CHAPTER 16- CRITICAL CARE.txt

4-8

2.5-4

800-1400

1500-2400

11+/- 4

7+/- 2

20-30/6-15

75 +/- 5

MAP = CO x SVR

CO/BSA

SVRI= SVR x BSA

• 1) kidney gets 25% of CO
• 2) brain gets 15% of CO
• 3) heart gets 5%

• 1) end-diastolic length
• 2) linearly related to end diastolic volume and filling pressure

1) resistance against the ventricle contracting (SVR)

• 1) determined by:
• 1- LVEDV
• 2- contractility
• 3- afterload

2) stroke volume = LVEDV- LVESV

stroke volume/ EDV

determined by preload and distensibility of the ventricle

determined by contractility and afterload

Cardiac output increases with HR up to 120-150 beats/min, then starts to go down because of decreased diastolic filling time

accounts for 15-30% of LVEDV

automatic increase in contractility secondary to increased afterload

automatic increase in contractility secondary to increased HR

• 1) Aortic mean and diastolic pressures are slightly greater than radial pressure.
• 2) Radial systolic pressure are slightly higher than mean aortic pressure.

O2 delivery = CO x arterial O2 content (CaO2) = CO x (Hgb x 1.34 x O2 saturation + 1[Po2 x 0.003])

• O2 consumption = CO x (CaO2-CvO2).
• CvO2= venous O2 content

• 1) normal O2 delivery-to-consumption ratio is 5:1
• 2) CO increases to keep this ratio constant
• 3) O2 consumption is usually supply independent (consumption does not change until low levels of delivery are reached).

• 1- increased CO2
• 2- increased temperature
• 3- increased ATP production
• 4- increased 2,3 DPG production
• 5- decreased pH

normal p50 (O2 at which 50% of O2 receptors are saturated) = 27mmHg

• 1) saturation of venous blood is normally 75%+/- 5%
• 2) occurs with increased shunting of blood or decreased O2 extraction (sepsis, cirrhosis, cyanide toxicity, hyperbaric O2, hypothermia, paralysis, coma, sedation)

Decreased SvO2 occurs with increased O2 extraction or decreased O2 delivery (decreased O2 saturation, decreased CO)

• 1- pulmonary hypertension
• 2- aortic regurgitation
• 3- mitral stenosis
• 4- high PEEP
• 5- poor LV compliance

should be placed in zone III (lower lung)

• 1- increase PEEP (will tamponade the pulmonary artery bleed)
• 2- mainstem intubate nonaffected side
• 3- can try to place Fogarty baloon down the affected side
• 4- may need thoracotomy and lobectomy

• 1) previous pneumonectomy
• 2) left bundle branch block

• R SCV 45cm
• R IJ 50cm
• L SCV 55cm
• LIJ 60cm

pulmonary vascular resistance can be measured only by using a swan-ganz catheter

• 1) increased ventricular wall tension
• 2) increased HR

are the primary determinants of myocardial O2 consumption--> can lead to myocardial ischemia

empties into pulmonary veins; thus, LV blood is 5mmHg (PO2) lower than pulmonary capillaries

1) 10-15mmHg normal in nonventilated patient

coronary venous blood (30%)

• 1) cardiovascular collapse
• 2) characteristically unresponsive to fluids and pressors

• 1) hyperpigmentation
• 2) weakness
• 3) weight loss
• 4) GI symptoms
• 5) increased K
• 6) decreased Na
• 7) fever
• 8) hypotension

• 1x- cortisone, hydrocortisone
• 5x- prednisone, prednisolone, methylprednisolone
• 30x- dexamethasone

