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6902 test 3 > Review > Flashcards

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1
Q

Normal pH

A

7.35-7.45

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2
Q

Normal CO2

A

35-45

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3
Q

Normal HCO3

A

22-26

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4
Q

pH ↓

PaCO2 ↑

A

Respiratory acidosis

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5
Q

pH ↓

PaCO2 ↓

A

metabolic acidosis

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6
Q

pH ↑

PaCO2 ↓

A

respiratory alkalosis

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7
Q

pH ↑

PaCO2 ↑

A

metabolic alkalosis

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8
Q

etiologies for respiratory acidosis

A 
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
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9
Q

etiologies for respiratory alkalosis

A

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

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10
Q

etiologies for metabolic alkalosis

A

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

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11
Q

base excess

A

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.

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12
Q

base excess more than +2 mEq

A

metabolic alkalosis.

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13
Q

A base excess less than -2 mEq/L

A

indicates a metabolic acidosis.

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14
Q

Lateral positioning CO2 arterial alveolar gradient

A

> 5 mmHg

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15
Q

Lung Zone 1

upright and awake

A

alveolar pressure > arterial pressure so the collapsible vessels are held closed and there is no flow

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16
Q

Lung Zone 2

upright and awake

A

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

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17
Q

Lung Zone 3

upright and awake

A

venous > alveolar
the collapsible vessels are held open.
The pressure gradient causing flow is arteriovenous and there is constant perfusion of alveoli

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18
Q

In the upright and awake patient, perfusion is greatest . . .
Ventilation is greatest . . .

A

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

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19
Q

Pleural pressure in the apex is more

A

negative and the alveoli are most distended

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20
Q

Base alveoli are

A

less distended and more compliant

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21
Q

Awake lateral pulmonary ventilation and perfusion

A

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

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22
Q

Anesthesia induction and lung ventilation/perfusion
Lateral patient
spontaneous breathing

A

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

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23
Q

Anesthesia induction and lung ventilation/perfusion
supine, paralyzed
mechanical ventilation

