Critical Care Flashcards
1
Q
MAP
A
CO x SVR
2
Q
Cardiac index
A
cardiac output / BSA
3
Q
cardiac output
A
kidney gets 25%
brain gets 15%
heart gets 5%
CO increases with HR up to 120-150 beats/min then starts to go down because of diastolic filling time
4
Q
Preload
A
end diastolic length, linearly related to end-diastolic volume (EDV) and filling pressure
5
Q
Afterload
A
resistance against the ventricle contracting (SVR)
6
Q
Strove volume
A
determined by LVEDV, contractility, and afterload
= LVEDV - LVESV
*atrial kick accounts for 15-30% of LVEDV
7
Q
Ejection fraction
A
stroke volume (LVEDV - LVESV) / EDV
8
Q
End diastolic volume (EDV)
A
determined by preload and distensibility of the ventricle
9
Q
End systolic volume (ESV)
A
determined by contractility and afterload
10
Q
Anrep effect
A
automatic increase in contractility secondary to increase afterload
11
Q
Bowditch effect
A
automatic increase in contractility secondary to increase heart rate
12
Q
O2 delivery
A
CO x arterial O2 content (CaO2) = CO x (Hgb x 1.34 x O2 saturation + 1 [PO2 x 0.003])
13
Q
O2 consumption (VO2)
A
CO x (CaO2 - CvO2); CvO2 = venous O2 content
- normal O2 delivery-to-consumption ratio is 5:1; CO increases to keep this ratio constant
- O2 consumption is usually supply independent (consumption does not change until low levels of delivery are reached)
14
Q
Right shift on oxygen-Hgb dissociation curve (O2 unloading)
A
increase CO2, increase temperature, increase ATP production, increase 2,3-dpg production, or decrease pH
15
Q
Increase SvO2 (saturation of venous blood, normally 75% +/- 5%)
A
occurs with increase shunting of blood or decrease O2 extraction (sepsis, cirrhosis, cyanide toxicity, hyperbaric O2, hypothermia, paralysis, coma, sedation)
16
Q
Decrease SvO2
A
occurs with increase O2 extraction or decrease O2 delivery (decrease O2 saturation, decrease cardiac output)
17
Q
Wedge
A
may be thrown off by pulmonary HTN, aortic regurgitation, mitral stenosis, mitral regurg, high PEEP, poor LV compliance
18
Q
Swan-Ganz catheter
A
should be placed in zone III (lower lung)
- hemoptysis after flushing Swan-Ganz catheter - increase PEEP, which will tamponade the pulmonary artery bleed, mainstem intubate nonaffected side; can try to place fogarty balloon down the affected side; may need thoracotomy and lobectomy
- relative contraindications - previous pneumonectomy, left bundle branch block
- approx catheter distances to wedge - R SCV 45cm, R IJ 50cm, L SCV 55cm, L IJ 60cm
19
Q
primary determinants of myocardial O2 consumption
A
increase ventricular wall tension and HR; can lead to myocardial ischemia
20
Q
Unsaturated bronchial blood
A
empties into pulmonary veins; thus LV blood is 5 mm Hg (P02) lower than pulmonary capillaries
21
Q
Alveolar - arterial gradient
A
10 - 15 mm Hg normal in nonvent pt
22
Q
blood with lowest venous saturation
A
coronary venous blood (30%)
23
Q
Acute adrenal insufficiency
A
cardiovascular collapse, characteristically unresponsive to fluids and pressors
24
Q
Chronic adrenal insufficiency
A
hyperpigmentation, weakness, weight loss, GI symptoms, increase K, decrease Na, fever, hypotension
25
Steroid potency
1X - cortisone, hydrocortisone
5X - prednisone, prednisolone, methylprednisolone
30X - dexamethasone
26
Neurogenic shock
loss of sympathetic tone
* usually have decrease heart rate, decrease blood pressure, warm skin
* tx: give volume 1st, then phenylephrine after resuscitation; give steroids for blunt spinal trauma with deficit
27
Hemorrhagic shock
initial alteration is increase diastolic pressure
28
Cardiac tamponade
* causes decreased diastolic ventricular filling and hypotension
* Beck's triad - hypotension, JVD, muffled heart sounds
* Echo - shows impaired diastolic filling of right atrium initially (1st sign of cardiac tamponade)
* pericardiocentesis blood does not form clot
* tx: fluid resuscitation initially; need pericardial window or pericardiocentesis
29
hemorrhagic shock
decrease CVP, PCWP, CO; increase SVRI
30
septic shock
decrease CVP, increase CO, decrease SVRI
| *severe septic shock that leads to cardiac dysfunction can cause decrease CO and increase SVRI
31
Cardiogenic shock
increase CVP and PCWP, decrease CO, increase SVRI
32
Neurogenic shock
decrease CVP and PCWP, decrease CO, decrease SVRI
33
Hypoadrenal shock
decrease CVP and possibly increase PCWP, decrease CO, decrease SVRI
