Critical Care - Absite

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Surgery - Absite Review Fichas sobre Critical Care - Absite, creado por Jennifer Huber el 19/06/2018.
Jennifer Huber
Fichas por Jennifer Huber, actualizado hace más de 1 año
Jennifer Huber
Creado por Jennifer Huber hace más de 6 años
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Normal Values for Cardiac Index 2.5-4L/min/m2
Normal Values for Cardiac Output 4-8L/min
Normal Values for CVP or Rt Atrial Pressure 2-6mmHg
Normal Values for Pulmonary Artery Pressure Systolic20-30mmHg Diastolic 8-12 mmHg Mean 25 mmHg
Equation to calculate MAP MAP = CO x SVR
Equation for Cardiac Index CI = CO/BSA
4 determinants for cardiac performance preload, afterload, contractility, HR
Preload ventricular end-diastolic volume or pressure
Afterload Resistance against the ventricle contracting (SVR)
Equation for Stroke Volume Stroke Volume = LVEDV - LVESV
Equation for Ejection Fraction Stroke Volume / LVEDV
End-Diastolic Volume determined by preload and distensibility of the ventricle
End Systolic Volume determined by contractility and afterload
Atrial Kick account for 20% of LVEDV
Anrep Effect Automatic increase in contractility secondary to increased afterload
Bowditch Effect automatic increase in contractility secondary to increased HR
Arterial O2 Content Equation CaO2 = Hb x 1.34 x O2 sat + (PO2 0.003)
Oxygen delivery equation O2 delivery = CO x arterial O2 content x 10
Oxygen Consumption Equation (VO2) VO2 = CO x (CaO2 - CvO2)
Normal Oxygen Delivery to consumption ratio 4 : 1
Causes of Right Shift (O2 unloading) Increased CO2 (Bohr), increased temp, increased ATP production, Increased 2,3-DPG production, acidic environment
Causes of increase oxygen saturation in venous blood increased shunting of blood, decreased oxygen extraction (sepsis, cirrhosis, cyanide toxicity, hyperbaric O2, hypothermia, paralysis, coma)
Causes of decreased venous oxygen saturation occurs with increased O2 extraction, malignant hyperthermia or decreased O2 delivery
What factors can affect wedge pressure? pulmonary HTN, mitral stenosis, mitral regurgitation, high PEEP, poor LV compliance
Where should a Swan-Ganz Catheter be placed? in zone III lower lung, had less respiratory influence on wedge pressure
What to do if you develop hemoptysis after flushing a Swan Ganz catheter? increase PEEP to tamponade the bleed mainstem intubate non-affected side place Fogarty balloon down mainstem of affected side Poss thoacotomy + lobectomy
Absolute contraindications for swan ganz catheter placement right sided mechanical valve
relative contraindication for placing a swan-ganz catheter previous pneumonectomy LBBB, recent PM, right sided endocarditis
Swan Ganz Catheter distances to wedge Rt SCV Rt IJ Lt SCV Lt IJ Rt SCV: 45cm Rt IJ: 50cm Lt SCV: 55cm Lt IJ: 60cm
When should wedge pressure be measured? at end-expiration
What are the 2 primary determinants of myocardial oxygen consumption? HR and increased ventricular wall tension
Normal range of Alveolar-arterial gradient 10-15mmHg
Blood with the lowest venous saturation coronary sinus blood (30%)
Blood with the highest venous saturation renal veins (80%)
Basic definition of shock Inadequate tissue oxygenation
MCC of adrenal insufficiency withdrawal of exogenous steroids
Acute Adrenal Insufficiency cardiovascular collapse, characteristicall unresponsive to fluids and pressors n/v, andominal pain, fever, lethargy, decreased glucose, increased potassium
Treatment for adrenal insufficiency dexamethasone
Steroid Potency 1x Cortisone, Hydrocortisone
Steroid Potency 5x prednisone, prednisolone, methylprednisolone
Steroid potency 30x Dexamethasone
Neurogenic Shock & treatment loss of sympathetic tone usually assoc with spine/head injury decreased HR, BP, warm skin tx: volume then phenylephrine
Treatment for Cardiogenic Shock Dobutamine, IABP
Beck Triad HoTN, JVD, muffled heart sounds
First sign of cardiac tamponade impaired diastolic filling of right atrium
Treatment of Cardiac Tamponade fluid resuscitate to temporize pericardial window, pericardiocentesis
Early Sepsis Triad Hyperventilation Confusion HoTN
Early Gram Negative Sepsis decreased insulin increased glucose (impaired utilization)
Late Gram Negative Sepsis Increased insulin, increased glucose 2/2 to insulin resistance
Neurohormonal Response to hypovolemia rapid: NE and epi sustained: renin, ADH, ACTH
Fat emboli petechia, hypoxia, confusion bone fractures sudan red stain
pulmonary emboli chest pain, dyspnea resp alkalosis, increase HR and RR HoTN and shock if massive
Where PEs usually arise from iliofemoral region
