Fiser Chapter 16 CRITICAL CARE Flashcards
(109 cards)
1
Q
Normal CO
A
4-8 L/min
2
Q
Normal CI
A
2.5-4 L/min/m^2
3
Q
Normal SVR
A
800-1400
4
Q
Normal PCWP
A
11 +/- 4 (7-15)
5
Q
Normal CVP
A
7 +/- 2
6
Q
Normal PAP
A
25/10
7
Q
Normal SvO2 (mixed venous O2 sat)
A
75
8
Q
MAP equation
A
MAP = CO x SVR
9
Q
CI equation
A
CI = CO/BSA
10
Q
Blood flow to organs
A
25% kidney
15% brain
5% heart
11
Q
EF equation
A
SV/LVEDV
(LVEDV-LVESV)/LVEDV
12
Q
Anrep effect
A
automatic increase in contractility 2/2 increased afterload
13
Q
Bowditch effect
A
automatic increase in contractility 2/2 increased HR
14
Q
CaO2 (arterial O2 content) equation
A
CaO2 = Hgb x 1.34 x O2 sat + (pO2 x 0.003)
15
Q
O2 delivery equation
A
CO x CaO2 x 10
16
Q
VO2 (O2 consumption) equation
A
VO2 = CO x (CaO2 - CvO2)
Normal O2 delivery-to-consumption ration 5:1
CO increases to keep this constant
O2 consumption is usually supply independent
17
Q
Right shift O2-Hgb dissociation curve causes (increased O2 unloading)
A
CADET
Increased CO2, ATP production, acidosis, 2,3-DPG production, elevation, temperature
Normal p50 (O2 at which 50% of O2 receptors saturated) = 27 mm Hg
18
Q
Causes of increased SvO2 (saturation of venous blood)
A
Normally 75%
Increased in shunt or decreased O2 extraction (sepsis, cirrhosis, CN tox, hyperbaric O2, hypothermia, paralysis, coma, sedation)
19
Q
Causes of decreased SvO2 (saturation of venous blood)
A
Normally 75%
Decreased in increased O2 extraction or decreased O2 delivery (decreased O2 sat, decreasedCO, malignant hyperthermia)
20
Q
Wedge may be thrown off by
A
Pulm HTN Aortic regurgitation Mitral stenosis Mitral regurgitation High PEEP Poor LV compliance
21
Q
Swan-Ganz cath placement
A
Zone III (lower lung)
R SCV 45 cm L SCV 55 cm
R IJ 50 cm L IJ 60 cm
PVR can be measured only with Swan-Ganz (not Echo)
Wedge pressure should be measured at end-expiration
22
Q
What do you do if there is hemoptysis after flushing Swan-Ganz cath?
A
Increase PEEP to tamponade pulmonary artery bleed
Mainstem intubate non-affected side
Fogarty balloon down mainstem on affected side
May need thoracotomy and lobectomy
23
Q
What are the relative contraindications to Swan-Ganz cath?
A
Previous pneumonectomy
Left bundle branch block
24
Q
Primary determinants of myocardial O2 consumption
A
Ventricular wall tension and HR
Increase can lead to MI
25
Normal alveolar-arterial gradient
10-15 mm Hg in normal nonventilated patient
26
What blood has the lowest venous saturation?
