Shock

Deepa Murali MS IV

Objectives
Definition Pathophysiology (cellular level) Clinical features Response Categories causes and treatment Approach to patient Hx and PE Treatment overview

Definition
John Collins Warren momentary pause in the act of death Samuel Gross a rude unhinging of the machinery of life A multifactorial syndrome resulting in inadequate tissue perfusion and cellular oxygenation affecting multiple organ systems.

 Cellular ischemia Tissue hypoxia, anaerobic metabolism. Free radical reperfusion injury - local vasoconstriction, thrombosis, regional malperfusion, release of superoxide radicals, direct cellular damage. Activation of inflammatory mediators -Activation of neutrophils, release of proinflammatory cytokines TNF, IL1 and PAF which results in celluar injury , organ dysfunction and failure.

Factors affecting O2 delivery

Oxygen Delivery DO2

DO2 is dependent on oxygen content (determines quality) in arterial blood (CaO2) & CO (determines quantity) FICK Formula for DO2: DO2 = CO X CaO2 X 10 CaO2 = (Hgb x 1.34 x SaO2) + (PaO2 x .003) 1.34 ml of O2 that can be bound by 1g HgB 0.003 solubility coefficient for O2 in plasma

Other formulas
CO = HR x SV SV affected by preload, afterload and contractility CO = MAP CVP/SVR CVP- central venous pressure/ RA pressure

Oxygen Delivery DO2

Cardiac Output CaO2 Heart Rate Stroke Volume

PaO2

SaO2

Hgb Synchrony

Preload

Afterload

Contractility

CVP PCWP

PVR SVR

EF%

Clinical features
1st Physiologic factor supply < demand Increased RR Increased HR 2nd Physiologic factor peripheral vasoconstriction Pale, cool skin Weakened peripheral pulses End Organ Perfusion fails Altered mental status Decreased urine output

Clinical manifestations
Cardio weak peripheral pulses, extremities cold&cyanotic, BP, CO, LOC, HR Pulm respiratory failure w/ ARDS, RR Neuro - LOC Renal acute renal failure w/ BUN/Cr GI sepsis or GI bleed Heme DIC , hyperglycemia

Stages of Shock
Compensated
The bodys compensatory mechanisms are able to maintain some degree of tissue perfusion.

Decompensated
The bodys compensatory mechanisms fail to maintain tissue perfusion (blood pressure falls).

Irreversible
Tissue and cellular damage is so massive that the organism dies even if perfusion is restored.

Compensated
Tachycardia Tachypnea Decreased capillary refill Pale, cool skin

Uncompensated
Hypotension Falling SaO2 Bradycardia Loss of consciousness Dysrhythmias

Irreversible - death

Response
Hematologic Activation of coagulation cascade and contracting bleeding vessels ( via local thromboxane A2 release) Platelets are activated Fibrin deposition and stabilization of clot Develop DIC Cardiologic Increase in NE release (due to sympathetic response) and decrease in basal vagal tone through baroreceptos in carotid arch, aortic arch, LA and pulmonary vessels) Increased HR, increased myocardial contractility, constricting peripheral blood vessels. Redistributing blood flow to vital organs.

Pulmonary Pulmonary arterioles constrict due to hypoxia, edema and mediator release. Develop pulmonary hypertension. Pulmonary blood flow and physiologic dead space Impaired gas exchange. Alveoli collapse/edema r/t surfactant production and capillary permeability. O2 diffusion leads to resp. failure w/ ARDS development. Neurologic Cerebral perfusion w/ CO and BP Deteriorating LOC

Renal Activation of renin-angiotensin-aldosterone system Stimulated by sympathetic nerve activation and renal artery hypotension Activation leads to vasoconstriction and increased Na and H2O retention. Neuroendocrine Release of ADH/vasopressin from the posterior pituitary which causes vasocontriction, and Na and H2O retention. GI Develop ischemic gut syndrome Develop paralytic ileus Increased changes of GI bleed

Categories
Hypovolemic shock as a cause of inadequate circulating volume as in hemorrhage Obstructive shock caused by extracardiac obstruction of blood flow as seen in cardiac tamponade Cardiogenic- shock caused by primary pump failure, as in decreased myocardial contraction after MI Distributive shock assoc. w/ maldistribution of blood flow, as in sepsis Endocrine shock as a result of hormonal pathology, either through underproduction or overproduction.

