References: Sabiston
Shock - the "rude unhinging of the machinery of life" -Gross
Definition: Inadequate organ perfusion and tissue oxygenation
1. Global decrease in O2 delivery
2. Flow maldistribution
Results in failure of electron transport and ATP production --> cell death
History
Bernard - first description of hemostasis
Cannon - coined term, described sympathetic response, toxin theory
Blalock - association of shock and reduced CO2, proposed 4 categories of shock
4 Categories of Shock:
Hypovolemic - hemorrhagic, dehydration - most common in surgery
Distributive - sepsis, neurogenic, anaphylactic
Cardiogenic
Obstructive - PTX, cardiac tampnade, PE
Clinical presentation - Oliguria, tachycardia, hypotension, cool mottled skin, depressed mental status
Tissue Oxygenation Variables
Arteral blood O2 content = blood contained on Hgb + blood disolved in plasma (negligible)
CaO2 = 1.34 x Hgb x SaO2 + 0.003 x PaO2
= 1.34 x 14 x 0.95 + 0.003 x 150 = 17.8 + 0.45 = 18.25 (normal 16-22 mL O2/dL)
***PaO2 is negligible - so don't base clinical decisions on PaO2
O2 Delivery = DO2 = CaO2 x CO = CaO2 x SV x HR = (16-22 mL/dL)(40-70 dL/min) = 640-1540 mL/min (average ~1000)
or if you use cardiac index, average DO2I ~ 500 mL/min/m2
Cardiac output = SV x HR
normally = (60-80 mL/beat)(60-90 beats/min) = (4-7 L/min (40-70 dL/min)
Cardiac Index = CO indexed to BSA in m2 = normally 2.5-3.5 L/min/m2
***Key parameters = Hgb, SaO2, CO - improve these, improve oxygen delivery
Oxygen consumption = VO2 = (CaO2 - CvO2) (CO)
Normals: CaO2 ~20 mL O2/dL, CvO2 ~15 mL O2/dL
VO2 = (1.34 x 15 x 0.95 - 1.34 x 15 x 0.75) x 60 = (19 - 15) mL O2/dL blood x 60 dL blood/min
= 240 mL O2/min (180 - 280)
Oxygen extraction ratio = the amount of oxygen extracted / the amount delivered = VO2/DO2
= 240 / 1000 = 0.24 (~ 0.25)
Ratio can increase up to ~ 0.50 (an SvO2 of ~50%) but further imbalance between DO2 adn VO2 results in tissue hypoxia (SHOCK!) = falling off the hemostatic curve
Most body systems have 75% reserve
Once Hgb loses 1 O2 molecule, it holds tighter to the other 3 - makes sense why it strips one hgb off
In sepsis extraction ratio can be impaired which potentiates decreased oxygen delivery
Treatment
Basics/Avoidance:
Increase DO2 by 1. increasing hgb and 2. increasing SaO2 3. Increase CO
Decrease O2 Consumptoion/Facilitate O2 Offloading by 1. Decrease physiologic stressors, 2. avoid alkalosis, hypothermia, old blood, 3. hypothermic arrest in future? suspended animation?
