ah2 exam 1

measures the amount of dissolved o2 in the plasma

pao2

what is normal pao2 and what is always horrible

80-100 but age dependent ; < 40

what is expected pao2

gauge of pulmonary function

what is fio2 × 5 formula

room air = 21% x 5 = expected pao2 ~105

types of supplemental oxygen

nasal cannula; nonrebreather mask; cpap / bi pap; endo-tracheal intubation

what is acid base balance for lungs

h20 + co2

what is acid base balance for kidneys

h + hco3

what is normal ph

7.35-7.45

what is normal co2

35-45

what is normal hco3

22-26

what is normal pao2

80-100

what is co2 an exchange of

o2 and exhalation

acid component of abg and respiratory component of abg

carbon dioxide

what happens when co2 increases

ph decreases and pt becomes acidotic

what happens when co2 decreases

ph increases and pt becomes alkalotic

what kind of relationship does co2 have w ph

reciprocal (one goes up, one goes down)

base component of abg and metabolic component of abg

bicarbonate (hco3)

how is bicarbonate (hco3) regulated

kidneys

what happens to ph when hco3 increases

it increases and pt becomes alkalotic

what happens to ph when hco3 decreases

it decreases and pt becomes acidotic

what is relationship between bicarbonate (hco3) and ph

same-directional

ph < 7.35 , co2 > 45

respiratory acidosis

what are causes of respiratory acidosis

copd and decreased respiratory rate (narcotics, od, coma)

ph > 7.45 , co2 < 35

respiratory alkalosis

what are causes of respiratory alkalosis

hyperventilating / anxiety ; pregnancy ; strenuous exercise

actions for respiratory alkalosis

sedation, paper bag breathing

actions for respiratory acidosis

improve ventilation

ph < 7.35 , hco3 < 22

metabolic acidosis

what are causes of metabolic acidosis

dka, burns, starvation, malnutrition, shock

what are actions for metabolic acidosis

treat underlying problem, increase bicarb

ph > 7.45, hco3 > 28

metabolic alkalosis

what are causes of metabolic alkalosis

severe vomiting, gastric sunctioning, excessive bicarb admin, excessive antacid use

what are actions for metabolic alkalosis

treat underlying problem, replace lost fluids

what is rome for ABG

Respiratory Opposite, Metabolic Equal

occurs when one component (respiratory or metabolic) adjusts to overcome primary disturbance

ABGs compensation

what happens to compensate for metabolic problems and occurs rapidly

lungs control co2

what happens to compensate for respiratory problems and occur slowly (24+ hours)

kidneys control hco3

ability to spontaneously initiate an impulse

automaticity

ability to respond to a stimulus

excitability

ability to transmit an impulse

conductivity

ability to contact after depolarization

contractility

cells at rest

polarized

cells stimulated by an impulse and causes muscle contraction

depolarized

the return to polarized state

repolarization

hr 60-100 ; impulse spreads through atria via internodal pathways

sa node - natural pacemaker

delay 0.08-0.12 seconds to allow for atrial depolarization ; back up pacer for SA node

impulse travels to AV node 40-60 BPM

what is cardiac conduction flow

sa node → av node → bundle of his → purkinje system

what does the stimulation of purkinje fibers cause

ventricular depolarization

shows rhythm: small electrodes applied to body, 6 on chest and 4 on extremities

12 lead

rhythm strips for ekg

telemetry monitoring

how long is ekg strip

6 seconds

how long is 1 big box of ekg

0.20 seconds

how long is 1 small box of ekg

0.04 seconds

generated by the SA node; electricity travels through atria; atrial depolaization

p wave

beginning og the p wave to the beginning of the QRS complex

pr interval

what does the pr interval show

heart block or conduction system disease

what is normal pr interval

0.12 seconds to 0.20 seconds

what is the pri formula

#of small boxes x 0.04

how is ventricular depolarization measured

beginning to end of QRS complex

what does a ventricular depolarization of less than 0.12 seconds mean

impulse was initiated from the SA / AV node

what does a ventricular depolarization of more than 0.12 seconds mean

impulse arises from ventricles

what does a prolonged conduction mean

wide QRS : bundle branch blocks

end of ventricular depolarization and beginning of ventricular repolarization

ST segment

what is evaluated in ST segment

shape and location

when is the ST element elevated

AMI, pre-infarction, and pericarditis

when is the ST element depressed

myocardial ischemia

repolarization of the ventricles

t wave

what can be seen following the T wave on a rare occasion

U wave

what does a U wave reflect

the repolarization of His-Purkinje fibers

represents the time necessary for ventricular depolarization and repolarization

q-t interval

what is the magic number for PRI

0.12-0.2

what is the magic number for QRS

0.08-0.12

what is the magic number for QTI

0.35-0.46

how do you determine rate

count beats in 6 second strip and multiply by 10

rapid atrial rate; no clearly defined p waves; irregular r to r intervals

a fib

what are causes of a fib

ischemia, heart disease, hyperthyroidism

what are actions for stable a fib

cardizem, digoxin, amiodarone

what are actions for unstable a fib

cardioversion

rapid atrial rate; individual p waves lost/sawtooth; v rhythm may be regular

a-flutter

what are actions for a flutter

iv adenosine to diagnose rhythm & calcium channel blocker or beta-blocker to slow HR

repeating wide uncoordinated spikes; heart is unable to pump effectively; HR > 100 bpm; no p waves; wide QRS complexes; +/- irregular rhythm

ventricular tachycardia

actions for stable ventricular tachycardia

lidocaine, amiodarone

actions for unstable ventricular tachycardia

shock

what to do when there is no pulse: ACLS for ventricular tachycardia

BLS plus epi shock and amiodarone shock

rapid unsynchronized pumping of the heart (quiver); no forward pumping of the blood: continuous undulating pattern without clear P waves, QRS waves, or T waves; irregular rhythm

ventricular fibrillation

what is ventricular fibrillation caused by

ischemic episode

action for ventricular fibrillation

defibrillation

what to do if pads are ready in ventricular fibrillation

shock first, then start CPR

movement of air in and out of the lungs

ventilation

what does ventilation require

patent airway and coordinated action of diaphragm and intra-costal muscles

cellular exchange of gasses at alveolar-capillary level

respiration

low content of oxygen in the blood

hypoxemia

not enough oxygen is reaching the body’s tissues

hypoxia

ventilation without perfusion

dead space

perfusion without ventilation

shunt

no ventilation or perfusion

silent unit

closure of collapse of alveoli

atelectasis

what causes atelectasis

increased secretions (mucous plugs), shallow respirations (immobility), impeded flow of air to area of lung

acute inflammation of lung parenchyma (caused by infectious agent) which leads to alveolar consolidation

pneumonia

what are cues for pneumonia

chest xr and blood / sputum cultures