Multisystem (Burns & shock) Flashcards
Protocols to follow like open heart surgery; order to doing stuff
Wax and wayne - may have to backwards
Resuscitative Phase:
Acute Care Phase
The rehabilitative phase of care of the patient with burns
Nursing management - phases of care
starts at the initial hemodynamic response to injury and lasts until capillary integrity is restored and fluid replacement has occurred. The goal is to maintain vital organ function and perfusion. Emergent interventions for inhalation injury, airway management, and hypovolemia are concurrently addressed.
Begins prehospital
Ends when wound closure is achieved
Resuscitative Phase:
begins after resuscitation (the onset of diuresis) and lasts until complete wound closure is achieved.
Start having third spacing
Fluid moving from extravascular and intravascular - wounds heal and not as edematous and start to heal
Acute Care Phase
starts from the admission of the patient and may last years, depending on future surgical procedures, therapy needs, contracture prevention, and psychological or emotional needs of the patient.
Long-term: years
Therapy to gain full range of motion
Skin grafts
After know will live
The rehabilitative phase of care of the patient with burns
Very beginning
In hospital setting
What kill first
Oxygenation Alterations
Fluid Resuscitation
Risk for Infection
Hyperkalemia:
Hypokalemia
Hyponatremia
Ineffective Tissue Perfusion
Invasive monitoring
Hypothermia
Laboratory assessment:
Resuscitative phase
Airway and Breathing
Have to have both to have adequate oxygenation and ventilation
What are we assessing? - Oxygenation Alterations
Lot airway - inhalation injury; burns inside mouth - swelling associated with that - mouth, tongue, pharynx - swell to point to completely occlude airway
Related to: - Oxygenation Alterations
Laryngeal and facial swelling
See face first
Specks black in oral cavity from soot of smoke
Breathing: carbon monoxide levels elevated because in environment on levels of high carbon monoxide - occupying spot on RBC
Edema
Burns
Severely chapped lips
Talking - listen to way speech is: hoarse; normal for you; normal voice - lower at glottis level with swelling - decompensate quickly
Assess depth and rate respirations - try compensate for low O2 levels - not getting enough in so increase RR
Assess: - Oxygenation Alterations
100% O2 on them no matter what
High carbon monoxide SpO2 inaccurate
If have burns on thorax (ant and post chest) - affects ability to move chest in and out - escharotomy - sharp scalpel and then spreads
Treatment: - Oxygenation Alterations
Deficient fluid volume
Fluid shifts - intracellular to extracelluar
Circulation: - Fluid Resuscitation
Hypovolemic shock - hypovolemia relative because fluid not where supposed to be
Burn shock - Fluid Resuscitation
hyperkalemia, hypokalemia, hyponatremia
Leaked out
Electrolytes in fluid that is being leaked out
Electrolyte imbalance: - Fluid Resuscitation
Very high risk
What is the most common source of infection?
What are some infection control measures?
Risk for Infection
Dirty environment when have injuries to dermis - try clean wounds but already in there on surface
Common source: Bacteria - from dermis, poor hand hygiene, stuff on the skin
What is the most common source of infection?
Wash hands
What are some infection control measures?
Causes:
release of potassium from damaged cells
metabolic acidosis
impaired kidney function caused by hemoglobinuria, myoglobinuria, or decreased renal perfusion.
Hyperkalemia:
Causes:
massive loss of fluids and electrolytes through the burn wounds
hemodilution from fluid resuscitation.
Inadequate replacement
diuresis
diarrhea
vomiting, nasogastric drainage,
long hydrotherapy sessions
Shift of potassium from the intravascular space to the cell after the acidosis has been corrected.
Hypokalemia
Causes:
the loss of sodium through the burn wound
the shift of fluid into the interstitial space
vomiting, nasogastric drainage
diarrhea
the use of hypotonic salt solutions during the early phase of resuscitation.