ICU Goal-Directed Therapy of Shock:
No survival advantage in 1980-90's studies - pounding them with resuscitation - supranormal oxygenation
? Problem = Missing "Golden Hour"
A period of global tissue hypoxia perpetuates 1. worsening inflammation, 2. endothelial activation, 3. Disruption of hemostasis between vascular tone, vascular permeability and coagulation
ER Goal Directed Therapy:
Rivers, et al. NEJM 2001 345:1368-77: Goal-directed approach (optimizing CVP, MAP, Hgb) achieved target ScvO2 in 95% vrs 60% of standard therapy
Early (<6hr) achievement of ScvO2>70% in septic patients associated with 20% reduction in mortality
Rivers was called personally every time a patient meeting the criteria entered the ED
The magnitude of physiologic response is determined by both the severity and duration of insult
Physiologic Compensatory Measures
Baroreflector reflexes - immediately
Dec arterial pressure --> dec baroreceptor firing (aortic arch, carotid body, atrium) ----
--> dec PNS discharge to heart
--> inc SA Nodal firing (chronotropism) and inc AV nodal conduction (dronotropism)
--> inc HR --> inc CO --> inc arterial pressure
--> inc SNS discharge to heart
--> inc SA Nodal firing (chronotropism), inc AV nodal conduction (dronotropism), inc cardiac contractility (Inotropism)
--> inc HR and SV
--> inc CO --> inc arterial pressure
--> inc SNS discharge to veins
--> inc venous tone --> inc venous return
--> inc SV --> inc CO --> inc arterial pressure
--> inc SNS discharge to arterioles
--> inc arteriolar constriction (can cause focal ischemia) --> inc TPR --> inc arterial pressure
Renal response to conserve volume - hours to days
Dec blood pressure --> inc renin secretion --> inc plasma renin
Angiotensinogen --[renin]--> angiotensin I --[ACE]--> angiotensin II
--> inc arteriolar constriction --> inc Total peripheral resistance --> inc BP
--> inc ADH secretion --> H2O reabsorption --> inc intravascular volume --> inc SV --> inc BP
--> inc aldosterone release --> inc Na+ reabsorption --> inc intravascular volume --> inc SV --> inc BP
Microcirculatory changes
Smaller, distal arterioles often paradoxically vasodilate with Shock
Effects of different, local vasoactive mediators
Combined with endothelial swelling and WBC aggregation can result in defect in peripheral O2 extraction
Most commonly seen with septic shock
Early resuscitation helps minimize such effects
Shock Progression - compensated, decompensated, irreversible (>50% shed blood return)
Once they fall off the physiologic curve, they fall very quickly
Mechanisms of Hypoxia-Induced Cell Death
Intracellular acidosis --> anaerobic metabolism --> lactate accumulation --> intracellular pH dec
--> derangements in cellular Ca++ signalling and impaired cell membrane ion exchange
Cellular swelling/necrosis --> depleted cell ATP --> dec cell membrane Na+/K+ ATPase --> intracellular Na+ accumulation
--> cellular edema --> organelle rupture
Apoptosis
4 Categories of Shock:
Hypovolemic - hemorrhagic, dehydration
CI dec, SVR inc, PVR nrml, SvO2 dec, right atrial pressure dec, right ventricular pressure dec, pulmonary artery pressure dec, pulmonary artery occlusion pressure dec
Most common type of shock in surgical patients, usually hemorrhagic
Four classes of hypovolemic shock:
Class 1 - EBL <15% (<750 mL), nrml UOP, nrml HR, nrml BP
Class 2 - EBL 15-30% (750-1500 mL), 20-30 mL/hr UOP, 100-120 HR, nrml BP
Class 3 - EBL 30-40% (1500 -2000mL), 5-15 mL/hr UOP, 120-140 HR, narrow PP
Class 4 - EBL >40% (>2000 mL), 0 mL/hr UOP, >140 HR, Hypotensive
***Classes unreliable thanks to paradoxical bradycardia, baseline bradycardia, baseline hypertension, beta blockers, calcium channel blockers, diabetes insipidus
Treatment covered in trauma lecture
Distributive - sepsis, neurogenic, anaphylactic
CI inc (usually actually dec), SVR dec, PVR nrml, SvO2 nrml-inc (usually actually dec), right atrial pressure nrml-dec, right ventricular pressure nrml-dec, pulmonary artery pressure nrml-dec, pulmonary artery occlusion pressure nrml-dec
Septic Shock
Mechanisms - Pathologic vasodilatation, relative and absolute hypovolemia (3rd spacing from inflammation), direct myocardial depression (25-30%), microvascular blood flow abnormalities (impaired extraction ratio)
Bacteremia --> inflammation and vasodilation
Inflammation --> vasodilation, myocardial depression and impaired microvascular flow
Vasodilation --> dec SR --> dec SV --> dec BP --> dec DO2 --> tissue hypoxia
myocardial depression --> dec SV --> dec BP --> dec DO2 --> tissue hypoxia
Impaired microvascular flow --> tissue hypoxia
***response to infection works locally but systemically causes problems
Treatment - crystalloid fluids, vasopressor support (when adequate filling pressures have been achieved but MAP <60-65 or are being achieved and BP is dramatically low - must give fluids!)
