Final Exam Flashcards
Shock
inadequate tissue perfusion; if untreated, results in cell death
a condition in which widespread perfusion to the cells is inadequate to deliver oxygen and nutrients to support vital organs and cellular function
ANY insult to the body can create a cascade of events resulting in poor tissue perfusion
Requires ongoing assessment
Hydration and oxygenation!
Cell death then tissue death then organ failure
physiologic responses common to all types of shock
hypoperfusion of tissues
hypermetabolism
activation of the inflammatory response (cascading event)
Vitals at least every 2 hours
Cellular function in cells (aerobic vs anaerobic)
Aerobic metabolism: yields more ATP–more efficient and effective in producing energy
Anaerobic metabolism: less ATP and accumulation of the toxic end product lactic acid (also seen with not enough perfusion, acidic pH and hyperventilation to compensate)
Cellular changes in shock
Anaerobic metabolism→ acid accumulation → increase permeability
Electrolytes and fluids seep out of and into the cell.
The sodium-potassium pump becomes impaired; cell structures, primarily the mitochondria, are damaged, and death of the cell results
Glucose is the primary substrate required for the production of cellular energy in the form of ATP.
SELF-PERPETUATING NEGATIVE SITUATION
Stress and cellular changes in shock
In stress statues, catecholamines, cortisol, glucagon, and inflammatory cytokines are released, causing hyperglycemia and insulin resistance to mobilize glucose for cellular metabolism→ more glucose is needed→ gluconeogenesis→ Need more energy → gluconeogenesis → hypermetabolic state → use proteins and fats to produce glucose (used up all the glucose) → proteolysis (breakdown of protein) → organ failure
Inflammatory process activates clotting cascade
3 major components of circulatory system
blood volume
cardiac pump
vasculature (need good tone)
they must work together to maintain adequate BP to perfuse body tissues
What is a good MAP
must exceed 65 mmHg for cells to receive the oxygen and nutrients needed to metabolize energy in amounts sufficient to sustain life
Stages of shock
(initial)
compensatory (stage 1)
progressive (stage 2)
irreversible (stage 3)
Better outcome when aggressive therapy begins within 3 hours of identifying a shock state, especially septic shock (gram + up, - down)
Fluids, treat underlying cause
Compensatory shock
normal BP
vasoconstriction
increased heart rate (usually 10% of baseline is a good indicator of possible shock)
blood shunts from skin, kidneys, and GI tract to brain, heart, and lungs
Cool pale skin, hypoactive bowel, low urine output
Met acid and resp alk
What to monitor and report in compensatory shock
Pt feel anxious or confused
vital signs–key indicators of hemodynamic status
BP: indirect measure of tissue hypoxia
report SBP< 100 mm Hg or drop in SBP of 40 mm Hg from the baseline or MAP less than 65 mmHg
AND
Notify MD promptly if two of the three following signs detected if the patient is concurrently diagnosed with an infection or if an infection is suspected:
Respiratory rate >=22/min
Altered mentation
Systolic BP<=100 mmHg
Pulse pressure
Correlates well with stroke volume
Pulse pressure=SBP-DBP
Normal pulse pressure: 40mmHg
Narrowing of pulse pressure: indicates decreased stroke volume
Systolic can keep dropping, diastolic stays around the same, causing narrow pp
Continuous central venous oximetry (ScvO2)
Normal 70%
With shock, more oxygen is consumed, ScvO2 will be lower
Obtained through a central catheter in the superior vena cava
Early interventions for compensatory shock
Identifying the cause of shock
IV fluids
oxygenation
Obtaining lab tests
pain control
sedating agents when needed
reducing anxiety
promoting safety
Progressive stage of shock
BP can no longer compensate: hypotensive (systolic less than 100 mmHg or a decrease of systolic BP of 40 mmHg from baseline)
Cardio effects of progressive shock
faster heart rate>150 bpm
failure of the cardiac pump
Possible MI
Levels of cardiac biomarkers increase
Respiratory effects of progressive shock
Respirations are rapid and shallow
Crackles are heard over the lung fields
Decreased pulmonary blood flow causes arterial oxygen levels to decrease and CO2 levels to increase
Hypoperfused alveoli stop producing surfactant and subsequently collapse
Pulmonary capillaries begin to leak, causing pulmonary edema, diffusion abnormalities (shunting), and additional alveolar collapse→ acute lung injury
ARDS
Neuro effects of progressive shock
Subtle changes in behavior→ become agitated→ confused→ signs of delirium→ lethargy increases→ lose consciousness
Renal effects of progressive shock
AKI from not enough perfusion to kidneys
Liver effects of progressive shock
Not able to metabolize medications and metabolic waste products (ammonia and lactic acid)
More susceptible to infection (liver fails to filter bacteria from the blood)
Elevated liver enzymes and bilirubin levels elevated (jaundice)
GI effects of progressive shock
stress ulcers–risk for GI bleeding.
