N400 Exam 1

ABG, CV physio, ADHF, ACS, Pulmonary

PaCO2

arterial CO2 that is correlated with ventilation

direct reflection of effectiveness of alveolar ventilation

reflects pulmonary participation

considered an acid

normal= 35-45

venous CO2

correlates to arterial bicarbonate (BMP)

does age affect your interpretation of ABGs

no; however age is a factor in interpreting oxygenation values

gerontologic A-B balance risk factors

multi-morbidities

polypharmacy

limited kidney/pulmonary function (compensation)

functional limitations

visual changes (med mistakes, falls)

pH

measurement of free H+ concentration in blood

normal 7.35-7.45

potentially fatal values= 6.8 or 7.8

HCO3

reflects renal participation

reflects the bicarbonate/ base level

normal = 22-26

base excess

reflects balance between all metabolic acids and bases

normal = ± 2

PaO2

reflects O2 immediately available to tissue

indicator of lung parenchymal function= diffusions across alveolar-capillary membrane

affected by paCO2, temp, and pH

normal= age dependent (100-# yrs over 40)

acceptable= 60-100

if on O2, expected= 5x FiO2

compensatory mechanisms

buffer system (may produce electrolyte imbalances; bicarb, phosphate, protein, hgb)

pulmonary system (acts within minutes; eliminates or retains CO2)

renal system (takes 24-48 hrs; eliminates or retains HCO3, eliminates acid; uses electrolytes to shift pH; handles acidosis fairly well but alkalosis is tolerated poorly)

causes of respiratory acidosis

obstructive pulmonary disease

oversedation

metabolic alkalosis

neurotrauma or dx

anesthesia

neuromuscular disorders

inadequate mechanical ventilation

pickwickian syndrome (obesity)

splinting

pneumothorax

flail chest

s/s of resp acidosis

tachypnea→ resp depression

tachydysrhythmias

HTN

lethargy, coma

muscle weakness

resp acidosis interventions

optimize ventilation (positioning, pain relief, correct oversedation, secretion removal, deep breathing, remove depressive factors/alkalosis)

inc rate or tidal volume if on mechanical ventilator

causes of resp alkalosis

hypoxia

early resp, insufficiency

PE, pneumonia, ARDS, PF

asthma

mechanical ventilation

CHF

anxiety, stress

pain, fever

metabolic acidosis

septicemia

brain injury

ASA

hepatic insufficiency

thyrotoxicosis

s/s of resp alkalosis

hyperventilation

light headedness

neuromuscular irritability

tetany, spasms, seizures

paresthesia

dysrhythmias

resp alkalosis interventions

tx underlying cause

mech vent: dec rate or tidal volume to inc CO2 retention

metabolic acidosis causes

anion gap acidosis (accumulation of acids)

non-anion gap acidosis (loss of bases)

anion gap acidosis causes

lactic acidosis

DKA

starvation ketoacidosis

alcoholic ketoacidosis

Renal failure

hyperkalemia

salicylate, ethylene glycol, methyl alcohol poisoning

shock

non-anion gap acidosis causes

diarrhea

pancreatic or duodenal fistula

ileostomy

hyperchloridemia

normal anion gap

8-16

s/s of metabolic acidosis

hyperventilation (compensation)

lethargy, drowsy, stupor, coma

dysrhythmias

muscle weakness

hyperkalemia (result of compensatory mechanisms)

metabolic acidosis interventions

tx cause

sodium bicarbonate or lactate

watch for hyperkalemia with tx

metabolic alkalosis causes

loss of acids: NG suction/vomiting, diuretics, hypokalemia, rapid correction of hypercapnia, excessive alkali intake, cushings disease, corticosteroid therapy, hyperchloridemia, burns

accumulation of bases: antacids, lactate, sodium bicarbonate

s/s of metabolic alkalosis

neuromuscular irritiability

fidgety, twitching, tetany, spasms, seizures

paresthesias

confused, irritable

dysrhythmias

metabolic alkalosis interventions

KCl

ammonium chloride (rare)

