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
mediastinal mass
complications
arrhythmias - stop manipulation
Innominate artery occlusion - stops blood flow to the right common carotid artery and right vertebral artery - change in art line waveform is clue. Reposition scope
Asymptomatic pts can crash under anesthesia
Turn pt lateral or prone
Avoid N2O - cysts can be air filled and grow and encroach on airway.
symptoms of mediastinal tumors
symptoms may develop due to pressure on the spinal cord, heart or heart lining (pericardium) and may include:
Coughing with or without blood, shortness of breath and hoarseness.
Night sweats, chills or fever.
Wheezing or a high-pitched breathing noise.
Unexplained weight loss and anemia.
Swollen or tender lymph nodes.
mediastinal dx
Chest x-ray
CT
MRI
Mediastinoscopy, a surgical procedure, with a biopsy of the tissue. A mediastinalscope is inserted into the mediastinum through a small incision in the chest. The scope has a camera on the end to give your doctor a clear view of the area. Tissue may be removed to perform a biopsy to test the cells for signs of cancer.
Under local while sitting up and spontaneously breathing is advisable
Awake FOB recommended
Helium-O2 mix can reduce turbulent airflow and improve oxygenation past the lesion
Mild ARDS
PaO2/FiO2 ratio (ratio calculated with CPAP or PEEP of >5 cm H2O)
201-300
ARDS treatment
Corticosteroids inhaled NO surfactant use ECMO Abx VTE prophylaxis early enteral feeding prone positioning
Avoid volume overload - fluid restriction 20 cc/kg
vent settings - high PEEP and high PIP
want to recruit alveoli and avoid right heart strain
Permissive hypercapnia - indicated by rising CVP
6-8 cc/kg
Plateau pressure <30 cm H2O
Moderate ARDS
ratio 101-200
Severe ARDS
ratio < 101
Stent management
Dual antiplatelet therapy for 6 weeks regardless of stent type after PCI
DES withhold elective surgery for 6 months
DES typically require 1 year before stopping dual antiplatelet therapy
BMS - 6 weeks after PCI or 12 weeks if was placed for ACS
Dual antiplatelet therapy
Aspirin AND
P2Y12 platelet inhibitor (clopidogrel, prasugrel, ticagrelor)
continued for 6 weeks after PCI
Causes of severe hypotension perioperatively
Sudden BLOOD LOSS (surgical) Impaired VENOUS RETURN (surgery / posture / high airway pressures / pneumothorax) VASODILATION (neuraxial block - assess block height, anaesthetic agents, drug reactions including ANAPHYLAXIS) EMBOLISM (Air / CO2 / orthopaedic / venous thromboembolism) CARDIAC DYSRHYTHMIA CARDIAC Dysfunction Ischaemia / Infarction Depressants (anaesthetic agents etc) Insufflating belly Cardiac tamponade Induction Carcinoid tumor will crash at induction
chronic bronchitis
COPD
constriction and resistance to flow with mucous production
Makes alveoli prone to atelectasis from plugging
Hypoventilation with little respiratory effort
Cyanosis
CO2 retention
Cor pulmonale
Normal lung volumes
HCT elevated in person with COPD. Why?
RBCs hypertrophy and produce more when exposed to chronic hypoxia
Treatment of COPD/Chronic bronchitis
Smoking cessation (> 8 weeks)
Long-acting B2 agonists
corticosteroids
anticholinergics
Anesthesia risks for COPD
Bronchospasm Auscultate lung for wheezes in pre-op Assess for RH failure Bronchodilators Antichlinergics to be inhaled before surgery stress dose steroids if oral use
PFTs are NOT required bc not a rik predictor
ALbumin and BUN can be part of risk predictor
ECHO for PHTN and RHF
When is pulm consult in COPD pt warranted?
hypoxemia on room air, HCO3 > 33 or PCO2 > 50, PHTN
Regional and COPD
preferred over GA as it reduces laryngospasm, bronchospasm, barotrauma, hypoxemia
What blocks to be avoided in COPD?