Coronary sinus blood (30%)
27
Shock definition
Inadequate tissue oxygenation
28
Adrenal insufficiency MCC
Withdrawal of exogenous steroids
29
Adrenal insufficiency manifestations
CV collapse, unresponsive to fluids and pressors
nausea, emesis, abdominal pain, fever, lethargy, decreased glucose, hyperkalemia
Tx: dexamethasone
30
Steroid potency
1x cortisone, hydrocortisone
5x prednisone, prednisolone, methylprednisolone
30x dexamethasone
31
Neurogenic shock symptoms and treatment
Loss of sympathetic tone
Spine or head injury
Decreased HR, BP, warm skin
Tx: Give volume first, then phenylephrine
32
Hemorrhagic shock initial alteration
Increased diastolic pressure
33
Cardiac tamponade mechanism of hypotension
Decreased ventricular filling
Echo: impaired diastolic filling of RA
34
Beck's triad
Hypotension, JVD, muffled heart sounds
Cardiac tamponade
35
Cardiac tamponade tx
Fluid resuscitation
Pericardial window or pericardiocentesis
36
Early sepsis triad
Hyperventilation
Confusion
Hypotension
37
Blood glucose in sepsis
Hyperglycemia often occurs just before clinically septic
Early GN sepsis: increased glucose, decreased insulin (impaired utilization)
Late GN sepsis: increased glucose and insulin (insulin resistence)
38
Hypovolemia neurohormonal response
Rapid: adrenergic release -> vasoconstriction and increased cardiac activity
Sustained: RAS -> renin from kidney -> vasoconstriction and water resorption; ADH from pituitary -> water reabroprtion; ACTH from pituitary -> cortisol
39
Sudan red stain
May show fat in sputum and urine in fat embolism
40
Where do most PEs arise from?
Iliofemoral region
41
If PE patient is in shock despite massive pressors and inotropes?
After heparin and Coumadin, consider open or percutaneous (suction catheter) embolectomy
42
Air emboli tx
Trendelenburg, role to left (keeps air in RV and RA), then aspirate air out with central line or PA catheter to RA/RV
43
IABP mechanism
- Inflates on T wave (diastole): improves diastolic BP, improves diastolic coronary perfusion
- Deflates on P wave (systole): decreases afterload
44
IABP contraindication
Aortic regurgitation
45
IABP catheter location
Just distal to L subclavian (1-2 cm below top of arch)
46
IABP uses
Cardiogenic shock after CABG or MI
| Refractory angina awaiting revasc
47
Alpha-1 receptor
Vascular smooth muscle constriction
Gluconeogenesis and glycogenolysis
48
Alpha-2 receptor
Venous smooth muscle constriction
49
Beta-1 receptor
Myocardial contraction and rate
50
Beta-2 receptor
- Relaxes bronchial smooth muscle
- Relaxes vascular smooth muscle
- Increases insulin, glucagon, and renin
51
Dopamine receptors
Relax renal and splanchnic smooth muscle
52
Dobutamine MoA
Beta-1: increases contractility mostly; tachycardia with higher doses
53
Milrinone MoA
Phosphodiesterase inhibitor: increases cAMP -> increased Ca flux and myocardial contractility; also vascular smooth muscle relaxation and pulmonary vasodilation
54
Phenylephrine MoA
Alpha-1 vasoconstriction
55
Norepinephrine MoA
Low dose: beta-1 increased contractility
High dose alpha-1 and alpha-2
Potent splanchnic vasoconstrictor
56
Epinephrine MoA
Low dose beta-1 and beta-2 increased contractility and vasodilation, but can decrease BP
High dose alpha-1 and alpha-2 vasoconstriction; increased cardiac ectopic pacer activity and myocardial O2 demand
57
Isoproterenol MoA
Beta-1 and beta-2 increased HR and contractility, vasodilation
SE: Very arrhythmogenic; increases heart metabolic demand, may actually decrease BP
58
Vasopressin MoA
V1- receptor vasoconstriction of vascular smooth muscle
V-2 receptor intrarenal water reabsorption at collecting ducts; extrarenal mediates factor VIII and vWF release
59
Nipride MoA
arterial vasodilator
CN toxicity; can check thiocyanate levels and metabolic acidosis
60
CN toxicity treatment
Amyl nitrite, then sodium nitrite
61
Nitroglycerin MoA
Venodilation with decreased myocardial wall tension by decreasing preload; moderate coronary vasodilator
62
Hydralazine MoA
alpha-blocker, lowers BP
63
Dopamine MoA
```
Dopamine receptors (renal)
Higher dose beta-adrenergic (heart contractility)
Higher dose alpha-adrenergice (vasoconstriction and increase BP)
```
64
Lung compliance
Change in volume/
Change in pressure
decreased in ARDS, fibrosis, reperfusion injury, edema, atelectasis
65
PEEP
Alveoli recruitment -> improves FRC and compliance -> best way to improves oxygenation
66
Pressure support
Decreases work of breathing
67
Prevent O2 radical toxicity by what
Keep FiO2 = 60%
68
When do you get barotrauma?
