Fiser Chapter 16 CRITICAL CARE Flashcards Preview

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Flashcards in Fiser Chapter 16 CRITICAL CARE Deck (109):
1

Normal CO

4-8 L/min

2

Normal CI

2.5-4 L/min/m^2

3

Normal SVR

800-1400

4

Normal PCWP

11 +/- 4 (7-15)

5

Normal CVP

7 +/- 2

6

Normal PAP

25/10

7

Normal SvO2 (mixed venous O2 sat)

75

8

MAP equation

MAP = CO x SVR

9

CI equation

CI = CO/BSA

10

Blood flow to organs

25% kidney
15% brain
5% heart

11

EF equation

SV/LVEDV

(LVEDV-LVESV)/LVEDV

12

Anrep effect

automatic increase in contractility 2/2 increased afterload

13

Bowditch effect

automatic increase in contractility 2/2 increased HR

14

CaO2 (arterial O2 content) equation

CaO2 = Hgb x 1.34 x O2 sat + (pO2 x 0.003)

15

O2 delivery equation

CO x CaO2 x 10

16

VO2 (O2 consumption) equation

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

Right shift O2-Hgb dissociation curve causes (increased O2 unloading)

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

Causes of increased SvO2 (saturation of venous blood)

Normally 75%
Increased in shunt or decreased O2 extraction (sepsis, cirrhosis, CN tox, hyperbaric O2, hypothermia, paralysis, coma, sedation)

19

Causes of decreased SvO2 (saturation of venous blood)

Normally 75%
Decreased in increased O2 extraction or decreased O2 delivery (decreased O2 sat, decreasedCO, malignant hyperthermia)

20

Wedge may be thrown off by

Pulm HTN
Aortic regurgitation
Mitral stenosis
Mitral regurgitation
High PEEP
Poor LV compliance

21

Swan-Ganz cath placement

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

What do you do if there is hemoptysis after flushing Swan-Ganz cath?

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

What are the relative contraindications to Swan-Ganz cath?

Previous pneumonectomy
Left bundle branch block

24

Primary determinants of myocardial O2 consumption

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