Hemodynamics Flashcards by Kelsey Klipfel

The flow of blood is ejected from the heart to circulate throughout the body in order to effectively oxygenate the tissues of the body
Blood flow
More cardiac cath lab side - look at valve areas and shunt sizes

Hemodynamics:

How well did you know this?

Not at all

Perfectly

Arterial pressures
Catheter that is inserted in an artery.
Continuous blood pressure measurement.

Intraarterial blood pressure monitoring (Arterial line)

How well did you know this?

Not at all

Perfectly

See lot with central venous catheter - get waveform and number from central vein
Have Swan-Ganz/PA catheter - translated to lower third of IVC/SVC
Catheter that is inserted in a vein – the distal tip of the catheter is in a central vein (superior or inferior vena cava)
Monitor alterations in fluid volume.

Central venous pressure monitoring (Central venous catheter)

How well did you know this?

Not at all

Perfectly

Fancy catheter
Have Introducer sheath in central vein - catheter put in - distal tip in PA
Multiple ports that do different things
Catheter that is inserted in a vein – the distal tip of the catheter is in the pulmonary artery.
Provide information about PA pressures (systolic, diastolic, mean), PAOP (Pulmonary Artery Occlusive Pressure), and CO. The location of the PA catheter provides access for measurement of mixed venous oxygen saturation.

Pulmonary Artery Catheter (PA catheter, Swan Ganz)

How well did you know this?

Not at all

Perfectly

What is the primary purpose of an arterial line?
The most common insertion sites are the radial artery (most common) and the femoral artery (coming out of procedure - usually accessed via this so just hook to continuous monitor).
What are patients with an arterial line most at risk for?

Intra-arterial BP monitoring

How well did you know this?

Not at all

Perfectly

Primary purpose: Continuous blood pressure
Will not infuse anything
May see with frequent ABGs
Can see continuous trends when giving meds that affect BP to see if getting better/worse or how long effect; transplant work up - put in PA catheter and start both dopamine and nitroprusside - see how long for PA to dilate out and then improve BP

What is the primary purpose of an arterial line?

How well did you know this?

Not at all

Perfectly

Allen’s test
Smaller arteries that supply distal arm and hand - ensure adequate flow - to provide arterial blood flow to hand
Occlude both radial and ulnar at the same time - palm blanch - release ulnar artery (since not getting catheter and see if supplies blood to whole hand - if only ½ turns pink, not enough flow to give adequate perfusion to whole hand: then think of other options
Can do popliteal - anywhere can get access

The most common insertion sites are the radial artery (most common) and the femoral artery (coming out of procedure - usually accessed via this so just hook to continuous monitor).

How well did you know this?

Not at all

Perfectly

Infection
Bleeding
Like big IV - 4 Fr - like 16/18 Gauge - not as flexible - if at a bend, need to keep area straight - make puncture site bigger and start bleeding

What are patients with an arterial line most at risk for?

How well did you know this?

Not at all

Perfectly

Once art line in - get nice waveform
Know what looks like - nice triangular up and down

Arterial pressure waveform interpretation

How well did you know this?

Not at all

Perfectly

Lot stuff
LV beating - ejection seeing
AO - aorta pressure - more defined than when in peripheral
↓ Arterial perfusion (pulse deficit)– PVC’s (less ejection), a. Fib (lose AV synchrony), tachyarrhythmias (filling time lower) - waveform less pronounced
↓LV function
Something wrong with LV
Pulsus alternans: later stages of CHF
Pulsus paradoxus: cardiac tamponade (gradual and monitor over time), pericardial effusion (gradual and monitor over time), or constrictive pericarditis (happens suddenly - fine until not)

What can affect the arterial waveform?

How well did you know this?

Not at all

Perfectly

When have an art line - make sure what seeing = accurate
Equipment is level
Abnormal - not something can fix easily
Squeezer or pigtail flushes it
A damped waveform can affect the arterial waveform.
The nurse must determine whether it is a patient problem or a problem with the equipment.

Dynamic response (AKA zeroing or square wave test)

How well did you know this?

Not at all

Perfectly

Seeing if it is optimal
Rarely see perfect waveforms
Optimal: when squeeze: get vertical line then level off (squared off); when let off, have refurb: oscillations (1-2)
Series of 1-2 oscillations
Oscillations 1-2 small boxes apart or < 0.8 sec
Fast flush
Square off
Look at how wide and how many oscillations are present after the square wave.

Optimal square wave test/dynamic response

How well did you know this?

Not at all

Perfectly

Squeeze and get vertical line, will square off; when let go, too many oscillations after - more than 2 and will be fatter
Care: systolic pressure not correct - overestimated; diastolic will be underestimated - still needs this and chronically underdamped - see order to just chart MAP because be accurate - cannot titrate meds based on diastolic underestimated but can on MAP
Characteristics
Causes
Corrective actions

Underdamped square wave test:

How well did you know this?

