Shock Part 1 Flashcards

1
Q

Pathophysiology of Shock

A

Activation of the sympathetic nervous system, inflammatory response, and the immune system

State of hypoperfusion

Derangement of compensatory mechanisms that results in further circulatory and respiratory dysfunction with subsequent multiple organ damage

Oxygen is consumed at a much greater rate than it is delivered.

***Compensatory mechanisms result in increases in heart rate, systemic vascular resistance (SVR), preload, and cardiac contractility.

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2
Q

Tissue oxygenation/perfusion

A

Cells usually take up 25% of oxygen delivered.

When cells can’t extract enough oxygen, the body turns to anaerobic metabolism, which can lead to lactic acidosis.

Cellular death can occur if this process isn’t reversed.

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3
Q

Systemic Inflammatory Response Syndrome

A

May be caused by any type of shock or other insults such as massive blood transfusion, traumatic injury, brain injury, surgery, burns, and pancreatitis and typically precedes septic shock

Local inflammatory response becomes a systemic response that results in an unregulated inflammatory response with widespread involvement of endothelial cells and a generalized activation of inflammation and coagulation.

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4
Q

SIRS

A

2 or more are required for it to be called SIRS

Temp >38 degrees C or <36 (>100.4 or <96.8)
HR > 90 bpm
RR > 20/min or PaCO2 <32mmHg
WBC >12,000 or <4,000

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5
Q

Stages of Shock

A
Stage 1 (nonprogressive)
Compensatory mechanisms are effective in maintaining relatively normal vital signs and tissue perfusion. 
Stage 2 (progressive)
Compensatory mechanisms begin to fail; metabolic and circulatory derangements become more pronounced.
Stage 3 (irreversible)
Irreversible cellular and tissue injury
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6
Q
Which type of shock state does not cause a relative hypovolemia?
A. Hypovolemic
B. Anaphylactic
C. Cardiogenic
D. Distributive
A

C. Cardiogenic

Rationale: Hypovolemic and distributive shock result in inadequate venous return to the heart, while cardiogenic shock is caused by the failure of the heart to pump effectively. Inadequate venous return may result from hypovolemia (dehydration, hemorrhage) or widespread vasodilation (sepsis, anaphylaxis, or loss of sympathetic tone with a spinal cord injury), which cause a relative hypovolemia.

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7
Q

Stage 1: Maintaining Cardiac Output

A

changes in LOC- restless, irritable
Falling/dropping SBP, narrowing pulse pressure
Tachycardia, “thready” or weak (bounding if septic)
Cool skin or diaphoretic (warm to hot if septic)
Slight decrease in urinary output

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8
Q

Stage 1: Failing Cardiac Output

A
AMS- confusion- lethargy
Failing/dropping SBP (less than, narrowing pulse pressure
Tachycardia, “thready” or weak
Cold &amp; clammy skin
Oliguria- decrease in urinary output
Tachypnea - dyspnea
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9
Q

4 Types of Shock States

A

Hypovolemic Shock – actual loss of intravascular volume (hemorrhaging/dehydration causes)

Cardiogenic Shock – pump failure

Obstructive Shock- physical obstruction of the great vessels or the heart itself

Distributive Shock:
Neurogenic
Septic
Anaphylactic

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10
Q

Hypovolemic Shock: Burn Shock

A

Interstitial tissue become reservoirs for fluids
Alterations in capillary permeability and/or decrease in colloidal osmotic pressure

Large area burns (20%) have generalized increase in permeability
Vasoconstriction leading to vascular hydrostatic pressure
Increased interstitial oncotic pressure, decreased interstitial hydrostatic pressure
All total massive hypovolemia & profound shock state
Require massive fluid resuscitation & transfusions

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11
Q

Management of Hypovolemic Shock

A

Diagnosis & treatment of the cause
Modified Trendelenberg (supine with legs elevated)
Control of hemorrhage
Infusions of colloids & crystaloids
If loss is >30%, blood volume is replaced

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12
Q
Which shock state requires careful administration of fluids?
A. Septic
B. Neurogenic
C. Anaphylactic
D. Cardiogenic
A

D. Cardiogenic

Rationale: Fluids should be managed to provide adequate filling pressure without overdistention of the ventricle. Left ventricular filling pressures are often elevated; therefore, diuresis or nitrate infusion may be indicated to achieve optimal preload.

