Shock Cases 2008

Marc Francis FRCPC

Case 1: Pediatric anaphylaxis

Type of shock:

  • Anaphylactic Shock (distributive)

Pathophysiology:

  • 2 stage process
  • Sensitization to allergen with IgE antibodies formed and upregulation of receptors and prepares mast cells for activation
  • Re-exposure with IgE – allergen interaction with release of preformed and newly synthesized mediators from mast cells and basophils
  • Type I or immediate hypersensitivity

Management goals:

  • Control massive histamine release
  • Return vasogenic tone to peripheral vasculature
  • Prevent bronchoconstriction
  • Rapid decrease in airway swelling to prevent need for airway capture in a difficult airway

Interventions:

  • Epinephrine IM 0.01mg/kg = 0.01cc/kg of 1:1000 IM
  • H1 (Benadryl) blockers 1-2mg/kg IV to max 100mg
  • Smooth muscle contraction
  • H2 (Ranitidine) 1mg/kg to max 50mg IV
  • Increases HR and contractility and bronchodilation
  • Fluids = 20cc/kg of NS
  • Ventolin nebulizer
  • Steroids = 1-2mg/kg of solumedrol IV
  • Racemic epi
  • Early ETT if required = triple set up
  • IV epinephrine can be life saving
  • Crash cart epi 1:10,000 and draw up in a 1 cc tuberculin syringe
  • Give 0.1cc aliquots every minute until effect
  • Can then start an infusion at 1ug/min-4ug/min

Pitfalls:

  • Not knowing the dose and volume of EPI
  • Giving EPI SC
  • generalized urticaria makes SC absorption very unpredictable
  • Difficult under stress
  • Not being aggressive early

Case 2: Anaphylaxis complicated by B-blockers

Type of Shock:

  • Anaphylactic or distributive

Pathophysiology:

  • Patients on B-blockers may be refractory to therapy with epinephrine and antihistamines
  • These patients may manifest with persistent hypotension, relative bradycardia and worsening bronchospasm despite adequate interventions for same

Management goals:

  • Attempt to increase positive inotropic and chronotropic cardiac effects using an alternative non-adrenergic pathway to increase the vasomotor tone and HR
  • Increase the bradycardia if unresponsive

Interventions:

  • Glucagon
  • Augments cAMP synthesis through a G-receptor that is independent of Alpha and Beta receptors
  • Initial dose 1-5mg IV over 5 mins and then an infusion at 5-15ug/min
  • Refractory Bradycardia may respond to 2nd line therapies
  • Transcutaneously pacing
  • Atropine 0.3-0.5mg IV
  • Isoproterenol 0.05-0.2ug/kg/min is the last line therapy for patient unresponsive to all the above

Potential pitfalls:

  • Failure to recognize that the patient is on a B-blocker or has a disease process which is commonly treated with B-blockers
  • Continual use of Epinephrine with no effect
  • Side effects of Glucagon therapy including nausea, vomiting, hypokalemia and hyperglycemia

Case 3: Blunt trauma with pelvic fracture

Type of Shock

  • Hemorrhagic

Pathophysiology:

  • Blood supply to the pelvis comes from the L and R internal iliac arteries
  • The venous system has many collateral branches and is without valves allowing for bidirectional flow
  • Most pelvic hematomas are venous in origin
  • Hemorrhage from pelvic fractures collect in the retroperitoneal space

Management goals:

  • Determine the grade of hemorrhagic shock
  • Restore the intravascular volume
  • Identify the source of the bleeding
  • Control the bleeding if able
  • Definitive management of the bleeding

Interventions:

  • Aggressive fluid resuscitation with level 1 infuser
  • 20cc/kg bolus of NS and then repeat same if not responding
  • Avoid lower limb IV sites in major pelvic fractures
  • Blood
  • after 40cc/kg of NS get the blood hung
  • This is not an indication for pressors  need to fill the tank
  • Rule out thoracic and external causes of blood loss
  • Pelvic binder in attempt to tamponade the bleeding
  • Stable patient = CT scanner
  • Unstable patient = ED FAST
  • In the hypovolemic patient with a pelvic fracture you need to determine if there is hemorrhage into the peritoneal cavity
  • Peritoneal blood = Laparotomy
  • Negative peritoneal blood = Likely retroperitoneal hematoma and they do worse with laparotomy need angiography for embolization vs mechanical stabilization
  • Note that external fixators have never been shown to decreases morbidity of mortality and are time consuming
  • Mobilize the angio team early as it takes time

