16 Critical Care Flashcards

1
Q

Mean arterial pressure

A

MAP = CO x SVR

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2
Q

Cardiac index

A

CI = CO/BSA

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3
Q

Define preload

A

Left ventricular end-diastolic length

Lineraly related to LV end diastolic volume and filling pressure

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4
Q

What percentage of CO does kidney get? Brain? Heart?

A

Kidney 25%
Brain 15%
Heart 5%

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5
Q

Define afterload

A

Resistance against the ventricle contracting

SVR

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6
Q

Define stroke volume

A

Determined by LVEDV, contractility and afterload

SV = LVEDV - LVESV

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7
Q

Define ejection fraction

A

EF = SV/LVEDV

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8
Q

Determinants of end-diastolic volume

A

Preload

Distensibility of the ventricle

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9
Q

Determinants of end-systolic volume

A

Contractility

Afterload

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10
Q

Define Anrep effect

A

Automatic increase in contractility secondary to increased afterload

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11
Q

Define Bowditch effect

A

Automatic increase in contractility secondary to increase heart rate

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12
Q

How do you determine the arterial O2 content?

A

CaO2 = Hgb x 1.34 x O2sat + (Po2 x 0.003)

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13
Q

How do you determine O2 delivery?

A

O2 delivery = CO x CaO2 x 10

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14
Q

How do you determine O2 consumption?

A

Vo2 = CO x (CaO2 - CvO2)

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15
Q

Normal O2 delivery-to-consumption ratio?

A

5:1
CO increase to keep this ratio constant
O2 consumption is supply independent (until very low levels of delievery are reached)

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16
Q

Causes of right shift of Oxyhemoglobin curve?

A
O2 unloading
Increased CO2
Increased 2,3-DPG
Increased temp
Increased ATP
Increased H+ ions (decreased pH)
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17
Q

Increased SvO2 occurs when:

A

Increased shunting of blood
Decreased oxygen extraction (i.e. sepsis, cirrhosis, cyanide toxicity, hyperbaric O2, hyptohermia, paralysis, coma, sedation)

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18
Q

Decreased SvO2 occurs when:

A

Increased O2 extraction

Decreased O2 delivery

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19
Q

Things that can effect pulmonary wedge pressure?

A
Pulmonary hypertension
Aortic regurgitation
Mitral stenosis
Mitral regurg
High PEEP
Poor LV compliance
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20
Q

Hemoptysis after flushing Swan-Ganz catheter?

A
Increase PEEP (tamponade the pulmonary artery bleed)
Mainstem intubate non-affected side
Fogarty balloon down mainstem on affected side
Possible thoracotomy and lobectomy
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21
Q

Relative CI to swan-ganz catheter?

A

Previous pnumonectomy

Left bundle branch block

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22
Q

Approximate Swan-Ganz catheter distance to wedge?

A

RSCV 45cm
RIJ 50cm
LSCV 55cm
LI 60cm

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23
Q

What is the only way to measure pulmonary vascular resistance?

A

Swan-Ganz catheter (NOT ECHO)

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24
Q

When should you take wedge pressure?

