Review Flashcards
Normal pH
7.35-7.45
Normal CO2
35-45
Normal HCO3
22-26
pH ↓
PaCO2 ↑
Respiratory acidosis
pH ↓
PaCO2 ↓
metabolic acidosis
pH ↑
PaCO2 ↓
respiratory alkalosis
pH ↑
PaCO2 ↑
metabolic alkalosis
etiologies for respiratory acidosis
Airway obstruction - Upper - Lower COPD asthma other obstructive lung disease CNS depression Sleep disordered breathing (OSA or OHS) Neuromuscular impairment Ventilatory restriction Increased CO2 production: shivering, rigors, seizures, malignant hyperthermia, hypermetabolism, increased intake of carbohydrates Incorrect mechanical ventilation settings
etiologies for respiratory alkalosis
CNS stimulation: fever, pain, fear, anxiety, CVA, cerebral edema, brain trauma, brain tumor, CNS infection
Hypoxemia or hypoxia: lung disease, profound anemia, low FiO2
Stimulation of chest receptors: pulmonary edema, pleural effusion, pneumonia, pneumothorax, pulmonary embolus
Drugs, hormones: salicylates, catecholamines, medroxyprogesterone, progestins
Pregnancy, liver disease, sepsis, hyperthyroidism
Incorrect mechanical ventilation settings
etiologies for metabolic alkalosis
Hypovolemia with Cl- depletion
GI loss of H+ - Vomiting, gastric suction, villous adenoma, diarrhea with chloride-rich fluid
Renal loss H+
Loop and thiazide diuretics,
Renal loss of H+: edematous states (heart failure, cirrhosis, nephrotic syndrome), hyperaldosteronism, hypercortisolism, excess ACTH, exogenous steroids, hyperreninemia, severe hypokalemia, renal artery stenosis, bicarbonate administration
base excess
This is the amount of strong base which would need to be added or subtracted from a substance in order to return the pH to normal (7.40).
A value outside of the normal range (-2 to +2 mEq/L) suggests a metabolic cause for the acidosis or alkalosis.
base excess more than +2 mEq
metabolic alkalosis.
A base excess less than -2 mEq/L
indicates a metabolic acidosis.
Lateral positioning CO2 arterial alveolar gradient
> 5 mmHg
Lung Zone 1
upright and awake
alveolar pressure > arterial pressure so the collapsible vessels are held closed and there is no flow
Lung Zone 2
upright and awake
arterial pressure > alveolar pressure but alveolar > venous pressure. A constriction occurs at the end of each collapsible vessel, and the pressure inside the vessel is equal to alveolar pressure, so the pressure gradient causing flow is arterial-alveolar. This gradient increases linearly with distance down the lung, and so does blood flow
Lung Zone 3
upright and awake
venous > alveolar
the collapsible vessels are held open.
The pressure gradient causing flow is arteriovenous and there is constant perfusion of alveoli
In the upright and awake patient, perfusion is greatest . . .
Ventilation is greatest . . .
in the base and decreases as you move towards the apex (head)
Ventilation is also greatest in the base and decreases towards the apex
Alveolar compliance is greatest in the base - when a breath occurs, most alveoli in the base receive this volume as they can distend down
Pleural pressure in the apex is more
negative and the alveoli are most distended
Base alveoli are
less distended and more compliant
Awake lateral pulmonary ventilation and perfusion
blood flow in zones 2 and 3 is less
pulmonary blood flow is greater in the dependent lung than non-dependent
no V/Q mismatch
Anesthesia induction and lung ventilation/perfusion
Lateral patient
spontaneous breathing
Induction causes a loss of lung volume in both lungs (reduced FRC)
Less Zone 3 available
Lung volumes reduce and change compliance where more pressure is required to generate volume changes
Non-dependent lung moves to a more favorable compliance
Perfusion is greater in dependent lung, but ventilation is better in the nondependent lung - creating V/Q mismatch
Anesthesia induction and lung ventilation/perfusion
supine, paralyzed
mechanical ventilation
FRC decreases further with loss of diaphragm contraction
V/Q mismatch worsens - PEEP can help restore
Open chest ventilation/perfusion
resistance to gas flow drops and large ventilator preferences goes to the nondependent lung
mediastinum shifts downward
The dependent lung is better fused but in it’s highest shunt state with lots of atelectasis, while the operative lung is in dead space
great vessel compression from the mediastinal weight can cause CO falls
Spontaneous ventilation would produce paradoxical chest wall movement
One lung ventilation
the nondependent lung TV can be diverted away to the well-perfused shunt dependent lung.