Diamox

tx cause

paO2/FiO2 ratio

only for pts on mech vent

higher number means better parenchymal function

normal= >300

SaO2

reflects total quantity of O2 available

normal= >95% on RA; but 92% acceptable

hallmark of ARF

hypoxemia

paO2 <55-60 or < 65-75 if paCO2= 25-35

paO2 <40= life threatening

SaO2 <90%

causes of hypoxemia

inadequate lung ventilation (alveolar hypoventilation)

impaired O2 diffusion (v/q mismatch or shunt)

dec pulmonary circulation

dec levels of inspired o2 (altitude)

dec blood o2 levels (anemia, CO poisoning, methemoglobinemia)

s/s of hypoxemia

restlessness, agitation, confusion (DO NO SEDATE W/O r/o hypoxemia, hypoglycemia, urinary retention)

tachypnea

hyperventilation= resp alkalosis

use of accessory muscles, flaring, retractions

dysrhythmias

hypoxemia interventions

airway

lowest FiO2 possible

tx underlying problem

Cardiac cycle

ventricular diastole late

atrial systole

isovolumic contraction

ventricular systole first phase

ventricular systole 2nd phase

isovolumic diastole/ v early diastole

late diastole

ventricular filling, AV valves open, nothing is contracting, 70% of ventricular volume returns

atrial contraction/systole

last 1/3 of diastole- 20-30% of ventricular filling volume

ATRIAL KICK

P wave

isovolumetric contraction

ventricles rapidly inc in pressure > atrial pressure (AV valves close= S1)

all valves now closed

QRS complex

ventricular systole/ first phase

ventricular pressure has increased above resistance created by aortic valve and arterial system

ventricular ejection/systole/2nd phase

SL valves open, ventricular ejection

isovolumetric relaxation= vent diastole early

ventricular pressure decreases < aortic

SL valves close (S2)

atrial filling increases atrial pressure > ventricular pressure

AV valves open

T wave

most basic physiologic need to stay alive

oxygen delivery created by CO and arterial O2 content

SV

mls ejected per beat

normal= 60-90mL/beat

made up of preload, afterload, and contractility

CO

amount of blood ejected/ min

HR x SV

normal= 4-8L/min

PAC or special A line

CI

CO in relation to BSA

normal= 2.5-4.5 L/m/m2

PAC or special A line

DBP

circulating volume and arteriolar resistance during diastole

low DBP indicated arterial vasodilation

pulse pressure

created by SV

pressure of blood on vessel walls during each beat

norm= 20-40

low PP is associated with low SV

SBP

DBP + PP

arterial pressure resulting from ejection of blood during ventricular systole

MAP

actual perfusion pressure

(2x DBP) + SBP/3

avg driving force of blood into vessels that go to the tissues

preload

stretch created by vol in ventricles just before they contract (LVEDV/RVEDV)

THE MOST IMPORTANT FACTOR IN DETERMINING SV AND CO

direct measurement: RAP/CVP thru a CVC or LAP/PAOP thru a PAC

factors affecting preload

circulating blood vol

venous return

ventricular compliance and contractility (atrial kick, filling time, vascular tone, intrathoracic pressure such as in CPAP, mech vent, pregnancy)

central venous catheter (CVC)

inserted subclavian, IJ or femoral vein

RAP measurement and access for infusions and blood sampling

normal 5-10 mmHg

measure of RVEDP

also used for LVEDP is no pure RV failure d/t pulm HTN or RV infarct or early pure LV failure

pulmonary artery catheter (PAC)

inserted via subclavian, IJ or femoral vein into the RA, RV or pulmonary artery

PA pressures and CO measurements and access for blood sampling (mixed venous blood)