Not at all

Perfectly

Extra oscillations
More than 2 little boxes apart
Narrow, peaked tracing

Characteristics - Underdamped square wave test:

How well did you know this?

Not at all

Perfectly

Long catheter length
Increased vascular resistance
See if on lot vasopressors - clamped done; constricted over catheter
Hypothermia protocol
After codes

Causes - Underdamped square wave test:

How well did you know this?

Not at all

Perfectly

Remove excess tubing - lot catheter - take the length off
Insert dampening device or filter
Never take vasoactive drugs off
Not discontinue hypothermia protocol - just chart underdamped

Corrective actions - Underdamped square wave test:

How well did you know this?

Not at all

Perfectly

Still have when squeeze straight line going up = may be tilted; square off, then go down
Not as many/none oscillations/squiggles
MAP always same - systolic underestimated and diastolic overestimated
Characteristics
Causes
Corrective actions

Overdamped square wave test

How well did you know this?

Not at all

Perfectly

Slurred upstroke
Loss of oscillations

Characteristics - Overdamped square wave test

How well did you know this?

Not at all

Perfectly

Seen lot
Air bubble - at transducer or in tubing
Kink in the tubing
Overly compliant tubing - tubing on long enough, very stiff tubing, older tubing just not as compliant
Blood clots/fibrin - catheter in vessel - not flushing enough; esp after draw ABG
Check Stopcocks - stop cock not at perfect 90 - needs to be perfect
No fluid in flush bag - lot flushing; look up and nothing in there
Low flush bag pressure - as flush - bag not as big so need to pump it up

Causes - Overdamped square wave test

How well did you know this?

Not at all

Perfectly

Correct the issue
Clear air or blood
Straighten tubing

Corrective actions - Overdamped square wave test

How well did you know this?

Not at all

Perfectly

Veins - Lower pressures - if same as normal BP, something wrong with lungs or valve on that side
Can get lot patho by looking at lumps and bumps
Central Venous Catheter: An indwelling catheter inserted into a large, central vein
Definition: Pressure created by volume in the right side of the heart. When the tricuspid valve opens, the CVP reflects filling pressures in the right ventricle.
Normal CVP: 2 – 5 mm Hg
Purpose
Insertion sites

Central venous pressure monitoring

How well did you know this?

Not at all

Perfectly

Central line
In IJ/subclavian

Central Venous Catheter: An indwelling catheter inserted into a large, central vein - Central venous pressure monitoring

How well did you know this?

Not at all

Perfectly

Measure fluid status
Preload - indicator of this; use other assessment with it; good indicator; preload is volume status - in overload/dehydrated

Purpose - Central venous pressure monitoring

How well did you know this?

Not at all

Perfectly

Internal jugular - not get first or second time go to femoral vein
Subclavian
Femoral vein - higher risk for infection esp if incontinent; movement inhibited some

Insertion sites - Central venous pressure monitoring

How well did you know this?

Not at all

Perfectly

Not without risk during dressing change Air embolus Thrombus formation Infection Nursing management

Central venous catheter complications

Leave stopcock open - will suck in air Broken catheter - see before insert - protocol is to flush before insertion Drawing up meds and not seeing fluid level and seeing air in syringe

Causes: - Air embolus

Acute sudden onset of respiratory distress: suddenly drop O2 sats; anxious - not exchanging O2 at that level; big enough: code - complete resp collapse followed by cardiac collapse

Signs & symptoms: - Air embolus

1-3 <1 min 1st. Cover the sight with an occlusive dressing - stop from getting bigger - cover catheter; bigger air embolus - more acutely ill; transparent occlusive dressing 2nd. Put on 100% O2 - increase cannula if present then Nonrebreather - not stay stable long 3rd. Drop on head and turn on left side so not move from RV - eventually reabsorb - do not want to go into pulmonary vasculature 4th. Notify PCP

Priority intervention: - Air embolus

Same thing as peripheral IV hard to flush - can put low dose alteplase in it to help break it up Causes Signs & symptoms: Priority intervention:

Thrombus formation

Operator error Not flushing enough after giving medications/administering blood or blood products

Causes - Thrombus formation

IV pump always beeping that occluded on pt side Not attached to continuous IV infusion - effort to push med Draw blood out - not get pulled out; very sluggish if can get it to pull back

Signs & symptoms: - Thrombus formation

Prevention: flush; Protocol: up to 20mL Can give thrombolytics if not contraindicated

Priority intervention: - Thrombus formation

Redness at the site, or red streaks around the site. Swelling or warmth at the site. Yellow or green drainage. Pain or discomfort. Fever.

