CCRN- Respiratory Flashcards
ABGs table
ROME-
Respiratory Opposite pH/CO2 (carbon dioxide)
Metabolic Equal pH/HCO3 (bicarb, base)
Acidosis 7.35 < pH > 7.45 Alkalosis
Alkalosis 35 < Co2 > 45 Acidosis (control by lungs)
Acidosis 22 < HCO3 > 26 Alkalosis (control by kidneys)
- **If pH w/in range, it’s always compensated
- *If pH <7.35, it’s uncompensated acidosis (pt is blowing off CO2)
*when H+ concentration ↑, the pH ↓
Respiratory Acidosis causes
Drugs
cardiac arrest
muscles weakness (MG, ALS)
COPD (retain CO2)
Respiratory Alkalosis causes
Hypoxemia CNS disorders (b/c alkalosis ↓ ICP) Salicylate overdose Cirrhosis Sepsis
Metabolic Acidosis causes
Ketoacidosis Lactic acidosis (↓BP) GI Loss (diarrhea) Renal failure
Metabolic acidosis can be measured by anion gap:
–difference b/w positive and negative ions
–normal: 5-15 mEq/L
(Na+ + K+) - (Cl- + HCO3-)
Metabolic Alkalosis causes
Blood transfusions
»the sodium citrate in banked blood converts to bicarb in the liver
Hypokalemia GI Loss (gastric acid) Contraction alkalosis (too much lasix, fluid deficit)
Acute Respiratory Failure- Hypocapneic
↓O2 + normal CO2 or ↓CO2
Ventilation/perfusion imbalance
Causes: Pulm edema PE Aspiration PNA Asthma ARDS PNA (aerated tissue turns semi-solid and conducts noise well, fremitus present)
Presentation:
tachypneic, Accessory muscle use, tachy early, brady late, HTN or hypo, cyanosis, anxious, agitated
***V/Q mismatch:
happens when part of your lung receives oxygen without blood flow or blood flow without oxygen. This happens if you have an obstructed airway, such as when you’re choking, or if you have an obstructed blood vessel, such as a blood clot in your lung.
CPAP or BiPAP
Acute Respiratory Failure- Hypercapneic
↓O2 + ↑CO2
Respiratory mechanical performance, exhalation issue
Causes: Drug overdose (CNS depression) COPD CVA Spinal cord (ALS, GB, MG) ↑ ICP
Presentation:
shallow breathing, clear lungs or not, progressive ↓ LOC
BiPAP- FiO2 + IPAP assist ventilation + EPAP assists oxygenation
In what respiratory condition does SHUNTING occur and what is it?
ARDS
-blood goes from R side of heart thru pulmonary vessels and never came in contact w/ alveoli, so blood returns to the arterial circulation with unoxygenated
»essentially ARDS is a separation of alveoli from the blood supply –NO GAS EXCHANGE occurs
***refractory hypoxemia b/c no matter how much O2 given, the pt will NOT get better (FiO2 100% will do nothing)»_space;»> PT NEEDS PEEP (pressure) to open alveoli!! The pressure inside distends the alveoli so that it touches the vasculature and gas exchg occurs.
!!! Keep pts with ARDS dry, minimal fluids.
Early stage of ARDS is tachypnea, normal PAWP, Resp alkalosis
Late stage is hypercapnia
How does shock lead to ARDS?
Shock causes capillary beds in lungs to vasoconstrict which will make blood flow stagnant, the epithelial wall is damaged then leaks and separates alveoli from the vessel d/t the fluid leakage into the space —lead to ARDS and NEED FOR PEEP!
How is Tidal volume set?
8-10ml/kg or about 2x normal TV
PaO2 vs PaCO2
PaO2 provides information on the oxygenation status, is a measurement of oxygen in arterial blood. It shows how well oxygen is able to move from the lungs to the blood (the PaO2 “sensors” in aortic arch–this is secondary control- if ↓ PaO2 sensed (hypoxemia), then ventilation stimulated (pt has increased rate and/or depth of breathing)
PaCO2 offers information on the ventilation status (chronic or acute respiratory failure).
PaCO2 is affected by hyperventilation (rapid or deep breathing), hypoventilation (slow or shallow breathing), and acid-base status.
