Conshock
description
Transcript of Conshock
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