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13
Q

Cardiogenic Shock: Systolic Dysfunction

A

Is the heart’s inability to pump blood forward
Usually affects the left ventricle because systolic pressure and tension are greater on the left side of the heart

Causes:
Myocardial Infarction
Blunt cardiac injury
Severe systemic or pulmonic HTN
Myocardial depression from metabolic problems
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14
Q

Cardiogenic Shock: Diastolic Dysfunction

A

Is the inability of the right or left ventricle to fill during diastole
Decreased filling of the ventricle = decreased stroke volume

Causes:
Cardiac tamponade
Cardiomyopathy

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15
Q

Cardiogenic Shock differs from Hypovolemia Shock

A

Differs from hypovolemic shock;

There is no decreased intravascular volume or vasodilation of the vascular bed,

The problem is pump failure

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16
Q

Cardiogenic Shock Clinical Manifestations

A

Deceased CO, as a result of decreased SV

Increase SVR or afterload due to catecholamine release

As the ventricle fails, LV volume at end of diastole (PAOP) begins to rise, leading to distention of ventricle & elevation of LV filling pressure (increased LA force)

Increased PA pressure

Increased PAOP (PWP)
O2 demand continues to rise resulting in end-organ dysfunction / failure / death
17
Q

Cardiogenic Shock Clinical Manifestations by System

A

CV: Increased HR, decreased BP, decreased cap refill, +/- chest pain, low CO
RESP: tachypnea, cyanosis, crackles, and rhonchi
RENAL: increase Na and water retention, decrease in renal bloodflow, decreased urine output
NEURO: decreased cerebral perfusion: anxiety, confusion, and agitation
SKIN: pallor, cool, and clammy
GI: decreased bowel sounds, n/v

18
Q

Diagnostic Findings for Cardiogenic Shock

A

Increased Cardiac Markers: Troponin I, CK-MB, and Troponin T, BNP
Increased blood glucose
Increased BUN
ECG: dysrhythmias will be present
Echo: left ventricular dysfunction
Chest X-Ray: pulmonary infiltrates will be present

19
Q

Cardiogenic Shock Treatment

A

No Trendelenberg, since the pump is already overloaded, and pulmonary congestion/edema is present

Elevate HOB to reduce afterload
Inotropic meds (dobutamine-Dobutrex) helps to increase contractility and reduce afterload

Diuretics to relieve pulmonary congestion/edema

20
Q

Cardiogenic Shock Treatment cont.d

A

Mechanical interventions:
Intra-aortic balloon pump
Ventricular assist device

Drugs that are used to decrease workload of the heart:
Nitrates-dilate coronary arteries
Diuretics-reduce preload
Vasodilators-reduce afterload
B-adrenergic blockers- reduce HR and contractility

21
Q

Distributive Shock

A

Characterized by abnormal distribution of the intravascular volume

Often complicated by loss of volume from increased capillary permeability

Vascular tone decreases

Relative hypovolemia related to massive vasodilation
Causes a decrease in preload, low CVP, and low PAWP

Major therapeutic goal
To stop the vasodilation & return circulating volume to the intravenous space to improve perfusion

Intravascular fluid resuscitation must occur before using vasoconstrictive agents such as Norepinephrine (Levophed)

22
Q

Neurogenic Shock

A

Caused by massive vasodilation as a result of loss of sympathetic vasoconstrictor tone in the vascular smooth muscles & impairment of autonomic function resulting in vasodilation.

Massive pooling of blood in the periphery
Decreased venous return (decreased pre-load)
Decreased CO
Inadequate end-organ perfusion
Acute hypotension

23
Q

Neurogenic Shock cont.d

A

Normally the body would increase HR to increase CO, but the parasympathetic nervous system dominates, resulting in blocking the sympathetic vasoconstriction and causing ***bradycardia (stimulation of the vagus nerve)

***You will see a significant decrease in CVP, PAWP, SV, CO/CI, BP when the pt is in neurogenic shock

24
Q

Neurogenic Shock Treatment

A

Replace fluids to increase CO, but be careful not to fluid overload the client
Norepinephrine , Vasopressin or Phenylephrine commonly used (cause vasoconstriction and thereby increase preload)

25
Q

Anaphylactic Shock

A

Life-threatening response to an allergen
Usually not with first exposure; antigens trigger a response with second exposure

Mostly due to insect venom (injected)
Drugs (injected or ingested) and foods are next most common; ASA and NSAIDs are common
Inhalation of antigens

26
Q

Anaphylactic Shock-Treatment

A

Anaphylactic Shock causes massive vasodilation
Epinephrine: alpha agonist-vasoconstriction
beta 1 agonist-increases HR/contractility
beta 2 agonist-broncodilation

***These patients will lose their airway quickly due to laryngeal edema. Airway is ALWAYS the first priority with this type of patient.