34
Early sepsis triad
hyperventilation, confusion, respiratory alkalosis
* early gram negative sepsis - decrease insulin, increase glucose (impaired utilization)
* late gram-negative sepsis - increase insulin, increase glucose (secondary to insulin resistance)
* hyperglycemia - often occurs just before patient becomes clinically septic
35
Fat emboli
signs include petechia, hypoxia, and confusion; sudan red stain may show fat in sputum and urine; most common with lower extremity (hip, femur) fractures
36
Pulmonary emboli
echo will show RV strain
*suspect PE and PA systolic pressures > 40, decrease PO2 and PCO2, respiratory alkalosis, chest pain, cough, dyspnea, increase heart rate
37
Air emboli
place patient head down and roll to left (keeps air in RV and RA), then aspirate air with central line or PA catheter to RA/RV
38
Intra-aortic balloon pump (IABP)
* inflates on T wave (diastole); deflates on P wave or start of Q wave (systole)
* aortic regurgitation contraindication
* place tip of catheter just distal to left subclavian (1-2 cm below the top of the arch)
* used for cardiogenic shock (after CABG, MI) or in patients with refractory angina
* decreases afterload (deflation during ventricular systole)
* improves SBP (inflation during ventricular diastole), which improves coronary perfusion
39
Alpha 1 receptor
vascular smooth muscle constriction; gluconeogenesis, glycogenolysis
40
Alpha 2 receptor
venous smooth constriction
41
Beta 1 receptor
myocardial contraction and rate
42
Beta 2 receptor
relaxes bronchial smooth muscle, relaxes vascular smooth muscle; increases insulin, glucagon, renin
43
dopamine receptors
relax renal and splanchnic smooth muscle
44
dopamine
* 0-5 ug/kg/min - dopamine receptors (renal)
* 6-10 ug/kg/min - beta-adrenergic (heart contractility)
* >10 ug/kg/min - alpha-adrenergic (vasoconstriction and increase BP)
45
dobutamine
* 5-15 ug/kg/min - beta-1 (increase contractility mostly)
| * >15ug/kg/min - beta-2 (vasodilation, increase HR)
46
Milrinone
* phosphodiesterase inhibitor (increase cAMP)
* results in increase calcium flux and increase myocardial contractility
* also causes vascular smooth muscle relaxation and vasodilation
47
Phenylephrine
*alpha-1, vasoconstriction
48
Norepinephrine
* low dose - beta-1 (contractility)
* high dose - alpha-1 and alpha-2
* potent splnachnic vasoconstrictor
49
Epinephrine
* low dose - beta-1 and beta-2 (increase contractility and vasodilation); can decrease BP at low doses
* High dose - alpha-1 and alpha-2 (vasoconstriction); increase cardiac ectopic pacer activity and myocardial O2 demand
50
Isoproterenol
* beta-1 and beta-2, increase heart rate and contractility, vasodilates
* side effects: extremely arrhythmogenic; increase heart metabolic demand (rarely used); may actually decrease BP
51
Vasopressin
* V-1 receptors - vasoconstriction of vascular smooth muscle
* V-2 receptors (intrarenal) - water reabsorption at collecting ducts
* V-2 receptors (extrarenal) - mediate release of factor VIII and von Willebrand factor
52
Nipride
arterial and venous dilator
* cyanide toxicity at doses > 3 ug/kg/min for 72 hours; can check thiocyanate levels and signs of metabolic acidosis
* tx: amyl nitrite, then sodium nitrite
53
Nitroglycerin
predominately venodilation, modest effect on coronaries; decrease myocardial wall tension by decrease preload
54
Hydralazine
alpha blocker
55
Lung compliance
change in volume / change in pressure
* high compliance means lungs easy to ventilate
* pulmonary compliance decrease in patients with ARDS, fibrotic lung diseases, reperfusion injury, pulmonary edema
56
Aging (re: lungs)
decrease FEV1 and vital capacity, increase functional residual capacity (FRC)
57
V/Q ratio
highest in upper lobes, lowest in lower lobes
58
Ventilator
* increase PEEP to improve oxygenation (alveoli recruitment) --> improves FRC
* increase rate or volume to decrease CO2
59
Normal weaning parameters
* negative inspiratory force (NIF) > 20
* FiO2 < 35%
* PEEP 5 (physiologic)
* pressure support 5
* RR < 24 / min
* HR < 120
* PO2 > 60 mm Hg
* PCO2 < 50 mm Hg
* pH 7.35 - 7.45
* saturations > 93%
* off pressors
* follows commands
* can protect airway
60
FiO2 < = 60%
prevents O2 radical toxicity
61
Barotrauma
* high risk if plateaus > 30 and peaks > 50
| * consider prophylactic chest tubes
62
PEEP