Systemic artery:
PaCO2 = 40
PaO2 = 100
SaO2 = 99%
PaO2 vs SaO2
PaO2 is the pressure exerted by O2 on the arterial wall. SaO2 is the percentage of hemoglobin binding sites that are occupied with O2. This is the main difference between PaO2 and SaO2
What does a decrease in pH stimulate?
A ↓pH is acidosis, primarily ventilation stimulated by brain stem with increased rate and/or depth of breathing
What is minute ventilation?
TV x RR
normal is 4L/min
An ↑ in minute ventilation = ↑ WOB
What increases alveoli dead space?
PE
-a clot means no blood flow past alveoli in that area of pulm circulation
Ventilation vs Perfusion
Treatment if an issue?
(V) ventilation: air into and out of lungs
(Q) perfusion: mvmt of blood thru pulm capillaries
Normal V/Q ratio: 0.8 ratio =
4L ventilation/min
————————–
5L perfusion/min
***V/Q mismatch:
happens when part of your lung receives oxygen without blood flow or blood flow without oxygen. This happens if you have an obstructed airway, such as when you’re choking, or if you have an obstructed blood vessel, such as a blood clot in your lung.
Seen with pneumonia, PE
Tx of mismatch»_space; give O2, then treat underlying problem
If a patient has a large R lung PNA, how should the pt lay?
GOOD LUNG DOWN! Lay on left side.
Otherwise all the blood goes to the bad lung and pt may become hypoxemic
Note: when pt laying supine, all blood is posterior.
Pathological vs Anatomical shunt
patho: ARDS
Physio: ASD, VSD
How does PEEP help?
-prevents expiratory pressure from returning to zero
-keeping expiratory pressure POSITIVE:
↑alveoli recruitment
↓surface tension of the alveoli, preventing atelectasis
↑driving pressure, extending time of gas transfer, allows fro a ↓in FiO2
Oxyhemaglobin-dissociation curve
|»_space;>LEFT shift
Left: aLkaLosis (both have L, things low are alkalosis!!!)
- Hgb “hold on” to O2 molecules
- Hgb has ↑ affinity for O2
> ↓Low PaCO2, high SaO2 (if ↓ PaO2 sensed (hypoxemia), then ventilation stimulated (pt has increased rate and/or depth of breathing)
↓coLd: Hypothermia
↓Low 2,3-DPG
»>bad for patient, SaO2 high but O2 stuck to Hgb
Note:
2,3-DPG. An organic phosphate in red blood cells that alters the affinity of hemoglobin for oxygen. Blood cells stored in a blood bank lose 2,3-diphosphoglycerate, but once they are infused, the substance is resynthesized or reactivated.
Oxyhemaglobin-dissociation curve
|»_space;>RIGHT shift
RIGHT: Acidosis -Hgb "release" O2 more easily to tissues -Hgb has ↓ affinity for O2 >↑ High PaCO2 (acidosis), low SaO2 >↑High: fever >↑High 2,3-DPG >>>>>Good for tissues, SaO2 low but O2 easily released
Note:
2,3-DPG. An organic phosphate in red blood cells that alters the affinity of hemoglobin for oxygen. Blood cells stored in a blood bank lose 2,3-diphosphoglycerate, but once they are infused, the substance is resynthesized or reactivated.
Carbon monoxide poisoning
Hgb carries O2 and CO2, when CO poisoning occurs the Hgb cannot carry O2»_space;» result TISSUE HYPOXIA
- **CO has a greater affinity for Hgb than O2 ~ 230x greater
- *A pulse ox will only tell you % of saturation of molecules. It will be CO with poisoning, not a representation of O2
Tx: 100% FiO2 until symptoms resolve and carboxyhemaglobin level is <10%
»if the CO level is 40%, the max amt of O2 carried by Hgb is 60%
High Anion gap causes
–difference b/w positive and negative ions
–normal: 5-15 mEq/L
(Na+ + K+) - (Cl- + HCO3-)
Increase w/ acidosis: Ketoacidosis Uremia Salicylate intoxication Methanol tox Alcoholic ketosis Lactic acidosis: shock, hypoxemia
COPD
expiratory flow low, V/Q mismatch d/t ventilation
chronic CO2 retention
COPD result in RV enlargement and high CVP
Mgmt:
-titrate FiO2 to PaO2>60 SpO2 >90%
inhaled Albuterol, anticholinergic (Ipratropium)
Gold std for dx of PE
pulmonary angiography
Pulmonary HTN
-defined as a PAP >25 at rest and a PAOP < 16mmHg at rest with secondary RHF
> cause RV failure
Tx:
- diuretics
- oxygen
- anticoags
- digoxin
- dilators (CCB or viagra/cialis)
ARDS/ ALI inflammation
- syndromes caused by acute conditions that trigger and inflammatory response»_space; resulting in increased permeability of the pulmonary capillary membrane, which allows a proteinaceous fluid into the interstitial and alveolar spaces “noncardiogenic pulm edema”
- dmg to Type II alveolar cells is one of the patho consequences and massive atelectasis occurs b/c these cells are responsible for the production of surfactant (which is needed to stabilize alveoli and keeps them open, ↑ lung compliance)
