Shock Flashcards
What is shock?
Inadequate oxygen delivery to meet metabolic demands resulting in global tissue hypo perfusion and metabolic acidosis.
Can shock occur with normal blood pressure?
YEP!
What happens to oxygen delivery during shock?
inadequate systemic O2 delivery activates autonomic responses to maintain systemic oxygen delivery.
Where does blood flow go during shock?
redirects tot he heart, kidneys and brain. Other beds are restricted.
explain the pathway from pain to shock
pain-> hemorrhage ->cortical perception of traumatic injury -> hormone and inflammatory mediators are released -> sympathetic nervous system releases catecholamines (NE, epi, dopamine, cortisol) -> vasoconstriction, increases in HR and increase CO -> RAAS ->decreased O2 delivery
What are 5 cellular responses to decreased systemic O2 delivery?
ATP depletion- ion pump dysfunction
- hydrolysis of cell membranes and cell death
- individual cells take up fluid
- depletion of intravascular fluid
- cell edema occludes adjacent capillaries
What is no reflow phenomenon?
prevents reversal of ischemia even with restoration of adequate macro-circulation
What is the bodies intrinsic goal during shock?
To maintain cerebral and cardiac perfusion.
What mediators do ischemic cells produce?
- lactate
- free radicals
- inflammatory factors (prostacyclin, thromboxane, prostaglandins, leukotrienes, endothelin, etc.)
What happens when the these mediators are released?
systemic metabolic lactic acidosis that overcomes the body’s compensatory mechanisms.
What is global tissue hypoxia?
endothelial inflammation and disruption. Inability of O2 delivery to meet demands.
When global tissue hypoxia (GTH) ensues, what is the result?
lactic acidosis, cardiovascular insufficiency, increased metabolic demands.
What happens to the central nervous system during GTH?
triggers a neuroendocrine response. Regional glucose uptake in the brain changes, reflexes and cortical activity are depressed (referable with mild hypo perfusion).
Failure to recover neurological function is a sign of poor prognosis.
What happens to the kidneys and adrenal glands during GTH?
Maintain GFR by selective vasoconstriction and concentration of blood flow in medulla and deep cortical area.
Prolonged hypotension -> decreased cellular energy -> inability to concentrate urine -> patchy cell death -> tubular necrosis -> renal failure
What happened to the heart during GTH?
cardiac function is well preserved in the late stages. Lactate, free radicals, and other humoral factors act as negative inotropes and, in a bleeding patient, may produce cardiac dysfunction as the terminal event in the shock spiral.
Trauma patient with cardiac disease….
Fixed stroke volume inhibits the body’s inability to increase blood flow in response to hypovolemia and anemia.
Tachycardia is the only option.
Shock in the elderly may therefor be rapidly progressive and not respond predictably to fluid administration.
What happens to the lung in GTH?
filter for the inflammatory by-products of the ischemic body. Immune complex and cellular factors accumulate in pulmonary capillaries.
Explain at the cellular level whats happening with the lungs?
Neutrophil and platelet aggregation, increased capillary permeability, destruction of lung architecture, ARDS, (the lung is the sentinel organ for the development of multi organ system failure in a traumatic patient)
Does pure hemorrhage, in the absence of hypoperfusion, produce pulmonary dysfunction?
NO
Is traumatic shock more than just a hemodynamic disorder?
yes
What happens to the gut during GTH?
One of the earliest organs affected by hypoperfusion. May be the prime trigger for MOSF. Intense vasoconstriction occurs early and frequently leads to “no reflow” phenomenon. Intestinal cell death -> breakdown in the barrier function in the gut -> increased translocation of bacteria to the liver and lung -> potentiation of ARDS.
What happens to the liver during GTH?
complex microcirculation; potential for repercussion injury during recovery from shock. Hepatic cells are metabolically active and contribute to the ischemic inflammatory response and to irregularities in blood glucose. Absence of liver after shock is almost always lethal.
What happens to skeletal muscle during GTH?