Hypovolemic shock - Intravascular volume

Hemorrhagic Ext blood loss -operative bleeding, GI or vaginal bleeding. Occult bleeding chronic GI hemorrhage, ruptured aortic aneurysms. Non hemorrhagic Uncompensated GI loss (protracted vomiting, high output fistula) Urinary loss Evaporative loss( from fever loss of intravascular vol, open body cavity surgery) Transudation of fluid in response to shock and resuscitation (trauma, pancreatitis, SBO).

Treatment
Oxygen Monitors IV access Fluid replacement crystalloids (isotonic LR or NS) vs colloids Pressor support (rarely needed) Correct underlying cause

Treatment
Fluid replacement:
Hypovolemia:
Isotonic crystalloids Colloids does not diffuse through capillary walls. osmotic pressure wherein fluid stays in vascular compartment

Hemorrhage:
Whole blood Packed RBCs HBOCs Isotonic Crystalloids

Obstructive Shock Resistance to cardiac output;

increased afterload; decreased SVR & MAP. Heart compensation w/ obstruction to atrial filling and/or outflow from the heart

1.

Cardiac Tamponade mechanical obstruction to normal CO and subsequent diminished systemic perfusion. Locally induced hypovolemic state. Acute Pericardial effusion trauma, ischemic myocardial rupture, aortic dissection. Pulmonary embolism CO restricted either by mechanical obstruction of pulmonary arterial tree or by pulmonary HTN. Venous air embolism Obstruction of pulmonary artery blood flow ensuing cardiac arrest. Examples from central access catheter and surgical procedures which are done 5 cm above RA. Tension pneumothorax Increased intrapleural pressure from an injury to lung or airways collapses the intrathoracic great veins and decreases venous filling and results in shock.

2. 3. 4.

5.

Treatment for Obstructive Shock

Address cause Pericardiocentesis Chest tube Thoracostomy Thrombolysis, embolectomy O2 therapy Fluid resuscitation and inotropes (temporary support)

Cardiogenic Shock Pump Failure

Acute MI Reduced contractility cardiomyopathy Ventricular outflow obstruction AS, Aortic dissection Ventricular filling anomalies- Atrial myxoma, MS Acute valvular failure AR, MR Cardiac dysrrhythmia Vfib, atrial dysrrhythmias hypoperfusion Ventricular septal defects VSD, rupture

Treatment
O2 therapy Increase preload Venous access- short, thin walled large bore IV catheters Pressor support Dobutamine Beta 1 adrenergic NE Alpha and beta adrenergic Dopamine - Renal and splanchnic vasodilation Beta adrenergic Alpha adrenergic Reduce afterload Nitroprusside, ACE inhibitors, IABP
Definitive therapy (fibrinolytic therapy, PTCA, CABG, ventricular assist device, cardiac transplant)

Distributive Shock
1. 2. 3. 4. 5. 6. 7. Septic shock Anaphylaxis Neurogenic SIRS TSS Addisonian Crisis Drugs nitrates, opiods, adrenergic blockers

Septic Shock
Septic shock is defined as a state of acute circulatory failure characterized by persistent arterial hypotension despite adequate fluid resuscitation or by tissue hypoperfusion (manifested by a lactate concentration greater than 4 mg/dL) unexplained by other causes.

Septic Shock
Decreased SVR and normal to low cardiac filling pressures Increased CO and SaO2 - scientific debate whether decreased cardiac perfusion is related to direct myocardial depression or cardiac ischemia. Gram negative bacteria -endotoxin lipopolysaccharide cell wall constituent of gram ve bacteria; TNF and IL 1 release results in activation of acute inflammatory cascade. Gram positive bacteria lipteichoic acid, superantigens Staph TSST and Strep pyrogenic exotoxin

Septic Shock
Signs: Early warm w/ vasodilation, often adequate urine output, febrile, tachypneic. Late-- vasoconstriction, hypotension, oliguria, altered mental status. Monitor/findings: Earlyhyperglycemia, respiratory alkylosis, hemoconcentration, WBC typically normal or low. Late Leukocytosis, lactic acidosis Very Late Disseminated Intravascular Coagulation & Multi-Organ System Failure.

Treatment of Septic Shock

Oxygenation IV fluids (crystalloids) Drainage of abscesses and excision of necrotic tissue Pressor support (dopamine, norepinephrine) Empiric antibiotics Gentamicin/tobramycin 3rd gen cephalosporin cefotaxime/ceftriaxone Pseudomonas ceftazidime Resistant Staph vancomycin Anaerobe - metronidazole NaHCO3? Steroids?