Plateaus > 30, peaks >50
So decrease Tv and consider pressure control ventilation
69
Excessive PEEP complications
- Decreased RA filling
- Decreased CO
- Decreased renal blood flow
- Decreased urine output
- Increased pulmonary vascular resistance
70
High frequency ventilation use
Kids
TE fistula
Bronchopleural fistula
71
TLC
TLC = FVC + RV
72
FRC
FRC = ERV + RV
Lung volume after normal exhalation
- Decreased by atelectasis, ARDS, contusion/trauma
- Improved with PEEP
73
Dead space
Area of lung ventilated but not perfused; normally to level of bronchiole (150 mL)
Increases with: Drop in CO, PE, pulm HTN, ARDS, excessive PEEP; can lead to hypercapnia
74
ARDS MoA
Neutrophils; increased proteinaceous material; increased A-a gradient; increased pulmonary shunt
MCC pneumonia
Other: sepsis, multi-trauma, severe burns, pancreatitis, aspiration, DIC
75
ARDS criteria
Acute onset
Bilateral pulmonary infiltrates
PaO2/FiO2 = 300
Absence of heart failure (wedge < 18 mm Hg)
76
Aspiration, increased damage associated with what
pH < 2.5, volume > 0.4 cc/kg
77
Mendelson's syndrome
chemical pneumonitis from aspiration of gastric secretions
78
Most frequent site of aspiration
superior segment of RLL
79
Fever, tachycardia, hypoxia in first 48hr postop
Atelectasis: collapse of alveoli resulting in reduced oxygenation
Increased in patients with COPD, upper abdominal surgery, obesity
Tx: IS, pain control, ambulation
80
What can throw off a pulse oximeter
```
Nail polish
Dark skin
Low-flow states
Ambient light
Anemia
Vital dyes
```
81
Causes of pulmonary vasodilation?
```
PGE1
Prostacyclin (PGI2)
Nitric oxide
Bradykinin
Alkalosis
```
82
Causes of pulmonary vasoconstriction?
```
Hypoxia
Acidosis
Histamine
Serotonin
TXA2
```
83
Causes of pulmonary shunting
Nitroprusside
Nitroglycerin
Nifedipine
84
MCC of postop renal failure
Intra-op hypotension
70% nephrons need to be damaged
85
FeNa
(urine Na/Cr) / (plasma Na/Cr)
Best test for azotemia
FeNa <1% in prerenal
FeNa >3% in parenchymal
86
Urine measurements in prerenal failure
```
Urine osmolarity >500
U/P osmolality >1.5
U/P creatinine >20
Urine sodium < 20
FeNa < 1%
```
87
Urine measurements in parenchymal failure
```
Urine osmolarity 250-350
U/P osmolality < 1.1
U/P creatinine < 10
Urine sodium > 40
FeNa > 3%
```
88
Oliguria tx
1. Volume load (CVP 11-15)
2. Diuresis trial
3. HD
89
Dialysis indications
```
AEIOU:
Acidosis
Electrolytes (hyperkalemia)
Ingestion (poisons)
Overload
Uremia (encephalopathy, coagulopathy)
```
90
CVVH compared to HD
Slower
Good for ill patients who cannot tolerate large colume shifts (septic shock)
Hct increases by 5-8 for each liter taken off
91
RAAS
1. hypotension, hypernatremia (sensed by macula densa), beta-adrenergic stiulation, or hyperkalemia -> JG apparatus releases renin
2. Renin converts Angiotensinogen (synthesized in liver) to ATI
2. ACE (from lung) converts ATI to ATII
3. ATII vasoconstricts and increases HR, contractility, glycogenolysis, gluconeogenesis; inhibits renin release
4. ATII also causes aldosterone release from adrenal cortex -> DCT -> upregulating NaK ATPase on membrane -> water reabsorbtion, Na re-absorbed, K secreted
