Chapter 39: Pts With Shock Flashcards
Hypovolemic shock
Total body fluid decreased
Hemorrhage
Dehydration
Fluid shifts: trauma, burns, anaphylaxis
Low circulating blood volume causes mean arterial pressure (MAP) decrease; inadequate total body oxygenation due to loss of RBCs
Commonly caused by hemorrhage (external or internal), dehydration (suction, diabetes insipidus, hyperglycemia), inadequate clotting, trauma, surgery, GI ulcer
Shock definition
Widespread abnormal cellular metabolism
Oxygenation and tissue perfusion needs not met
“Whole-body” response; “syndrome”
Any problem impairing oxygen delivery to tissues and organs can start shock, lead to life-threatening emergency
Cardiogenic shock
Actual heart muscle is unhealthy; pumping is directly impaired
Myocardial infarction most common cause, valve problems, myopathies, ventricular dysrhythmias, cardiac arrest, myocardial degeneration
Fluid volume not affected
Direct pump failure
Decreased CO and MAP
Distributive shock
Blood volume distributed to interstitial tissues where it cannot circulate, deliver oxygen (fluid shifted from central vascular)
Total volume normal or increased
Caused by loss of sympathetic tone, blood vessel dilation, pooling of blood in venous and capillary beds, capillary leak > decreased MAP
Neural-induced distributive shock: head trauma, anesthesia, opioids, sedatives > decreased MAP
Chemical-induced distributive shock: sepsis, anaphylaxis, capillary leak,
Obstructive shock
Impaired ability of normal heart muscle to pump effectively
Conditions outside heart prevent either adequate filling of heart or adequate contraction of healthy heart muscle (cardiac function decreased by noncardiac factors)
Cause is indirect pump failure.
Central volume decreased: Pericarditis most common cause and
Cardiac tamponade. pulm HTN, tension pneumothorax, thoracic
tumor,
Total fluid not affected
Stages of shock
Initial
Nonprogressive
Progressive
Refractory
Initial stage
Baseline MAP decreased by <10 mm Hg
Increased SNS stimulation
Heart and respiratory rate increased from baseline, or slight increase in diastolic blood pressure may be the on,y objective manifestation of this early stage of shock
Adaptive responses of vascular constriction, increased heart rate
O2 90-95%
Nonprogressive stage
MAP decreases by 10 to 15 mm Hg
Continued SNS stimulation
Chemical compensation: Kidney and hormonal adaptive mechanisms activated renin, aldosterone, ADH, epi, norepinephrine > vasoconstrict, decreased urine, stimulation of thirst
Tissue hypoxia in nonvital organs, skin GI
Acidosis and hyperkalemia
Stopping conditions that started shock and supportive interventions can prevent shock from progressing. Cellular effects are reversible.
Thirst and anxiety. Objective: Restlessness, tachycardia, increase respirations, decreased urine, falling systolic, rising diastolic, narrow pulse pressure, cool extremities, 2 to 5% decrease in oxygen.
Progressive stage
Sustained decrease in MAP of >20 mm Hg from baseline
Anoxia of vital organs
Vital organs develop hypoxia
Moderate acidosis, hyperkalemia, tissue ischemia
Life-threatening emergency
Conditions causing shock must be corrected within 1 hour of progressive stage onset
Subjective include severe thirst and deeper anxiety. They have a feeling of something bad to happen. Immediate confusion. Objective includes a rapid week pulse, low blood pressure, pallor to cyanosis, cool moist skin, anuria, 5 to 20% decrease in oxygen, low Ph O2 75-80%
Refractory stage/irreversible stage
Too little oxygen reaches tissues; cell death and tissue damage result
Body cannot respond effectively to interventions; shock continues
Rapid loss of consciousness, nonpalpable pulse, cold, dusky extremities; slow, shallow respirations; unmeasurable oxygen saturation
Severe tissue hypoxia with ischemia and the process. Release of myocardial depressant factor from the pancreas. Buildup of toxic metabolites. Multiple organ dysfunction syndrome. Death.
Therapy is not effective in saving the patient’s life, even if the cause of shock is corrected and MAP temporarily returns to normal. So much damage has occurred in vital organs. Manifestations include rapid loss of consciousness, nonpalpable pulse, cold mottled dusky extremities, slow shallow respiration, unmeasurable o2 sat.
Health promotion and maintenance
Can usually be prevented Avoid trauma and hemorrhage ØProper safety equipment ØSeat belts ØAwareness of hazards in home/workplace Secondary prevention ØAssess for early manifestations Patient teaching Drink adequate fluids Assess for shock in a patient who develops a change in mental status, increasing pain, or an increase in anxiety. Teach manifestations of shock.
