20-30mmHg

Elevate = high pulmonary vascular resistance, when CO is high

Decrease = pulmonary vasodilaiton

Normal PA diastolic pressures and its fxn

Normal = 8-15mmHg

Fxn: reflects LV end-diastolic pressure in healthy patients

What disease process does an increased PADP-PCWP gradient signify? What value associates with it? What can it not be treated with?

ARDS! a gradient >5 is common w/ ARDS and a high PVR.

CANNOT be treated /w diuretics, just don’t hurt lungs more!

Normal PCWP

4-12mmHg

Most common cause of increased PCWP? decreased PCWP?

Increased: Left ventricular failure

Decreased: hypovolemia

Hypovolemia: CVP, PAP, PCWP

All low

Tricuspid and pulmonic valve stenosis: CVP, PAP, PCWP

CVP: high

PAP: normal/low

PCWP: normal

cor pulmonale, pulmonary hypertension, ARDS, pulmonary emboli: CVP, PAP, PCWP

CVP: high

PAP: high

PCWP: normal

LV failure, mitral and aortic valve stenosis, and hypervolemia: CVP, PAP, PCWP

CVP: high

PAP: high

PCWP: high

Preload, after load and SV definitions

Preload = how much heart STRETCHES to fill @ end diastole just before contraction.

Afterload = pressure/RESISTANCE heart overcomes to move blood during systole

SV = amount of blood pumped by one ventricle in a single heartbeat.