MAP <60 is associated with compromised coronary, renal and CNS perfusion in animal models
ER Goal directed therapy as discussed above
General - early maximization of DO2, aggressive fluid resuscitation, NE (other pressors as needed), treat underlying problem (surg, atbx, etc.)
(More info in sepsis lecture)
Norepinephrine (Levophed) = DOC
Prospective randomized trial demonstrating significant difference in BP normalization (97 vs 31%) and survival (59 vs 17%) with NE compared to Dopamine
Increased survival compared to dopamine and epi in early SvO2 optimization trial
"Renal Dose" Dopamine is a myth
With sufficient fluid resuscitation, renal and splanchnic hypoperfusion is not seen
Dobutamine useful in conjunction with NE in low cardiac output sepsis
Vasopressin 0.03-0.04 units/min may help in some cases with suboptimal response to high dose NE
Phenylephrine (pure alpha agonist, doesn't effect HR) may be useful in patients with tachyarrhythmias
Neurogenic Shock - hypotension as result of spinal cord trauma, present in complete and incomplete injuries
C/T Spine trauma --> loss of alpha adrenergic tone --> vasodilation (--> dec DBP) --> dec venous return --> dec SBP
Injuries above T5 --> interrupt SNS to heart --> inappropriately normal or low HR
***Spinal shock is different - it is the initial phase of spinal cord injury, flacid muscles/absent reflexes below level of injury, must pass prior to completeness of injury being determined
Treatment - up to 40cc/kg IVF bolus, think bleeding until proven otherwise, maximize O2 and perfusion, neosenephrine prn (SBP < 90, impaired mentation, oliguria), usually resolves in 24-48 hrs
Central cord syndrome - effects grey matter, weak hands, little stronger arms, LE normal
Anaphylactic Shock
Anaphylaxis - IgE mediated systemic hypersensitivity reaction
Anaphylactoid reaction - mast cell mediated systemic hypersensitivity reaction
Anaphylactic shock - extreme reaction with airway compromise and hypotension
DX - acute onset + hives, pruritis, flushing, edema + respiratory compromise or hypotension (cutaneous sxs present in 90%)
Two of the following: Respiratory compromise, hypotension, crampy abdominal pain and/or vomiting
Treatment
Only real treatment, EPI - 0.5 mg Epi IV or IM, repeat Q5min prn, drip for refractory cases
Vasoconstriction (alpha 1), increased CO (Beta 1), bronchodilation (beta 2) and mast cell stabilization
Respiratory support
Crystalloid boluses
EPI only treatment, rest is supportive/2nd line:
Glucagon 1-2 mg IV over 5 min then 10mcg/min if on beta blocker
Albuterol Nebs
Antihistamines - benadryl 50mg IV, zantac 50 mg IV
Steroids - methylprednisolone 125 mg IV
Cardiogenic -
CI dec, SVR inc, PVR nrml, SvO2 dec, right atrial pressure inc, right ventricular pressure inc, pulmonary artery pressure inc, pulmonary artery occlusion pressure inc
Extensive acute MI = most common cause (or smaller MI with underlying LV dysfunction)
Complicates 5-10% of MIs
Usually within 24hrs (most within 7)
Treatment - RECOGNIZE!!