Bacteria translocation (due to GI ischemia)
Hematologic effects of progressive shock
Disseminated intravascular coagulation DIC: inflammatory cytokines activate the clotting cascade–widespread clotting and bleeding occur simultaneously
Management of progressive shock
IV fluids and medications to restore tissue perfusion
mechanical ventilation
Optimizing intravascular volume
Supporting the pumping action of the heart (IABP)
Improving the competence of the vascular system
Early enteral nutritional support (like burns)
Glycemic control, medications to reduce the risk of GI ulceration and bleeding
Preventing complications of progressive shock
monitor s/s of infection
aseptic techniques
frequent oral care
aseptic suction technique
turning and elevating the HOB at least 30 degrees
Promoting rest and comfort in progressive shock
priority
conserve the patient’s energy
not be warmed too quickly (vasodilation–leads to drop in BP)
Protect the patient from temperature extremes (excessive warmth or cold, shivering)
Preventing delirium in progressive shock
Assess once a shift
Frequent orientation activities
Assessing and treating pain
Promoting sleep
Providing early mobilization activities
Limiting sedation (especially sedation with benzodiazepines, e.g, lorazepam [Ativan]).
Irreversible stage of shock
organ damage is so severe that the patient does not respond to treatment and cannot survive
BP remains low
renal and liver failure (release of necrotic tissue toxins, metabolic acidosis)
Nursing management of irreversible shock
offer brief explanations to the patient about what is happening is essential even if there is no certainty that the patient hears or understands what is being said
General management strategies of shock
support of the respiratory system with supplemental oxygen and/or mechanical ventilation to provide optimal oxygenation
fluid replacement to restore intravascular volume
vasoactive medications to restore vasomotor tone and improve cardiac function
nutritional support to address the metabolic requirements that are often dramatically increased in shock–skeletal muscle mass will be broken down first
Insufficient fluid replacement in shock
higher incidence of morbidity and mortality from lack of tissue perfusion
Excessive fluid replacement in shock
systemic and pulmonary edema–ARDS
abdominal compartment syndrome (ACS): too much pressure in the abdomen and the abdominal wall cannot expand anymore
can make breathing difficult, check liver function to differentiate from ascites, also we’re giving so much fluid and it’s everywhere in the abdomen now whereas ascites you can just take the fluid out
Crystalloid solutions in shock
electrolyte solutions
Commonly used: 0.9% sodium chloride solution (NS) and lactated Ringer’s solution.
Isotonic solutions disadvantage: diffuse into the interstitial space
Hypertonic solution: 3% NaCl–for TBI patient (brings down ICP, also used in TB)
These don’t stay in vasculature for long
Colloid solutions in shock
electrolyte solutions
Commonly used: 0.9% sodium chloride solution (NS) and lactated Ringer’s solution.