**Acute onset w/ precipitating event in both
**Bilateral infiltrates consistent w/ pulm edema, both
**PAOP < 18mmHg must be present in both!
>>>The difference is PaO2/FiO2 regardless of the level of PEEP:
–if < or = 200 it is ARDS
–If 201-300 it is ALI
What does refractory hypoxemia mean?
Pt given 100% FiO2 and hypoxemia still present
What is meant by no lung reserve?
FRC- Functional reserve capacity?
With ARDS and destruction of the Type II alveolar cells,
**massive atelectasis, ALVEOLAR COLLAPSE
↓ lung compliance (stiff)
↑ WOB
↓ FRC
How does prone positioning help?
- helps deliver blood flow to underperfused lung units, thereby improving ventilation/perfusion
- keeps alveolar open»_space; improving gas exchange and preventing further injury
Treatment for ARDS
- PEEP 15cm H2O or greater (may need pressors for hypotension)
- lower Vt to 5-6ml/kg –> permissive hypercapnia to prevent volutrauma
- prone
- DVT and stress ulcer prophylaxis
!!!NO STEROIDS!!!
spontaneous or traumatic pneumothorax
- air can’t exit
- outside air enters from chest wall and lung air enters from parietal pleura
*trachial deviation towards affected side if present
-mediastinum remains midline, no shift
decrased or absent breath sounds on affected side
TENSION PNEUMO
TENSION PNEUMO - >>>>LIFE THREATENING *MEDIASTINAL deviation AWAY from affected side -JVD -hypotension -tachycardia
Hemothorax
Tracheal deviation toward the unaffected side
blood has dull percussion
absent breath sounds on affected side
Ventilator
-Assist-control (AC) mode
- set TV at set breath rate
- also set TV with triggered spontaneous breaths efforts above the set breath rate, however ALL BREATHS ARE MACHINE BREATHS
Ventilator
-Sync intermittent mandatory ventilation (SIMV)
- set TV at set breath rate
- all breaths above set rate by the patient are at the patient’s own breath rate
Ventilator
-Pressure support ventilation (PSV)
-frequently used during weaning to REDUCE THE WOB and to overcome imposed work of ETT and vent circuit
- the pt receives an increase in air pressure during inspiration to augment (boost) the spontaneous Vt
- this is a pt triggered mode, so if pt paralyzed or sedated it won’t be triggered)
- rate, Vt, inspiratory flow rate, inspiratory time are determined by the pt effort
> > when wean off, the PEEP is decreased by 5 q4h, so if pt does not tolerate, go back up by 5
Cause for high pressure vent alarms
agitation coughing secretions aspiration kinked/occluded ETT or vent circuit Bronchspasm or mucosal edema Decreased lung compliance (ARDS) Pneumothorax
Cause for low pressure vent alarms
Vent circuit disconnect or leak
inadequate Vt
cuff leak
Chest tube leak
Pt on CPAP for SBT, how is readiness to extubate assessed?
divide RR by TV in liters
If < 105 breaths/min/L the pt is ready
Emphysema
A lung disease which results in shortness of breath due to destruction and dilatation of the alveoli.
Due too the long term high pressure, can cause cor pulmonale (RHF)»_space; increased CVP
**If present in young population with no smoking hx, test for alpha-1 antititrypsin deficiency
How can vital capacity predict pt being taken of mech vent?
minimum Life sustaining VC is 15ml/kg
What medication is given for pulmonary arterial HTN?
Epoprostenol (glycine) (Flolan)
with PPV, what happens to CO2?
decreases
As pulmonary ventilation increases, CO2 is exhaled