measures: PAS, PAD, RAP, PAOP

use has dramatically dec d/t poor risk/benefit ratio except in critically ill

normal PAS

20-30mmHg

normal PAD

8-15mmHg

normal PAOP

6-12mmHg

pulmonary capillary wedge pressure

most sensitive measure of LVEDP

if not available, PAD may be used

CVC or PAC

swan-ganz

balloon= wedging, never use more than 1.5 mL, do not inflate for more than 10 sec, stop if blood noted(red)

distal= PA , used for mixed venous, do not use for meds(yellow)

proximal= RA/CVP pressure, access to venous blood draw(blue)

thermistor (purple)= CO

VIP= fl, some meds

measures continuous CO

central line complications

electrical hazards, infection, pneumo/hydrothorax

hemorrhage= d/c, dislodgement, open stopcock

air embolism= low r sided intracardiac pressures< atmospheric air leading to air sucked in and occludes RV outflow track leading to circulatory collapse (TURN ON LEFT SIDE STAT, helps to prevent air from traveling to r side of heart into pulm arteries)

pulmonary embolism= thrombi, fragment, plaque

ventricular irritability= CVP too long, or PAC insertion or displacement

(Full barrier precautions during insertion, flat or trendelenburg during insertion or care, visible at all times, monitor breath sounds, and ECG)

PAC complications

displacement into RV or persistent wedge

balloon rupture

PA rupture

pulmonary infarction

catheter knotting

(KNOW WAVEFORMS)

low preload indicates

hypovolemia or dec venous return which leads to low SV and CO

tx with fl and/or vasopressors

high preload indicates

hypervolemia or dec ventricular compliance/contractility which leads to dec SV, CO and pulmonary congestion

tx with diuretics, vasodilators, fl removal via dialysis or ultrafiltration

assessing preload responsiveness

passive leg raise

stroke volume variation (SVV) or pulse pressure variation (PPV)

bedside echo, IVC ultrasound, esophageal doppler

passive leg raise

if BP goes up after a bolus given it means the pt would be responsive to tx; reversible inc in venous return of around 300 mL blood bolus that lasts 2-3 min

SVV or PPV

more than 13-15% drop in SV or PP during ventilation with positive pressure

need A line

predicts preload responsiveness

afterload

ventricular wall stress created by resistance against which the ventricles must pump

the force ejection must oppose (vascular resistance

THE MAJOR FACTOR AFFECTING MYOCARDIAL WORKLOAD AND MVO2 (myocardial oxygenation consumption)

factors affecting afterload

valve function

vascular tone (primary physiological factor): vascular health/condition, ANS (neurohormonal) stimulation, meds

direct measurement of afterload

Pulmonary vascular resistance (PVR)= RV

systemic vascular resistance (SVR)= LV

normal SVR

800-1400 dynes/sec/cm5

need A line and CVC or PAC

Arterial line

radial, attached to noncompliant tubing which is attached to a transducer which attaches to fl bag

measures oscillations in the artery to give BP

The waste collector prevents waste loss and iatrogenic anemia

measures: SBP, DBP, MAP

may be up to 10-15mmHg>cuff pressures

20 gauge

non dominant hand preferred (DO THE ALLEN TEST)

A line wave= QRS with corresponding a wave, dicrotic notch

map goal

>60-65

to maintain minimal perfusion of vital organs (needed for it but no guarantee of it)

A line complications

electrical hazards, infection

hemorrhage= d/c, dislodgement, open stopcock

peripheral limb ischemia= embolization, vasospasm

radial nerve palsy

low afterload indicates

vasodilation which leads to dec BP, blood flow and preload

tx w fl and vasopressors

high afterload indicates

vasoconstriction or valve stenosis which leads to inc myocardial workload

tx with vasodilators and aggravating factors

contractility

force of muscular contraction (inotropy)

affected by: preload, afterload, muscular ability (viable muscle mass, O2 supply/demand), myocardial metabolic state, neurohormonal influences)

