Shock

Definition

Multi system organ hypoperfusion Tissue hypoperfusion

Rapid Clinical Evaluation

Mean BP < 60mmHg or SBP < 90 mmHg Altered mental status Oliguria (< 30 cc/hr) Lactic acidosis

Cardiogenic Shock (1)

Left ventricular failure– Systolic dysfunction– Diastolic dysfunction– Valvular dysfunction– Cardiac dysrhythmias

Right ventricular failure

Cardiogenic Shock (2)

Low cardiac output:– Echo / radionuclear study: Reduced EF;

thermodilution: CI < 2.2 L/min/m2

Elevated LVEDP:– PA cath: Elevated CVP, RAP, PCWP (>

18mmHg)

PE:– Hypotension, JVE(+), basal rales, S3

Decreased Venous Return

Hypovolemic shock Neurogenic shock Compression of heart Obstruction of veins

Hypovolemic Shock

Decreased intravascular volume – decreased venous return

Endogenous catecholamines compensate up to 25% reduction in intravascular volume

Orthostasis: BP drops 10 mmHg, PR rises 30 beats/min.

“No reflow” phenomenon: > 40% blood loss > 2hr – cannot be resuscitated!

Shock in Trauma

Hypovolemia “Third spacing” Inflammatory mediators – SIRS

(resembling septic shock) Myocardial depressant substances Myocardial contusion

Neurogenic Shock

Decreased tone of venous capacitance bed – decreased venous return

E.g. C-spine cord injuries

Compression of the Heart

Cardiac tamponade, tension pneumothorax – decreased venous return

PE: JVE (+), high RA pressure Cardiac tamponade:

– Echo: Pericardial fluid, diastolic collapse of atria and RV, inspiratory right-to-left septal shift.

– PA cath: Equal RA, RV diastolic, PA diastolic, and PA occlusion pressures

Obstruction of Veins

Decreased venous return IVC obstruction SVC obstruction Tension pneumothorax

Septic Shock (1)

Reduced arterial vascular tone and reactivity – high cardiac output hypotension

Septic shock: 2/3 G(-) bacilli G(-) bacteremia: 1/3 Septic shock Lactic acidosis

– Abnormal distribution of blood flow – mismatch between O2 supply and demand

– Cellular defect in metabolism

Septic Shock (2)

Hypoperfusion– Redistribution of blood flow (major)– Myocardial depressant factor of sepsis (minor)– Non-survivors Diastolic dysfunction

Septic Shock (3)

Treatment:– Mainstay: IV crystalloids + Early antibiotics– Surgical drainage of abscesses– Vassopressors: Dopamine / Levophed– Colloids: Be cautious in ARDS– Steroids: Not recommended– Antiendotoxin antibodies

Initial Management

Primary survey A – B – C

Resuscitation O2 – IV – Monitors

Vital signs BP – PR - RR

Etiology Rate – Volume – Pump

Primary survey: A – B – C

Airway intubation + Mechanical ventilation– Airway protection – External masks O2 delivery not reliable– Increase FiO2 and PEEP– Sedation and paralysis (respiratory muscle

fatigue Metabolic acidosis)– Intervene early and fast if unconscious, RR >

30/min, abdominal paradoxical respiratory motion, accessory muscle use

Resuscitation: O2 – IV – Monitors

O2– Airway intubation + Mechanical ventilation

IV– Hypovolemia: 2 or more 16# or larger IV, large

bore CVP (trauma kit), X-match blood products

Monitors– ECG; BP (A-line); SpO2; Foley; NG– ABGs; echocardiography

Volume or Vasoactive drugs?

Cardiologist-intensivists:– PA cath and vasopressors as priority– Delay volume expansion

Surgical/anesthesiologist-intensivists:– Vasopressors accompany volume therapy to

raise BP quickly Common pitfalls:

– Inadequate circulating volume long after the 1st hour of urgent resuscitation!

Volume or Vasoactive drugs?

Working diagnosis of cardiogenic shock:– 250 cc NS in 20 min– Frequent reassessments for end points:

• Increased BP and pulse pressure• Increased JVP or CVP, new gallop or extra heart

sounds, lung edema

– Vasoactive drugs only after volume infusion be pushed to a discernable “to much”:

• Dobutamine 2-10 ug/kg/min (inotropy)• Dopamine 2-5 ug/kg/min (renal perfusion)

Definitive Therapy Hypovolemia: Volume expansion Hemorrhage: Surgical/endoscopic hemostasis Sepsis: Volume + Antibiotics +/- Drainage AMI: Surgical reperfusion / IABP Tamponade: Pericardiocentesis Pneumothorax: Pleurocentesis/thoracostomy Bradycardia: TCP/Atropine/Dopamine/Adrenaline Tachycardia: Cardioversion/Lidocaine/verapamil Lactic acidosis: Hyperventilation (PaCO2 to

25mmHg), NaHCO3 if pH < 7.0, hemodialysis.

Case 55Y female: Confused, BP 80/50, PR 135,

RR 24, dry skin, clear BS, cold limbs. Tx: 3L NS total

– BP normalize Hypovolemia• Seek bleeder or cause of dehydration

– BP low, fever 39.5C, warm limbs Sepsis• Antibiotics, septic work-up, +/- Dopamine

– BP low, rales, S3, JVE, cool limbs Cardiogenic shock

• Vasoactive drugs

Goal of Therapy (1)

Tables of normal hemodynamic values are frequently misleading:– E.g. Septic shock:

• “Numerically normal” CO too low

• “Numerically normal” BP over-hydration (lung edema, ARDS) or over-vasoconstriction (increased O2 demand and worsened tissue hypoxia)

Goal of Therapy (2) Intubation + Mechanical ventilation +/- Sedation /

paralysis to rest respiratory muscles PEEP Reduced venous return in cardiogenic

shock Increased cardiac output Adequate volume infusions to make vasoactive

drugs more effective Adequate Hb / Hct to increase O2-carrying

capacity Hyperventilate / NaHCO3/ HD to correct lactic

acidosis

Outcome

Cardiogenic shock– 90% mortality with medical tx alone– Predictors: blood lactate (> 5 mmol/L), cardiac

output, arterial pressure

Septic shock– MSOF mortality > 60%– Predictors: cardiac output, high blood bacterial

concentrations, failure to mount a febrile response, age, preexisting illness

Thank You