16 Critical Care Flashcards
Mean arterial pressure
MAP = CO x SVR
Cardiac index
CI = CO/BSA
Define preload
Left ventricular end-diastolic length
Lineraly related to LV end diastolic volume and filling pressure
What percentage of CO does kidney get? Brain? Heart?
Kidney 25%
Brain 15%
Heart 5%
Define afterload
Resistance against the ventricle contracting
SVR
Define stroke volume
Determined by LVEDV, contractility and afterload
SV = LVEDV - LVESV
Define ejection fraction
EF = SV/LVEDV
Determinants of end-diastolic volume
Preload
Distensibility of the ventricle
Determinants of end-systolic volume
Contractility
Afterload
Define Anrep effect
Automatic increase in contractility secondary to increased afterload
Define Bowditch effect
Automatic increase in contractility secondary to increase heart rate
How do you determine the arterial O2 content?
CaO2 = Hgb x 1.34 x O2sat + (Po2 x 0.003)
How do you determine O2 delivery?
O2 delivery = CO x CaO2 x 10
How do you determine O2 consumption?
Vo2 = CO x (CaO2 - CvO2)
Normal O2 delivery-to-consumption ratio?
5:1
CO increase to keep this ratio constant
O2 consumption is supply independent (until very low levels of delievery are reached)
Causes of right shift of Oxyhemoglobin curve?
O2 unloading Increased CO2 Increased 2,3-DPG Increased temp Increased ATP Increased H+ ions (decreased pH)
Increased SvO2 occurs when:
Increased shunting of blood
Decreased oxygen extraction (i.e. sepsis, cirrhosis, cyanide toxicity, hyperbaric O2, hyptohermia, paralysis, coma, sedation)
Decreased SvO2 occurs when:
Increased O2 extraction
Decreased O2 delivery
Things that can effect pulmonary wedge pressure?
Pulmonary hypertension Aortic regurgitation Mitral stenosis Mitral regurg High PEEP Poor LV compliance
Hemoptysis after flushing Swan-Ganz catheter?
Increase PEEP (tamponade the pulmonary artery bleed) Mainstem intubate non-affected side Fogarty balloon down mainstem on affected side Possible thoracotomy and lobectomy
Relative CI to swan-ganz catheter?
Previous pnumonectomy
Left bundle branch block
Approximate Swan-Ganz catheter distance to wedge?
RSCV 45cm
RIJ 50cm
LSCV 55cm
LI 60cm
What is the only way to measure pulmonary vascular resistance?
Swan-Ganz catheter (NOT ECHO)
When should you take wedge pressure?
End-expiration
Ventilatory method does not matter
Primary determinants of myocardial O2 consumption?
Increased ventricular wall tension
Heart rate
Normal A-a gradient in a non-ventilated patient?
10-15mmHg
Blood with lowest venous saturation?
Coronary sinus blood (30%)
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
Steroid potency?
1x - cortisone, hydrocortisone
5x - prednisone, prednisolone, methylprednisolone
30x - dexamethasone
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
Initial alteration in hemorrhagic shock?
Increased diastolic pressure
Cardiac tamponade
Causes cardiogenic shock
Decreased ventricular filling
ECHO shows impaired diastolic filling of right atrium first (weakest wall)
Tx: Rescucitation, pericardial window/pericardiocentesis
Beck’s triad
Hypotension
Jugular venous distention
Muffled heart sounds
Decreased CVP/PCWP
Decreased CO
Increased SVR
Hemorrhagic shock
Decreased CVP/PCWP
Increased CO
Decreased SVR
Septic shock (hyperdynamic)
Increased CVP/PCWP
Decreased CO
Increased SVR
Cardiogenic (i.e. MI, cardiac tamponade)
Decreased CVP/PCWP
Decreased CO
Decreased SVR
Neurogenic (i.e. head or spinal cord injury)
Adrenal insufficiency
Early sepsis triad
Hyperventilation
Confusion
Hypotension
Early gram-negative sepsis
Decreased insulin Increased glucose (impaired utilization)
Late gram-negative sepsis
Increased insulin Increased glucose (insulin resistance)
Neurohormonal response to hypovolemia - Rapid
Epinephrine and norepinephrine release
Adrenergic release
Results in vasoconstriction and increased cardiac activity
Neurohormonal response to hypovolemia - Sustained
Renin (from kidney - vasconstriction and water resorption)
ADH (from pituitary - reabsorption of water)
ACTH (from pituitary - increases cortisol)
Fat emboli
Petechia, hypoxia, confusion
Sudan red stain may show fat in sputum and urine
Most common from LE fractures, orthopedic procedures
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
Most common source of PEs?
