Shock

Shock Basics

Systemic inflammatory response syndrome (SIRS)- widespread inflammation that occurs within the body

Shock- acute, widespread process of impaired tissue perfusion

  • Low BP (MAP<60/SBP <90) and signs of poor perfusion

  • Initial (no symptoms) -> compensatory (starts seeing symptoms - ↑ HR and glucose), progressive, refractory

Multiple organ dysfunction syndrome (MODS)- failure within multiple body systems



Meds

  • Vasoconstrictors to increase SVR – epi, norepi, phenylephrine, vasopressin

  • Vasodilators to decrease afterload – nitroprusside, nitro, hydralzine 

  • Positive inotrops to increase contractility – dobutamine, milrinone, dopamine (increases HR)

  • Antidysrhythmics – amio, procainamide, lidocaine, labetalol

Hypovolemic

Most common – loss of circulation volume and significant decrease in preload

  • Mild – loss of about 15-20% volume, slight anxiety

  • Moderate – loss of about 20-30% volume, compensation and hits progressive stage around 30%

  • Severe – loss of about 30-40% (2L) volume, typically refractory in nature

Causes – vomiting, diarrhea, bleeding

Management 

  • Correct the cause. Restore perfusion, replace volume, prevent complications

  • Blood loss – rapid blood infusion

  • Third spacing – albumin to pull fluid into vascular spaces

  • Fluid loss – NS or LR

  • Monitor intake/output and daily weight

Cardiogenic

Usually see decreased contractility 

CO/CI low and wedge high

See high numbers of this in women and diabetics

Most common with MI that results in loss of 40% or more of functional myocardium (lower rates with early revas)

Compensatory vasoconstriction increases workload on heart and decreases perfusion through coronary arteries

Echo can be used to confirm diagnosis (shows estimate of wedge and CO/EF)

Manifestations – SBP <60, weak thready ulse, diminished heart sounds, cool, pale, moist skin, decreased cardiac output, increased wedge pressure, tachypnea, urine output <30mL/hr, chest pain, signs of pulm edema

Management

  • Identify and treat etiological factors of HR

  • Positive inotropes (milrinone, dobutamine, dopamine)

  • Diuretics for preload reduction (furosemide)

  • Antidysrhythmic to prevent electrical problems (amio)

  • Mechanical circulatory support devices (intra-aortic balloon pump, percutaneous VAD, ECMO)

Intra-aortic Balloon Pump

  • Used less frequently now

  • Sausage-shaped balloon wrapped around the end of a catheter inserted in the descending thoracic aorta – just distal to the subclavian artery

  • Diastolic augmentation – inflation during diastole – pushes blood backward into coronary arteries improving oxygen supply and pushes blood towards the peripheral vascular system

  • Afterload reduction – deflation during squeeze – just before the opening of the aortic valve and creates a vacuum to pull blood out of the LV and decreases afterload

  • Wean before removal ideally (1:1 -> 1:2 -> 1:3)


  • Contraindications – aortic valve insufficiency, severe peripheral vascular disease, aortic aneurysm 

  • Helium is used to fill balloon so it doesn’t have the possibility to cause an air embolism

  • Closed circuit – if blood does get into balloon it will cause a huge clot that will need open heart removal (call MD if you see blood in the tubing

  • Will need bed rest if in femoral

  • Do frequent neurovas checks

  • If the balloon goes back too far is can block renal arteries (check for decreased urine output)

  • If the balloon is pushed too far in it will block aorta flow and caused decreased perfusion

  • If the wedge goes up and CO goes down – the timing isn’t right

  • Complications – artery occlusion, aortic dissection, thrombosis, bleeding, balloon perforation, mispositioning, timing complications

Temporary VAD

  • Need volume in order to use or the vessel and RBC will get destroyed

  • Cannot go home on this device

  • Axial flow pumps the draw blood from one area and ejects it proximally (in LV or RV)

  • Cannot be used in patients with mechanical aortic valves

  • Can offer between 3-5 L/min of support

  • Monitor for signs of catheter migration, platelet destruction, and bleeding

  • Purge – there is a little bit of counter flow going around the fan blades so platelets don’t  clump to them

  • Use dextrose because NS will erode and rush the blades

  • WATCH FOR BLEEDING AND HIT (clots and bleeding so hold pressure and start them on direct thrombin inhibitor)

ECMO

  • Can be venoarterial (VA – only one we use for cardiogenic shock) or venovenous (VV – use for respiratory failure no cardio support)

  • Vasoactive drugs are weaned off to allow the myocardium time to rest

  • Need anticoagulation but bleeding is highest complication

  • 2nd highest risk is cloting and limb ischemia

  • Complications – cardiac tamponade, sepsis, limb ischemia, bleeding

  • Must be weaned off

  • May or may not have a pulse

  • Could get up with central but must lay flat with peripheral

Limit myocardial oxygen demand (analgesics, anxiety meds, control afterload and dysrhythmias, limit activities, calm quiet environment)

Distributive – Widespread Vasodilation

Anaphylactic Shock

  • First remove the allergen and then epi (promotes bronchodilation, vasocontriction, and myocardial contractility, inhibits further release of biochemical mediator) – limited response in patients receiving beta-blocks

  • Meds that can be given after epi – inhaled beta-adrenergic agents for bronchospasms, diphenhydramine slow IV push, famotidine (H2 blocker), corticosteroidss

  • Due to histamines, tryptasem cytokine

  • Can be minutes to hours after exposure to allergen 

  • Manifestations – profound vasodilation, increased capillary permeability, laryngeal edema, bronchoconstriction, excessive mucous secretions, coronary vasoconstriction, cutaneous reactions, gastrointestinal reactions

  • Get fluids if they are hypotensive after epi

  • Usual causes – IV contrast, blood, anti-venim, IGG

Neurogenic Shock

  • Caused by spinal cord injury (cervical spine) or head injury -lack of sympathetic tone

  • Causes - massive peripheral vasodilation, inhibition of baroreceptor response, and impaired thermoregulation (cutaneous blood vessels dilate and constrict to maintain body temperature, BRADYCARDIA, hypotension, warm/dry skin, decreased SVR

  • Management – fluid resuscitation, vasopressors, atropine or pacing, prophylaxis to prevent DVTs due to venous pooling

Septic Shock

  • Can be caused by bacteria, fungus, or a virus 

  • Neutrophils are over activated (mast cells and plasma enzyme cascades are triggered, containment to localized infection fails – systemic release of cytokines, mediators, and activated cells 

  • Endothelial damage and coagulation dysfunction – at risk for Acute Respiratory Distress Syndrome

  • Intrinsic Risk Factors – male, advanced age, coexisting disease, substance abuse, malnutrition

  • Extrinsic Risk Factors – invasive devices, wounds, surgical/invasive procedures, immunosuppressive therapy

  • Manifestations - ↑ HR, ↓ BP, change in sensorium, decreased urine output, ↑ temp, decreased SVR, late sign is hypothermia 

  • Fluid first then vasoconstrictors!

  • First hour – lactate level, blood cultures, broad-spectrum antibiotics, NS or LR at 30 mL/kg, vasopressors if hypotensive after fluid resuscitation (MAP > 65)

  • Monitor for DIC – like HIT but without the Heparin

Obstructive

Notify the MD? We cannot do any of the effective interventions

Causes – cardiac tamponade, tension pneumothorax, superior vena cava syndrome – tumor compressing, pulmonary embolism