Shock Flashcards
Shock: Defined
Lack of oxygen to the tissues that results in cells using anaerobic metabolism resulting in production of lactic acid (higher lactic high probability of mortality)
Lactic acid will also be produce with hypoxemia
When this state persists there will be an impaired organ function, irreversiable cell damage and death, hypotension, and oliguria (decreased urine output)
Classificiations of Shock
Hypovolemic
- Decreased BP caused by a decrease of blood volume
- Can be due to loss of blood or loss of fluid in general.
Cardiogenic
- Decreased BP caused by failure of the heart’s ability to pump blood forward
Distributive
- Widespread vasodilation( Decreased SVR) resulting in a relative hypovolemia
- Can be septic, anaphylactic or neurogenicin origin
Obstructive
- Decreased BP caused by an impedance to the filling of the heart or an obstruction to blood leaving the heart
Hypovolemic Shock Defintiion
The state where inadequate tissue perfusion results from lack of blood volume and corresponding decreased CO
Very common in COPD Exasterbationdue to the decrease appeities
Hypovolemic Shock Etiology
Can be due to acute blood loss or signifiant fluid loss
-
Acute Blood Loss (can be internal or external)
- Trauma
- GI bleed-Internal so it is easy to miss at first
- Vascular (ruptured AAA)
- Pregnancy related-placenta previa, ruptured ectopic pregnancy
- Most hypovolemic shock is due to this “hemorrhagic shock”
-
Significant fluid loss
- Extensive burns
- Inadequate fluid intake
- Excessive diarrhea
- Excessive vomiting
Hypovolemic Stage One
- Blood loss < 10% Circulating blood volume is decreased but not enough to cause serious effects
- Signs & Symptoms:
- None; comparable to a blood donation
Hypovolemic Stage Two
- Blood loss ~ 10-25%
- Compensatory mechanisms maintain BP (increase HR and SVR)
- Tissue perfusion is maintained at an adequate level to prevent cell damage
- Signs & Symptoms:
- Minimal increase in HR but < 100 bpm
- Slightly ¯BP (but still in normal range)
- Mild evidence of peripheral vasoconstriction (Cool hands/feet)
Hypovolemic Stage Three
- Blood loss ~25 – 35%
- Unfavorable signs appear as compensatory mechanisms can no longer maintain BP
- Impaired blood flow to the vital organs
- Cells and their enzyme systems are damaged
- Capillary permeability
Signs & Symptoms:
- Tachycardia
- Decrease in pulse pressure
- BP low to low/normal
- Lactic acidosis
- Altered LOC
- Diaphoretic
- Pallor
- Oliguria
- Extreme thirst
- Rapid deep respirations
Hypovolemic Stage Four
Irreversible stage
Sustained hypoperfusion leads to irreversible multi-system organ failure
Even if blood volume is restored and vital signs stabilized, death will likely ensue due to MSOF
Hypovolemic Shock
Lab Findings
- Hemoglobinand hematocrit
- If due to blood loss: decreased Hbg, and possibly Hctif the patient has been fluid resuscitated
- If due to fluid loss: Increased Hbg and Hctdue to hemoconcentration(same # of cells in a ¯volume)
- Increased lactate levels
- Due to poor peripheral circulation
- Cells are not receiving oxygen and \using anaerobic metabolism
- pH will correlate with the severity of the acidosis
Hypovolemic Shock
Management
Main goal = Fluid Resuscitation!!
- Blood or blood products
- Administered based on Hbgand Hctlevels
- IV fluids
- Crystalloids (e.g., NS, Ringer’s lactate)
- Colloids (e.g., Pentaspan, albumin)
Supportive Care
- Oxygen and/or mechanical ventilation as required
- Frequent monitoring of:
- Vital signs: especially HR and BP
- Urine output
Cardiogenic Shock Definition
The state where inadequate tissue perfusion results from cardiac dysfunction/failure and the resultant decrease in CO.
Cardiogenic Shock Etiology
- Myocardial infarction**
- Cardiogenicshock is most often associated with anterior MI
- Myocardial contusion
- Myocarditis
- End-stage cardiomyopathy
- Prolonged cardiopulmonary bypass
- Valvular dysfunction
- Cardiac arrhythmias
- Vtach, bradyarrhythmias, tachyarrhythmias
- CAD
Cardiogenic Shock Clinical Manifestations
The “classic” shock symptoms:
- Thirst
- Hypotension
- Cool and clammy skin
- Cyanosis
- Poor mentation
- Oliguria/anuria
Also the S & S related to heart failure:
- Peripheral edema, JVD, hepatomegaly, ascites…
- Pulmonary edema, frothy pink secretions, tachypnea…
Cardiogenic Shock Lab Findings
- Increased lactate will correspond with a decreased pH
- Due to the hypoperfusion of cells using anaerobic metabolism
- Increase cardiac enzyme
- if MI occuring
Normal Lactate
- 5 to 19.8 mg/dL
- 5 to 2.2 mmol/L
Cardiogenic Shock
Management
Reduced preload but optimizing fluid volume
- Diuretics, nitroglycerin, morphie
Reduce afterload
- B-blockers, ACE inhibitors, nitroglycerin
Inotropic Drugs (Ex. Epi, Aminodarone, dig)
- Used with caution as result in increased afterload and tachycardia (both which increase demand on the heart!)