• 1) loss of sympathetic tone
• 2) Usually have decreased HR, decreased BP, warm skin
• 3) Treatment:
• 1- give volume 1st
• 2- phenylephrine after resuscitation
• 3- give steroids for blunt spinal trauma with deficit

increased diastolic pressure

• 1) causes decreased diastolic ventricular filling and hypotension
• 2) Beck's triad:
• 1- hypotension
• 2- jugular venous distention
• 3- muffled heart sounds
• 3) Echocardiogram shows impaired diastolic filling of right atrium initially (1st sign of cardiac tamponade)
• 4) pericardiocentesis blood does not form clot
• 5) Treatment:
• 1- fluid resuscitation initially
• 2- need pericardial window or pericardiocentesis

• 1) confusion
• 2) hyperventilation
• 3) respiratory alkalosis

• 1) decreased insulin
• 2) increased glucose
• (impaired utilization)

• 1) increased insulin
• 2) increased glucose
• (secondary to insulin resistance)

hyperglycemia

• 1) Signs include:
• 1- petechia
• 2- hypoxia
• 3- confusion
• (can also be similar to pulmonary embolism)

2) Sudan red stain may show fat in sputum and urine

3) Most common with lower extremity (hip/femur) fractures/orthopaedic procedures

• 1) echo will show RV strain
• 2) suspect PE with:
• 1- PA systolic pressures >40
• 2- decreased PO2 and PCO2
• 3- respiratory alkalosis
• 4- chest pain
• 5- cough
• 6- dyspnea
• 7- increased HR

1) place patient head down and roll to left (keeps air in RV and RA), then aspirate air would with central line or PA catheter to RA/RV

• 1) inflates on T-wave (diastole)
• 2) deflates on P wave or start of Q wave (systole)
• 3) aortic regurgitation is a contraindication
• 4) place tip of the catheter just distal to left subclavian (1-2 cm below the top of the arch)
• 5) used for cardiogenic shock (after CABG, MI) or in patient with refractory angina
• 6) decreases afterload (deflation during ventricular systole)
• 7) Improves SBP (inflation during ventricular diastole, which improves coronary perfusion

• 1) vascular smooth muscle constriction
• 2) gluconeogenesis
• 3) glycogenolysis

venous smooth muscle constriction

myocardial contraction and rate

• 1) relaxes bronchial smooth muscle
• 2) relaxes vascular smooth muscle
• 3) increases insulin, glucagon, rennin

relax renal and splanchnic smooth muscle

• 1) (2-5ug/kg/min initially, 20-50 mg/kg/min for high dose)
• 2) 0-5 ug/kg/min - dopamine receptors (renal)
• 3) 6-10 ug/kg/min- beta-adrenergic (heart contractility)
• 4) >10ug/kg/min- alpha-adrenergic (vasocontriction and increased BP)

• 1) 3ug/kg/min initially
• 2) 5-15ug/kg/min- beta-1 (increased contractility mostly)
• 3) >15ug/kg/min- beta-2 (vasodilation and increased HR)

• 1) phosphodiesterase inhibitor (increased cAMP)
• 2) results in increased calcium flux and increased myocardial contractility
• 3) also causes vascular smooth muscle relaxation and vasodilation

1) alpha-1, vasocontriction

• 1) 4ug/min initially
• 2)low dose- beta-1 (increased contractility)
• 3) high dose- alpha-1 and alpha-2, potent splanchnic vasocontrictor

• 1) 2ug/min initially
• 2) Low dose- beta-1 and beta-2 (increased contractility and vasodilation)
• 3) can decrease BP at low doses

• 4) High Dose- alpha-1 and alpha-2 (vasocontriction)
• - increased cardiac ectopic pacer activity and myocardial O2 demand

• 1) 1-2 ug/min initially
• 2) beta-1 and beta-2, increases HR and contractility, vasodilates
• 3) Side Effects:
• 1- extremely arrhythmogenic
• 2- increases heart metabolic demand (rarely used)
• 3- may actually decrease BP