Interscalene bc hit the phrenic nerve and can be detrimental
supraclavicular can also cause same effect
Thoracic epidurals and central brachial plexus blocks can affect the intercoastal muscles
When is GA required in COPD?
upper abdominal and intrathoracic surgeries
If a COPD pt becomes unstable under GA, consider what?
Pneumothorax
Bronchopleural fistula
Tendency to auto peep can increase intrathoracic pressure, impede preload, and compress the pulmanry vasculature of the heart
GA and COPD considerations
Use Sevo, des but Des can cause irritation of the J receptors of the bronchi and increase airway resistance
No N2O bc can cause tension pneumothorax and worsen PVR
Humidified air
Low TV with peak pressures < 30
Avoid high O2
If auto-peep, increase I:E ratio
Consider TIVA to circumvent concerns of prolonged emergence due to air trapping of inhalation agents
VSD with normal (low) PVR
Left to right shunt
magnitude depends on PVR
No cyanosis
most close spontaneously
VSD with high PVR
PVR increases due to chronic high flow leading to remodeling of the pulmonary vasculature
PVR exceeds SVR and a right to left shunt occurs
Cyanosis
Eisenmenger’s syndrome
non-surgical at this pt
Fallot’s tetralogy
- VSD
- RV hypertrophy
- Pulmonary stenosis
- Overridng aorta
Right to left shunt
Cyanosis
Increasing SVR reduces the shunt and improves oxygenation
Hypotension worsens the shunt
Acyanotic lesions
left to right shunt
shunting causes increased PVR and remodeling
PHT, RVH, CHF
ASD
PHTN- which can reverse flow of shunt to right to left and cause cyanosis
ASD with sig L to R need to be repaired before PHTN develops. Once developed, surgery not indicated
atrial arrhythmias - afib
LVH
systolic murmur with split S2 (delayed PV closure)
PM
ASD shunt calculation
Pulmonary to systemic flow < 1.5:1, asymptomatic
VSD shunt calculation
Pulmonary to systemic flow < 1.4:1
VSD Anesthesia
treat like CHF with PHTN
PDA
connects the left pulmonary artery to descending aorta
allows blood to shunt right to left intrautero to bypass the lungs
After delivery, the PDA should close and seal within one month
When open, causes left to right shunting
Heart failure and endocarditis
Ligation performed before age 5
Ventilation difficult due to prematurity and HTN
RLN damage
Phrenic nerve injury
COX inhibitors reduce PGE1 to help promote closure
Transposition of the great vessels
LV empties into the Pulmonary artery and RV empties into the aorta
L-transposition
RA-MV-LV-PV -pulmonary circulation - LA - RV - aortic valve
Anesthesia and shunting disorders
elminminate bubbles
when PVR:SVR is > 1.5:1, then limit pulmonary blood flows.
Maintain CO
Ketamine preferred at induction bc increase PVR, contractility
Minimize drugs that increase SVR and lower PVR for L to R
Cor pulmonale
complication from PHTN
Causes RHF - the right ventricle to enlarge and pump blood less effectively than it should.
Cor pulmonale anesthesia
avoid increasing PVR (precipitants include hypoxemia, hypercarbia, acidosis, nitrous oxide
In severe cases, beta-agonists may be required to overcome PVH, but with the concomitant risk of myocardial ischemia.
Phosphodiesterase inhibitors (amrinone, milrinone) may be needed as they can both improve ventricular function and induce vasodilation (thus reducing afterload).
