Shock Part 1 Flashcards
Pathophysiology of Shock
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.
Tissue oxygenation/perfusion
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.
Systemic Inflammatory Response Syndrome
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.
SIRS
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
Stages of Shock
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
Which type of shock state does not cause a relative hypovolemia? A. Hypovolemic B. Anaphylactic C. Cardiogenic D. Distributive
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.
Stage 1: Maintaining Cardiac Output
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
Stage 1: Failing Cardiac Output
AMS- confusion- lethargy Failing/dropping SBP (less than, narrowing pulse pressure Tachycardia, “thready” or weak Cold & clammy skin Oliguria- decrease in urinary output Tachypnea - dyspnea
4 Types of Shock States
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
Hypovolemic Shock: Burn Shock
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
Management of Hypovolemic Shock
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
Which shock state requires careful administration of fluids? A. Septic B. Neurogenic C. Anaphylactic D. Cardiogenic
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.
Cardiogenic Shock: Systolic Dysfunction
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
Cardiogenic Shock: Diastolic Dysfunction
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
Cardiogenic Shock differs from Hypovolemia Shock
Differs from hypovolemic shock;
There is no decreased intravascular volume or vasodilation of the vascular bed,
The problem is pump failure
Cardiogenic Shock Clinical Manifestations
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
Cardiogenic Shock Clinical Manifestations by System
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
Diagnostic Findings for Cardiogenic Shock
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
Cardiogenic Shock Treatment
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
Cardiogenic Shock Treatment cont.d
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
Distributive Shock
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)
Neurogenic Shock
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
Neurogenic Shock cont.d
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
Neurogenic Shock Treatment
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)