A

End-expiration

Ventilatory method does not matter

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25
Primary determinants of myocardial O2 consumption?
Increased ventricular wall tension | Heart rate
26
Normal A-a gradient in a non-ventilated patient?
10-15mmHg
27
Blood with lowest venous saturation?
Coronary sinus blood (30%)
28
Adrenal insufficiency
MCC - withdrawal of exogenous steroids Acute: cardiovascular collapse, unresponsive to fluids or pressors, nasuea/vomiting, abdominal pain, fever, lethargy, decreased glucose, hyperkalemia Tx: Dexamethasone
29
Steroid potency?
1x - cortisone, hydrocortisone 5x - prednisone, prednisolone, methylprednisolone 30x - dexamethasone
30
Neurogenic shock
Loss of sympathetic tone Associated with spine or head injury Decreased HR, decreased BP, warm skin Tx: give volume 1st, phenylephrine after resuscitation
31
Initial alteration in hemorrhagic shock?
Increased diastolic pressure
32
Cardiac tamponade
Causes cardiogenic shock Decreased ventricular filling ECHO shows impaired diastolic filling of right atrium first (weakest wall) Tx: Rescucitation, pericardial window/pericardiocentesis
33
Beck's triad
Hypotension Jugular venous distention Muffled heart sounds
34
Decreased CVP/PCWP Decreased CO Increased SVR
Hemorrhagic shock
35
Decreased CVP/PCWP Increased CO Decreased SVR
Septic shock (hyperdynamic)
36
Increased CVP/PCWP Decreased CO Increased SVR
Cardiogenic (i.e. MI, cardiac tamponade)
37
Decreased CVP/PCWP Decreased CO Decreased SVR
Neurogenic (i.e. head or spinal cord injury) | Adrenal insufficiency
38
Early sepsis triad
Hyperventilation Confusion Hypotension
39
Early gram-negative sepsis
``` Decreased insulin Increased glucose (impaired utilization) ```
40
Late gram-negative sepsis
``` Increased insulin Increased glucose (insulin resistance) ```
41
Neurohormonal response to hypovolemia - Rapid
Epinephrine and norepinephrine release Adrenergic release Results in vasoconstriction and increased cardiac activity
42
Neurohormonal response to hypovolemia - Sustained
Renin (from kidney - vasconstriction and water resorption) ADH (from pituitary - reabsorption of water) ACTH (from pituitary - increases cortisol)
43
Fat emboli
Petechia, hypoxia, confusion Sudan red stain may show fat in sputum and urine Most common from LE fractures, orthopedic procedures
44
Pulmonary emboli
``` Chest pain and dyspnea Decreased PO2 and PCO2 Respiratory alkalosis Increased HR and RR Hypotension and shock if massive ``` Tx: HEparin, coumadine; consider open or percutaneous emboliectomy if in shock despite massive pressors and inotropes
45
Most common source of PEs?
Iliofemoral region
46
Treatment of air emboli?
Patient head down and roll to left (keeps air in RV/RA) | Aspirate air out with central line to RA/VA
47
When does an intra-aortic balloon pump inflate? Deflate?
Inflates on T wave (diastole) | Deflates on P wave (systole)
48
CI to intra-aortic balloon pump?
Aortic regurgitation
49
Uses/effect of intra-aortic balloon pump?
Used for cardiogenic shock (after CABG or MI) Refractory angina awaiting revascularization Decreases afterload (deflation during ventricular systole) Improves diastolic BP (inflation during ventricular diastole) Which improves diastolic coronary perfusion
50
Alpha-1 receptors
Vascular smooth muscle constriction Gluconeogenesis Glycogenolysis
51
Alpha-2 receptors
Venous smooth muscle contriction
52
Beta-1 receptors
Myocardial contraction and rate (ionotrope and chronotrope)
53
Beta-2 receptors
Relaxes bronchial smooth muscle Relaxes vascular smooth muscle Increases insulin, glucagon, renin
54
Dopamine receptors
Relaxes renal and splanchnic smooth muscle
55
Dopamine (2-5ug/kg/min initially)
2-5ug/kg/min - dopamine receptors (renal) 6-10ug/kg/min - beta-adrenergic (heart contractility) >10ug/kg/min - alpha-adrenergic (vasoconstriction and increased BP)
56
Dobutamine (3ug/kg/min initially)
Beta-1 receptors | Increased contractility, tacycardia with higher doses
57
Milrinone
Phosphodiesterase inhibitor - increases cAMP Results in increased Ca flux and increased myocardial contractility Vascular smooth muscle relaxation and pulmonary vasodilation
58
Phenylephrine (10ug/kg/min initially)
Alpha-1 | Vasoconstriction
59
Norepinephrine (5ug/min initially)
Low doses - Beta-1 (increased contractility) | High dose - Alpha-1 and Alpha-2 (veno and vaso constriction)
60
Epinephrine (1-2ug/min initially)
Low dose - Beta-1 and B-2 (increased contractility and vasodilation; can decrease BP at low dose) High dose - Alpha-1 and Alpha-2 (veno and vaso constriction; can increase cardiac ectopic pacer activity and myocardial O2 demand)
