Sepsis / Shock Flashcards
shock
complex pathophysiologic process that often results in MODS and death, all types of shock involve inadequate tissue perfusion and acute circulatory shock
causes of shock are classified according to
the pathophysiologic cause and hemodynamic profile
cause of shock
- hypovolemic
- cardiogenic
- distributive; septic, anaphylactic, neurogenic
compensation in shock
neuroendocrine responses in response to ineffective circulating blood volume
compensation in shock
neuroendocrine responses in response to ineffective circulating blood volume
what response occurs during compensation shock
SNS “fight or flight”
why does “fight or flight” occur during compensation shock
compensation for increase venous return, CO, and oxygen delivery
progression of shock stages
initial stage, compensatory stage, progressive stage, refractory stage
progression through each stage varies with
the pts condition, duration of initiating event, response to therapy, and correction of underlying cause
clinical manifestations of all shock states are the result of
inadequate oxygen delivery and activation of compensatory mechanisms
traditional parameters for assessment of shock states
- appearance
- VS
- LOC
- decrease urinary output
objective parameters when assessing shock states
- arterial pH
- serum lactate
- base excess and base deficit
how would arterial pH be affected in a pt experiencing shock
acid or alkaline state of the arterial output
how would serum lactate be affected in a pt experiencing shock
lactic acidosis -> anaerobic metabolism
how would base excess and base deficit be affected in a pt experiencing shock
base deficit indicates a buildup of lactic acidosis from impaired tissue oxygenation
general management of shock states
- oxygen therapy
- fluid resuscitation
- vasoactive pharmacotherapy
- nutritional support
- hypovolemic shocl
why provide oxygen therapy to shock pts
to improve oxygen delivery to hypoxic tissues
why provide fluid resuscitation to shock pts
to restore intravascular volume (restoring preload and increase CO of oxygen delivery)
why provide vasoactive pharmacotherapy to shock pts
to restore vasomotor tone and improve cardiac function; used when fluid resuscitation has not adequately improved the pts perfusion status
why provide nutritional support to shock pts
to address the metabolic requirements which are greatly increased in shock
hypovolemic shock occurs when
inadequate circulating volume results in inadequate CO to meet tissue oxygenation
hypovolemic shock results from
an absolute fluid volume deficit or relative fluid volume deficit
absolute hypovolemia
loss of fluid from the intravascular space resulting from an external loss of fluid from the body or from internal shifting of fluid from the intravascular to the extravascular space
relative hypovolemia
vasodilation produces an increase in vascular capacitance relative to circulating volume
in hypovolemic shock decrease blood volume leads to ______________ leads to _____________ leads to ____________ leads to ____________
decrease blood volume leads to decrease venous return -> decrease SV decrease which leads to CO and results in altered tissue perfusion
clinical manifestations of hypovolemic shock are dependent on the
severity of fluid loss and the pts ability (age and health) to compensate for it
clinical manifestations of hypovolemic shock
- increase HR
- decrease bp as volume loss increases
- dry mouth
- pale
- cool, clammy skin
- poor cap refill
- faint/absent peripheral pulses
- low urine output
management of hypovolemic shock
- secure pts airway
- support breathing
- control bleeding
- restore fluid volume
- primary prevention of shock
- targeted treatment at the cause of shock and restoring intravascular volume
what is cardiogenic shock
occurs when the heart’s ability to contract and pump blood is impaired and the supply of oxygen is inadequate for the heart and tissues
cardiogenic shock most often is seen in pts with a
MI
cardiogenic shock is decreased cardiac contractility -> ________ -> ____________ and __________
decrease SV and CO -> pulmonary congestion -> systemic tissue perfusion and decrease coronary artery perfusion
clinical manifestations of cardiogenic shock
- decrease BP
- tachypnea
- cyanosis
- pulmonary crackles and wheezes
- increased respiratory distress as fluid overload occurs
- increase HR
- increase CVP
- increase PAWP
- decreased urine output