Cardiovascular manifestations
Decreased cardiac output/ MAP
Increased pulse, thready pulse
Decreased blood pressure
Narrowed pulse pressure
Postural hypotension
Low central venous pressure
Flat neck and hand veins in dependent positions
Slow capillary refill
Diminished peripheral pulses
Increased heart rate is the earliest manifestation
Systolic is not always decreased. When vasoconstriction is present, diastolic increases but systolic remains the same.
Respiratory manifestations
Increased respiratory rate
Shallow depth of respirations
Decreased Paco2
Decreased Pao2
Cyanosis, especially around lips and nail beds
The depth increases when lactic acidosis is present
Multiple organ dysfunction syndrome
MODS
Sequence of cell damage caused by massive release of toxic metabolites and enzymes
Microthrombi form
Occurs first in liver, heart, brain, kidney
Myocardial depressant factor from ischemic pancreas.
Once the damage has started, the sequence becomes a vicious cycle as more dead cells break open and release harmful metabolites.
Neuromuscular manifestations
CNS changes
Early: anxiety, restless, increasedthirst
Late: decreased CNS lethargy-coma, general muscle weakness, diminished or absent muscle reflexes, sluggish pupils
Renal manifestations
Decreased urine output is early sign
Increased specific gravity
Sugar and acetone present in urine
Can tolerate hypoxia in anorexia for up to one hour without permanent damage. Afterwards they are at risk for acute tubular necrosis and kidney failure
Integumentary manifestations
Cool Pale Mottled-cyanotic Moist and clammy (normal fluid does not evaporate) Mouth dry, pastry
Dark skin assess pallor in the mucous membranes. Patients will appear darker with an underlying reddish glow. With lite skin it is first noticed in the extremities and the central trunk area. They will progress to an overall grayish blue color
GI manifestations
Decreased motility
Diminished or absent bowel sounds
N&V
constipation
Nonsurgical management
Maintain tissue oxygenation, increase vascular volume to normal range, support compensatory mechanisms
Oxygen therapy
IV therapy
ØNS or RL. Crystalloids
NS expands plasma volumes
RL (Na, cl,ca,k,lactate which buffers acidosis)
Colloids: whole blood, PRBCs, improve H&H, plasma(restores pressure with normal H&H), albumin, platelets. Restore osmotic pressure
Drug therapy: increase venous return, improve contractility, dilate coronary arteries
Ensure a patent airway. Start IV catheter. Administer oxygen, elevate the patients feet keeping his or her head flat or elevated to 30°, examine for overt bleeding, apply pressure if needed, administer meds, increased rate of fluids, do not leave the patient
Assess pulse, blood pressure, pulse pressure, central venous pressure, respiratory rate, skin and mucosal color, oxygen saturation, mental status, and urine output every 15 minutes until patient is improved.
Drug therapy
Vasoconstrictors
ØDopamine: ^CO
ØEpinephrine
ØNorepinephrine(levophed):
ØPhenylephrine
Agents enhancing contractility: inotropic agents, dobutamine
Agents enhancing myocardial perfusion: sodium nitroprusside/nitropress. Monitor vitals q 15 min, vasodilation, careful if volume depleted.
Septic shock
Complex type of distributive shock—bacterial/fungal infection progresses to dangerous condition within days
Sepsis—widespread infection coupled with general inflammatory response (SIRS systemic inflammatory response syndrome); triggered when infection escapes local control. Leads to extensive vascular and tissue changes that impair oxygenation. Widespread dilation and blood pooling. Acute respiratory distress syndrome may occur.
Mild hypotension, decreased urine, increased RR, temp varies, thrombi leads to hypoxia leads to reduced organ function.
Possible bacteremia. H&H normal until late septic. Fibrinogen levels and platelet counts are low from DIC. There might take is above normal when there’s acidosis. Activated protein C will be low. Plasmid D dimer levels rise.
Oxygenation and tissue perfusion
Related to MAP. It is effected by total blood volume, cardiac output, size of the vascular bed.
^total blood volume ^CO raise MAP
Increase in size vascular bed(dilation of vessels), decrease in MAP
Increases in sympathetic stimulation cause constriction. Decreases cause dilation.
The effects of hypotension and anaerobic cellular metabolism result in the features of shock.
Risk for sepsis
Malnutrition, immunosuppression, large open wounds, mucous membrane fissures in contact with bloody dressings, GI ischemia, invasive procedures, malignancy, >80 yo, infection with resistance microorganisms, chemo, alcoholism, DM, chronic kidney disease, transplant, hepatitis, HIV/aids.
Bacterial infection that escapes local control. Possible fungal infection. There is a genetic risk because of differences in immune systems.
Severe sepsis
All tissues hypoxic, some organs are dysfunctioning, thrombi formation widespread used all the platelets>DIC, liver releases glucose>hyperglycemia, CO increased rapid HR increased systolic BP, no cyanosis, WBCs no longer elevated, it may even be low.
Low O2, rapid RR, decreased or absent urine, change in cognition
- low o2 sat, increased RR, decreased or absent urine, change in cognition and affect,