Hyponatremia
Ensure end organ perfusion adequate
About blood and components of blood not in vascular space - in tissue - not circulating
Kidney
Cerebral
Gastrointestinal
Peripheral
Ineffective Tissue Perfusion
Related to
Hgb - Hemoglobinurea - extra Hgb circulating - big molecules of kidneys not like filtering it out
Hypoperfusion cause kidney issue
Hypovolemia
Assess:
Muscle breakdown and myoglobin in urine - urine looks brown raspberry iced tea color
Kidney
Related to
End organ perfusion
Not have blood in vascular space - not circulate to head - hypoperfuse brain
Associated with head injury - in environment long enough and face planted - head injury
Carbon monoxide poisoining and Hypoxemia and Electrolyte balance
Assess:
Baseline neuro assessment - LOC - before and throughout stay
Know carbon monoxide levels elevated - as come down neuro levels should improve
Cerebral
Related to
Paralytic ileus is a common GI complication that can be related to hypokalemia, the sympathetic response to severe trauma, or decreased tissue perfusion related to hypovolemia
Ileum not have peristalsis so have bowel obstructions - because of K - need K at this level to make it work
Assess:
bowel sounds in all 4 quads, high risk for GI bleeding - high risk for having more liquid stool; peristalsis above and below blockage; not necessary whole ileum and what get past ileum is water so have watery stools - one first see with eyes that is a problem
Circumferential abdominal burns:
Burns in thorax and have swelling - see swelling - swells outwards and inwards - smushing guts: intraabdominal compartment syndrome
assess for abdominal compartment syndrome. Is caused by intra-abdominal hypertension (IAH) - pressure in abdominal cavity. IAH is an IAP greater than or equal to 12 mm Hg (normal 5 to 7 mm Hg).
First see swelling - pushing on all organs under it
Important structure - aorta then get CV sys - decrease CO, preload
Assess for
Gastrointestinal
Quantify with special catheter with extra ports - push saline in bladder and put up to transducer and up to abdominal cavity
If it >12 focus assessment - decrease output, more incidence of ileus and other organ dysfunc
Pressing on aorta - issues with venous return - BP down - not have preload - no BP - compound with lack circulating volume - crump fast
Need be symptomatic first - now radar and assessing for other probs - pressure 20 not package deal of escharotomy
Increased pressure see - Decreased cardiac output, decreased tidal volume, increased peak pulmonary pressure, decreased urine output, and hypoxia.
Measured with a transurethral bladder pressure catheter
Surgical decompression (escharotomy - burn and cut through hard eschar tissue) of the abdomen may be required for IAP > 20 to 25 mm Hg accompanied by a taut, tense abdomen and signs of organ dysfunction - HAVE TO HAVE SX - actively treat need sx
Not have obvious burns - fasciotomy to give room to swell
Assess for
Burns all around - squeezing effect
Compensatory mechanisms - not lot fluid circulating - now constrict to get BP with what do have
Combining burn with vasoconstriction - issues with perfusion to extremities
Related to vasoconstriction secondary to hypovolemia
Assess CMS on all extremities.
Circumferential burns: Assess for pulselessness, pallor, pain, paresthesia, paralysis, and poikilothermy (defn: the inability to maintain a constant core temperature independent of ambient temperature)
Doc CMS to distal extremity
Pulses start weaker and sides getting cooler - emergency - cont swell and get worse
An escharotomy may be needed to allow the underlying tissue to expand - straight line and swelling spreads it
In deeper wounds, a fasciotomy (incision into the fascia) may be necessary - swelling deeper - all through levels dermis to muscle and cut between to open fascia so muscle can swell somewhere
Peripheral
Need to do this when caring for them
Invasive monitoring includes direct measurement of CVP, pulmonary artery pressure, arterial pressure, core temperature, cardiac output, SVR, and PVR.
Arterial line is considered if serial and frequent arterial blood gas values are required for respiratory management or for hemodynamic instability requiring the titration of vasoactive medications.
Lot ABGs
Central venous catheters: to deliver the massive volume of fluids required.
Pulmonary artery catheters are placed only when necessary for optimal care.
May or may not get this
Go straight to invasive montioring - need to know CVP and need bigger access - large bore IV
Invasive monitoring
Look at CVP - quantify preload so ensure vena cava not getting smushed; vascular volume
No way to prevent it from going intravascular to extravascular but we can monitor it
Monitor fluid resuscitation
Take a lot volume - Judge if adequately/enough volume
Look at all hemodynamics
Invasive monitoring includes direct measurement of CVP, pulmonary artery pressure, arterial pressure, core temperature, cardiac output, SVR, and PVR.
Package deal with getting this
Getting lot fluid very quickly and need large vein to accept it at that speed
Using Rapid infusers used/pressure bag
Central venous catheters: to deliver the massive volume of fluids required.
What causes hypothermia in this population?
Probs managing temp
Not have intact dermis and what is there is damaged and ineffective - heat is kept in body here - hard regulate temp
Burn units very hot - ambient air warmer - not cool for staff (gowned up for infection control)
Dressings off - issues with regulation
The patient’s core temperature should be maintained between 37.6° C (99.6° F) and 38.3° C (101° F).