***After airway management and Epinephrine, can give Diphenhydramine and/or anti-toxin if available for insect/snake bites.

27
Q

Septic Shock Findings

A
Changes in LOC
Tachypnea
**Fever; hypothermia
Decreased urinary output
Decreased bowel sounds
Diminished peripheral pulses
Metabolic acidosis
**Lactic acid> 4mols/L (grey tube)
28
Q

Treating Septic Shock

A

Problem: Patient is extremely vasodilated in septic shock. SVR low, BP low, CO low, tachycardic.

Ensure adequate hydration and fill vascular bed—IV fluid boluses to maintain CVP in normal (or slightly higher than normal) range—about 6-10 mmHg. Utilize blood products if indicated by lab values, or normal saline.

Pressors to cause vasoconstriction (Norepinephrine, Vasopressin, Phenylephrine drips)

Check ABGs and lactic acid often.

Intubate and ventilate patient (usually required)

Monitor blood sugars every hour—usually require insulin drip—stress response

29
Q

Shock/SIRS/MODS

A

Hypermetabolic response:
Glycogen stores converted to glucose rapidly
When glycogen is exhausted, amino acids converted to glucose.
Fatty acids used for fuel
Catecholamines and glucocorticoids released—hyperglycemia and insulin resistance
End result? Catabolic state and lean muscle loss

30
Q

Shock/SIRS/MODS metabolic effects

A

Hypermetabolism results in liver dysfunction.

Body unable to convert lactate to glucose- lactic acidosis occurs

31
Q

Disseminated Intravascular Coagulation (DIC)

A

A serious bleeding and thrombotic disorder
Abnormally initiated and accelerated clotting
Subsequently, it uses up all available clotting factors and platelets, which may lead to uncontrollable hemorrhage

****Common Major cause: Sepsis, endotoxins releasing
Initiated by a thrombosis

Tissue necrosis/Impaired perfusion

32
Q

DIC Treatment

A

Replace clotting factors if actively bleeding—FFP, platelets, cryoprecipitate

Heparin—increases neutralization of thrombin

Check PT/INR, H&H
***If high PT/INR: FFP, Vit K, platelets if needed

33
Q

A note about septic shock

A

Vasopressive support in septic shock to maintain BP

34
Q

Spider bite: Black Widow

A

venom is neurotoxic that initially produces severe pain that progresses to N&V, abdominal cramping, HTN, dyspnea, paresthesias, and tachycardia within 2-3 hours.

Symptoms mimic abdominal emergencies (perforated ulcer, appendicitis, pancreatitis).

Tx with ice to the area to slow venom, IV, O2, and treat muscle spasms with Ca gluconate, valium or robaxin.

35
Q

Spider bite: Brown Recluse

A

venom is cytotoxic and causes a local reaction (itching, erythema) that progresses to a ulcerating necrotic wound with bluish purpura ring.

may have systemic effect such as fever, chills, joint pain, malaise, and N&V.

Tx. Each reaction- cleanse wound, analgesics, antihistamines, antibiotics, corticosteroids, and tetanus shot. Surgical debridement with grafting or hyperbaric O2 therapy if needed.

36
Q

Tick bites

A

Tick bites can carry Lyme disease, Rocky Mountain spotted fever and tick paralysis by release of neurotoxin.

Tx: Remove tick, cleanse area. Doxycycline (Vibramycin) is the drug of choice for Lyme disease and Rocky Mountain spotted fever if confirmed.

37
Q

Snake Bites

A

S&S- localized pain, swelling, and bruising with loss of function and necrosis.
Systemic reactions include N&V, dizziness, GI bleeding, respiratory problems, and tachycardia.

Tx by preventing the spread of the venom.

Elevate limb, administer crystalloids to prevent hypotension. Tylenol for pain and assess for compartment syndrome (fasciotomy if necessary). Can try antivenom administration but often fails due to incomplete dosage.