Anaphylaxis Massive vasodilation, SVR,

capillary permeability

Dermatologic reaction urticaria, pruritus Respiratory obstruction processes stridor, bronchoconstriction, angioedema Low CVP and CO

Treatment of Anaphylaxis
Avoidance Airway (have low threshold for early intubation) Oxygenation and ventilation Epinephrine (IV, IM, Subcutaneously) IV Fluids (crystalloids) Antihistamines
Benadryl Zantac

Steroids Beta agonists Aminophylline -bronchodilator Pressor support (dopamine, dobutamine or epinephrine)

Neurogenic Shock Massive vasodilation due to

loss of sympathetic tone / vasomotor control Hypotension, bradycardia, hypothermia Sympathetic outflow is disrupted resulting in unopposed vagal tone (circulatory collapse) Autonomic dysfunction as result of spinal cord injury above upper thoracic level with corresponding hypotension, bradycardia and warm, dry skin. Not to be confused with spinal shock - phenomena surrounding physiologic or anatomic transection of the spinal cord that results in temporary loss or depression of all or most spinal reflex activity below the level of the injury.

Treatment for Neurogenic Shock

ABCs Judicial fluid resuscitation with crystalloid Solumedrol therapy O2 therapy Consider vasopressor support with dopamine or dobutamine Atropine for bradycardia Monitor V/S, u/o, LOC, skin and hemodynamics Transfer patient to regional spine center

Other forms of Distributive Shock

SIRS TSS Addisonian crisis Pancreatitis Burns

Endocrine Shock
Hypothyroidism Decreased CO due to lower inotropic activity in assoc. with bradycardia. HTN increase in vascular resistance Decreased ventilatory drive in response to hypoxemia and hypercapnia

Thyrotoxicosis High output heart failure Previous cardiac or coronary artery disease Increased HR,EF and CO leads to myocardial ischemia Tachyarrhythmias Afib and supraventricular tachycardia

Approach to Patient
History Know cardiac disease hx CHF, pericardial, coronary disease Recent fever or infection Drugs diuretics or antihypertensives Predisposing conditions to PE Possible bleeding site Hospitalized pts, indwellin catheters, recent surgery. Accidental allergen exposure Influenzalike illness (fever, arthralgias, myalgias) and a desquamating rash Abdominal pain or tenderness or pulsatile mass Women of childbearing age ruptured ectopic pregnancy Immunosuppressive therapy

PE
Jugular vein Flat distributive shock Distended cardiogenic & obstructive shock Paradoxical pulses cardiac tamponade Evidence of CHF, murmurs Assymetry of pulses aortic dissection Tenderness or rebound in abd pancreatitis or peritonitis High pitched bowel sounds intestinal obstruction Fever, chills

Skin lesions Petechiae or purpura N.meningitidis Ecthyma gangrenosum P. aeruginosa Generalized erythroderma - TSS due to S.aureus or S.pyogenes

Lab work
Hematocrit, WBC, electrolytes Platelet count, PT,PTT, DIC screen Arterial blood gas resp alkalosis (hyperventilation) then met.acidosis (increase in lactic acidosis) Blood cultures, urinalysis, gram stain and cultures of appropriate sites EKG MI, arrythmia CXR - CHF, tension pneumothorax, aortic dissection, pneumonia Echo - cardiac tamponade, CHF

PCW pressure (desired range 1215 mmHg); Mean PCW < 6 mmHg suggests oligemic or distributive shock; PCW > 20 mmHg suggests left ventricular failure. CVP (desired range 1012 cmH2O) Urine output ( 30ml/hour)

Initial Assessment - ABC

Airway:
Does pt have mental status to protect airway? GCS less than eight means intubate Airway is compromised in anaphylaxis

Breathing:
If pt is conversing with you, A & B are fine Place patient on oxygen

Circulation:
Vitals (HR, BP) 2 large bore (#16g) IV, start fluids (careful if cardiogenic shock), put on continuous monitor

ABCDE
In a trauma, perform ABCDE, not just ABC Deficit or Disability
Assess for obvious neurologic deficit Moving all four extremities? Pupils? Glascow Coma Scale (V6, M5, E4)

Exposure
Remove all clothing on trauma patients

Treatment
Monitoring Fluid resuscitation Vasoactive agents

Activated Protein C (Xigris)

Inactivates Factors Va and VIIIa Inhibits thrombin (decreases inflammation)
Inhibits platelet activation, neutrophil recruitment, and mast cell degranulation

