Critical Care Flashcards
Formula for MAP
MAP = DBP + 1/3 x (SBP-DBP)
Normal range for CO
4-8 L/min
Normal range for CI
2.5 to 4 L/min
Normal range for SVR
800-1400 dyn s/(cm5)
Normal range for PCWP
7-15 mm Hg
Normal range for CVP
2-6 mm Hg
Normal range for PA pressure
20-30/6-15 mm Hg
Normal range for mixed SvO2
70% +/- 5
What is SVO2
Oxygen saturation of blood in RV/PA that serves as indirect measure of peripheral oxygen supply and demand
Factors that influence SVO2
Oxygen delivery
Oxygen extraction
Approx % of CO that goes to kidney
25%
Approx % of CO that goes to brain
15%
Approx % that goes to heart
5%
If patient receives air embolus
Roll patient to LEFT and place head DOWN (trendelenberg) to keep air in RA/RV. Attempt to aspirate air with central catheter/PA catheter
Relative contraindications for PA catheter placement
LBBB
Previous pneumonectomy
Treatment for hemoptysis after PA catheter placement
Imbed pull PA catheter slightly back and reinflate balloon
Increase PEEP to help tamponade
Mainstem intubate non affected side
Attempt made to place fogarty catheter down affected side; if recalcitrant, may need thoracotomy and lobectomy
What West zone of lung is desired location for PA catheter?
Zone III
Pa > Pv > PA (pressure in aa > pressure in veins > pressure in alveoli)
Which portion of lung has highest V/Q ratio?
Upper lobes
Which portion of lung has lowest V/Q ratio
Lower lobes
At what point in respiratory cycle is PCWP most accurate in ventilated patient
End expiration
At what point in respiratory cycle is PCWP most accurate in NON ventilated patient
Peak inspiration
What conditions make wedge pressure unreliable
Aortic regurg high PEEP Mitral stenosis Mitral regurg Poor LV compliance Pulm HTN Pulm disease (ARDS) Tamponade PTX
PA catheters allow direct measurement of which parameters?
CVP RA pressure PA pressure LVEDVP PAWP SVO2
What is an IABP?
Mechanical device that consists of cylindrical balloon that actively deflates in systole increasing forward blood flow by reducing after load and actively inflates in diastole increasing blood flow to the coronary arteries resulting in decreased myocardial oxygen demand and increased CO
When does balloon from IABP inflate on ECG?
T wave (diastolic)
When does balloon from IABP deflate on EKG?
P wave or start of Q wave (systole)
Indications for IABP
Bridge to heart transplant for patients with LV failure
Cariogenic shock
Percutaneous coronary angioplasty
Post-CT surgery
Pre sop use for high risk patients (unstable angina with stenosis >70% main coronary artery)
Reversible intracardial mechanical defects complicating infarction
Unstable angina pectoris
Ventricular dysfunction with EF <35%
Absolute CI to IABP
Aortic regurgitation
Aortic dissection
Severe aortoiliac occlusive disease
Relative contraindications to IABP
Prosthetic vascular grafts in aorta
Aortic aneurysm
Aortofemoral grafts
Desired location for tip of IABP
1-2 cm below top of aortic arch just distal to left subclavian
What is preload
End diastolic length of cardiac myocytes which is linearly related to end diastolic volume and filling pressure
What 3 things determine SV?
LVEDV (preload)
Contractility
Afterload
How is EF calculated
Stroke volume/EDV
How is stroke volume calculated?
LVEDV - LVESV
Normal O2 delivery to consumption ratio
5 to 1
Primary determinants of myocardial O2 consumption
HR, increased ventricular wall tension
Normal range for alveolar:arterial gradient
10-15 mm Hg
What shifts O2-Hgb dislocation curve to LEFT
Decrease temperature
Decrease DPG
Decrease pCO2
Increase pH
What shifts O2-Hgb dissociation curve to RIGHT
Increase temperature
Increase DPG
Increase pCO2
Decrease pH
When does BP begin to decrease (what stage of shock)
Class III
When does pulse pressure begin to decrease (class of shock)
Class II
What class of shock do you start to see tachycardia
Class II
What class of shock do you see RR 30-40?
Class III
What class of shock is UOP 5-15 mL/hr
Class III
What is formula for O2 content of blood
[Hb + SaO2 x 1.34] + [0.003 x PaO2]
What is formula for O2 delivery?
CaO2 x CO; [(Hb x SaO2 x 1.34) + (0.003 x PaO2)] x (HR x SV)
What is formula for O2 consumption
VO2 = CO x (CaO2 - CVO2) x 10
Can be rearranged to estimate mixed venous saturation
How many mL O2 will gram of hemoglobin is fully saturated with oxygen?
1.34 mL of O2 is bound to each gram of Hgb
Manipulation of what factors increase O2 delivery?
