Shock

Outline Definition of Shock Signs and Symptoms of Shock Categorization of Shock The PA Catheter Replacement Fluids Vasopressors and Inotropes Example Cases

What is Shock? Shock is a physiologic state characterized by a systemic impairment in oxygen delivery as a result of reduced tissue perfusion, almost universally mediated by low blood pressure.

What is Shock? The general physiologic mechanisms of how shock leads to irreversible cell damage and death include: Cell membrane ion pump dysfunction Intracellular edema Leakage of intracellular contents into the extracellular space Inadequate regulation of intracellular pH

Signs/Symptoms of Shock Cardiovascular – Hypotension Nervous – Agitation  Delirium  Coma Pulmonary – Tachypnea; hypoxia Epidermal – Cool, clammy skin; peripheral cyanosis Kidneys – Oliguria; increased BUN/Cr ratio GI – Ileus, hemorrhage; hepatic dysfunction Hematologic – Coagulopathy  DIC Diffuse Cellular Injury – Lactic acidosis

Physiologic Description of Shock Pressure Gradient = Flow x Resistance (i.e. Ohm’s Law  V=IR) Perfusion Pressure = MAP – CVP Perfusion Pressure = CO x SVR Perfusion Pressure = HR x SV x SVR SV is dependent upon preload, afterload, and myocardial contractility

Categories of Shock Hypovolemic Decreased Preload (from an extracardiopulmonary process) Decreased SVR Decreased Contractility Decreased Preload (from an intracardiopulmonary process) Distributive Cardiogenic Obstructive

Etiologies of Shock Cardiogenic Hypovolemic Distributive Obstructive – Heart failure – Myocarditis – Arrhythmias – Paplillary muscle rupture – Acute AI Obstructive – Massive PE – Tension pneumothorax – Cardiac tamponade Hypovolemic Loss of blood volume Loss of plasma volume Distributive SIRS / Sepsis Anaphylaxis Myxedema Coma Neurogenic Shock

The Pulmonary Artery (PA) Catheter http://www.edaya.com

The PA Catheter The PA catheter allows measurement of 3 types of data: 1. Central venous, pulmonary artery, and pulmonary capillary occlusion (or “wedge”) pressures 2. Cardiac output and vascular resistence 3. Sampling of mixed venous blood Situations in which PA catheters are most helpful: 1. Guiding the management of severe CHF 2. Estimating fluid status in non-cardiogenic pulmonary edema 3. Diagnosing pulmonary hypertension 4. Diagnosing right heart infarction

The PA Catheter As the catheter is “floated” from either the internal jugular or subclavian veins, and advanced from the RA to the RV, and from the RV to the PA, a number of specific pressure waveforms should be observed.

The PA Catheter Right Atrium

The PA Catheter Right Ventricle

The PA Catheter Pulmonary Artery

Pulmonary Capillary Wedge Pressure (PCWP) The PA Catheter Pulmonary Capillary Wedge Pressure (PCWP)

Replacement Fluids IV replacement fluids can be divided into two categories based on whether they do or do not have a tendency to stay intravascular: Crystalloid – Normal saline, lactated Ringer’s, D5W Colloid – Fresh frozen plasma, albumin

Replacement Fluids Although there are theoretical reasons to favor colloids over crystalloids for volume resuscitation in patients with shock, no data to date has shown any significant outcome difference. Therefore, crystalloid is almost always the preferred choice, given its decreased cost and decreased risk.

Vasopressors and Inotropes Vasopressors – Act to increase SVR, and subsequently increase BP. Inotropes – Act to increase CO. BP may either be increased or decreased. Together, vasopressors and inotropes are colloquially known as “pressors”.

Vasopressors and Inotropes A given drug may have an effect on multiple receptors, and which receptors it interacts with may be dose dependent. Hypovolemia must be corrected prior to the institution of vasopressor therapy. Therefore, pressors are generally not helpful in hypovolemic shock. A given agent may affect systemic blood pressure through both direct actions, as well as indirect reflex actions.

Vasopressors and Inotropes Drug Alpha-1 Beta-1 Beta-2 Dopa. Effect on SVR Effect on HR Effect on contractility Typical Dose Phenylephrine +++ ↑↑ ↔ / ↑ ↔ 20-200 μg/min Vasopressin (mechanism of action poorly understood) 0.01-0.04 U/min Norepinephrine ++ ↑ 0.5-20 μg/min Epinephrine ↓ (low dose) ↔ / ↑ (high dose) 2-10 μg/min Dopamine 0.5 – 2 5 – 10 10 – 20 (μg/kg/min) + 1-20 μg/kg/min Dobutamine 0 / + ↓ 2.5-20 μg/kg/min Isoproternol 1-10 μg/min Milrinone (acts as a phosphodiest- erase inhibitor) Load: 50 μg/kg over 10 min Maintenance: 0.375 – 0.75 μg/kg/min

Vasopressors and Inotropes (Generalized Summary) Phenylepherine Norepinepherine Epinepherine Dopamine Dobutamine Milrinone ↑ SVR No effect on contractility ↓ SVR ↑ Contractility

Case 1 A 35 year old construction worker is brought in to the ER 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.

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.

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 ill-appearing, cachectic, and non-responsive. His neurologic exam is non-focal. Aside from the vital sign abnormalities, his cardiac and respiratory exams are unremarkable.

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. Vitals now: HR=130, BP 82/64, RR=28, O2 sat=94% on 2L. Vitals 5hrs ago: HR=84, BP 134/70, RR=20, O2 sat=99% on 2L.

Case 5 You are on-call in the ICU, and are paged in the middle of the night regarding a patient 3 days post-op from a CABG that had been complicated by a intraoperative cardiac arrest from ventricular fibrillation. He continues to be on pressors and is intubated, due to concerns regarding hemodynamic instability in the immediate post-op period, which continues to be incompletely explained. His nurse has noted that his blood pressure has been trending downward over the past 6 hours, requiring progressively higher doses of dopamine to maintain mean arterial pressures (MAP) of 60mmHg. His exam is notable for a 2/6 systolic murmur over the right upper sternal border, and coarse crackles at the left lung base. As you have never examined him before, you have no idea if these findings are old or new. His CXR from the previous morning was notable only for mild pulmonary edema, that you remember the team did not seem particularly worried about.

Case 5 (continued) Time HR MAP CO (L/min) SVR (dynes/sec/cm5) Dopa (μg/kg/min) Dobut Epi (μg/min) 12pm 90 72 3.5 1460 5 4 2 8pm 105 68 3.8 1260 10pm 113 64 4.2 1100 6 12am 118 58 4,9 865 8 2am 123 56 6.1 670 12