*improves FRC and compliance by keeping alveoli open --> best way to improve oxygenation
63
Excessive PEEP complications
decrease RA filling, decrease CO, decrease renal blood flow, decrease urine output, and increase pulmonary vascular resistance
64
High frequency ventilation
used a lot in kids; tracheoesophageal fistula, bronchopleural fistula
65
Inverse ratio ventilation
helps reduce barotruama
* normal 1:2 I:E phase
* go to 2:1
66
Total lung capacity
lung volume after maximal inspiration
| TLC = FVC + RV
67
Forced vital capacity
maximal exhalation after maximal inhalation
68
Residual volume
lung volume after maximal expiration (20% TLC)
69
Tidal volume
volume of air with normal inspiration and expiration
70
Functional residual capacity
lung volume after normal exhalation
* FRC = ERV + RV
* surgery (atelectasis ), sepsis (ARDS), and trauma (contusion, atelectasis, ARDS) all decrease FRC
71
Expiratory reserve volume
volume of air that can be forcefully expired after normal expiration
72
Inspiratory capacity
maximum air breathed in from FRC
73
FEV1
forced expiratory volume in 1 second (after maximal inhalation)
74
Minute ventilation
TV x RR
75
Restrictive lung disease
```
decrease TLC (Total lung capacity), decrease residual volume (RV), decrease FVC (Forced vital capacity)
*FEV1 can be normal or increase
```
76
Obstructive lung disease
increase TLC, increase RV, decrease FEV1
| *FVC can be normal or decreased
77
Dead space
normally to the level of the bronchiole (150mL); increase with drop in cardiac output, PE, pulmonary HTN, ARDS, excessive PEEP; can lead to high CO2 buildup
*area of lung that is ventilated but not perfused
78
COPD
increase work of breathing due to prolonged expiratory phase
| *work of breathing normally 2% of total body VO2
79
ARDS
mediated by cellular inflammatory processes, increase proteinaceous material, increase gradient, increase shunt
*most common cause is sepsis
80
Acute lung injury
acute onset
bilateral pulmonary infiltrates
PaO2/FiO2 < = 300
PAOP < 18 mm Hg or no clinical evidence of LAH (left arterial hypertension
81
Acute respiratory distress syndrome
acute onset
bilateral pulmonary infiltrates
PaO2/FiO2 < 200
PAOP < 18 mm Hg or no clinical evidence of LAH (left arterial hypertension
82
SIRS
*mediated by TNF-alpha and IL-1; temperature > 38 or < 36, RR > 20, PC02 < 32, WBC > 12,000 or < 4,000, HR > 90
83
Endotoxin (lipopolysaccharide - LipidA)
most potent stimulus of SIRS
84
SIRS
Sepsis
Septic Shock
MOD
```
SIRS:
*temp > 38 or < 36
*HR > 90
*WBC > 12000 or < 4000
*RR > 20 or PaCO2 < 32
SEPSIS:
*sirs with infection
SEVERE SEPSIS
*sepsis with organ dysfunction
SEPTIC SHOCK
*septic and arterial hypotension despite fluid
MOD
*progressive but reversible dysfunction of 2 or more organs
```
85
Pulmonary organ dysfunction
need for mechanical ventilation; PaO2:FiO2 ratio < 300 for 24 hours
86
Cardiovascular organ dysfunction
need for inotropic drugs to maintain adequate tissue perfusion or CI < 2.5 L/min/m^2
87
Kidney organ dysfunction
creatinine > 2 times baseline on 2 consecutive days or need for renal replacement therapy
88
Liver organ dysfunction
bilirubin > 3 mg / dL on 2 consecutive days or PT > 1.5 control
89
Nutrition organ dysfunction
10% reduction in lean body mass; albumin < 2.0 g/dL or total lymphocyte count < 1,000
90
CNS organ dysfunction
GCS < 10 without sedation
91
Coagulation organ dysfunction
platelet count < 50,000 / uL; fibrinogen < 100 mg/dL or need for factor replacement
92
Aspiration
pH < 2.5 and volume > 0.4 cc/kg associated with increase degree of damage
*most frequent site is posterior portion of RUL and superior portion of RLL
93
Mendelson's syndrome
chemical pneumonitis from aspiration of gastric secretions
94
Atelectasis
bronchial obstruction and respiratory failure are main causes
* most common cause of fever in first 48 hours after operation
* fever, tachycardia
* increased in patients with COPD, upper abdominal surgery, obesity
* tx: incentive spirometry
95
Things that throw off a pulse ox
nail polish, dark skin, low flow states, ambient light, anemia, vital dyes
96
Pulmonary vasodilation
bradykinin, PGE1, prostacyclin (PGI2), nitric oxide
| *alkalosis
97
Pulmonary vasconstriction
histamine, serotonin, TXA2, epinephrine, norephinephrine, hypoxia, acidosis
98
Pulmonary shunting
occurs with nitroprusside (Nipride), nitroglycerin, and nifedipine
99