- “Inodilators” a better choice as also decrease demand
- Some Beta agonists (dobutamine), dopaminergics(dopamine), phosphodiesteraseinhibitors (milrinone).
Assisting the heart
- IABP or ventricular assist device
Distributive Shock Definition
The state where inadequate tissue perfusion results from a “maldistribution” of blood due to a reduced SVR.
Characterized by loss of blood vessel tone resulting in a relative hypovolemia
Widespread vasodilation results in an increase in the amount of blood the vasculature can hold (especially the venous system)
This causes pooling of the blood away from the heart and central circulation and reduced venous return
While the circulating blood volume is normal it is insufficient to provide adequate cardiac filling
Types of Distributive Shock
There is three types of distributive shock
- Neurogenic shock
- Anaphylactic shock
- Septic Shock - Infection in the blood and can lead to ARDS
Distributive Shock
Loss of Vessel Tone
The loss of vessel tone is from one of two mechanisms:
- Decreased sympathetic control over vessel tone
- Presence of vasodilatorysubstances in the blood
Distributive Shock-Neurogenic Shock
Etiology
Due to defect in the vasomotor center of the brain or blockage of the sympathetic impulses
Caused by:
- Head injury
- Spinal cord injuries
- Spinal anesthesia
- General anesthesia
- Depressant drugs
Distributive Shock-Neurogenic Shock
Hemodynamic Parameters
Decreased SVR
Decreased CVP
Decreased PAP and PAWP as blood pools in periphery decreasing venous return
Decreased CO 2°to Decreased HR and Decreased venous return
Distributive Shock-Neurogenic Shock
Clinical Manifestations
Bradycardia
- Due to imbalance between S and PS stimulation
Skin is usually warm and dry
- With other shock types it tends to be cool and clammy 2° to peripheral vasoconstriction—here we have vasodilation
•Hemodynamic parameters
§¯¯SVR
§¯CVP (and ¯PAPs, ¯PAWP) as blood pools in periphery decreasing venous return
¯CO 2°to¯HR and ¯venous return
Distributive Shock-Neurogenic Shock
Lab Findings
If prolonged
- Lactic acidosis and corresponding¯pH
Distributive Shock-Neurogenic Shock
Management
Fluid management
Sympathomimetic agents
For vasoconstricting effects to increase SVR
For positive chronotropic effects to increase HR
Distributive Shock-Anaphylactic Shock
Etiology
Immune mediated reaction to an antigen
- The allergen triggers WIDESPREAD mast cell degranulation which releases vasodilator substances into the blood (histamine, leukotrienes and others)
- Result is massive vasodilation, pooling of the blood in the peripheral vessels and increased permeability of the capillaries
Distributive Shock-Anaphylactic Shock
Potential Allergens
- Drugs
- Penicillin, cephalosporins
- Foods
- Nuts, shellfish, eggs
- Venoms
- Insects: bees, wasps, fire ants, spiders
- Animals: snakes, jellyfish, lizards
- Animal antigens
- Blood products
- Latex
Distributive Shock-Anaphylactic Shock
Clinical Maniestations
- Itching, urticarial (Hives, pale red rash, itchy)
- Choking
- Wheezing
- Chest tightness
- Dyspnea
- General edema, swollen tongue/throat
- Decreased BP, and thus weak pulses
- Tachycardia
- Cyanosis
- Nausea, vomiting, abdominal cramping
- GI symptoms more common with food allergy reactions
Distributive Shock-Anaphylactic Shock
Management
-
AIRWAY**
- Intubate if impending loss of airway
- Oxygen
- Bronchodilators
- Epinephrine
- Antihistamines
- Corticosteroids
- Fluid resuscitation
Distributive Shock-Septic Shock
Most common type of distributive shock
Sepsis with hypotension despite fluid resuscitation
Bacteremia
Presence of bacteria in blood stream
SIRS
Systemic hyperinflammatory response to a variety of severe clinical insults
Sepsis
SIRS caused by infection
Severe Sepsis
Sepsis associated with organ dysfunction
Multi-organ dysfunction syndrome (MODS)
Altered organ function; homeostasis cannot be maintained without intervention
Sepsis Pathophysiology
Microcirculatory damage
- Tissue hypoxia despite adequate fluid resuscitation
- Results in lactic acidosis and metabolic acidosis
- Leads to organ dysfunction
Sepsis Hemodynamics
Increased HR, increased CO, decreased SVR (assuming adequate fluid loading)
Reduced oxygen extraction due to damage in the microvasculature
Increased oxygen consumption due to high metabolic needs
Thus, SVO2can be increased or decreased!