Air Emboli, what to do head down, foll to left to keep air in RV and RA aspirate air with central line
How Intra-aortic balloon pump works inflates on T wave (diastole) deflates on P wave (systole) decreases afterload, improves DBP, improves diastolic coronary perfusion
When to use IABP? cardiogenic shock after CABG or MI in patients with refractory angina awaiting revascularization, pre-op in high risk patients, acute MR, ventricular septal ruptures
Where to place an IABP catheter tip distal to left subclavian (1-2cm below the top of the arch)
absolute contraindications for IABP aortic dissection, severe aortoiliac disease, aortic regurgitation
relative contraindications for IABP vascular grafts, aortic aneurysms
alpha-1 receptors vascular smooth muscle constriction
alpha-2 receptors venous smooth muscle constriction
beta-1 receptors myocardial contraction and rate
beta-2 receptors relaxes bronchial smooth muscle, relaxes vascular smooth muscle, increases renin
dopamine receptors relax renal and splanchnic smooth muscle
Dopamine 2-5mcg/kg/min affects what renal dopamine receptors
Dopamine 6-10mcg/kg/min affects what beta-adrenergic receptors heart contractility and HR
Dopamine >10mcg/kg/min affects what alpha adrenergic receptors, vasoconstriction and increased BP
Dobutamine starts at what rate? what does it affect? 3mcg/kg/min beta-1, increases contractility, tachycardia with higher doses
Milrinone phosphodiesterase inhibitor increases cAMP causes increase of calcium and myocardial contractility pulm vasodilation
Phenylephrine, intial dose and effects 10mcg/min alpha-1, vasoconstriction
Norepinephrine, starting dose and effects 5mcg/minute alpha-1, alpha-2, some beta-1 potent splanchnic vasoconstrictore
Epinephrine initial dose effects of low dose vs high dose 1-2mcg/min Low: beta-1 & 2, increases contractility and vasodilation, can decrease BP High: alpha1 & 2, vasoconstriction increases cardiac ectopic pacer and myocardial O2 demand
Isoproterenol initial dose and effects 1-2mcg/min initially beta-1 &2, increase HR + contractility, vasodilates
side effects of isoproterenol extremely arrhythmogenic increase heart metabolic demand, may decrease BP
Vasopressin V-1 receptors arterial vasoconstriction
Vasopressin V-2 receptors (intrarenal) water reabsorption at collecting ducts
Vasopressin V-2 Receptors (extrarenal) mediate release of factor VIII and vWF
Nipride arterial vasodilator cyanide toxicity at doses >3mcg/kg/min for 72hrs; check thiocyanate levels
Treatment for cyanide toxicity amyl nitrate then sodium nitrite
Nitroglycerin predominately venodilation with decreased myocardial wall tension from decreased preload; moderate coronary vasodilator
Hydralazine alpha-blocker lowers BP
Equation for pulmonary compliance change in volume / change in pressure
diseases in which pulmonary compliance is decreased ARDS, fibrotic lung diseases, reperfusion injury, pulmonary edema, atelectiasis
How aging affects lung function decreases FEV1 and vital capacity increases functional residual capacity
V/Q ratio highest in upper lobes lowest in lower lobes
With ventilation, how do you improve oxygenation? increase PEEP - improves FRC increase FiO2
On ventilator, how do you decrease CO2/improve ventilation? increase rate or volume
Normal Weaning Parameters Neg inspiratory force >20, FiO2 <40%, PEEP of 5, pressure support 5, RR <24/min, HR <120bpm, PO2 >60mmHg, PCO2 <50mmHg, pH 7.35-7.45, sat >93%, off pressors, follows commands, can protect airway
Pressure support patient initiates every breath and the ventilator delivers support with the preset pressure value inspiratory pressure held constant
Excessive PEEP complications decreases right atrial filling decreased BP, decreased RBF and U/O, increased wedge pressure, increase pulmonary vascular resistance
Total Lung Capacity TLC = FVC + RV
Forced Vital Capacity maximal exhalation after maximal inhalation
Residual Volume Lung Volume after Maximal expiration (20%)
Tidal Volume volume of air with normal inspiration and expiration
Functional Residual Capacity lung volume after normal exhalation ERV + RV
Expiratory reserve volume volume of air that can be forcefully expired after normal expiration
Inspiratory Capacity maximum air breathed in from FRC
FEV1 forced expiratory volume in 1 sec after maximal inhalation
Minute ventilation TV x RR
Restrictive Lung Disease effects on TLC, RV, FVC, FEV TLC, RV and FVC are decreased FEV1 can be normal or increased
Obstructive Lung Disease effects on TLC, RV, FEV1 and FVC TLC, RV increase FEV1 decreases FVC normal or decreased