Signs & symptoms: - Infection

Single most crucial step a nurse can take to help prevent central line-associated bloodstream infections is performing proper hand hygiene. Other interventions focus on dressing management, bathing practices, access of intravenous infusion sets, blood draws, and management of port line occlusions Perform hand hygiene Apply appropriate skin antiseptic Ensure that the skin prep agent has completely dried before inserting the central line Remove a central line as soon as it is no longer needed

Priority intervention: - Infection

Volume assessment Central venous catheter removal

Nursing management

Physical assessment findings Preload: CVP - 2-5: number on screen: assess pt after seeing low/high number

Volume assessment

What is the optimal position for the patient to be in? Are in the bed - if complication cannot put on left side When do you pull the catheter (inhale or exhale)? Exhale/holding breath About intrathoracic pressure When inhaling - if tract - can suck air in threw that and get embolus Pulling out quick Prevents air embolus: exhale; occlusive dressing, stopcock closed Volume assessment: CVP Most common complications Air embolus Bleeding

Central venous catheter removal

Common Decreased fluid in vasculature

Signs and symptoms: - Bleeding

Right sided probs - CVP high and good stream coming out - someone who is bleeding - Hold firm pressure; occlude and let go until see oozing and add more pressure Holding pressure on veins/arteries not 100% occlussive because affecting blood flow - arterial - cold; venous - cause issues Put firm pressure

Priority intervention: - Bleeding

Hemodynamics = blood flow

Pulmonary Artery Pressure Monitoring (Hemodynamics)

Ultimately want to know CO CO = amount of blood pumped by each ventricle in one min; volume/min; product of SV (amount of blood pumped in one heartbeat) x HR Increase in SV or HR increases CO Ventricles do not eject all blood contain in one beat EF = 60% typical from body 100 mL usually in ventricles = end diastolic volume (EDV); at end of diastole/filling 40 mL left = end systolic volume (ESV) - at end of systole/contraction SV = EDV - ESV; dependent on contractility (force of contraction of heart muscle), preload (EDV - according to Frank-Starling mechanism - greater the stretch the greater the force of contraction), afterload (resistance ventricle must overcome to eject blood; includes: vascular pressure (pressure in LV - must be greater than systemic pressure for aortic valve to open; pressure in RV must exceed pulmonary pressure to open pulmonary valve) Damage to valves - presents higher resistance and HTN does as well - leads to lower blood output

CO determinants

Affects CO Elevated heart rate Slow heart rate Why is this important to know?

Decreases filling time and BP; arterial waveforms lower What contributes to an elevated heart rate? External stimuli Sympathetic nerve response Excitement Drug related How do we manipulate the heart rate? Taking away external stimuli Give medications - beta blockers, calcium channel blockers Most drugs not soley chronotropic - may be primary response to chronotropic to lower HR; but also other components but need to pick best option for it

Elevated heart rate

What contributes to a slow heart rate? damage to your heart due to aging or heart diseases (such as heart attack), cardiomyopathy or myocarditis. Hypothyroidism. a malfunction in the heart's sinus node, its natural pacemaker How do we manipulate the heart rate? Atropine - common Stable - dopamine - lot chronotropic effects - keep HR up Pacemaker

Slow heart rate

Contributes to CO

Why is this important to know?

Volume Fluid status Preload: Volume of blood in the ventricle at end-diastole What is left 2 numbers: PAOP and CVP Left Ventricle Preload Right Ventricle Preload Frank-Starling Law: Ejection fraction (EF): Low preload is associated with: How does a low preload affect the cardiac output? Assessment findings If preload is low what medications are given? High preload is associated with: How does a high preload affect blood pressure? Assessment findings If preload is high what medications are given?

Preload

Measured by pulmonary artery occlusive pressure (PAOP) Normal PAOP (pulmary artery occlusive pressure): 5- 12 mm Hg

Left Ventricle Preload

Measured by the central venous pressure (CVP) Normal CVP: 2 – 5 mm Hg

Right Ventricle Preload

Preload contributes to CO; affects stretch for it to recoil to eject - affects how dilated LV The more you stretch the muscle fiber in diastole, or the more volume in the ventricle, the stronger the next contraction will be in systole until a physiological limit has been reached In the heart, it is the ability to increase the force of contraction that converts an increase in venous return to an increase in stroke volume. Stroke volume must match venous return, or the heart will fail.

Frank-Starling Law:

The percentage of preload volume ejected from the left ventricle per beat. Normal: 50-70% Hyperdynamic EF (80-100%) - something fundamentally wrong with LV Not all of the preload volume is ejected

Ejection fraction (EF):

Lower Filling pressure, or less volume of blood at end-diastole

Low preload is associated with:

If do not have adequate filling pressures - CO will go down - translating to BP being lower Extreme dehydration or lot blood on ground - BP low - give volume - no vasopressors - nothing to squeeze

How does a low preload affect the cardiac output?

s&s dehydration Not perfusing organs - mainly kidneys (be first) - urine output first - not enough to filter to get adequate output; and have low BP; earlier part - on cusp being low - orthostatic hypotension ↓urine output, hypotension, orthostatic hypotension

Assessment findings

NS Fluids Losing blood: blood Need to fill tank with something Start with NS/LR - albumin - blood unless know frank blood - know blood prob RBC carries O2 to perfuse end organs

If preload is low what medications are given?