• 1) V1 receptors- vasocontriction of vascular smooth muscle
• 2) V2 receptors (intrarenal)- water reabsorption at collecting ducts
• 3) V2 receptors (extrarenal)- mediate release of factor VIII and von willebrand factor

arterial and venous dilator

• 1) at doses >3ug/kg/min for 72 hours
• 2) can check thiocyanate levels and signs of metabolic acidosis
• 3) treatment: amyl nitrite, then sodium nitrite

• 1) predominantly venodilation
• 2) modest effect on coronaries
• 3) decreased myocardial wall tension by decreasing preload

alpha blocker

• Compliance: (change in volume)/(change in pressure)
• - high compliance means lungs are easy to ventilate
• - Pulmonary compliance decreases in patients with:
• 1) ARDS
• 2) fibrotic lung diseases
• 3) reperfusion injury
• 4) pulmonary edema

• Aging-
• 1) decreases FEV1 and vital capacity
• 2) increases functional residual capacity

V/Q ratio- highest in upper lobes, lowest in lower lobes

• 1) improve oxygenation (alveoli recruitment)
• 2) improves FRC

decrease CO2

• 1- negative inspiratory force (NIF) >20
• 2- FiO2 <35%
• 3- PEEP 5 (physiologic)
• 4- pressure support 5
• 5- RR <24/min
• 6- HR <120 beats/min
• 7- PO2 >60mmHg
• 8- PCO2 <50mmHg
• 9- pH 7.35-7.45
• 10- saturations >93%
• 11- off pressors
• 12- follows comands and can protect airway

decreases the work of breathing (inspiratory pressure is held constant until minimum volume is achieved)

prevents O2 radical toxicity

high risk if plateaus >30 and peaks >50 --> consider prophylactic chest tube

• 1) improves FRC and compliance by keeping alveoli open
• 2) its the best way to improve oxygenation

• 1) decreased RA filling
• 2) decreased CO
• 3) decreased renal blood flow
• 4) decreased urine output
• 5) increased pulmonary vascular resistance

used a lot in kids; tracheoesophageal fistula, bronchopleural fistula

helps reduce barotrauma (normal 1:2 I:E phase; go to 2:1)

• 1) lung volume after maximal inspiration
• 2) TLC= FVC +RV

1) maximal exhalation after maximal inhalation

lung volume after maximal expiration (20% TLC)

1) volume of air with normal inspiration and expiration

• 1) lung volume after normal exhalation
• 2) FRC= ERV + RV

• 1- surgery (atelectasis)
• 2- sepsis (ARDS)
• 3- trauma (contusion, atelectasis, ARDS)

volume of air that can be forcefully expired after normal expiration

maximum air breathed in from FRC

forced expiratory volume in 1 second (after maximal inhalation)

Minute ventilation = TV x RR

• Decreased TLC
• Decreased RV
• Decreased FVC
• FEV1 can be normal or increased

• Increased TLC
• Increased RV
• Decreased FEV1
• FVC can be normal or decreased

• 1) normally to the level of the bronchiole (150mL)
• 2) increases with:
• 1- drop in cardiac output
• 2- PE
• 3- pulmonary HTN
• 4- ARDS
• 5- excessive PEEP
• 3) can lead to high CO2 buildup
• 4) area of lung is ventilated but not perfused

• 1) increased work of breathing due to prolonged expiratory phase
• 2) work of breathing normally 2% of total body VO2

• 1) mediated by cellular inflammatory processes
• 2) increased proteinaceous material
• 3) increased gradient
• 4) increased shunt
• 5) most common cause is sepsis

• Acute Lung Injury
• 1) Acute onset
• 2) Bilateral pulmonary infiltrates
• 3) PaO2/FiO2 <300
• 4) PAOP <18 mmHg or no clinical evidence of LAH

• Acute Respiratory Distress Syndrome
• 1) all of the above criteria with PaO2/FiO2 <200

1) Mediated by TNF-alpha and IL-1

• Criteria for SIRS:
• 1) Temperature >38C or <36C
• 2) RR >20/min or PCO2 <32mmHg
• 3) WBC >12 or <4
• 4) HR >90