CPP
Diastolic Arterial Pressure - LV End Diastolic Pressure
or
MAP - ICP
If LVEDP increase or DAP pressure decreases, then subendocardial tissue becomes at risk during diastole
Brain gets 20% of cardiac output from ICA and vertebral arteries
CBF
remains constant due to autoregulation (60-160 mmHg) and collateral circulation through the Circle of Willis
HTN shifts autoregulation to the right
normal CBF can be cut in half before ischemia occurs (50 ml/100g/min)
CVP
a wave
end diastole
atrial contraction
CVP
c wave
early systole
Tricuspid bulging
CVP
v wave
Late systole
Systolic filling of the atrium
CVP
x descent
Mid systole
Atrial relaxation
CVP
y descent
Early diastole
Early ventricular filling
Calculating oxygen content of arterial blood
CaO2 = ( Hgb * 13.4 * O2Sat / 100 ) + ( PaO2 * 0.031 )
Greater radicular artery
Spinal cord blood supply
1 anterior spinal artery - Motor - from GRA
2 posterior spinal arteries - Sensory
Artery of Adamkiewicz/GRA
comes from intercostal branch of T8-L2 and provides 2/3 blood flow to the anterior spinal cord
injury can be complication from lung resection or aortic cross clamp/dissection
CRT
cardiac resynchronization therapy
Used for CHF pts caused from asynchrony and conduction blocks
3 pacing leads in RA, RV and coronary sinus
When:
1. LVEF < 35%
2. QRS prolongation
NYHA 3-4
Heart transplant medications
HR dependent and cannot take preload/afterload changes
Etomidate induction with narcotics
RSI with succ or roc
Glucocorticoids perioperatively
Separation from CPB with isoproterenol or epi (Direct acting agents)
Epicardial pacing
Volume status essential coming off pump
Pulmonary vasodilation with NO, prostaglandin, milrinone (and reduce PVR)
Vasopressin
Drugs to avoid with heart transplant
Indirect agents (ephedrine, anticholinergic drugs) ineffective
N2O bc of PHTN
Avoid histamine releasing drugs (morphine, atracurium)
Creatinine increase with heart transplant pt
cyclosporine or tacrolimus induced nephrotoxicity
Hemodynamic goals with CPB
Before cannulation SBP 90-100 mmHg or MAP < 70
After cannulation, SBP can be raised if needed
Hypotension common when bypass is initiated due to hemodilution reducing SVR
If MAP cannot be raised > 30 mmHg, aortic dissection considered
CPB flow is 50-60 ml/kg/min with pressure of 50-70 mmHg. Hypertension means more anesthetic needed
Coming off bypass - mg to prevent arrhythmias. Pressors needed including positive inotropes
BP is lowered to MAP of 70 or systolic of 90 mmHg before the venous cannula is removed
Aortic dissection management
Vascular access - transfuse
Art line to still perfused limb away from CPB site
Goal: no HTN or worsen dissection
HR 60
Vasodilation to SBP < 120
Heparin dose
300-400 units/kg body weight prior to circuit
Confirm with ACT 3-5 minutes
ACT must be >400 or 450
Protamine dose
1 mg for each 100 units of heparin
Ischemia detection
Nuclear Imaging/MRI (perfusion abnormalities)
Increase in LVEDP and Decrease in Compliance
3. TEE - systolic dysfunction/RWMA
4. ECG changes
5. Clinical symptoms
6. infarct/shock
Biomarkers
- Myoglobin and CK
- Troponin
- CKMB
TV
500 mL
Vital capacity
5500 mL
Inspiratory reserve volume
3300 cc
Expiratory reserve volume
1700 cc
Inspiratory capacity
3800 cc
Total lung capacity
7300 cc
FRC
3800 cc
Residual volume
800 cc
Mild asthma
<80% FEV1
>2 days/week but not daily
Short acting B2-agonist use for symptom control
Moderate asthma
FEV1 60-80%
Daily
Short acting b2 agonist for symptom control
Add inhaled low dose steroid
Severe asthma
FEV <60%
Several times/day
B2-agonsit use for symptom control
increase inhaled low dose steroid
Add inhaled long acting Beta 2 agonist
Add leukotriene receptor antagonist
For very severe add oral steroid at lowest dose possible
Asthma treatments
inhaled corticosteroids oral/IV agents short acting Beta agonists Long acting beta agonists Leukotriene modified
Bronchial dilators with more than 10% increase in FEV1 are considered responders