High Filling pressure, or more/too much volume of blood at end-diastole.

High preload is associated with:

BP high with high preload

How does a high preload affect blood pressure?

Right or left CHF sx depending on which chamber effected LV affected: left CHF sx; crackles bilaterally in lungs Tachypnea, Tachycardia, Cough, Bibasilar crackles, Gallop rhythms (S3 and S4), Increased pulmonary artery pressures, Hemoptysis, Cyanosis, Pulmonary edema, Fatigue, Dyspnea, Orthopnea, Paroxysmal nocturnal dyspnea, Nocturia RV affected: rt CHF sx; JVD extended Peripheral edema, Hepatomegaly, Splenomegaly, Hepatojugular reflux, Ascites, Jugular venous distention, Increased central venous pressure, Pulmonary hypertension, Weakness, Anorexia, Indigestion, Weight gain, Mental changes Volume overload

Assessment findings

Least invasive - prob intake Fluid restriction (IV and oral) - lot meds: double or quad strength so volume decreased; decrease fluid intake; volume intaking less Venous dilators: Nitroglycerine - dilates venous sys so more room for extra fluid to go; holds more since bigger Diuretics - get fluid off

If preload is high what medications are given?

Have bidirectional flow with an incompetent valve; measuring flow going back and forth in volume PAOP indirect measurement of LA - leftsided preload - looking at volume of blood in LV; incompetent valve - increase pressure in chamber before it

A patient with mitral regurgitation (MR) has an elevated PAOP. Why is the PAOP elevated?

Low

A patient presents to the ED with 4 days of vomiting and diarrhea. How does this impact preload?

High SOA - left sided Anasarca - right sided; any edema = right

A patient presents to the ED with shortness of air and anasarca. He states he has missed his last 3 dialysis appointments. How does this impact preload?

Decrease

A patient is on a nitroglycerine drip for chest pain. Will the preload increase or decrease?

Low Decreased Look for PAOP or CVP since fluid status

A patient is in the MSTICU post open cholecystectomy. Vital signs are BP: 92/20, HR: 90, RR 20, Spo2 98% on 40% FIO2, Temp 98.9˚F. He has a central line where Central Venous Pressure is monitored – CVP: 1 mm Hg. What is this patient's fluid status?

s&s agree: BP; HR little high Not enough O2 to organs - circulate more what have Increase HR - brain Decreased BP RR can increase

Are there any compensatory mechanisms present?

Urine output: low Hypotensive Echocardiogram: EF/CO: low Everything low

Expected assessment findings?

Look at left side with the PAOP - not just drop one in to look at left side Central line - get all right-sided pressures

If the patient has a PA catheter, what other measure could you look at?

Fluids Bleeding - Hgb dropped - give blood products Post-op: dry side since NPO - not enough to do this

How would you raise/lower the CVP?

Vascular tone - constricted or dilated Definition: The pressure the ventricle generates/has to generate to get the valve open to get the blood out; to overcome the resistance to ejection created by the arteries and arterioles. Is calculated/calculation – not a waveform Left Ventricle Afterload Right Ventricle Afterload High SVR Elevated SVR: Low SVR:

Afterload

Measurement of the resistance of blood flow through the systemic vasculature Measured as Systemic Vascular Resistance (SVR) The normal value is 800 to 1400 dynes-sec-cm−5 800 to 1400 dynes-sec-cm−5

Left Ventricle Afterload

All about pulmonary vasculature Measurement of the resistance of blood flow through the Pulmonary vasculature Measured as Pulmonary Vascular Resistance (PVR)

Right Ventricle Afterload

High afterload - arteries that are constricted All about resistance and what LV can overcome Normal, health heart Left ventricle dysfunction:

High SVR

SVR elevated - compensatory mechanism to get BP higher Not much impact of cardiac output May increase blood pressure

Normal, health heart

Decreased contractility (MI), global damage: cardiomyopathy, or regionally damage (MI) Something wrong with LV - Big MI/CHF - LV cannot work any harder to overcome increased resistance for someone who has increases SVR - BP decreases More effort Lowers cardiac output Lowers blood pressure

Left ventricle dysfunction:

Caused by too much arterial constriction - all about arteries Too clamped down/SVR too high - need consider if let ride since perfusing head leave, but maladaptive need treat it To lower SVR Continuous infusions of vasodilators Sodium nitroprusside/Nipride High-dose nitroglycerin - arterial; usually avoid since lot AE; liver metabolites issues; low-dose - impacts venous system

Elevated SVR:

Too dilated out - not any resistance from arteries - BP low Need fill extra space by giving volume Caused by too much arterial dilation. To increase SVR First give volume, then vasopressors Fluids (to fill the dilated vascular bed) - NS Once extravascular space filled then do arterial constrictors Vasoconstrictors: Norepinephrine - Increases MAP by vasoconstriction of the peripheral vasculature. Nursing considerations: Frequent assessment of the peripheral circulation is required when medications that increase SVR are used because excessive vasoconstriction will negatively affect tissue perfusion. Since actively restricting/intentionally squeezing - arteries small enough to where getting blue extremities - need to assess peripheral circulation

Low SVR:

Not a normal assessment Cool and clammy - dermis/skin not perfused as well; one cue arteries too constricted > 3 sec - another cue that arteries too constricted and not perfusing distally Something wrong with LV - LV not functioning well Acute event - body tries to compensate with comp mechanisms - but not lot thought - maladaptive - does not work Increased SVR

The nurse is assigned a patient who had a MI 2 days ago, he is cool and clammy. Capillary refill is > 3 seconds. What are these symptoms indicative of?

Decreased CO Came in with pneumonia - would be unchanged since nothing with heart unless sepsis

What is the effect on cardiac output? ↓ or ↑ or unchanged

Sodium nitroprusside High-dose Nitroglycerine

How should the afterload be manipulated?

SVR going to change - arterial dilator - lower SVR causing higher BP BP high PA pressure high CVP high CO normal SVR: high Ignore PVR

The nurse is caring for a client in the ICU. The hemodynamics for this client are: Arterial blood pressure 175/90 mm Hg; Pulmonary artery (PA) pressure: 48/18 mm Hg; Central venous pressure (CVP): 6 mm Hg; Cardiac output (CO): 2.3 L/min; Systemic vascular resistance (SVR): 1580 dynes-sec-cm−5; Pulmonary vascular resistance. If sodium nitroprusside is initiated, what hemodynamic value should change? Higher or lower? Why?

SVR - would not give - increase - vasoconstrictor

If norepinephrine is initiated, what hemodynamic value should change? Higher or lower? Why?

CVP - increase it; need something that messes with venous tone

If a fluid bolus is initiated, what hemodynamic value should change? Higher or lower? Why?

Sodium nitroprusside - arterial - messes with arteries; does not touch veins Biggest problem: address SVR If clamping down - need something to unclamp them first - so not cause more issues later on

Which medication(s) should be given to this patient?

SVR low

Too dilated

SVR high

Too constricted

Estimated by SV and PAOP or CVP. Definition: The force with which the heart muscle contracts. How well myocardium contracts Is calculated – not a waveform Left and right ventricular stroke work index values. These values estimate the force of ventricular contraction Possible causes of High Left & Right ventricular stroke work index (LVSWI & RVSWI) Possible causes of Low Left & Right ventricular stroke work index (LVSWI & RVSWI) Medications that increase contractility - increase work index - LVWSI Medications given to decrease contractility - LVWSI How does the nurse know if the patient’s contractility is responding to treatment? Summary

Contractility

How well myocardium contracts Is calculated – not a waveform

Definition: The force with which the heart muscle contracts.

Left ventricle: left ventricular stroke work index (LVSWI) Condition impacts: HF and MI Amount of work the left ventricle performs with each heartbeat. LVSWI: 50-62 g-m/m2 Right ventricle: right ventricular stroke work index (RVSWI) RVSWI: 7.9 – 9.7 g-m/m2

Left and right ventricular stroke work index values. These values estimate the force of ventricular contraction

Considering everything preload/afterload prob or CNS related Increased volume in the ventricle (↑ the stretch of the ventricle) Low systemic vascular resistance (contractility is augmented) CNS stimulation (exercise, fever, infection, pain, anxiety)

Possible causes of High Left & Right ventricular stroke work index (LVSWI & RVSWI)

Overdistended ventricle (Volume overload in the ventricle) - Overstretched it and some point not go back to normal size since so stretched out - overextended it High systemic vascular resistance (↑ resistance to ventricular ejection) Hypoxemia (negative inotropic effect) - adequate O2 for it to work; global effect; severely hypoxemic Decreased myocardial function (CHF, MI, cardiomyopathy) Electrolyte imbalance - K, Mg big ones

Possible causes of Low Left & Right ventricular stroke work index (LVSWI & RVSWI)

Dopamine Dobutamine Milrinone Some afterload reduction as well

Medications that increase contractility - increase work index - LVWSI

Beta blockers Propranolol Metoprolol

Medications given to decrease contractility - LVWSI

Giving drugs to affect contractility - + inotropes - increase BP - very few drugs that affect one of them Once start meds increase contractility - increase BP - get more ejection out so BP going higher Beta blockers to decrease contracility - BP go down - chronotropic effects on HR; but if elevated - primary purpose decrease contractility to decrease BP

How does the nurse know if the patient’s contractility is responding to treatment?