- pale, cool, clammy skin
goals of cardiogenic treatment
- limit further myocardial damage and preserve the healthy myocardial tissue
- improve cardiac function by ↑ myocardial contractility and ↓ ventricular afterload or both (achieved by ↑ oxygen supply to the heart muscle while ↓ oxygen demands)
management of cardiogenic shock
- prevention of cardiogenic shock
- monitoring hemodynamic status
- administering fluids and medications
- enhancing safety and concern
pharmacologic management of cardiogenic shock
- oxygen
- analgesia
- antiplatelet and beta blockers
- vasoactive medications
- diuretics
- antiarrhythmic medications
distributive shock
the body’s ability to adjust vascular tone is impaired (due to endothelial insult or loss of SNS response) and blood volume is abnormally displaced in the vasculature
classifications of distributive shock
- Septic shock
- Neurogenic shock
- Anaphylactic shock
septic shock is characterized by
- altered fluid volume r/t vasodilation
- increased capillary permeability
- maldistribution of circulating volume
bacteremia
presence of bacteria in the blood
infection
presence of microorganisms that trigger an inflammatory response
what does SIRS stand for
systemic inflammatory response syndrome
what is SIRS
a syndrome resulting from a severe clinical insult that indicates an systemic inflammatory response
sepsis
a systemic response to infection that may occur post burn, surgery, or serious illness
sepsis is the presence of SIRS plus the presence of
an infectious source
severe sepsis
defined as sepsis plus at least one of the following signs
- areas of mottled skin
- cap refill > 3 sec
- decreased urinary output
- lactate > 2mmol/L
- abrupt change in mental status
- platelet count of <100 000 or DIC
- acute lung injury (ALI) or ARDS
- cardiac dysfunction
septic shock
Shock associated with sepsis; defined as severe sepsis, plus one of the following
- MAP < 60 mmHg post fluid resuscitation
- Need for vasoactive medication in order to maintain MAP of > 60 mmHg
clinical manifestations of septic shock
- Temperature (> 38.3°C or < 36°C)
- Heart rate > 90/min
- Tachypnea
- Altered mental status (d/t hypoxia)
- Significant edema or positive fluid balance (> 20 mL/kg over 24 hr)
- Hyperglycemia (plasma glucose > 7.7 mmol/L) in the absence of diabetes
inflammatory variables
- leukocytosis - increased WBC (neutrophils)
- elevated plasma C reactive protein
- increase plasma procalcitonin
goal of sepsis management
The goal of management is the identification and elimination of the cause of the infection and aggressive cardiopulmonary support
managing sepsis
- fluid resuscitation
- pharmacologic therapy
- nutritional therapy and glycemic control
why fluid resuscitation in pts with sepsis
increased CVP, increased BP
what pharmacological therapy for pts with sepsis
- if fluid administration fails to increase BP and restore organ perfusion
- vasopressor or inotropic agents
- hydrocortisone, activated protein C
why nutritional therapy and glycemic control for sepsis pts
- malnutrition further impairs patient’s compensatory mechanisms
- glycemic control decreased mortality
two types of shock from spinal cord injury
- spinal shock
- neurogenic shock
clinical manifestations of spinal and neurogenic shock are related to
lost sympathetic innervation & unopposed parasympathetic innervation with a triad of expected signs (hypotension, bradycardia & hypothermia)
treatment goals of spinal and neurogenic shock
- Maintain stability of spine
- Optimize oxygen delivery
- Restore intravascular volume
anaphylactic shock
- Severe, systemic allergic reaction to allergens including food, drugs, blood products, insect venom, and latex
- A combination of massive vasodilation and ↑ capillary permeability results in a ↓ in venous return, ↓ in CO, and a ↓ in oxygen delivery
- Involves multiple organ systems, but most life threatening are those involving the cardiovascular and pulmonary systems
anaphylactic shock onsets rapidly within ________ or slowly __________
5-30 min ; 6-12 hrs
clinical manifestations of anaphylaxis
- Respiratory distress due to laryngeal edema, bronchospasm
- Dizziness, chest pain, facial swelling
- Wheezing, stridor
- Pruritis, urticaria, angioedema
- Anxiety
- LIFE THREATENING
goals of treatment for anaphylaxis
- *Maintain an airway
- *Support blood pressure
- Oxygen as necessary
- Early intubation if necessary, why?