Most common cause of postop renal failure
hypotension
| *70% nephrons need to be damaged before renal dysfunction occurs
100
FeNa
(urine Na / Cr) / (plasma Na / Cr) --> best test for azotemia
101
Prerenal cause of acute renal failure
FeNa < 1%, urine Na < 20, BUN / Cr ratio > 20, urine osmolality > 500 mOsm; otherwise consider renal cause of azotemia
102
Oliguria
1st - make sure patient is volume loaded (CVP 11-15 mm Hg)
2nd - try diuretic trial --> furosemide (lasix) / butanamide
3rd - dialysis if needed
103
Indications for dialysis
fluid overload, increase K, metabolic acidosis, uremic encephalopathy, uremic coagulopathy, poisoning
104
Hemodialysis vs CVVH
HD - rapid, causes large volume shifts
| CVVH - slower, good for ill pts who cannot tolerate the volume shifts (septic shock)
105
Renin
released in response to decrease pressure sensed by juxtaglomerular apparatus in kidney
* also released in response to increase Na concentrations sensed by macula densa
* beta adrenergic stimulation and hyperkalemia also cause release
* converts angiotensinogen (synthesized in liver) to angiotensin I
* angiotensin-converting enzyme (lung) - converts angiotensin I to angiotensin II
* adrenal cortex - releases aldosterone in response to angiotensin II
* Distal Convoluted Tubule - aldosterone acts here to reabsorb more water by increase Na/K (ATPase on membrance, K secreted)
* Angiotensin II - also vasoconstricts, increases HR, contractility, permeability, glycogenolysis, and gluconeogenesis; inhibits renin release
106
Atrial natriuretic peptide or factor
released from atrial wall with atrial distention
* inhibits Na and water resorption in collecting ducts
* also a vasodilator
107
Antidiuretic hormone
* ADH, vasopressin
* released by posterior pituitary gland when osmolality is high
* acts on collecting ducts for water resorption
* also a vasoconstrictor
108
Renal toxic drugs
* NSAIDs - cause renal damage by inhibiting prostaglandin synthesis, resulting in renal arteriole vasoconstriction
* Aminoglycosides - direct tubular injury and laterrenal vasoconstriction
* Myoglobin - direct tubular injury; tx: alkalinize urine
* Contrast dyes - direct tubular injury; tx: premedicate with N-acetylcysteine and volume
*efferent limb of kidney controls GFR
109
Brain death
* precludes diagnosis - uremia, temperature < 30, BP < 70/40, desaturation with apnea test, drugs (phenobarbital, pentobarbital), metabolic derangements
* must exist for 6-12h --> unresponsive to pain, absent caloric oculovestibular reflexes, absent oculocephalic reflex, positive apnea test, no corneal reflex, no gag, fixed and dilated pupils
* EEG - electrical silence; MRA - can be used, will show no blood flow to brain
* Apnea test - disconnected from ventilation; CO2 > 60 mm Hg or increase in CO2 by 20 is a positive test for apnea; if arterial pressure drops to < 60 or patient desaturates, the test is terminated
* can still have deep tendon reflexes with brain death
110
Carbon monoxide
can falsely increase O2 saturation reading on pulse ox
* binds Hgb directly (creates carboxyhemoglobin)
* can usually correct with 100% on vent (displaces carbon monoxide); may need hyperbaric O2 if really high
* abnormal carboxyhemoglobin > 10%; in smokers > 20%
111
Methemoglobinemia
* from nitrites such as hurricaine spray; nitrites bind Hgb) - 02 sat reads 85%
tx: methylene blue
112
Critical illness polyneuropathy
motor > sensory neuropathy; occurs with sepsis; can lead to failure to wean from vent
113
Xanthine oxidase
in endothelial cells, forms toxic oxygen radicals with reperfusion, involved in reperfusion injury
*also involved in metabolism of purines and breakdown to uric acid
114
DKA
* nausea and vomiting, thirst, polyuria, abdominal pain, increase glucose, increase ketones, decrease Na, increase K
* tx: insulin and eventually glucose, so pt does not bottom out, isotonic solutions, K+ (although initial K will be high, it will be driven back into cells by insulin), HCO3- for pH < 7.25
115
ETOH withdrawal
HTN, tachycardia, delirium, seizures after 48 hours
| *tx: thiamine, folate, Mg, K, B12, PRN lorazepam (Ativan)
116
ICU or hospital psychosis
* generally occurs after third postoperative day and is frequently preceded by lucid interval
* need to rule out metabolic (hypoglycemia, DKA, hypoxia, hypercarbia, electrolyte imbalances) and organic (MI, CVA) causes