Contractility: The force with which the heart muscle contracts Factors that impact contractility Significant factors related to contractility that can be measured by the PA catheter Hypoxemia acts as a negative inotrope because the myocardium must have oxygen available to the cells to contract efficiently.

Summary

Preload volume as measured by PAOP - no stretch for recoil for elasticity SVR - not have it for pumping; makes it harder Myocardial oxygenation Amount of myocardium available to contract. Positive and negative inotropic medications Amount of functional myocardium available to contribute to contraction. Electrolyte balance

Factors that impact contractility

Preload filling pressures As volume in the ventricle rises, contractility increases. If the ventricle is overdistended with volume, contractility falls. SVR Change in resistance to ventricular ejection. If SVR is high, contractility is decreased. If SVR is low, contractility is augmented

Significant factors related to contractility that can be measured by the PA catheter

Low BP sx: dizziness, lethargy High HR: anxious (can feel it), diaphoretic CO - relates to low BP SVR: slow cap refill; skin cool and clammy because arterioles clamped down to nothing LVSWI sx: dizziness, lethargy

The nurse is caring for a patient in the CICU who is has a pulmonary artery (PA) catheter. Using the following hemodynamic values, determine what is going on with this patient.

High end of normal

Preload ↑, ↓, or normal?

SVR High

Afterload ↑, ↓, or normal?

Looking at LVSWI and RVSWI Decreased

Contractility ↑, ↓, or normal?

Try have adequate perfusion HR - high SVR for the BP

Any compensatory mechanisms?

MI and CHF all about LVSWI (low) Either end stage CHF or had big anterior wall MI

Possible causes?

Try decrease SVR so ailing LV can pump easily - give sodium nitroprusside for increased SVR Help CO - on cusp of being low - compensatory mechanisms in place - start milirinone, dopamine, doputamine to help LVSWI up to normal so perfusing If has doppled pulses, SVR - is vascular tone - if cannot palpate historically not having issue - dealing with dilation/constricting arteries - constricting in distal lens, need look at SVR

Anticipated treatment(s)?

LV preload

PAOP

LVSWI RVSWI

Contractility

Measuring afterload

SVR

Cardiac output measurement with a pulmonary artery catheter Definition: The amount of blood (Liters/minute) ejected from the ventricle in one minute. Measured 2 ways

CO measurement

In a healthy resting human adult, normal CO= 4 - 6 L/min; normal Cardiac Index (CI)= 2.2 - 4 L/min/m2

Definition: The amount of blood (Liters/minute) ejected from the ventricle in one minute.

Fick - variety of numbers - measuring/how get CO - beginning/end of cycle Thermodilution PA catheter - injecting cold saline so calculate CO - thermodiluation - thermisters and insert saline just above ring and measures temp and as passes thermistor does calculation and difference makes calculation for CO Specific quantity of cold fluid is injected into the proximal port Inject rapidly and smoothly Cold bolus passes thru RV then is ejected into the PA Computer plots the difference in blood temp and bolus temp on a time/temperature curve

Measured 2 ways

Endogenous catecholamines: Stress, exercise - compensatory response - more CO to supply O2 to the muscles Exogenous catecholamines: Epinephrine, isoprel (right heart work up; not respond to transplants; use to increase HR), dobutamine, dopamine, milrinone - medications; stress test - dopamine until HR response Positive inotropes: digitalis, amrinone Hyperthyroidism - systemic probs Anemia - systemic probs

What can cause increased CO?

Inadequate left ventricular filling. Inadequate left ventricular ejection. LV not func as well

What can cause decreased CO?

Decreased Decreased filling time Output is less

During a run of paroxysmal supraventricular tachycardia, the nurse would expect the CO to increase, remain unchanged, or decrease? Why:

Right sided valve issue Low Affecting preload to LV Stenotic valve - not as much blood ejected - leaflets stenosed and not opening as much so not as much blood to LV to have adequate preload

A patient is admitted for a tricuspid valve repair secondary to tricuspid stenosis. The nurse would expect the CO to be elevated or low? Why?

Same as with low BP Dizzy and lethargic Also have low EF; left sided prob - left HF prob; right sided - right HF prob Decreased CO and CHF s&s - same

What are the clinical manifestations of decreased CO?

decreased cardiac output (e.g., diminished peripheral pulses, hypotension) End organ perfusion - not circulating O2 blood adequately; end organs not getting oxygenated blood/perfused adequately CV: see if have extensive CAD, chest pain with exertion but as soon as sit down fine; left and right sided HF sx Neuro: Brain not perfused - start with dizziness, confusion, irritation Lose cortex first then into higher functions (then to ataxic) GU/GI: Bump in creatinine after urine output GU: perfusion to gut esp if underlying issues - constipation issues; mesenteric artery problems Pulm: Start seeing some ventilation probs - see more left-sided HF probs with crackles Renal: Kidneys easiest tell us Output decrease - drop first then creatinine Hepatic: Not go right to jaundice Labs and look at liver panels; ALT, AST

What assessment finding would indicate a decreased CO is affecting tissue prefusion?