61
Isoproterenol (1-2ug/min initially)
B-2 and B-2 (increased contractility, vasodilates) | AE: extremely arrhythmogenic, increased heart metabolic demand, may actually decrease BP
62
Vasopressin
``` V1 receptors - vasocontriction of vascular smooth muscle V2 receptors (intrarenal) - water reabsoprtion at collecting ducts V2 receptors (extrarenal) - mediate release of factor VII and vWF ```
63
Nipride
Arterial vasodilator Cyanide toxicity at dose >3ug/kg/min for 72hrs Check thiocyanate levels and signs of metabolic acidosis
64
Treatment for cyanide toxicity
Amyl nitrate | Then sodium nitrite
65
Nitroglycerin
Predominately venodilation with decreased myocardial wall tension from decreased preload Moderate coronary vasodilator
66
Hyrdalazine
a-blocker | Lower BP
67
Compliance
Change in volume / change in pressure High compliance means lungs are EASY to ventilate Decreased: ARDS, fibrotic lung disease, reperfusion injury, pulmonary edema, atelactasis
68
Effect of aging on the lungs?
Decreased FEV1 Decreased vital capacity Increased functional residual capacity
69
V/Q ratio
Ventilation/perfusion ratio Highest in upper lobes Lowest in lower lobes
70
Why does increasing PEEP improve oxygenation?
Increased alveoli recruitment | Improves FRC
71
How to you decrease CO2?
Increase respiratory rate | Increase tidal volume
72
Normal weaning parameters?
``` NIF > 20 FiO2 < 40% PEEP 5 Pressure support 5 RR < 24 HR <120 PO2 > 60mmHg PCO2 < 50mmHg pH 7.35-7.45 Saturation >93% Off pressors Follows commands Can protect airway ```
73
Puts you at risk for barotrauma? How do you decrease the risk?
Plateau > 30 Peak > 50 Need to decrease TV Consider pressure control ventilation
74
Complications of excessive PEEP?
``` Decreased RA filling Decreased CO Decrease renal blood flow Decease urine output Increase pulmonary vascular resistance ```
75
Total lung capacity
Lung volume after maximal inspiration | TLC = FRC + RV
76
Forced vital capacity
Maximal exhalation after maximal inhalation
77
Residual volume
Lung volume after maximal expiration (20% TLC)
78
Tidal volume
Volume of air with normal inspiration and expiration
79
Functional residual capacity
Lung volume after normal exhalation | FRC = ERV + RV
80
What can decrease functional residual capacity?
Surgery (atelectasis) Sepsis (ARDS) Trauma (contusion, atelectasis, ARDS)
81
Expiratory reserve volume
Volume of air that can be forcefully expired after normal expiration
82
Inspiratory capacity
Maximum air breathed in from FRC
83
FEV1
Forced expiratory volume in 1 second after maximal inhalation
84
Minute ventilation
MV = TV x RR
85
Decreased TLC Decreased RV Decreased FVC
Restrictive lung disease | FEV1 can be normal or increased
86
Increased TLC Increased RV Decreased FEV1
Obstructive lung disease | FVC can be normal or decreased
87
Dead space
``` Normally to the level of the bronchiole (150mL) Area of lung that is ventilated but not perfused Increases with: - Drop in CO - PE - Pulmonary HTN - ARDS - Excssive PEEP ```
88
COPD breathing changes
Increased work of breathing due to prolonged expiratory phase
89
ARDS
Mediated by PMNs, increased proteinaceous material, increased A-a gradient, increased pulmonary shunt Causes: Pnuemonia*, sepsis, multi-trauma, severe burns, pancreatitis, aspiration, DIC
90
Diagnostic criteria for ARDS
Acute onset Bilateral pulmonary infiltrates PaO2/FiO2 <300 Absence of heart failure (Wedge <18mmHg)
91
Mendelson's syndrome
Chemical pneumonitis from aspiration of gastric secretions
92
Atelectasis
Collapse of alveoli resulting in reduced oxygenation Sx: Fever, tachycardia, hypoxia Tx: IS, pain control, ambulation
93
What can make a pulse-ox inacurate?
Nail polish, dark skin, low-flow state, ambient light, anemia, vital dyes
94
Causes pulmonary vasodilation?
PGE1 Prostacyclin (PGI2) Nitric oxde Bradykinin
95
Causes pulmonary vasoconstriction?
HYpoxia Acidosis Histamine Serotonin, TXA2
96
Alkalosis - effect on pulmonary vasculature?
Pulmonary vasodilator
97
Acidosis - effect on pulmonary vasculature?
Pulmonary vasoconstrictor
98
Drugs that cause pulmonary shunting?
Nitroprusside Nitroglycerin Nifedipine
99
Most common cause of postoperative renal failure?
Intra-op hypotension
100
Amount of nephron that needs to be damaged before renal dysfunction?
70%
101
FeNa
Fractional excretion of sodium (Urine Na/Cr) / (plasma Na/Cr) Best test for azotemia
102
``` Urine Osm >500 U/P osmolality >1.5 U/P creatinine >20 Urine sodium <20 FeNa < 1% ```