Blocks cytokine production Inhibits cell adhesion Anti-apoptotic actions

Apoptosis (i.e. GI epithelial cell) induces anergy

Immediate Goals in Shock

Hemodynamic support MAP >60mm Hg CI > 2.2 L/min/m2 Maintain O2 delivery Hgb > 9g/dl Arterial saturation > 92% Supplemental O2 & mechanical ventilation Reversal of O2 dysfunction Decrease lactate < 2.2mM/L Maintain urine output >.5L/h

Shock

CVP SVR

HR

CO

PCWP

Hypovolemic Cardiogenic Obstructive Neurogenic Septic

Case 1
A 35 year old construction worker is brought in to the ER immediately following a 20-30 foot fall off a ladder. His past medical history is unknown. On exam, his vitals are: HR=120, BP=82/45, and RR=8. He is on a backboard and in a cervical collar. He withdraws from painful stimuli, but is otherwise non-responsive. Upon a quick superficial examination, he has an obvious fracture of his right femur and numerous mild lacerations.

Questions
What type of shock? What are the sources of blood loss? What is initial treatment of choice? If he fails to respond to the initial treatment, should a pressor be considered? If so, which one?

Case 2
A 68 year old woman is brought to the ER by ambulance after developing severe shortness of breath 30 minutes ago. Although her symptoms were initially only respiratory in nature, upon arriving in the ER she is now complaining of lightheadedness and nausea. Vitals are as follows: HR=95, BP=84/36, RR=32, O2 sat=89% on 2L, temperature=36.5. Exam is otherwise significant for loud bilateral crackles, an S3. She is mildly agitated, but otherwise has a grossly intact neurologic exam.

Questions
What type of shock? What is the best initial test? What is the initial tx of choice?

I. Hemodynamic support Dopamine is probably the best initial pressor of choice, as it will improve both BP and CO. If the patient fails to improve with dopamine, a second pressor can be added (norepinepherine or dobutamine, depending on the patients BP), though serious consideration should be made regarding insertion of an intra-aortic balloon pump. All patients in cardiogenic shock should also have a PA catheter inserted to help guide therapy. Although small (~250cc) fluid boluses can be given to some patients with cardiogenic shock, they should be avoided in this patient, as she is already experiencing significant respiratory compromise. II. Ventilatory support Oxygen is the best treatment to improve her oxygenation and comfort. Other therapies typically used for pulmonary edema (diuretics, nitrates, morphine) should be avoided as it will likely worsen her hypotension. If her pulmonary status continues to worsen despite supplemental oxygen, she should be placed on either non-invasive positive pressure ventilation (NIPPV) or be intubated. III. Revascularization She should receive aspirin and heparin. A call should immediately be made to cardiology to discuss the need for emergent catheterization vs. IIb/IIIa inhibitor vs. thrombolytics (dependent upon results of the EKG and availability of the cath lab)

Case 3
A 76 year old nursing home patient is brought to the ER by ambulance after becoming progressively incoherent over the preceding 24 hours. His past medical history is unavailable. On exam, his vitals are: HR=127, BP=78/45, RR=24, O2 sat=97% on RA, temp=34.7. He is acutely illappearing, cachectic, and non-responsive. His neurologic exam is non-focal. Aside from the vital sign abnormalities, his cardiac and respiratory exams are unremarkable.

Questions
What type of shock? Initial tx? Assume that 1 hour has past since initial presentation to the ER, and the results of the tests are consistent with a diagnosis of urosepsis. After 2.5L of normal saline, the patients BP remains at 83/50 with a HR of 122. What additional steps should be undertaken at this time?

Case 4
As the on-call intern, you are called on a cross-cover patient on another service for low blood pressure and shortness of breath. All you initially know about the patient is that they are a 64 year old man who was admitted for an uncomplicated NSTEMI 4 days ago, who was supposed to be discharged to home tomorrow. The patient had been feeling fine all day until 10 minutes ago when he very acutely developed shortness of breath. He is now complaining of lightheadedness and is developing a visibly waning level of consciousness. Vital signs now: HR=130, BP 82/64, RR=28, O2 sat=94% on 2L. Vital signs 5hrs ago: HR=84, BP 134/70, RR=20, O2 sat=99% on 2L.

Questions
What are the most likely etiologies causing this patients hypotension? As additional help is arriving, you perform a quick physical exam. Lung sounds are clear, heart sounds are distant, JVP is elevated, and no murmurs are present. With this additional information, what diagnosis becomes the most likely? What additional therapy is most appropriate as arrangements are made for emergent pericardiocentesis?