Iliofemoral region
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
When does an intra-aortic balloon pump inflate? Deflate?
Inflates on T wave (diastole)
Deflates on P wave (systole)
CI to intra-aortic balloon pump?
Aortic regurgitation
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
Alpha-1 receptors
Vascular smooth muscle constriction
Gluconeogenesis
Glycogenolysis
Alpha-2 receptors
Venous smooth muscle contriction
Beta-1 receptors
Myocardial contraction and rate (ionotrope and chronotrope)
Beta-2 receptors
Relaxes bronchial smooth muscle
Relaxes vascular smooth muscle
Increases insulin, glucagon, renin
Dopamine receptors
Relaxes renal and splanchnic smooth muscle
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)
Dobutamine (3ug/kg/min initially)
Beta-1 receptors
Increased contractility, tacycardia with higher doses
Milrinone
Phosphodiesterase inhibitor - increases cAMP
Results in increased Ca flux and increased myocardial contractility
Vascular smooth muscle relaxation and pulmonary vasodilation
Phenylephrine (10ug/kg/min initially)
Alpha-1
Vasoconstriction
Norepinephrine (5ug/min initially)
Low doses - Beta-1 (increased contractility)
High dose - Alpha-1 and Alpha-2 (veno and vaso constriction)
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)
Isoproterenol (1-2ug/min initially)
B-2 and B-2 (increased contractility, vasodilates)
AE: extremely arrhythmogenic, increased heart metabolic demand, may actually decrease BP
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
Nipride
Arterial vasodilator
Cyanide toxicity at dose >3ug/kg/min for 72hrs
Check thiocyanate levels and signs of metabolic acidosis
Treatment for cyanide toxicity
Amyl nitrate
Then sodium nitrite
Nitroglycerin
Predominately venodilation with decreased myocardial wall tension from decreased preload
Moderate coronary vasodilator
Hyrdalazine
a-blocker
Lower BP
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
Effect of aging on the lungs?
Decreased FEV1
Decreased vital capacity
Increased functional residual capacity
V/Q ratio
Ventilation/perfusion ratio
Highest in upper lobes
Lowest in lower lobes
Why does increasing PEEP improve oxygenation?
Increased alveoli recruitment
Improves FRC
How to you decrease CO2?
Increase respiratory rate
Increase tidal volume
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
Puts you at risk for barotrauma? How do you decrease the risk?
Plateau > 30
Peak > 50
Need to decrease TV
Consider pressure control ventilation
Complications of excessive PEEP?
Decreased RA filling Decreased CO Decrease renal blood flow Decease urine output Increase pulmonary vascular resistance
Total lung capacity
Lung volume after maximal inspiration
TLC = FRC + RV
Forced vital capacity
Maximal exhalation after maximal inhalation
Residual volume
Lung volume after maximal expiration (20% TLC)
Tidal volume
Volume of air with normal inspiration and expiration
Functional residual capacity
Lung volume after normal exhalation
FRC = ERV + RV
What can decrease functional residual capacity?
Surgery (atelectasis)
Sepsis (ARDS)
Trauma (contusion, atelectasis, ARDS)
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 second after maximal inhalation
Minute ventilation
MV = TV x RR
Decreased TLC
Decreased RV
Decreased FVC
Restrictive lung disease
FEV1 can be normal or increased
Increased TLC
Increased RV
Decreased FEV1
Obstructive lung disease
FVC can be normal or decreased
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
COPD breathing changes
Increased work of breathing due to prolonged expiratory phase
ARDS
Mediated by PMNs, increased proteinaceous material, increased A-a gradient, increased pulmonary shunt
Causes: Pnuemonia*, sepsis, multi-trauma, severe burns, pancreatitis, aspiration, DIC
Diagnostic criteria for ARDS
Acute onset
Bilateral pulmonary infiltrates
PaO2/FiO2 <300
Absence of heart failure (Wedge <18mmHg)
Mendelson’s syndrome
Chemical pneumonitis from aspiration of gastric secretions
Atelectasis
Collapse of alveoli resulting in reduced oxygenation
Sx: Fever, tachycardia, hypoxia
Tx: IS, pain control, ambulation
What can make a pulse-ox inacurate?
Nail polish, dark skin, low-flow state, ambient light, anemia, vital dyes
Causes pulmonary vasodilation?
PGE1
Prostacyclin (PGI2)
Nitric oxde
Bradykinin
Causes pulmonary vasoconstriction?
HYpoxia
Acidosis
Histamine
Serotonin, TXA2
Alkalosis - effect on pulmonary vasculature?
Pulmonary vasodilator
Acidosis - effect on pulmonary vasculature?