Potential Pitfalls:

  • Delay in blood in hemorrhagic shock
  • Using pressors in hemorrhagic or hypovolemic shock when you have not given adequate volume
  • Failure to identify the source of bleeding
  • Surgical involvement in major unstable pelvic fractures when there is no peritoneal bleeding and angiography is what is required

Case 4: Neoplastic Cardiac Tamponade

Type of shock:

  • Obstructive

Pathophysiology

  • Neoplastic pericarditis can result from any number of malignancies
  • Decompensated cardiac function comes from a marked rise in intrapericardial pressure seen with a rapid accumulation of fluid
  • Chronic and slow effusions usually are not hemodynamically unstable
  • Radiation pericarditis and scar formation is a well known complication of radiotherapy

Management goals:

  • Rule out other causes of hypotension, CP and dyspnea
  • Hemorrhage
  • PE
  • MI
  • Restore the intravascular volume in an attempt to overcome the constriction
  • Rapid removal of the pericardial fluid
  • Diagnostic studies and longterm therapeutic measures to prevent re-accumulation of the effusion

Interventions:

  • FAST US looking for pericardial effusion is essential
  • Remember that a very large effusion that is chronic may not be the cause of tamponade
  • Likewise a small accumulation of fluid in a constrictive pericardium can result in tamponade
  • Prepare for immediate pericardiocentesis in the hemodynamically unstable patient
  • Supportive therapy with fluid bolus 1 liter of NS and 100% O2 by non-rebreather mask
  • Pericardiocentesis
  • U/S guided is always preferred
  • patient at 45deg angle seated
  • pre-medicate with atropine
  • 18 gauge spinal needle (8 - 12 cm long) with a 3 way stop cock
  • insert b/w xiphoid and L costal margin at 30-45deg angle
  • aim for L shoulder tip
  • enter b/w 6-8 cm
  • free flowing abundant blood suggests cardiac puncture
  • can use an 8 french central line kit once in for ongoing drainage
  • If patient can be hemodynamically stabilized with fluids then this is always better done under U/S guidance by radiology and insertion of a pigtail catheter
  • Diagnostic work-up of fluid
  • Biochemical and cytologic analysis for future management

Potential pitfalls:

  • Not thinking about tamponade in the oncology patient who presents with SOB and CP
  • Improper treatment for submassive or massive PE could be fatal!!!
  • Failure to recognize that even a small effusion can lead to tamponade in a constrictive pericardium
  • Neoplastic constrictive pericardium
  • Radiation pericarditis
  • Performing ED pericardiocentesis and exposing patient to risks of procedure on a stable chronic effusion

Case 5: Neurogenic Shock

Type of shock:

  • Distributive

Pathophysiology:

  • Disruption of sympathetic autonomic ganglia leading to loss of vasomotor tone and lack of reflex tachycardia
  • Hypotension
  • Due to loss of sympathetic tone thus vasodilation and decreased SVR
  • Usually only lesions at or above T6 because below this leaves enough intact sympathetics to maintain BP
  • Bradycardia (absolute or relative)
  • Due to unopposed parasympathetic (VAGAL) tone to the heart
  • Usually only occurs with lesions at or above T4 because sympathetic innervation to heart is at T4

Management Goals:

  • This is a diagnosis of exclusion requiring a rule out of all other causes of hypotension first
  • Address the hypotension with fluids +/- pressors
  • Manage the airway as required realizing that intubation may have an even more profound effect on hypotension and bradycardia with a significant vagal stimulus
  • Prevent secondary spinal cord injuries

Interventions:

  • C-spine collar
  • Most are mild and will respond to fluid resuscitation alone
  • Severe hypotension and bradycardia are seen in 20-30% and are most common in high c-spine fractures
  • These will require fluid resuscitation and vasopressors
  • Something with Alpha squeeze will be required
  • Epinephrine 1:10,000 1cc until effect
  • Phenylephrine 10mg in 100cc minibag and draw up in 10 cc syringe with 1ml = 100mcg q2-5mins
  • Premedication with atropine for intubation 1.0mg IV and expect a transient worsening with same with vasopressors hung in anticipation
  • Foley cath for all spinal cord injuries to prevent bladder distenstion
  • NG tube to address atonic GI tract

Potential Pitfalls:

  • Failure to rule out all other potential causes of shock before explaining hypotension by neurogenic shock
  • Failure to recognize the significant additional unopposed vagal stimulus from intubation and not anticipating it’s deleterious effects
  • Continuing to push fluids in cases of high c-spine injuries where pressors are required
  • This can precipitate or worsen non-cardiogenic pulmonary edema which these patients are at high risk for

Case 6: MI with hypotension and acute pulmonary edema

Type of shock:

  • Cardiogenic shock vs Hypovolemic shock

Pathophysiology

  • Normal cardiac index is 2.5-4.0L/min/m2
  • Coronary perfusion in patients with coronary artery disease depends on the pressure gradient between the aorta and the LV chamber in diastole
  • The combination of decreased BP and increased filling pressures leads to a dramatic ↓↓ in coronary perfusion
  • There are two main classes of shock in the patient with hypotension and pulmonary edema
  • Volume depleted (25%)
  • Hypotension and decreased perfusion
  • +/- pulmonary edema
  • Low cardiac index CI <2.2 L/min/m2
  • Low left sided filling pressures (PAOP <15mmHg)
  • Cardiogenic shock (75%)
  • Hypotension and decreased perfusion
  • Uniformly have pulmonary edema
  • True cardiogenic shock have lost as much as 40% of their ventricular mass
  • Low cardiac index (<2.2L/min/m2)
  • High left sided filling pressures (PAOP>15mmHg)
  • Very difficult to differentiate between these two patient groups based on physical exam alone as they present the same and no access to pulmonary artery cath in the ED

Management Goals:

  • Hypovolemic
  • Fluid challenge alone in these patients will restore hemodynamic stability
  • Vasopressors should not be required if no cardiogenic component
  • Hemodynamic monitoring
  • Cardiogenic shock
  • Inotropic and vasopressor therapy
  • Mechanical support
  • Intubation and mechanical ventilation
  • Reperfusion therapies
  • Hemodynamic monitoring
  • Pressors
  • Goal to increase BP
  • Required for maintaining coronary perfusion
  • Potential Significant negative effects
  • Increase afterload
  • Decreased CO
  • Increase myocardial demand
  • Can exacerbate dysrhythmias

Interventions:

  • Judicious fluid challenge is a reasonable first step
  • 250cc saline boluses over 5-10 mins
  • Repeat if the resp status is not deteriorating
  • If hypovolemia is contributing to the hypotension this should restore BP and perfusion without need for pressors
  • Although this carries a potential risk in true cardiogenic shock small fluid bolus is unlikely to have a severe negative impact
  • Inotropic agents
  • Ensure that patient is adequately volume repleted first
  • Norepiniphrine is probably pressor of choice
  • Raises BP and α-constrictor effect will increase coronary perfusion
  • Little effect on contractility so no increase myocardial O2 demand
  • Temporizing only
  • Dopamine
  • Easily accessible in ED
  • Dose dependant effect on peripheral vascular tone (ie don’t start at 5!!!)
  • Positive inotropic agent = good
  • Positive chronotropin agent = bad
  • Dobutamine
  • Mostly B2 agonist with some B1 and some α activity
  • Inotropic = good
  • Vasodilator = problematic
  • Amrinone/Milrinonoe
  • Phosphodiesterase inhibitors
  • Increase CO and decrease LV pressures without producing significant changes in HR and BP
  • Early intubation
  • Addresses the hypoxia
  • Reverses the metabolic +/- respiratory acidosis which has a negative inotropic effect on the heart and its contractility
  • Use hemodynamically stable induction agents and lower doses if required
  • May require no drugs at all
  • Anticipate transient worsening in hemodynamic parameters and pre-load with medications or have inotropes hung and ready
  • Mechanical support
  • Intra-aortic ballon pump
  • Anti-ischemic therapies
  • Hold Beta-blockers
  • Hold nitrates
  • Reperfusion strategies
  • Lytics
  • Angioplasty
  • Shock trial would indicate the early PCI vs medical stabilization is best
  • Get the cath lab involved early
  • CABG

Potential pitfalls:

  • Failure to recognize that hypovolemia and pulmonary edema can co-exist
  • Using pressors before ensuring that the patient is fully volume resuscitated
  • Selecting inotropic agents in cardiogenic shock that have significant chronotropic side effects or that have the potential to increase myocardial oxygen demand
  • Using anti-ischemic therapies in patients who are borderline hypotensive and inducing cardiogenic shock
  • Delaying life-saving reperfusion therapies with prolonged attempts at medical stabilization