MCC of increased dead space excessive PEEP
Other causes of increased dead space PE, pHTN
What is a shunt? What causes it? poor ventilation but good perfusion atelectiasis, mucus plug, ARDS
What is ARDS? inflammation of lung parenchyma mediated primarily by PMNs, get increased proteinaceous material, increased A-a gradient, increased pulmonary shunt
ARDS Criteria Acute onset bilateral pulmonary infiltrates PaO2/FiO2 <300 wedge <18mmHg
Mendelson's Syndrome chemical pneumonitis from aspiration of gastric secretions
MCC of hypoxia early post-op atelectasis
Tx for atelectasis incentive spirometer, pain control and ambulation
How do patients develop fevers secondary to ateletasis? alveolar macrophages release IL-1
Factors causing pulmonary vasodilation PGE1, Prostacyclin, inhaled nitric oxide, sildenafil (heehee)
Causes for pulmonary vasoconstriction hypoxia, acidosis, histamine, serotonin, TXA2
MCC of poor urine output post-op hypovolemia
MCC of post-operative renal failure hypotension intra-op
% of nephrons that need to be damaged to cause renal dysfunction 70%
Best test to determine azotemia FeNa fractional excretion of sodium
Equation for FeNa (urine Na/Cr) / (Plasma Na/Cr)
Prerenal RF Urine Osm, BUN:Cr, UNa, FeNa Urine Osm: >500 BUN:Cr >20 Urine Na: <20 FeNa: <1%
Parenchymal RF Urine Osm, BUN:Cr, UNa, FeNa Urine Osm: 250-350 BUN:Cr <10 Urine Na: >40 FeNa: >3%
Treatment for Oliguria 1st: volume load 2nd: diuretic trial 3rd: dilaysis
MCC of renal ATN HoTN intra-op
Causes of Post-renal Oliguria obstructive uropathy ureteral obstruction severe BPH
Indications for Dialysis fluid overload, hyperK, metabolic acidosis, uremic encephalopathy, uremeic coagulopathy, poisoning
How much does Hct increase per liter taken off during dialysis? 5
Continuous Veno-Venous Hemofiltration (CVVH) temporary treatment for patients with acute renal failure who are unable to tolerate hemodialysis and are unstable
When is Renin Released? decreased pressure sense in juxtaglomerular apparatus increased Na conc in macula densa beta-adrenergic stim & hyperK
Effects of Renin converts angiotensinogen to angiotensin I
Aldosterone acts on distal convoluted tubule to resorb water by upregulating Na/K ATPase Na resorbed, K secreted
Effects of AngII vasocontricts as well as inhibits renin release
Atrial Natriuretic Peptide released from atrial wall with atrial distention inhibits Na and water resorption in collecting ducts vasodilator
what part of the kidney controls GFR? efferent limb
Antidiuretic Hormone (ADH) released by posterior pituitary when osmolality is high collecting ducts for water resorption vasoconstrictor
Renal Toxic Drugs NSAIDs Aminoglycosides Myoglobin Contrast Dyes
How NSAIDs affect Kidneys inhibits prostaglandin synthesis, results is renal arteriole vasoconstriction
Aminoglycosides effects on kidneys direct tubular injury
Mediators of SIRS IL-1, TNF-alpha
Causes of SIRS shock, infection, burns, multitrauma, pancreatitis, ARDS,
Most important stimulus for SIRS endotoxin, LPS - lipid A
SIRS Criteria Temp >38C or <26C HR >90 RR >20bpm or PaCO2 <32 WBC >12,000 or <4,000
Multisystem Organ Dysfunction Progressive but reversible dysfunction of 2 or more organs arising from an acute disruption of normal homeostasis
What must exist for 6-12 hours before someone is considered brain dead? unresponsive to pain, absent cold caloric oculovestibular reflexes, absent oculocephalic reflex (patient doesn't track) no spontaneous respirations, no corneal reflexes, no gag reflex, fixed and dilated pupils, +apnea test
Results of EEG and MRA in brain dead person MRA - no blood flow to brain EEG - electrical silence
Apnea test and brain death patient disconnected from ventilator for 10 minutes CO2 > 60mmHg or increase CO2 > 20 at the end of the test
Affinity to Hb, O2 vs CO CO has 250x more affinity than oxygen
Abnormal levels of carboxyHb in smokers vs nonsmokers smokers: >20 nonsmokers >10
Tx for methemoglobinemia methylene blue
cyanide toxicity disrupts the electron transport chain; can't utilize oxygen; get left to right shunt
treatment for cyanide toxicity amyl nitrite, then sodium nitrite hydroxycobalamin
critical illness polyneuropathy motor > sensory neuropathy occurs with sepsis can lead to failure to wean from vent
xanthine oxidase in endothelial cells forms toxic radicals with reperfusion involved in metabolism of purines to uric acid
ICU psychosis generally POD#3 and is frequently preceded by lucid interval
MCC of delayed discharge after cardiac surgery AFib
Mostrar resumen completo Ocultar resumen completo

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