Not metabolically active during shock; tolerates ischemia well. Skeletal muscle mass -> of lactic acid and free radicals.
sustained ischemia ->increased intracellular Na and free water -> further depletion of intravascular and interstitial fluid.
What is Multiorgan dysfunction syndrome
progression of physiologic effects as shock ensues. cardiac depression, reap distress, renal failure, and DIC.
Result is end organ failure.
Symptoms of shock
pallor, diaphoresis, hypotension, tachycardia, prolonged cap refill, diminished urine output, narrowed pulse pressure
diagnosis of shock
physical exam (VS, mental status, skin color, temp, pulses)
infectious source
labs (cbc, chemistries, lactate, coags, cultures, ABG)
further studies that should be performed
CT of head, lumbar puncture, wound cultures, acute and series, and/pelvis CT or US, cortisol level, fibrinogen, FDPs, d-dimer
what historical questions do you ask for the pt in shock
recent illness, fever, chest pain, SOB, and pain, commodities, medications, toxins/ingestions, recent hospitalizations or surgeries, baseline mental status.
physical exam for a pt in shock
vitals, CNS (mental status), skin (color, temp, rashes, sores), CV (JVD, heart sounds), reap (lung sounds, RR, o2 sats, ABG), GI (and pain, rigidity, guarding, rebound), renal (urine output)
Is this pt in shock? Patient looks ill Altered mental status Skin cool and mottled or hot and flushed Weak or absent peripheral pulses SBP <110 Tachycardia
yepperz!
If you can palpate a pulse at the neck, radial, femoral or tibial you know the BP is at least…..
neck-60
radial- 70
Femoral- 80
Tibial- 90
Types of shock
hypovolemic, septic, cardiogenic, anaphylactic, neurogenic, obstructive
What type of shock is this? 68 yo M with hx of HTN and DM presents to the ER with abrupt onset of diffuse abdominal pain with radiation to his low back. The pt is hypotensive, tachycardic, afebrile, with cool but dry skin
hypovolemic
types of hypovolemic shock
non-hemorrhagic and hemorrhagic
causes of non-hemorrhagic shock
Vomiting Diarrhea Bowel obstruction, pancreatitis Burns Neglect, environmental (dehydration)
causes of hemorrhagic shock
GI bleed Trauma Massive hemoptysis AAA rupture Ectopic pregnancy, post-partum bleeding
How do you care for hypovolemic shock?
ABC’s, 2 large bore IV’s or a central line, crystalloids (NS or LR),
PRBC’s (O neg or cross matched, 1:1:1), Control any bleeding, definitive treatment
tests to be done pre-op on shock patients
ABG/lactate CBC Electrolytes BUN, Creatinine Coagulation studies Type and cross-match AND As indicated CXR Pelvic x-ray Abd/pelvis CT Chest CT GI endoscopy Bronchoscopy Vascular radiology
What type of shock is this?
An 81 yo F resident of a nursing home presents to the ED with altered mental status. She is febrile to 39.4, hypotensive with a widened pulse pressure, tachycardic, with warm extremities
septic shock
what is important to know about hypotension for septic shock?
Hypotension secondary to Sepsis that is resistant to adequate fluid administration and associated with hypoperfusion
what is the criteria for SIRS
Temp > 38 or < 36 HR > 90 RR > 20 or PaCO2 < 32 WBC > 12 or < 4 Plus the presumed existence of infection Blood pressure can be normal
refractory hypotension in septic shock
after bolus of 20-40ml/Kg patient still has the following
SBP <65mmHg
decrease of 40mmHg from baseline
clinical signs of septic shock
hyperthermia or hypothermia, tacycardia, wide pulse pressure, low blood pressure (SBP <90), mental status change
BEWARE OF COMPENSATED SHOCK
ancillary studies for shock
cardiac monitor, pulse ox, CBC, chem 7, coags, LFTs, lipase, UA, ABG with lactate, blood cultures, urine culture, CXR, foley cath
treatment for septic shock
2 large bore IV’s, NS IV bolus 1-2L wide open (if not contraindicated), supplemental O2, empiric antibiotics
refractory hypotension in septic shock
after bolus of 20-40ml/Kg patient still has the following
SBP <65mmHg
decrease of 40mmHg from baseline
So what do you do if you have persistent hypotension in these people?
if no response ager 2-3L start a vasopressor (norepi, dopamine,etc) and titrate to effect. Goal is a MAP >60, consider adrenal insufficiency: hydrocortisone 100mg IV.