Severe Sepsis Pathophysiology
- Persistent hypotension despite fluid resuscitation
- Presence of perfusion abnormalities
- e.g., oliguria, altered mental status, altered skin perfusion
- Increased CO
- Affects 10-15 % of ICU patients and has a mortality rate of 50-60%.
- One half of the infections were nosocomial!
Spetic Shock
Clinical Manifestations
- Fever, usually preceded by chills
- 15-20% of patient present with hypothermia
- Skin is warm, flushed
- Cool, clammy extremities in end-stage
- Tachypnea +/- hyperventilation
- Tachycardia
- Hypotension (due to the ¯SVR)
- Altered mental status
- Oliguria
Spetic Shock
Lab Findings
- Increased WBC (often; but can be decreased!)
- Blood gases
- Precursor: Increased pH due to Decreased PaCO2 2°to hyperventilation
- Once in shock: decrerased pH due to lactate levels
- Mixed venous: decreased or increased PvO2 or SvO2
- Positive blood cultures
- Clotting abnormalities (clotting time)
- Thrombocytopenia
Spetic Shock
Mangement for the infection
- Treat the infection, if there is one!
- Antibiotic agents specific to the infectious agent
Spetic Shock
Mangement - Circulatory support
- Fluid resuscitation
- Vasopressors (compensate for the decreased SVR
- Positive Inotropes (to help with the cardiac dysfunction)
Spetic Shock
Mangement - Immunomodulation
- Drugs that limit the pro-inflammatory cytokines
- Possibly corticosteroids (new evidence pending
Spetic Shock
Mangement - Respiratory Support
- Oxygenation and mechanical ventilation as required
Obstructive Shock
Definition
The state where inadequate cardiac output results from an impedance to either cardiac filling or an obstruction to emptying.
Obstructive Shock
Etiology
- Impedance to heart filling
- Cardiac tamponade
- Obstruction to heart emptying
- PE
- Tension pneumothorax
- Diaphragmatic hernia
Obstructive Shock
Clinical Manifestations
There will also be the S & S of the underlying cause!!
The “classic” shock symptoms:
- Thirst
- Hypotension
- Tachycardia
- Cool and clammy skin
- Cyanosis
- Poor mentation
- Oliguria/anuria
Also JVD due to blood backing up
Obstructive Shock
Management
Treat the problem!
Pericardiocentesis
Thoracentesisand chest tube
Thrombolyticsfor PE
Sx (surgery)for diaphragmatic hernia
If the causative agent is not quickly diagnosed then prognosis is very poor!
Cardiac Output
The amount of blood that is pumped out of each ventricle.
4-6 L/min
Systemic Vascular Resistance (SVR) Normal
1200-1600 dynes.sec.cm^ -5
Central Venous Pressure
Reflects the preload on the right side of the heart
CVP 2-8 mmHg
Pulmonary Artery Pressure (PAP)
(20-30)/(6-15) mmHg
Pulmonary wedge Pressure (PAWP)
4-12
Obstructive Shock
Hemodynamic Parameters
CVP: Big Increase
PAP: Big Increase
PAWP: Can increase or decrease
BP: Decrease
CO: Decrease
HR: Incraese
SVR: Increase
Neurogenic Shock
Hemodynamic Parameters
CVP: Decrease
PAP: Decrease
PAWP: Decrease
BP: Decrease
CO: Decrease
HR: Decrease
SVR: decrease
Septic Shock
Hemodynamic Parameters
CVP: Decrease
PAP: Decrease
PAWP: Dcrease
BP: Decrease
CO: Increase
HR: Increase
SVR: Big decrease
Cardiogenic Shock
Hemodynamic Parameters
CVP: Increase
PAP: Big Increase
PAWP: Big Increase
BP: Decrease
CO: Decrease
HR: Increase
SVR: Big increase
Hypovolemic Shock
Hemodynamic Parameters
CVP: Big Decrease
PAP: Big Decrease
PAWP: Big Decrease
BP: Decrease
CO: Decrease
HR: Increase
SVR: Big increase