Isotonic solutions disadvantage: diffuse into the interstitial space
Hypertonic solution: 3% NaCl–for TBI patient
Colloid solutions in shock
large-molecule IV solutions
Contain molecules that are too large to pass through capillary membranes, remain within the intravascular compartment longer
Albumin: expensive
Vasoactive meds
Inotropic
vasodilators
vasopressors
when given must monitor vital signs frequently (every 15 minutes until stable, or more often if indicated)
must be given through a central line–tissue necrosis and sloughing
should be tapered and weaned–should not stop abruptly (titrated the dosage)
When patients are on this for long, fingers and toes can be necrotic
Inotropic meds and examples
dobutamine, dopamine, epinephrine, milrinone
Inotropic meds pros and cons
(+) Increase contractility
(-) Increase oxygen demand of the heart
Vasodilator examples
Nitroglycerin, nitroprusside
Vasodilator pros and cons
(+) Reduce preload and afterload (makes pumping easier)
(-) cause hypotension
Vasopressor examples
norepinephrine, dopamine, epinephrine, vasopressin
Vasopressor pros and cons
(+) increase blood pressure
(-) increase cardiac workload
Nutritional support in shock
May require more than 3000 calories daily
Skeletal muscle mass broken down first
Enteral feeding is preferred
Hypovolemic shock
decreased intravascular volume
reduction of 15-30% of intravascular fluid
750-1500 mL of blood loss in a 70-kg person
due to either fluid loss or shifting (dehydration, edema, ascites…)
Management of hypovolemic shock
fluid replacement
two IV lines (alternative: intraosseous catheter)
Blood products
Modified Trendelenburg position–fluid redistribution (Knee straight, trunk horizontal, head slightly elevated)
Nursing management of hypovolemic shock
temperature should be monitored to ensure rapid fluid resuscitation does not cause hypothermia
Pharm therapy in hypovolemic shock indications
If fluid fails to reverse hypovolemic shock, then vasoactive medications that prevent cardiac failure are given
Also given to reverse cause of dehydration
Pharm therapy in hypovolemic shock
Insulin for hyperglycemia (hyperglycemia can lead to dehydration)
Desmopressin (DDAVP) for diabetes insipidus
Antidiarrheal for diarrhea
Antiemetic for vomiting
Cardiogenic shock
when the heart’s ability to contract and to pump blood is impaired and the supply of oxygen is inadequate for the heart and tissues
Coronary and noncoronary causes of cardiogenic shock
MI
Stress to myocardium (hypoxemia, acidosis, hypoglycemia, hypocalcemia, tension pneumothorax)
Cardiomyopathies
Valvular damage
Cardiac tamponade
Dysrhythmias
Patho of cardiogenic shock
Impaired tissue perfusion weakens the heart and impairs its ability to pump
Reduced ejection fraction
Fluid accumulates in the lungs
Clinical manifestations of cardiogenic shock
angina
dysrhythmias
fatigue
express feelings of doom
show signs of hemodynamic instability
Medical management of cardiogenic shock
increasing cardiac contractility
decreasing ventricular afterload
correction of underlying causes
First line treatment of cardiogenic shock
O2 (NC 2-6 L/min Sats > 90%)
Pain control–IV morphine
hemodynamic monitoring
laboratory marker monitoring (BNP, cardiac enzymes, ECG)
fluid therapy
Dobutamine for cardiogenic shock
Inotropic: increasing the strength of contractility
Decrease pulmonary and systemic vascular resistance
Nitro for cardiogenic shock
Low dose: venous vasodilation–reduce preload
Higher dose: arterial vasodilation–reduce afterload and improve blood flow to the myocardium
Dopamine for cardiogenic shock
Use with dobutamine and nitroglycerin to improve tissue perfusion
Low dose: Improve contractility (2-8 𝛍g/kg/min)
Higher dose: > 8 ưg/kg/min vasoconstriction (not desirable; titrate carefully)
Other vasoactive meds for cardiogenic shock
Norepinephrine, epinephrine, milrinone, vasopressin, and phenylephrine
They stimulate different receptors of the sympathetic nervous system.