What type of shock is this? A 55 yo M with hx of HTN, DM presents with “crushing” substernal CP, diaphoresis, hypotension, tachycardia and cool, clammy extremities
Cardiogenic
defining features of cardiogenic shock
SBP < 90 mmHg
CI < 2.2 L/m/m2
PCWP > 18 mmHg
What are the signs of cardiogenic shock?
Cool, mottled skin Tachypnea Hypotension Altered mental status Narrowed pulse pressure Rales, murmur
What can cause cardiogenic shock?
AMI Sepsis Myocarditis Myocardial contusion Aortic or mitral stenosis Hypertrophic cardiomyopathy Acute aortic insufficiency
Pathophys of cardiogenic shock
- Often after ischemia, loss of LV function
- Lose 40% of LV -> clinical shock ensues
- CO reduction = lactic acidosis, hypoxia
- Stroke volume is reduced
- Tachycardia develops as compensation
- Ischemia and infarction worsens
treatment of cardiogenic shock for RV infarct
Fluids and Dobutamine (no NTG)
treatment of cardiogenic shock for acute mitral regurg or VSD
Pressors (Dobutamine and Nitroprusside)
Ancillary tests for cardiogenic shock
EKG
CXR
CBC, Chem 10, cardiac enzymes, coagulation studies
Echocardiogram
How do you treat a patient with cardiogenic shock?
- Goals- Airway stability and improving myocardial pump function
- Cardiac monitor, pulse oximetry
- Supplemental oxygen, IV access
- Intubation will decrease preload and result in hypotension
- Be prepared to give fluid bolus*
treatment of cardiogenic shock for AMI
- Aspirin, beta blocker, morphine, heparin
- If no pulmonary edema, IV fluid challenge
- If pulmonary edema
- *Dopamine – will ↑ HR and thus cardiac work
- *Dobutamine – May drop blood pressure
- *Combination therapy may be more effective
- PCI or thrombolytics
What type of shock is this?
A 34 yo F presents to the ER after dining at a restaurant where shortly after eating the first few bites of her meal, became anxious, diaphoretic, began wheezing, noted diffuse pruritic rash, nausea, and a sensation of her “throat closing off”. She is currently hypotensive, tachycardic and ill appearing.
Anaphylactic
What is anaphylaxis?
a severe systemic hypersensitivity reaction characterized by multisystem involvement
***IgE mediated
SO what does anaphylactoid mean?
clinically indistinguishable from anaphylaxis, do not require a sensitizing exposure
***Not IgE mediated
Symptoms of anaphylaxis
First- Pruritus, flushing, urticaria appear
Next- Throat fullness, anxiety, chest tightness (decreased compliance, increased peak airway pressures, shortness of breath and lightheadedness
Finally- Altered mental status, respiratory (wheezing) distress, hypotension, tachycardia, circulatory collapse
Who is at the highest risk for death from anaphylaxis?
poorly controlled asthmatics
previous anaphylaxis
What are the reoccurrence rates?
40-60% for insect stings
20-40% for radiocontrast agents
10-20% for penicillin
Most common causes of anaphylaxis?
Neuromuscular blocking agents (most common in anesthetized patients) Antibiotics* Heparin* Protamine* Insects Food
What does the “lump in my throat” or “hoarseness” signify for these patients?
heralds life threatening laryngeal edema
what is a biphasic phenomenon?
occurs in up to 20% of patients- symptoms return 3-4 hours after initial reaction has cleared
How long does it take for anaphylaxis to show symptoms?
60 minutes
clinical diagnosis of anaphylaxis
airway compromise, hypotension, involvement of the cutaneous, GI, or reap systems.
look for drug, food, or insect exposure
***labs are worthless
SO how do you treat this anaphylaxis?