Prerenal azotemia
103
``` Urine Osm 250-350 U/P osmolality <1.1 U/P creatinine <10 Urine sodium >40 FeNa > 3% ```
Parenchymal azotemia
104
Treatment of oliguria
Make sure patient is volume loaded (CVP 11-15mmHg) Try diuretic trial (Lasix) Dialysis if needed
105
Indications for dialysis
``` Fluid overload Hyperkalemia Metabolic acidosis Uremic encephalopahty Uremic coagulopathy Poisoning ```
106
Renin
Released in response to decreased pressure (JGA), increased Na (macula densa) concentration, beta-adrenergic stimulation and hyperkalemia
107
Aldosterone
Acts at distal convoluted tubule to reabsorb water by up-regulating the Na/K ATPase (Na re-absorbed, K secreted)
108
Effect of Angiotensin II
``` Stimulates release of aldosterone Vasoconstricts Increases HR Contractility Glycogenolysis Gluconeoenesis Inhibits renin ```
109
Atrial natriuretic peptide
Released from atrial wall with atrial distention Inhibits Na and water resoprtion in the collecting ducts Vasodilator
110
Antidiuretic hormone (ADH, vasopressin)
Released by posterior pituitary gland when osmolality is high Acts on collecting ducts for water resorption Vasoconstrictor
111
What controls GFR?
Efferent limb of the kidney
112
Renal toxic drugs
NSAIDs (inhibit PGE - renal arteriole vasoconstriction) Aminoglycoside (direct tubular injury) Myoglobin (DTI) Contrast dye (DTI)
113
Causes of SIRS
``` Shock Infection Burn Multi-trauma Pancreatitis Severe inflammatory responses ```
114
What is the most potent stimulus for SIRS?
Endotoxin (lipopolysaccharide - Lipid A) | Stimulates TNF release
115
Effect of TNF-a and IL-1 release?
SIRs | Capillary leakage, microvascular thormbi, hypotension, eventually end-organ dysfunction
116
Criteria for SIRS
Temp >38 or < 36 HR >90 RR >20 or PaCO2 <32 WBC >12000 or < 4000
117
Diagnostic criteria: end organ dysfunction. | Pulmonary
Need for mechanical ventilation | PaO2:FiO2 ratio <300 for 24hrs
118
Diagnostic criteria: end organ dysfunction. | Cardiovascular
Need for ionotropic drugs | CI <2.5 L/min/m2
119
Diagnostic criteria: end organ dysfunction. | Kidney
Creatinine >2x baseline on 2 consecutive days | Need for dialysis
120
Diagnostic criteria: end organ dysfunction. | Liver
Bilirubin >3mg/dL for 2 days | PT > 1.5
121
Diagnostic criteria: end organ dysfunction. | Nutrition
10% reduction in lean body mass albumin 2.0 Total lymphocyte count <1
122
Diagnostic criteria: end organ dysfunction. | CNS
GCS <10 without sedation
123
Diagnostic criteria: end organ dysfunction. | Coagulation
Platelet count < 50 Fibrinogen <100 Need for factor replacement
124
Diagnostic criteria: end organ dysfunction. | Host defenses
WBC < 1000 | Invasive infection including bacteremia
125
What precludes a diagnosis of brain death?
Temp <32 BP <90 Drugs (i.e. phenobarbital, pentobarbital, ETOH) Metabolic derangemetns (hyperglycemia, uremia) Desaturation with apnea test
126
What must exist for 6-12 hours to diagnose brain death?
``` Unresponsive to pain Absent cold caloric oculovestibular reflexes Absent oculocephalic reflex No spontaneous respirations No corneal reflex No gag reflex Fixed and dilated pupils Positive apnea test ``` Still have deep tendon relfexes with brain death
127
Apnea test
Patient is pre-oxygenated, catheter delivering O2 at 8L/min is placed at the carina through the ET-tube and CO2 should be normal before the start of the test - Disconnect from vent for 10 minutes - CO2 > 60mmHg or increase in CO2 by 20 is POSITIVE for apena
128
What is a negative result for an apnea test?
``` BP drops (<90mmHg) Patient desaturates (<85%) Spontaneous breathing ```
129
Carbon monoxide
Can increase O2 sats on pulse-ox Carboxyhemoglobin - HA, nausea, confusion, coma, death (<10% in normal, <20% in smokers) Corrects with 100% O2
130
Methemoglobinemia
From nitrates O2 sat reads 85% Tx: methylene blue
131
Critical illness polyneuropathy
Motor > sensory neuropathy Occurs with sepsis Causes failure to wean from ventilation
132
Xanthine oxidase
Is in endothelial cells Forms toxic oxygen radicals with reperfusion Also involved in metabolism of purines to uric acid
133
DKA
Nausea/vomiting, thirst, polyruia, increased glucose, increased ketones, decreased sodium, increased potassium TX: normal saline and insulin
134
ETOH withdrawal
HTN, tachycardia, delirium, seizures (After 48hrs) | Tx: Thiamine, folate, B12, Mg, K, PRN lorazepam
135
ICU psychosis
``` Third POD day - preceded by lucid interval Address metabolic (hypoglycemia, DKA< hypoxia, hypercarbia, electrolyte imbalances) and organic (MI, CVA) causes ```