Heat is lost through open burn wounds by means of evaporation and radiation
Hypothermia can occur during initial treatment, hydrotherapy, dressing changes, and immediately after surgery.
Hypothermia
Need serial labs
Laboratory values, when paired with the physical assessment, provided a complete picture of the patient’s end organ perfusion, electrolyte assessment, and complete blood count.
Watch labs because shift of fluids - electrolytes follow fluid; electrolytes within norm limits (cardiac and neuro issues); gut needs adequate K for adequate peristalsis; always electrolyte probs with phase - package deal with phase and fluid location
White blood cell counts usually are monitored for elevation, a sign of sepsis. However, it is not unusual for the white blood cell count to fall to less than 5000/mm3 within 48 hours after injury.
High risk for infection
Not all septic infections get but high risk
Hemoglobin and hematocrit data can be useful in the resuscitative phase to guide fluid administration.
Serum chemistry to assess kidney function and electrolyte balance.
End organ perfusion - Cr and BUN
Which electrolytes do we need to focus on?
Hyperkalemia
Hypokalemia
Na
What causes the electrolyte imbalance?
Hyperkalemia - Release K from damaged cells - damaged and releasing contents into vascular space; get from acidotic state; Kidney func - Taking kidneys with myoglobinurea and lower perfusion - messes with K
Hypokalemia - massive amount fluids giving to maintain adequate amount of perfusion
Na - lost through burn wound; shift from intravascular to extravascula
Laboratory assessment:
electrical shock - through the muscle to break it down
Burn highest risk for having myoglobinurea -
First degree - redness to the face and neck
Second degree - patchy white areas that blanch with pressure
Third degree - pale with charred areas
An 80 Kg patient presents to the emergency department with redness to the face and neck, the upper chest and back are pale with charred areas, and the left upper (front & back) and right lower (top only) arm are red with patchy white areas that blanch with pressure. IV fluids are running through 2 large bore IVs. NG tube is to low intermittent suction. Blood is sent to the lab. The patient is agitated but answers questions appropriately. Their voice is hoarse. When speaking to the patient, the nurse notices that the patient has singed nose hairs and black, carbon deposits on their lips.
Which type of burns does this patient have?
Yes
voice is hoarse
singed nose hairs and black, carbon deposits on their lips
Does this patient have any signs or symptoms of an inhalation injury?
Face - 4.5
Thorax - 18%
Left upper (front and back) - 4.5
Right lower (top only) - 2.25
29.25%
What is the % of the surface area burned?
Stable - nothing with ABCs concerning
100% O2 and start fluid resuscitation - A before C
Assess ABCs <20sec
Lot issues with airway so anticipate and consider intubation before diff intubation because massive amount edema in oral airway and glottis
What intervention should the nurse anticipate next?
Not care about Sat prob - reading carbon monoxide and O2 on RBC - finger probe - getting 100% oxygen
Have both airway and breathing
Breathing - shallow respirations with poor chest wall excursion
Airway - expiratory wheezing; anything from oral cavity to mainstem bronchus
MAP soft
HR elevated as comp mechanism
Issues with oxygenation and ventilation - not in good place
The patient is put on 100% high-flow oxygen via a non-rebreather mask and transported to the burn unit. 4 hours later, the nurse assesses the patient again. Neuro: The patient is lethargic but is oriented to person, place, and time. CV: S1,S2, no advantageous heart tones. Right arm: doppled pulse, warm, reddened skin tone, 3/10 pain, no numbness/decreased sensation reported. left arm: doppled pulse, pale, cool 9/10 pain, + tingling, decreased sensation. lungs are course throughout with expiratory wheezing, rapid, shallow respirations with poor chest wall excursion. Urine output is 30 ml/hr and is a dark red color. Vital signs: BP 101/48 (65), HR 128, RR 28, SaO2 91% ABG: pH 7.32 PaCO2 50 HCO3 20 PaO2 76
Is this assessment concerning? Why/Why not?
Raspberry tea colored urine
Muscle break down
What does the urine color indicate?
Both burns were second degree
Left arm was circumferential - smushing in on vascular bed but also nerves smushing - so have sensory probs
Great enough pressure - affecting nerves - not that forgiving; first pins and needles, then no feeling, then painful; perfusion back - painful for awhile
Why is the left arm more painful than the right?