Greatest increase of O2 delivery with increasing Hgb content and SaO2
Can also increase oxygen delivery by raising CO by increasing either HR or SV
Equation for oxygen extraction ratio
VO2/DO2
Normal is 25-30%
Treatment for vfib/pulseless v tach
1 shock monophonic 360 or biphasic 100-200 J
CPR with additional counterchecks
Epi 1 mg Iv and repeat q 3-5 min or vasopressin 40U IV
Consider amiodarone (300 mg IV), lidocaine (1-1.5 mg/kg), magnesium (1-2 gIV)
Treatment for asystole/PEA
Verify with lead rotation
Epi 1 mg IV and repeat q3-5 or vasopressin 40units IV
Consider atropine 1 mg IV q3-5 up to 3 doses
Treatment for UNSTABLE bradycardia
Transcutaneous pacing
If not immediately available, give atropine 1 mg and epi 2-10 mg/min
In which pts with fib is anticoagulation unnecessary
Fib for <48 hrs
What is tx for fib with hemodynamic INSTABILITY
Cardioversion and anticoagulation
Tx of fib withOUT hemodynamic instaiblity
Rate control (amid, CCB, beta blockers, digoxin) and correct not underlying cause; anticoagulation
10 for 0.08 rule of acid base balance
pH falls by 0.08 for every increase of PaCO2 by 10 mm Hg
What is 35-45 rule of blood gas values
pH = 7.35 to 7.45 corresponds to pCO2 35-45
Most common cause of post op renal failure
Hypotension
What lab results suggest pre renal cause of ARF
Bun/Cr ratio >20
FENa < 1%
urine Na <20/24 hrs
urine osmolality >500 mOsm
What is formula for FENa
UNa x pCr / pNa x urine Cr
What does FeNA <1% indication
Pre renal due to decreased renal blood flow
What does FENa > 3%
Intrinsic kidney damage (ATN, severe obstruction of both kidneys)
What are indications for ialysis
fluid overload Metabolic acidosis Hyperkalemia Poisoning Uremic coagulopathy or encephalopathy
Advantages of intermittent hemodialysis over CRRT
Lower cost
Lower risk of systemic bleeding
Facilitates transport for other interventions
More suitable for severe hyperK
Advantages of CRRT over intermittent hemodialysis
Better fluid control Better hemodynamic stability Fewer cardiac arrhythmias Improved nutritional support Better pulmonary gas exchange
Disadvantages of intermittent hemodialysis over CRRT
Availability of dialysis staff
Inadequate fluid control
Inadequate dialysis frequency
Inadequate nutritional support
More difficult hemodynamic control
Potential complement activation by non biocompatible membranes
Not suitable for pts with intracranial HTN
Disadvantages of CRRT over intermittent hemodialysis
Greater cost Greater vascular access problems Higher risk of systemic bleeding Long term immobilization of patient More filter problems (clotting, rupture)
How much steroids should patient be on preoperatively to have presumed HPA axis suppression
20 mg prednisone or equivalent per day for 3 weeks or longer
How much preoperative steroid supplementation should you give a patient with HPA axis suppression undergoing moderate operation (open chole, LE revascularization)
50-75 mg/d of hydrocortisone equivalent for 1-2 days
How much preoperative steroid supplementation should you give a patient with HPA axis suppression undergoing a major operation (colectomy, cardiac surgery)
100-150 mg/d hydrocortisone equivalent for 2-3 days
How much preoperative steroid supplementation should you give a patient iwht acute adrenal insufficiency
100 mg hydrocortisonne IV q6 -8 hours tapered as the patient’s condition stabilizes
Rapid ACTH stim test: normal response
If baseline cortisol doubles
If baseline cortisol is >34 mg or incremental increase >9 in patients iwht baseline between 15-34
alpha 1 receptors
Vascular smooth muscle constriction
Gluconeogenesis
Glycogenolysis
Alpha 2 receptors
Venous smooth muscle constriction
Beta 1 recpetors
Myocardial contraction and rate
Beta 2 receptors
Relaxes bronchial smooth muscle
Relaxes vascular smooth muscle
Insulin secretion
Role of dopamine receptors
Relaxation of renal and splanchnic smooth muscle
Site of action of intermediate dose (4-10) dopamine
++beta 1
+alpha 1
Increase isotropy with some vasoconstriction
What is site of action of high dose (>10) dopamine
+++ alpha 1 agonist
Marked arteriolar vasoconstriction increasing afterload
What is site of action of epinephrine?
Low dose beta 1 and beta 2 (incr contractility, increase vasodilation)
High dose alpha 1 and alpha 2 (vasoconstriction)
What is site of action of norepinephrine?
Low dose B1 (incr contractility)
High dose a1 and a2 (vasoconstriction)
What is site of action of vasopressin
V1: vasoconstriction of vascular smooth muscle
V2: water reabsorption in collecting ducts of kidney
V3: immediate release of vWf and factor VIII
What is site of action of phenylephrine?
a1 (vasoconstriction)
What is site of action of dobutamine
B1 (5-15) and B2 agonist (>15)
Incr isotropy, incr chronotropy, decrease SVR
What is site of action and effect of isoproterenol?