A

FRC decreases further with loss of diaphragm contraction

V/Q mismatch worsens - PEEP can help restore

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24
Q

Open chest ventilation/perfusion

A

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

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25
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
26
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)
27
HPV inhibitors
``` NTG SNP Dobutamine CCB Isoproterenol ``` ``` Alkalosis Excessive Vt Excessive PEEP Hemodilution Hypervolemia Hypocapnea Hypothermia Shunt fraction <20 or > 80 ```
28
Drugs that cause HPV
``` Dopamine Norepi Serotonin histamine hypoxia endothelin leukotriene thromboxane prostaglandin epinephrine phenylephrine *Vasopressin does NOT ```
29
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
30
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
31
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
32
correct position of left DLT ventilation through the bronchial lumen produces breath sounds
left lung
33
correct position of right DLT ventilation through the bronchial lumen produces breath sounds
Right lung
34
DLT too shallow ventilation through the bronchial lumen produces breath sounds
both lungs
35
DLT too deep in the right bronchus ventilation through the bronchial lumen produces breath sounds
Right middle and lower lobes
36
DLT too deep in the left bronchus ventilation through the bronchial lumen produces breath sounds
Left lung
37
correct position of left DLT Ventilating through the tracheal lumen produces breath sounds
Right lung
38
correct position of right DLT Ventilating through the tracheal lumen produces breath sounds
Left lung
39
DLT too shallow Ventilating through the tracheal lumen produces breath sounds
diminished or absent if bronchial cuff obstructs trachea; or both lungs
40
DLT too deep in right bronchus Ventilating through the tracheal lumen produces breath sounds
Left lung or right upper lobe
41
DLT too deep in left bronchus Ventilating through the tracheal lumen produces breath sounds
Left lung
42
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
43
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
44
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.
45
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.
46
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
47
Mild ARDS
PaO2/FiO2 ratio (ratio calculated with CPAP or PEEP of >5 cm H2O) 201-300
48
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
49
Moderate ARDS
ratio 101-200
50
Severe ARDS
ratio < 101
51
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
52
Dual antiplatelet therapy
Aspirin AND P2Y12 platelet inhibitor (clopidogrel, prasugrel, ticagrelor) continued for 6 weeks after PCI
53
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 ```
54
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
55
HCT elevated in person with COPD. Why?
RBCs hypertrophy and produce more when exposed to chronic hypoxia
56
Treatment of COPD/Chronic bronchitis
Smoking cessation (> 8 weeks) Long-acting B2 agonists corticosteroids anticholinergics
57
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
58
When is pulm consult in COPD pt warranted?
hypoxemia on room air, HCO3 > 33 or PCO2 > 50, PHTN
59
Regional and COPD
preferred over GA as it reduces laryngospasm, bronchospasm, barotrauma, hypoxemia
60
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
61
When is GA required in COPD?
upper abdominal and intrathoracic surgeries
62
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
63
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
64
VSD with normal (low) PVR
Left to right shunt magnitude depends on PVR No cyanosis most close spontaneously
65
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
66
Fallot's tetralogy
1. VSD 2. RV hypertrophy 3. Pulmonary stenosis 4. Overridng aorta Right to left shunt Cyanosis Increasing SVR reduces the shunt and improves oxygenation Hypotension worsens the shunt
67
Acyanotic lesions
left to right shunt shunting causes increased PVR and remodeling PHT, RVH, CHF
68
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
69
ASD shunt calculation
Pulmonary to systemic flow < 1.5:1, asymptomatic
70
VSD shunt calculation
Pulmonary to systemic flow < 1.4:1
71
VSD Anesthesia
treat like CHF with PHTN
72
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
73
Transposition of the great vessels
LV empties into the Pulmonary artery and RV empties into the aorta
74
L-transposition
RA-MV-LV-PV -pulmonary circulation - LA - RV - aortic valve
75
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
76
Cor pulmonale
complication from PHTN Causes RHF - the right ventricle to enlarge and pump blood less effectively than it should.
77
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).
78
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
79
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)
80
CVP | a wave
end diastole atrial contraction
81
CVP | c wave
early systole | Tricuspid bulging
82
CVP | v wave
Late systole | Systolic filling of the atrium
83
CVP | x descent
Mid systole | Atrial relaxation
84
CVP | y descent
Early diastole | Early ventricular filling
85
Calculating oxygen content of arterial blood
CaO2 = ( Hgb * 13.4 * O2Sat / 100 ) + ( PaO2 * 0.031 )
86
Greater radicular artery
Spinal cord blood supply 1 anterior spinal artery - Motor - from GRA 2 posterior spinal arteries - Sensory
87
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
88
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
89
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
90
Drugs to avoid with heart transplant
Indirect agents (ephedrine, anticholinergic drugs) ineffective N2O bc of PHTN Avoid histamine releasing drugs (morphine, atracurium)
91
Creatinine increase with heart transplant pt
cyclosporine or tacrolimus induced nephrotoxicity
92
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
93
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
94
Heparin dose
300-400 units/kg body weight prior to circuit Confirm with ACT 3-5 minutes ACT must be >400 or 450
95
Protamine dose
1 mg for each 100 units of heparin
96
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 1. Myoglobin and CK 2. Troponin 3. CKMB
97
TV
500 mL
98
Vital capacity
5500 mL
99
Inspiratory reserve volume
3300 cc
100
Expiratory reserve volume
1700 cc
101
Inspiratory capacity
3800 cc
102
Total lung capacity
7300 cc
103
FRC
3800 cc
104
Residual volume
800 cc
105
Mild asthma
<80% FEV1 >2 days/week but not daily Short acting B2-agonist use for symptom control
106
Moderate asthma
FEV1 60-80% Daily Short acting b2 agonist for symptom control Add inhaled low dose steroid
107
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
108
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

6902 test 3 (1 decks)

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