Preload Goal of therapy: Fluids

CVP 1 mm Hg

Preload Left Goal of therapy: Bring it down High preload - need give fluid somewhere to give - nitroglycerin and diuretics - give somewhere to go then get rid of it

PAOP 22 mm Hg

Low Goal of therapy: Get up Look at other numbers and other assessment Everything contributes to CO See what causing it - preload, afterload, contractility

Cardiac Output 1.2 L/min

Preload High Right Goal of therapy: Decrease Fluid restriction Diuretics Nitroglycerin to dilate venous bed

CVP 12 mm Hg

Afterload Goal of therapy: Decrease Sodium nitroprosside - arterial dilator SVR - dealing with arteries

SVR 2000 dynes-sec-cm−5

Contractility Goal of therapy: Increase Positive inotropes: dopamine, dobutimanine, milrinone

LVSWI 38 g-m/m2

Definition and explanation Average perfusion pressure created by arterial BP during the cardiac cycle. The normal cardiac cycle is ⅓ systole and ⅔ diastole. These three components are divided by 3 to obtain the average perfusion pressure for the whole cardiac cycle Normal range 70-100mmHg

MAP

Definition and explanation Pressure created by volume in the right side of the heart. When the tricuspid valve is open, the CVP reflects filling pressures in the RV. clinically, the CVP is often used as a guide to overall fluid balance Normal range 2-5mmHg

CVP

Definition and explanation Pressure created by the volume in the left side of the heart. When the mitral valve is open, the PAOP reflects filling pressures in the pulmonary vasculature and pressures in the left side of the heart are transmitted back to the catheter “wedged” into a small pulmonary arteriole Normal range 5-12mmHg

PAOP

Definition and explanation Amount of blood pumped out by a ventricle over 1 min. Clinically, it can be measured using the thermodilution CO method, which calculates CO in L/min Normal range 4-6L/min (at rest)

Definition and explanation Mean pressure difference across the systemic vascular bed divided by blood flow. Clinically, SVR represents the resistance against which the LV must pump to eject its volume. Ths resistance is created by the systemc arteries and arterioles As SVR increases, CO falls. SVR is measured in Wood units or dyn times s times cm-5. If the number of Wood is multiplied by 80, value is converted to dyn times s times cm-5 Normal range 10-18 Wood units or 800-1400 dyn times s times cm-5

SVR

Definition and explanation Amount of work the LV performs with each heartbeat. The hemodynamic formula represents pressure generated (MAP) multiplied by volume pumped (SV). a conversion factor is used to change mL/mmHG to g-m. Always represented as an indexed volume; increases or decreases because of changes in the pressure (MAP) or volume pumped (SV) Normal range 50-62g-m/m2

LVSWI

Definition and explanation Amount of work the RVperforms with each heartbeat. The hemodynamic formula represents pressure generated (PAPm) multiplied by volume pumped (SV). a conversion factor is used to change mHG to g-m. Always represented as an indexed value (BSA chart). Similar to LCWI, RCWI increases or decreases because of changes in the pressure (PAPm) or volume pumped (SV) Normal range 7.9-9.7g-m/m2

RVSWI

Fancy Central venous catheter with multiple lumens and functions Long and variety of lumens Color coding always the same on all catheters Diagnosis and evaluation of cardiac dysfunction, cardiogenic shock, management during and after heart surgery, transplant work-up, measure valve areas AO - in ventricle - pulling back into aorta to see if systolic pressure stayed same; if dropped = incompetent aortic valve Right arterial (RA) pressure Pulmonary artery (PA) pressure Pulmonary artery occlusive pressure (PAOP) Cardiac output (CO) Indications Complications PA Catheter waveform interpretation

Pulmonary Artery (PA) Catheter

Measurement of CVP/preload

Right arterial (RA) pressure

Below 30 Like arterial pressure Where stays; colored yellow

Pulmonary artery (PA) pressure

Measurement is obtained after the balloon on the distal tip of the catheter is briefly inflated. Intermittent; when need it, inflate balloon at distal tip - get waveform; <10 sec - can cause pulm infarct; min amount of time as necessary Tell if incompetent valve Should not see RV - See this - pull blood out to see shunt - pull back on RA because put in tach arrhythmia; RV ignore - see go to tach arrhythmia

Pulmonary artery occlusive pressure (PAOP)

Measurement is obtained after injecting cold fluid the proximal port.