Pulmonary vasoconstrictor
Drugs that cause pulmonary shunting?
Nitroprusside
Nitroglycerin
Nifedipine
Most common cause of postoperative renal failure?
Intra-op hypotension
Amount of nephron that needs to be damaged before renal dysfunction?
70%
FeNa
Fractional excretion of sodium
(Urine Na/Cr) / (plasma Na/Cr)
Best test for azotemia
Urine Osm >500 U/P osmolality >1.5 U/P creatinine >20 Urine sodium <20 FeNa < 1%
Prerenal azotemia
Urine Osm 250-350 U/P osmolality <1.1 U/P creatinine <10 Urine sodium >40 FeNa > 3%
Parenchymal azotemia
Treatment of oliguria
Make sure patient is volume loaded (CVP 11-15mmHg)
Try diuretic trial (Lasix)
Dialysis if needed
Indications for dialysis
Fluid overload Hyperkalemia Metabolic acidosis Uremic encephalopahty Uremic coagulopathy Poisoning
Renin
Released in response to decreased pressure (JGA), increased Na (macula densa) concentration, beta-adrenergic stimulation and hyperkalemia
Aldosterone
Acts at distal convoluted tubule to reabsorb water by up-regulating the Na/K ATPase (Na re-absorbed, K secreted)
Effect of Angiotensin II
Stimulates release of aldosterone Vasoconstricts Increases HR Contractility Glycogenolysis Gluconeoenesis Inhibits renin
Atrial natriuretic peptide
Released from atrial wall with atrial distention
Inhibits Na and water resoprtion in the collecting ducts
Vasodilator
Antidiuretic hormone (ADH, vasopressin)
Released by posterior pituitary gland when osmolality is high
Acts on collecting ducts for water resorption
Vasoconstrictor
What controls GFR?
Efferent limb of the kidney
Renal toxic drugs
NSAIDs (inhibit PGE - renal arteriole vasoconstriction)
Aminoglycoside (direct tubular injury)
Myoglobin (DTI)
Contrast dye (DTI)
Causes of SIRS
Shock Infection Burn Multi-trauma Pancreatitis Severe inflammatory responses
What is the most potent stimulus for SIRS?
Endotoxin (lipopolysaccharide - Lipid A)
Stimulates TNF release
Effect of TNF-a and IL-1 release?
SIRs
Capillary leakage, microvascular thormbi, hypotension, eventually end-organ dysfunction
Criteria for SIRS
Temp >38 or < 36
HR >90
RR >20 or PaCO2 <32
WBC >12000 or < 4000
Diagnostic criteria: end organ dysfunction.
Pulmonary
Need for mechanical ventilation
PaO2:FiO2 ratio <300 for 24hrs
Diagnostic criteria: end organ dysfunction.
Cardiovascular
Need for ionotropic drugs
CI <2.5 L/min/m2
Diagnostic criteria: end organ dysfunction.
Kidney
Creatinine >2x baseline on 2 consecutive days
Need for dialysis
Diagnostic criteria: end organ dysfunction.
Liver
Bilirubin >3mg/dL for 2 days
PT > 1.5
Diagnostic criteria: end organ dysfunction.
Nutrition
10% reduction in lean body mass
albumin 2.0
Total lymphocyte count <1
Diagnostic criteria: end organ dysfunction.
CNS
GCS <10 without sedation
Diagnostic criteria: end organ dysfunction.
Coagulation
Platelet count < 50
Fibrinogen <100
Need for factor replacement
Diagnostic criteria: end organ dysfunction.
Host defenses
WBC < 1000
Invasive infection including bacteremia
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
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
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
What is a negative result for an apnea test?
BP drops (<90mmHg) Patient desaturates (<85%) Spontaneous breathing
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
Methemoglobinemia
From nitrates
O2 sat reads 85%
Tx: methylene blue
Critical illness polyneuropathy
Motor > sensory neuropathy
Occurs with sepsis
Causes failure to wean from ventilation
Xanthine oxidase
Is in endothelial cells
Forms toxic oxygen radicals with reperfusion
Also involved in metabolism of purines to uric acid
DKA
Nausea/vomiting, thirst, polyruia, increased glucose, increased ketones, decreased sodium, increased potassium
TX: normal saline and insulin
ETOH withdrawal
HTN, tachycardia, delirium, seizures (After 48hrs)
Tx: Thiamine, folate, B12, Mg, K, PRN lorazepam
ICU psychosis
Third POD day - preceded by lucid interval Address metabolic (hypoglycemia, DKA< hypoxia, hypercarbia, electrolyte imbalances) and organic (MI, CVA) causes