Ventilation to the operative lung is now the shunt lung, but HPV reduces this by 50% to divert lung back to the dependent lung
PaO2 is higher in the lateral position with OLV than when supine
Any blood to the deflated lung is shunt flow and causes PaO2 to decrease
Hypoxic Pulmonary Vasoconstriction
Reflex where the pulmonary vasculature constricts in response to alveolar hypoxia
Reduces flow to the shunt lung in OLV
Can increase PVR up to 300% and become chronic
PA remodeling occurs (cor pulmonale and PHTN)
HPV inhibitors
NTG SNP Dobutamine CCB Isoproterenol
Alkalosis Excessive Vt Excessive PEEP Hemodilution Hypervolemia Hypocapnea Hypothermia Shunt fraction <20 or > 80
Drugs that cause HPV
Dopamine Norepi Serotonin histamine hypoxia endothelin leukotriene thromboxane prostaglandin epinephrine phenylephrine *Vasopressin does NOT
OLV
key points
Lower lung volume - 6-8 ml/kg if pt not auto-peeing pressure limit is 25 cm H2O Permissive hypocapnia - 60-70 PaCO2 Volatile agents <1 1.5 MAC N2O avoided b/c increase PVR
transcutaneous CO2 monitoring
Central line
Regional anesthesia and OLV
can reduce opiate use, reduce atelectasis, resp failure
Cannot be sole technique
Does NOT inhibit HPV as this is a local autoregulated event
End of surgery OLV
Lungs are reinflated with slow breaths
holding peak pressures to 30-40 cm H2O
Deflate the bronchial cuff as soon as possible
The effects of OLV are not immediately reversed and hypoxemia is common
*some places uses prostacyclin, NO and phenylephrine to constrict the operative lung
correct position of left DLT
ventilation through the bronchial lumen produces breath sounds
left lung
correct position of right DLT
ventilation through the bronchial lumen produces breath sounds
Right lung
DLT too shallow
ventilation through the bronchial lumen produces breath sounds
both lungs
DLT too deep in the right bronchus
ventilation through the bronchial lumen produces breath sounds
Right middle and lower lobes
DLT too deep in the left bronchus
ventilation through the bronchial lumen produces breath sounds
Left lung
correct position of left DLT
Ventilating through the tracheal lumen produces breath sounds
Right lung
correct position of right DLT
Ventilating through the tracheal lumen produces breath sounds
Left lung
DLT too shallow
Ventilating through the tracheal lumen produces breath sounds
diminished or absent if bronchial cuff obstructs trachea; or both lungs
DLT too deep in right bronchus
Ventilating through the tracheal lumen produces breath sounds
Left lung or right upper lobe
DLT too deep in left bronchus
Ventilating through the tracheal lumen produces breath sounds
Left lung
Mediastinal masses
appraoch
scope passes in front of trachea but hehind the thoracic aorta
close to left common arotid, left subclavian, innominate artery, innominate veins, vagus nerve, LRNL, superior vena cava, aortic arch
Mediastinal masses
prep
Large bore IVs
Blood readily available T & S
External defib pads due to the risk of arrhythmias
Art line on the right side and/or SPO2 monitor
NIBP on right arm
Check PFTS
Flow volume loops
evidence of tracheal/bronchial compression
CT scan