- Fluid resuscitation
- If hypotensive, to restore vascular volume
- Drug therapy
- Stopping the hypersensitivity response and reversing manifestations of the response
- Obstructive Shock
obstructive shock
A physical obstruction to blood flow, either in the heart or major blood vessels resulting in a ↓ in CO and ultimately, a ↓ in tissue perfusion
causes of obstructive shock
- Pulmonary Embolism
- Early initiation of anticoagulant therapy (heparin)
- Tension Pneimothorax
- Trapped air is decompressed (needle or chest tube)
- Cardiac Tamponade
- Emergency removal of pericardial fluid (pericardiocentesis)
- MODS: Multiple Organ dysfunction syndrome
- SIRS: Systemic Inflammatory response Syndrome
causes of obstructive shock
- Pulmonary Embolism
- Early initiation of anticoagulant therapy (heparin)
- Tension Pneimothorax
- Trapped air is decompressed (needle or chest tube)
- Cardiac Tamponade
- Emergency removal of pericardial fluid (pericardiocentesis)
- MODS: Multiple Organ dysfunction syndrome
- SIRS: Systemic Inflammatory response Syndrome
causes of obstructive shock
- Pulmonary Embolism
- Early initiation of anticoagulant therapy (heparin)
- Tension Pneimothorax
- Trapped air is decompressed (needle or chest tube)
- Cardiac Tamponade
- Emergency removal of pericardial fluid (pericardiocentesis)
- MODS: Multiple Organ dysfunction syndrome
- SIRS: Systemic Inflammatory response Syndrome
causes of obstructive shock
- Pulmonary Embolism
- Early initiation of anticoagulant therapy (heparin)
- Tension Pneimothorax
- Trapped air is decompressed (needle or chest tube)
- Cardiac Tamponade
- Emergency removal of pericardial fluid (pericardiocentesis)
- MODS: Multiple Organ dysfunction syndrome
- SIRS: Systemic Inflammatory response Syndrome
causes of obstructive shock
- Pulmonary Embolism
- Early initiation of anticoagulant therapy (heparin)
- Tension Pneimothorax
- Trapped air is decompressed (needle or chest tube)
- Cardiac Tamponade
- Emergency removal of pericardial fluid (pericardiocentesis)
- MODS: Multiple Organ dysfunction syndrome
- SIRS: Systemic Inflammatory response Syndrome
causes of obstructive shock
- Pulmonary Embolism
- Early initiation of anticoagulant therapy (heparin)
- Tension Pneimothorax
- Trapped air is decompressed (needle or chest tube)
- Cardiac Tamponade
- Emergency removal of pericardial fluid (pericardiocentesis)
- MODS: Multiple Organ dysfunction syndrome
- SIRS: Systemic Inflammatory response Syndrome
SIRS stimulates an overwhelming __________
inflammatory, immunologic, and hormonal response similar to that seen in sepsis patients
although SIRS presents clinically like sepsis the difference is that
there is NO identifiable source of infection
SIRS -> _______ -> ________
SIRS -> sepsis -> septic shock
SIRS -> _______ -> ________
SIRS -> sepsis -> septic shock
SIRS can lead to
MODS
This inflammatory, systemic response is manifested by two or more of the following conditions:
- Temperature >38 or <36
- HR >90
- RR >20, or Pa CO₂ <32
- WBC > 12,000/mm3 or < 4,000/mm3
MODS
Severe organ dysfunction of at least two organ systems lasting at least 24 to 48 hours in the context of sepsis, trauma, burns, or severe inflammatory conditions
MODS can result from SIRS or any type of
shock due to inadequate tissue perfusion
two MODS pathways
primary
secondary
4 factors that lead to pathologic changes associated with MODS
Uncontrolled systemic inflammation
- Pro-inflammatory mediators initiate a systemic, inflammatory response
Tissue hypoxia
- Patient may appear to have adequate oxygenation but regional tissue hypoxia may occur
Unregulated apoptosis (cell death)
- ↓ levels of certain immune cells (↑ susceptibility) and ↑ levels of other immune cells that ↑ tissue damage
Microvascular coagulopathy
- Abnormal clotting in the small blood vessels resulting in micro-thrombosis and obstruction of blood flow
clinical manifestations of MODS
- Difficult to identify because much of organ damage occurs at the cellular level & therefore, can’t be directly measured or observed
- Most common types of organ dysfunction are ARF and ARDS
focus of MODS is
prevention