Mechanical ventilation, support BP, protect the heart, treat underlying problem
Dobutamine - dec preload, inc contractility, dec afterload,
Vasodilators - dec preload, dec afterload, dec myocardial VO2
Aortic balloon - dec preload, dec afterload, dec myocardial VO2 - improves coronary perfusion
Dopamine - inc preload, inc contractility, inc afterload, inc heart rate, inc myocardial VO2
Pressors
Need central line for administration and A line for monitoring
Alpha-1 - on blood vessels cause vasoconstriction
Beta-1 - on heart, improve transmission of electrical impulses (coronotropic) and ionotropic
Beta-2 - on vessels cause vasodilation
Dopaminergic
Phenylephrine - Alpha-1 (+++), Beta-1 (0), Beta-2 (0), Dopaminergic (0) - SVR (++), CO (nrml/+)
Norepinephrine - Alpha-1 (+++), Beta-1 (++), Beta-2 (0), Dopaminergic (0) - SVR (++), CO (nrml/+)
Epinephrine - Alpha-1 (+++), Beta-1 (+++), Beta-2 (++), Dopaminergic (0) - SVR (- w/ low dose, + w/ high dose), CO (++)
Dopamine 0.5-2.0 mcg/kg/min - Alpha-1 (0), Beta-1 (+), Beta-2 (0), Dopaminergic (++) - SVR (0), CO (+)
Dopamine 5.0-10.0 mcg/kg/min - Alpha-1 (+), Beta-1 (++), Beta-2 (0), Dopaminergic (++) - SVR (+), CO (+)
Dopamine 10.0-20.0 mcg/kg/min - Alpha-1 (++), Beta-1 (++), Beta-2 (0), Dopaminergic (++) - SVR (++), CO (0)
Dobutamine - Alpha-1 (0/+), Beta-1 (+++), Beta-2 (++), Dopaminergic (0) - SVR (-), CO (+)
Isoproterenol - Alpha-1 (0), Beta-1 (+++), Beta-2 (+++), Dopaminergic (0) - SVR (-), CO (+)
Blunt cardiac injury (cardiac contusion) - bent steering wheel, sternal pain/bruising, sternal fx
Blunt chest trauma --> cardiac bruising --> cardiac arrhythmias
Dx: EKG changes - sinus tach, ST/T wave changes, RBBB
Treatment: ACLS, observation, cardiac eval with ECHO (new murmurs, persistent EKG changes)
Obstructive - obstruction of cardiac outflow tract - PTX, cardiac tampnade, PE - acutely life-threatening, essential to recognize, easy to treat
CI dec, SVR nrml-inc, PVR inc, SvO2 dec, right atrial pressure inc, right ventricular pressure inc, pulmonary artery pressure inc, pulmonary artery occlusion pressure nrml-dec
Tension pneumothorax - acutely life threatening, essential to recognize, easy to treat - one way leak from - sealing off open pneumothorax, rib fractures poking lung, bronchial injury, CVL complication, barotrauma
One way valve in chest wall --> air is pumped into pleural space but can't escape --> complete lung collapse (--> hypoxia) --> mediastinal shift (--> tracheal deviation) --> decreased venous return to heart --> obstructive shock --> death
Dx: Respiratory distress, hypoxia, absent breath sounds, crepitus, tracheal deviation
Treatment: immediate decompression (needle), chest tube, +/- surgery (rare)
Needle thoracentesis - 2nd intercostal space, midclavicular line, over top of rib, long large bore angiocath
Cardiac Tamponade - muffled heart tones, hypotension, distended neck veins - BECK's Triad
Penetrating Injury (--> non-contained bleeding --> death)
Blood contained in pericardial sac (--> muffled heart tones) --> pressure on heart
--> decreased CO (hypotension and obstructive shock)--> back-up of venous blood --> distended neck veins
Dx: Clinical suspicion, CXR - globular heart, FAST, Pericardial Window
Treatment: pericardiocentesis, ER Thoracotomy, Subxiphoid window
Pulmonary Embolism
High suspicion in high risk Pts, sudden onset of hypoxia associated with movement, hypoxia w/ normal a-a gradient and normal CXR, unexplained tachycardia
EKG findings: RBBB, S1Q3, acute cor pulmonale
ECHO - R ventricular dysfunction
Dx - D-dimer sensitive but not specific, LE venous duplex, V/Q scan, pulmonary CTA, conventional angiography
Treatment - vent support; support BP with NE, Vasopressin or Dopamine; thrombolytics (speeds lysis, no strong data, 3% risk of intracranial hemorrhage); embolectomy
Venous Air Embolism
Air (only takes 5 cc) introduced to venous circulation travels to the right atrium, then right ventricle and if large enough causes obstruction in the RV outflow tract or travels into pulmonary circulation and causes a pulmonary air embolism
Treatment; pull back from catheter
If arresting - follow ACLS for arrest (chest compressions break up air), +/- thoracotomy
If not arresting - L decubitous positioning, head down, 100% FiO2 - try to trap bubble in R atrium where it can slowly break down