B1 and B2 agonist
Incr isotropy, incr chronotropy, incr vasodilation of skeletal and mesenteric vascular beds, extremely arrhythmogenic
What is milrinone
a phosphodiesterase inhibitor that causes vasodilation, vascular smooth muscle relaxation and leads to increased cAMP –> increased calcium flux –> increased myocardial contractility
What CV drug is arterial and venous dilator: nitride or nitroglycerin
Nitride is arterial and venous dilator (NTG is predominately VENOdilator)
What is treatment for cyanide toxicity
Inhaled amyl nitrite then IV sodium nitrite followed by thiosulfate
What is atrial natriuretic factor
Vasodilator that is released from atrial wall with atrial distention that inhibits sodium and water resorption in collecting ducts
What is most potent stimulant for SIRS
Endotoxin (LPS lipid A)
What happens to insulin and glucose with early gram negative sepsis
Decreased insulin
Increased glucose
Impaired utilization
What happens to insulin and glucose with late gram negative sepsis
Increased insulin
Decreased glucose
Insulin resistance
What is the early sepsis triad
Confusion , hyperventilation, respiratory alkalosis
What is the diagnostic triad of ARDS
PCWP <18 mm Hg
Xray of chest with bilateral infiltrates
PF ratio <200
What concentration of O2 –> O2 toxicity
FiO2 >60% for 48 hours
What are main causes of CO2 retention
Increased dead space ventilation
Hypoventilation
Increased CO2 production
What is total lung capacity
Lung volume after maximal inspiration
TLC = forced vital capacity (FVC) + residual volume (RV)
What is FVC
Volume of air maximally exhaled after maximal inhalation
What is RV
Lung volume after maximal exhalation
What is tidal volume
Volume of air with normal inspiration and expiration
What is function residual capacity
Lung volume after normal exhalation
FRC = expiratory reserve volume (ERV) + RV
What is ERV
Volume of air that can be forcefully expired after normal expiration
What is inspiratory capacity
The maximal amount of that that inspired from FRC
What is FEV1
Forced expiratory volume after maximal inhalation in 1 second
What are advantages of PEEP
Prevention of alveolar collapse/atelectasis
Decreased shunt fraction
Improved gas exchange
Increased pulmonary compliance
What are side effects of excessive peep
Decreased preload l--> decreased CO Barotrauma Increased intracranial pressure Decreased compliance Decreased gas exchange Fluid retention
What is dead space
Portion of inspired air that does not participate in gas exchange (large airways/ET tube)
What increases dead space
Undwrperfusion (PE, pulmonary artery vasoconstriction, low CO)
Overventilation (excessive peep, emphysema)
What is shut fraction
Portion of pulmonary venous gas that does not participate in gas exchange
Increased airway resistance seen in
Airway/ET tube obstruction ARDS Bronchospasm CHF (pulm edema) Mucus plug
Low UOP and increased peak airway pressures
Abdominal compartment syndrome
Tension PTX
How can you manipulate ventilation to decrease pCO2
increase minute ventilation
How can you increase PO2 in a ventilated patient
Increase PEEP
Increase FIO2
Why does increasing the FiO2 in a patient with a high shunt fraction have minimal effect on arterial PO2?
If >50% shunt fraction the oxygenated blood is already at maximal oxygen absorption
What is minute ventilation
Total lung ventilation per minute
Tidal volume x RR
Can be measured by expired gas collection for period of 1-3 minutes
What is the normal range of minute ventilation
5-10 L /min
What is CPAP
Patient breathes on their own with continuous positive pressure delivered during inspiration and expiration with no volume breaths given by the ventilator
What is pressure support ventilation
A mode that overcomes resistance of vent circuit to decrease work of breathing
Ventilator only delivers pressure during initiated breath
What is IMV mode on ventilator
Patient can breathe on their own above the mandatory rate without assistance from vent
Otherwisise vent will deliver mandatory breath at predetermined rate
What is SIMV
Delivers mandatory breath synchronously with patients initiated breath
If patient does not initiate a breath the ventilator delivers a predetermined mandatory breath
What is AC mode
Ventilator assets the patient by delivering a breath when the patient imitates a breath
Otherwise the ventilator takes control if patient does not initiate a breath and delivers a breath at a predetermined rate
What medications can be delivered through an ET tube
Narcan Atropine Vasopressin Epi Lidocaine (NAVEL)
Acetylcysteine, albuterol
Extubation criteria –> NIF
NIF < -20 cm H2O
What adjustments should you make to TPN in patient with hypercapnia, RQ > 1 and difficulty getting off the vent
Decrease amount of carbs in diet
Carbs have highest CO2 production
What is most sensitive predictor for successful extubation
RSBI < 100
More likely to cause increased auto-PEEP
Pressure controlled inverse ratio ventilation
Lower-normal CI and high wedge pressure
Cariogenic shock
High CI and lower SVR
Distributive shock
Decreased CVP, PCWP and CO
Hypovolemic