• Sepsis
• 1) SIRS with clinical evidence of infection
• 2) Sepsis with organ dysfunction

• Septic Shock
• 1) sepsis and arterial hypotension despite adequate volume resuscitation

• MOD
• 1) progressive but reversible dysfunction of 2 or more organs arising from an acute disruption of normal homeostasis

Pulmonary: Need for mechanical ventilation; PaO2/FiO2 <300 for 24hrs

Cardiovascular: Need for inotropic drugs to maintain adequate tissue perfusion or CI <2.5

Kidney: Creatinine >2 times baseline on 2 consecutive days or need for renal replacement therapy

Nutrition: 10% reduction in lean body mass; albumin <2g/dL or total lymphocyte count <1,000/uL

CNS: glasgow coma scale <10 without sedation

Coagulation- platelet count <50k/uL, fibrinogen <100mg/dL or need for factor replacement

Host defenses: WBC <1,ooo/uL or invasive infection including bacteremia

• 1) pH <2.5 and volume >0.4cc/kg associated with increased damage
• 2) Mendelson's syndrome- chemical pneumonitis from aspiration of gastric secretions
• 3) Most frequent site is the posterior portion of RUL and superior portion of RLL

• 1) bronchial obstruction and respiratory failure are the main causes
• 2) most common cause of fever in first 48 hrs after operation
• 3) increased in patients with COPD, upper abdominal surgery, and obesity
• 4) fever, tachycardia
• 5) Treatment: incentive spirometer

• Lots of things can through off a pulse oximeter:
• - nail polish
• - dark skin
• - low-flow states
• - ambient light
• -anemia
• - vital dyes

• 1) bradykinin
• 2) PGE1
• 3) prostacyclin (PGI2)
• 4) nitric oxide

• 1) histamine
• 2) serotonin
• 3) TXA2
• 4) epinephrine + norepinephrine
• 5) hypoxia
• 6) acidosis

pulmonary vasodilator

pulmonary vasocontrictor

• 1) nitroprusside (nipride)
• 2) nitroglycerin
• 3) nifedipine

hypotension

70%

FeNa= (urine Na/Cr)/(plasma Na/Cr) --> best test for azotemia

• 1) FeNa <1%
• 2) Urine Na <20
• 3) BUN/Cr ratio >20
• 4) urine osmolality >500mOsm
• otherwise consider renal cause of azotemia

• 1st- make sure patient is volume loaded (CVP 11-15mmHg)
• 2nd- try diuretic trial --> furosemide (lasix)/butanamide
• 3rd- dialysis if needed

• 1) fluid overload
• 2) high K
• 3) metabolic acidosis
• 4) uremic encephalopathy
• 5) uremia coagulopathy
• 6) poisoning

• - rapid
• - causes large volume shifts

• - slower
• - good for ill patietns who cannot tolerate the volume shifts (septic shock, etc)
• - Hct increases by 5-8 for each liter taken off

• Advantages:
• 1) lower risk of systemic bleeding
• 2) facilitates transport for other interventions
• 3) More suitable for severe hyperkalemia
• 4) lower cost

• Disadvantages
• 1) availability of dialysis staff
• 2) more difficult hemodynamic control
• 3) inadequate dialysis dose (frequency)
• 4) inadequate nutritional support
• 5) not suitable for patients with intracranial hypertension
• 6) no removal of cytokines (theoretical)
• 7) potential complement activation by nonbiocompatible membranes

• Advantages:
• 1) better hemodynamic stability
• 2) fewer cardiac arrhythmias
• 3) improved nutritional support
• 4) better pulmonary gas exchange
• 5) better fluid control

• Disadvantages:
• 1) greater vascular access problems
• 2) higher risk of systemic bleeding
• 3) long-term immobilization of patient
• 4) more filter problems (rupture/clotting)
• 5) greater cost