direct measurement of contractility

ejection fraction (EF)= ratio of SV to end diastolic volume- % ejected

CO/CI

Stroke work index (SWI)= most sensitive

normal EF

57-73%

<50%= serious dysfunction

<35%= profound dysfunction

normal SWI

50-62g-m/m2

need a line and PAC, or CVP

thermodilution CO on PAC

thermistor in distal port of PAC monitor blood Temp

bolus of cold or room temp fl is injected into RA through the proximal port

computer calculates the change in temp and calculates flow rate

limitations: wide fluctuations in pt temp, PAC position, technique

CCO: pulse contour

from an A line

uses PP to estimate SV

uses that estimate and HR to calculate CO

interventions for low contractility

optimize preload and afterload

optimize O2, pH, lytes, coronary circulation

inotropes if necessary

mechanical assist device if needed to maintain life

causes of low contractility

preload is too high or too low

afterload is too high or too low

ventricular failure

low contractility results in

dec SV and CO

pulmonary congestion

Low CO/CI

evidenced by low BP, tachycardia, metabolic acidosis

dec SV

preload dec or inc too much

afterload inc or dec so much that preload is low

dec contractility

high CO/CI

evidenced by high BP, bounding pulses

tachycardia, inc SV

preload inc to a point

afterload dec to a point

contractility increased

critical closing pressure

point at which vessel collapses and flow stops

normal=20 mmHg

sympathetic stimulation= 60 mmHg

direct measurement of perfusion

tissue oxygenation (PAC/ special CVP)

serum lactate, ABGs (metabolic acidosis)

organ function

ensuring accuracy of hemodynamic monitoring

zeroing

leveling (fast flush square wave test)

pt positioning (releveling with changes)

zeroing

open transducer to air, then ‘zero’ the display system

calibrates the equipment to atmospheric pressure

BUT SYSTEM MUST BE LEVEL WITH THE HEART

ensures accuracy

leveling

the transducer air/fluid interface (stopcock) must be level with the heart (phlebostatic axis)

this eliminates effects of hydrostatic forces on the observed hemodynamic pressures

If it is below the LA it raises the pressure

if it is above the LA it it decreases the pressure

phlebostatic axis

level of LA

4th ICS and ½ AP diameter

mark chest with washable felt pen

Fast flush square wave test

tests the accuracy of the system to reproduce pressures

determines the ability of the transducer to correctly reflect pressures

perform at beginning of each shift and PRN

results: expected, dampened or underdampened

expected fast flush square wave test

1-2 oscillations within 0.12 seconds

dampened fast flush square wave test

no ringing- blunted

no oscillations below baseline

false low SBP and false high DBP

causes: large air bubbles in system, compliant tubing, loos or open connections, low fluid level in flush bag

underdampened fast flush square wave test

numerous oscillations above and below baseline

artificially spiked

false high SBP and false low DBP

causes: small air bubbles, tubing too long, defective transducer

regulation of cardiac performance and tissue perfusion

PNS (AcH to slow HR)

SNS (catecholamines to inc HR + adrenergic receptors alpha and beta)

RAAS (inc BP)

intrinsic regulation

alpha receptors

mediate smooth muscle contractions and VASOCONSTRICTION

mostly involved in stimulation of cells and constriction of blood vessels

beta receptors

mediate vasodilation, smooth muscle relaxation, bronchodilation, and excitatory cardiac function (faster and more forceful)

alpha 1 receptors

vasoconstriction

alpha 2 receptors

feedback/vasodilation

reduce sympathetic outflow to peripheral vessels

beta 1 receptors

inc HR, inc contractility

inc renin

vasoconstriction heart and bvs

most in pericardial area

beta 2 receptors

most in lungs

bronchodilation

intrinsic regulation

bodys protective mechanism of shunting blood to vital organs only during times of stress and low blood volume, etc. (brain, heart, lungs, kidneys)

IV vasopressors

NE (Levophed): alpha and beta

phenylephrine (Neosynephrine): alpha

dopamine: alpha and beta

IV vasodilators

nitroglycerin

nitroprusside