- **Stop triggering agent!
- ABC’s
- Angioedema and respiratory compromise require immediate intubation (if not already intubated)
- IV, cardiac monitor, pulse oximetry
- IVFs, oxygen
- Epinephrine
Second line
- Corticosteriods
- H1 and H2 blockers
Medications to treat anaphylactic shock
Epinephrine, 0.1 mg - 0.3 mg IM/IV of 1:1000
Repeat every 5-10 min as needed
Caution with patients taking beta blockers- can cause severe hypertension due to unopposed alpha stimulation
For CV collapse, 1 mg IV of 1:10,000
Vasopressin Adult, IV, 1-2 U initially for hypotension; 40 U IV for cardiac arrest
Phenylephrine Adult, bolus IV, 0.1-1 mg (maximum) repeated every 10-15 min; infusion IV, 40 mg diluted in 250 mL
Norepinephrine Adult, infusion IV, 0.05 μg/kg/min or 2-4 μg/min
Methylene blue Adult, bolus IV, 0.5-2 mg/kg; infusion IV, 0.5 mg/kg/h
More medications
Corticosteroids
- Methylprednisolone 125 mg IV
- Prednisone 60 mg PO
Antihistamines
- H1 blocker- Diphenhydramine 25-50 mg IV
- H2 blocker- Ranitidine 50 mg IV
Bronchodilators
- Albuterol nebulizer
- Atrovent nebulizer
- Magnesium sulfate 2 g IV over 20 minutes
Glucagon
- For patients taking beta blockers and with refractory hypotension
- 1 mg IV q5 minutes until hypotension resolves
So what do you do with anaphylactic patients after you have treated them?
- All patients who receive epinephrine should be observed for 4-6 hours
- If symptom free, discharge home
- If on beta blockers or h/o severe reaction in past, consider admission
What type of shock is this?
A 41 yo M presents to the ER after an MVC complaining of decreased sensation below his waist and is now hypotensive, bradycardic, with warm extremities
neurogenic
What is neurogenic shock?
- Occurs after acute spinal cord injury
- Sympathetic outflow is disrupted leaving unopposed vagal tone
- Results in hypotension and bradycardia
- Spinal shock- temporary loss of spinal reflex activity below a total or near total spinal cord injury (not the same as neurogenic shock, the terms are not interchangeable)
How long does neurogenic shock last?
1-3 weeks
What if the injury is T1 or higher?
can disrupt the entire sympathetic system
higher injury= worse paralysis
treatment of neurogenic shock
Remember c-spine precautions
Fluid resuscitation
- Keep MAP at 85-90 mm Hg for first 7 days
- Thought to minimize secondary cord injury
- If crystalloid is insufficient use vasopressors
Search for other causes of hypotension
For bradycardia
- Atropine
- Pacemaker
What type of shock is this?
A 24 yo M presents to the ED after an MVC c/o chest pain and difficulty breathing. On PE, you note the pt to be tachycardic, hypotensive, hypoxic, and with decreased breath sounds on left
obstructive
tension pneumothorax
-Air trapped in pleural space with 1 way valve, air/pressure builds up
-Mediastinum shifted impeding venous return
-Chest pain, SOB, decreased breath sounds
-No tests needed!
Tx: Needle decompression, chest tube
Cardiac tamponade
-Blood in pericardial sac prevents venous return to and contraction of heart
-Related to trauma, pericarditis, MI
-Beck’s triad: hypotension, muffled heart sounds, JVD
-Diagnosis: large heart CXR, echo
Tx: Pericardiocentisis
Pulmonary embolism
-Virscow triad: hypercoaguable, venous injury, venostasis
-Signs: Tachypnea, tachycardia, hypoxia
-Low risk: D-dimer
-Higher risk: CT chest or VQ scan
Tx: Heparin, consider thrombolytics
Aortic stenosis
- Resistance to systolic ejection causes decreased cardiac function
- Chest pain with syncope
- Systolic ejection murmur
- Diagnosed with echo
- Vasodilators (NTG) will drop pressure!
- Tx: Valve surgery