• 1) released in response to decreased pressure sensed by the juxtaglomerular apparatus in kidney
• 2) also released in response to increased Na concentrations sensed by the macula densa
• 3) beta-adrenergic stimulation and hyperkalemia also cause release
• 4) converts angiotensinogen (synthesized in liver) to angiotensin I
• 5) angiotensin-converting enzyme (lung)- converts angiotensin I to angiotensin II
• 6) adrenal cortex- releases aldosterone in response to angiotensin II
• 7) Distal convoluted tubule- aldosterone acts here to reabsorb more water by increased Na/K ATPase on membrane (potassium secreted)

• 1) vasoconstricts
• 2) increases HR + contractility
• 3) increases permeability
• 4) glycogenolysis + gluconeogenesis
• 5) inhibits renin release

• 1) released from atrial wall with atrial distention
• 2) inhibits Na and water resorption in the collecting ducts
• 3) also a vasodilator

efferent limb of kidney controls GFR

• 1) NSAIDS- causes renal damage by inhibiting prostaglandin synthesis, resulting in renal arteriole vasocontriction
• 2) Aminoglycosides- direct tubular injury and later renal vasoconstriction
• 3) Myoglobin- direct tubular injury
• Tx: alkalinize urine
• 4) Contrast dyes- direct tubular injury
• Tx: premedicate with N-acetylcysteine and volume

• Precludes Diagnosis:
• 1) uremia
• 2) temperature <30C
• 3) BP <70/40mmHg
• 4) desaturation with apnea test
• 5) drugs (phenobarbital, pentobarbital)
• 6) metabolic derangements

• 1) must exist for 6-12 hours:
• 1- unresponsive to pain
• 2- absent caloric oculovestibular reflexes
• 3- absent oculocephalic reflex
• 4- positive apnea test
• 5- no corneal reflex
• 6- no gag reflex
• 7- fixed and dilated pupils

EEG- electrical silence

MRA- can be used--> will show no blood flow to brain

• 1) disconnect from ventilation
• 2) CO2 >60mmHg or increase in CO2 by 20 is positive test for apnea
• 3) if arterial pressure drops to <60 or patient desaturates, the test is terminated

you can still have deep tendon reflexes with brain death

• 1) can falsely increase oxygen saturation reading on pulse oximeter
• 2) binds hemoglobin directly (creates carboxyhemoglobin)
• 3) can usually correct with 100% oxygen on ventilator (displaces carbon monoxide), may need hyperbaric O2 if really high

• 1) from nitrites such as Hurricain spray; nitrites bind Hgb
• 2) O2 saturation reads 85%
• 3) Tx: methylene blue

• 1) motor > sensory neuropathy
• 2) occurs with sepsis; can lead to failure to wean from ventilation

• 1) in endothelial cells, forms toxic oxygen radicals with reperfusion, involved in reperfusion injury
• 2) also involved in the metabolism of purines and breakdown to uric acid

• 1) nausea + vomiting
• 2) thirst
• 3) polyuria
• 4) abdominal pain
• 5) increased glucose
• 6) increased ketones
• 7) increased K
• 8) decreased Na

• Treatment:
• 1- insulin and eventually glucose, so patient does not bottom out
• 2- isotonic solutions
• 3- K+ (althuogh initial K wil be high, it will be driven back into cells by insulin)
• 4- HCO3- for pH <7.25

• 1) HTN
• 2) tachycardia
• 3) delirium
• 4) seizures after 48hrs

• Treatment:
• 1) Thiamine
• 2) folate
• 3) B12
• 4) K
• 5) Mg
• 6) PRN lorazepam (ativan)

• 1) generally occurs after 3rd postoperative day and is frequently preceded by lucid interval
• 2) need to rule out metabolic (hypoglycemia, DKA, hypoxia, hypercarbia, electrolyte imbalances) and organic (MI, CVA) causes