92
ANP
Atrial distention -> ANP release from atrial wall -> inhibits Na and water resorption in collecting ducts; also vasodilation
93
ADH
High osmolality -> posterior pituitary releases ADH -> water resorption in collecting ducts; also vasoconstrictor
94
Efferent limb of kidney
Controls GFR
95
DCT
where ATII acts to upregulate NaK ATPase and cause Na, water reabsorbtion and K secretion
96
Renal toxic drugs
NSAID: inhibits prostaglandin synthesis, causing renal arteriole vasoconstriction
Aminoglycosides: direct tubular injury
Myoglobin: direct tubular injury (Tx: alkalinize urine)
Contrast dyes: direct tubular injury (Tx: pre-hydration best; HCO3-, NAC)
97
SIRS most potent stimulus
Endotoxin (lipopolysaccharide - lipid A)
Major components: TNF-alpha and IL-1
Results in capillary leakage, microvascular thrombi, hypotension, end-organ dysfunction
98
SIRS definition
Temp > 38 or <36
HR > 90
RR > 20 or PaCO2 < 32
WBC >12 or <4
99
Shock definition
Arterial hypotension despite adequate volume resuscitation
| Inadequate tissue oxygenation
100
Multi organ dysfunction definition
Progressive but reversible dysfunction of 2 or more organs arising from an acute disruption of normal homeostasis
101
Brain death preclusions
```
Temp <32
BP <90
Drugs (phenobarb, pentobarb, EtOH)
Metabolic derangements (hyperglycemia, uremia)
Desaturation with apnea test
```
102
Brain death definition
6-12 hours of:
- Unresponsive to pain
- Absent cold caloric oculovestibular reflexes
- Absent oculocephalic reflex (patient doesn't track)
- No spontaneous respirations
- No corneal reflex
- No gag reflex
- Fixed and dilated pupils
- Positive apnea test
*Can still have deep tendon reflexes with brain death
103
Brain death on EEG or MRA
EEG: Electrical silence
MRA: No blood flow to brain
104
Apnea test
Pre-oxygenation, and CO2 should be normal prior
Catheter delivering O2 at 8L/min is placed at carina through ETT-Disconnect from vent for 10 minutes
Positive test meets brain death criteria: CO2 >60 or increase in CO2 by 20
Negative test and cannot declare brain death, so put back on vent: If BP drops <90, desaturates <85%, or spontaneous breathing occurs
105
Carbon monoxide poisoning
- Falsely normal oxygen saturation on pulse ox
- Binds Hgb directly, creates carboxyhemoglobin
- HA, nausea, confusion, coma, death
- Can usually correct with 100% oxygen on vent
- Abnormal carboxyhemoglobin >10% (smokers >20%)
106
Methemoglobinemia
- From nitrites such as Hurricaine spray
- Nitrites bind Hgb
- O2 sat reads 85%
- Tx: Methylene blue
107
Critical illness polyneuropathy
Motor > sensory neuropathy
Occurs with sepsis
Can lead to failure to wean from vent
108
Reperfusion injury
Xanthine oxidase: In endothelial cells, forms toxic oxygen radicals with reperfusion
XO also involved in the metabolism of purines and breakdown to uric acid
Most important mediator of reperfusion injury is PMNs
109
EtOH withdrawal
HTN, tachy, delirium, seizures after 48hr
Tx: thiamine, folate, B12, Mg, K, PRN lorazepam