Antiarrhythmic meds for cardiogenic shock
Used to stabilize HR
Mechanical assistive devices for cardiogenic shock
Intra-aortic balloon pump
Left and right ventricular assist devices
Total temporary artificial hearts
Cardiopulmonary bypass system
Circulatory shock
Also known as distributive
blood volume pools in peripheral blood vessels (abnormal displacement of blood volume)
lack of vascular tone:
septic shock
neurogenic shock
anaphylactic shock
Lack of vascular tone in circulatory shock
central regulatory mechanisms (sympathetic tone, constriction)
local regulatory mechanisms (cellular biochemical mediators)
Massive arterial and venous dilation
Septic shock
Most common type of circulatory shock
caused by widespread infection
most common cause of death in noncoronary ICUs in the U.S.
Gram-negative bacteria: most common (e. coli)
gram-positive bacteria: Staphylococcus aureus, MRSA
Fungal infections, viral infections
Site of infection not always identified
Risk factors of septic shock
Immunosuppression (cancer, HIV/AIDS, organ transplant)
Extremes of age (<1 yr and >65 yr)
Malnourishment
Chronic illness
Invasive procedures
Emergent and/or multiple surgeries
Patho of septic shock
immune and inflammatory response cause increased capillary permeability and poor tissue perfusion
Systemic inflammatory response syndrome (SIRS): Clots formation
Early stage septic shock
hyperthermia and fever, with warm and flushed skin and bounding pulses; elevated RR
Cloudy urine (e. coli)
Warm phase
Late phase (true septic shock)
BP drops and skin becomes cool, pale, and mottled.
Pulse ox!
Ventilator/intubation possible
Cold phase
Medical management of septic shock
identify and treat patients in early sepsis within 3 hours (sepsis bundle chart, tells us when there’s a major change in vitals from baseline)
fluid replacement therapy
pharmacological therapy
nutritional therapy: initiated within 24 to 48 hours of ICU admission
Nursing management: Sepsis-Related Organ Failure Assessment Score (SOFA)
Neurogenic shock
vasodilation due to a loss of balance between parasympathetic and sympathetic stimulation–predominant parasympathetic stimulation
Caused by spinal cord injury, spinal anesthesia, or other nervous system damage. can be caused by lack of glucose
venous pooling in the extremities and peripheral vasodilation (dry warm skin)**
S/S of neurogenic shock
Low BP
low HR
(Low CO)
dry, warm skin
pt does not perspire in the paralyzed portions of the body (neurogenic shock can also be caused by spinal cord injury)
Management of neurogenic shock
closely observe for an abrupt onset of fever
elevate and maintain the HOB at least 30 degrees to prevent neurogenic shock when the patient receives spinal or epidural anesthesia (prevent the spreading of medication up through the spinal cord)
supportive care
Higher risk for VTE, evaluated for DVT
Monitor closely for internal bleeding among patients with a spinal cord injury (they may not report pain caused by internal injuries.)
Anaphylactic shock
caused by a severe allergic reaction when patients who have already produced antibodies to a foreign reaction
an antigen-antibody reaction provokes mast cells to release potent vasoactive substances, such as histamine or bradykinin, causing widespread vasodilation and capillary permeability
rapid onset of hypotension, neurologic compromise, respiratory distress, and cardiac arrest
1st time exposure antibodies formed
2nd time anaphylactic shock
Medical management of anaphylactic shock
Fluid management
IM epinephrine
IV diphenhydramine
Albuterol
Multiple organ dysfunction syndrome (MODS)
A complication of any form of shock, but is most commonly seen in patients with sepsis.
Rapid assessment with early recognition and response to shock states and sepsis is essential to the patient’s recovery
dysfunction of one organ system is associated with 20% mortality, and if more than four organ fail, the mortality is at least 60%.
Progression of MODS
usually begins in the lungs, and cardiovascular instability as well as failure of the hepatic, GI, renal, immunologic, and CNS (hearing last to go)
Medical management of MODS
prevention is the top priority
elderly: early signs are changes in mentation and a gradual rise in temperature (mental status first)
Controlling the initiating event
Promoting adequate organ perfusion
Providing nutritional support
Maximizing patient comfort