Cardiac output (CO)

Get information to make a diagnosis Work up heart transplants - dilate out PA and get normal pressures - decrease right sided - so not take out new heart Component of fluid volume status Dx for shunts and incompetent valves - regurgent/stenotic Observe response to therapies inotropes/vasodilators/vasoconstrictors

Indications

In the heart - more cardiac wise comps Cardiac complications Pulmonary complications Infection

Complications

Ventricular dysrhythmias Endocarditis - something in heart can go through it - through RV to PA Valvular damage - stenotic valve - hard go through so typ stop; can damage valves Cardiac rupture - aggressive enough - punch through RV (wall thin) Cardiac tamponade

Cardiac complications

Chest pain (angina) Dizziness. Pounding heartbeat (palpitations) Lightheadedness. Shortness of breath.

Ventricular dysrhythmias

Aching joints and muscles. Chest pain when you breathe. Fatigue. Flu-like symptoms, such as fever and chills. Night sweats. Shortness of breath. Swelling in the feet, legs or belly. A new or changed whooshing sound in the heart (murmur)

Endocarditis - something in heart can go through it - through RV to PA

dyspnea, chest pain, hypotension, cold extremities, and occasionally mental status changes

Cardiac rupture - aggressive enough - punch through RV (wall thin)

Anxiety, restlessness. Sharp chest pain that is felt in the neck, shoulder, back, or abdomen. Chest pain that gets worse with deep breathing or coughing. Problems breathing. Discomfort, sometimes relieved by sitting upright or leaning forward. Fainting, lightheadedness. Pale, gray, or blue skin.

Cardiac tamponade

Rupture of a PA - inflating balloon to get PAOP - not using syringe came with PA thrombosis, embolism or hemorrhage Infarction of a segment of lung.

Pulmonary complications

PA waveform Normal systolic pressure is 20 to 30 mm Hg and diastolic pressure is 10 mm Hg (20 -30)/10 mm Hg PA occlusion waveform (wedge) (left ventricle preload) Normal pressure is 5 to 12 mm Hg

PA Catheter waveform interpretation

Venous pressures - not have muscular wall - waveforms affected by intrathoracic pressure; all venous pressures not have perfect waveform - vary with inspiration and expiration; just make sure level Patient position The patient does not need to be flat for accurate pressure readings to be obtained. Respiratory variation Because patients remain on PEEP for treatment, they remain on it off during measurement of PA pressures. In this situation, the trend of PA readings is more important than one individual measurement.

PA catheter nursing management

All Pulmonary artery diastolic pressure (PADP) and PAOP (wedge) tracings are subject to respiratory interference. Positive-pressure, volume-cycled ventilator. Will push it up Vent valley During the positive-pressure inhalation phase, the increase in intrathoracic pressure may “push up” the PA tracing, producing an artificially high reading During inhalation with spontaneous breaths, negative intrathoracic pressure “pulls down” the waveform, producing an erroneously low measurement To minimize the impact of respiratory variation, the PADP is read at end-expiration On roller coaster with waveforms - need know where end-expiration is - that one waveform is where measure it

Respiratory variation

Measure pressures at end-expiration. Spontaneous respirations: Measure at the tip of the curve or “patient peak” Own respiratory effort - measure at the tip of the curve Intrathoracic pressure decreases during spontaneous inspiration Negative deflection on waveforms Intrathoracic pressure increases during spontaneous expiration Positive deflection on waveform Mechanical Ventilation: Measure at bottom of curve or “vent valley” Messing with intrathoracic pressure - translates to intrathoracic pressures - completely changes it - changing with inspiration and expiration - at valley Intrathoracic pressure increases during positive pressure ventilations (inspiration) Positive deflection on waveforms Intrathoracic pressures decrease during positive pressure expiration Negative deflection on waveforms

PA catheter waveform

Looks like roller coaster - watch go across screen and get pattern Take in breath - baseline goes down; exhale - goes back up; watch it - focus on diastole Where do you measure the PA pressure? Get top of the hump and bottom; report 30/10 Spontaneous Pick waveform at peak of waveform before trending down Get at the top before go back down Top one Ventilator with PEEP Always increased intrathoracic pressure - measure - right before goes up Not normal change in intrathoracic pressure - falsely elevating - + pressure throughout inspiration and expiration throughout breathing - lose normal rhythm of breathing Do: end expiration at pt peak but before go up Measure it right before puff air - one measure - end expiration - ventilator causing hump; goes up and gets wonky waveform; before go up Last one before end expiration when get hump Exhalation before starts trending up

PA pressure

Do not label Venous pressure Same intrathoracic variations Instead 1 pump, series of pumps When on vent - more bumps Vent valley Pt peak before trending down Intermittent measurement Not a continuous measurement. - cause infarct The balloon on the distal tip of the PA catheter is briefly inflated to get the PAOP measurement. Indirect measurement of the left atrial pressure (Preload).

Pulmonary artery occlusive pressure (PAOP)