Priority: airway: losing his airway - if we can do tube - tube him; if not trach him - going 4 hours - deteriorating quickly; prepare for intubation - kit and bed ready and pt ready
2. Not able to expand in burns: crusty and constricted - hard sided luggage - not expand to get extra stuff in; burn circumferential on chest - can go in - affects ability to breath; do escharotomy bedside; scalpel - getting through crust and swelling exands out to wound - makes chest func again - more wall excursion: classic when burns on front and back
Intubate for airway; prepare for escharotomy for breathing
3. Circulation: arm not getting perfusion (pale, cool skin) - must perfuse it; volume resucictation - ensure doing this adequately; fasciotomy
Must do all 3 together
If crust start with escharotomy (third degree); fasciotomy (second degree burns - cut up so expand)
What should the nurse prepare for next?
Extravascular fluid going back into intravascular fluid - more stable - not requiring as much fluid resuscitation
The acute care phase begins after resuscitation (the onset of diuresis) and lasts until complete wound closure is achieved.
Impaired Tissue Integrity
Skin Substitutes mimic the native epidermis and dermis
Temporary substitutes:
Permanent substitutes
Definitive Burn Wound Closure
Acute care phase
Still issue with this
Still have wounds healing
Prevent anything that stops the process of healing
What factors affect the healing of the burn wound?
Wound Cleansing
Hydrotherapy facilitates the removal of debris and loose eschar
Wound Care:
Topical Antibiotic Therapy
Wound Debridement:
Mechanical Debridement:
Enzymatic debridement: Topical proteolytic is applied to the wound.
Surgical debridement.
Impaired Tissue Integrity
Not get an infection - natural flora on skin
Inconteninet - E coli from stool
Diabetic - higher risk for infection
CHF and bad CO need good CO to perfuse areas to heal
tissue hypoxia
More aggressive when debriding eschar tissue - once gone - open wound again - higher risk for infection
Daily dressing change - peeling off of burnt skin or scab
What factors affect the healing of the burn wound?
Gently clean with gauze dressing, pat dry, and apply topical ointment
Cleaning wounds
Abx ointment and nice dressings
Wound care detailed
Cleaning burns - cleaning and putting abx ointment on
Wound Cleansing
Measures to reduce pain (analgesics, opiates, sedatives) and hypothermia are required
Gentler way of debriding
Taking off dead tissue instead scrubbing
Imp to be gone so heal
Painful - premedicated and medication tweaked during procedure
Hydrotherapy facilitates the removal of debris and loose eschar
Not want wounds to dry - want moist environment - bacteria loves it
Maintaining a moist wound environment while preventing wound infection is the standard of care.
Apply a topical antimicrobial agent, followed by a primary nonstick dressing. An outer layer is applied to provide increased absorption, compression, and occlusion
Using silver-impregnated dressings can reduce dressing change frequency - bacteria not grow on silve
Wound Care:
Used to control bacterial colonization
Protocol and physician based
Abx base
Most silver based creams - silver impregnated 4x4s because bacteria not grow on silver
The most used topical antibiotics are SSD (Silvadene cream), mafenide acetate cream (Sulfamylon), bacitracin ointment, and silver impregnated into the primary dressing
Topical Antibiotic Therapy
Removal of nonviable tissue (eschar) that has no blood supply, and polymorphonuclear leukocytes, antibodies, and systemic antibodies cannot reach these areas.
Ambiguous - what debride - color with blue dye so know gotten deep enough and whole area
Ensure get whole surface necessary
Wound Debridement:
nonviable tissue is manually removed using scissors and forceps.
Mechanical Debridement:
Softens the eschar and dissolves devitalized tissue while sparing healthy tissue.
Promote the separation of eschar, which can lead to earlier wound closure.
Eschar hard as rock - put enzyme in it to digest it away
Enzymatic debridement: Topical proteolytic is applied to the wound.
A surgical procedure to remove nonviable tissue down to bleeding viable tissue with an electric dermatome or surgical knife.
In OR
Sometimes in room
Go lot deeper
Very painful
Need general anesthesia
Surgical debridement.
Dermis may or may not come back - not regenerate if full-thickness - Get into grafts
Nice pink and scarred then products
Long process - with grafts never baseline - always distortment - sometimes lot scar
Skin Substitutes mimic the native epidermis and dermis
Designed for placement on partial-thickness or clean, excised wounds.
Cover open wound to help prevent infection
Most long-term
Temporary substitutes:
provide a permanent skin replacement
Permanent substitutes
Long-term; deeper 2nd degree and 3rd degree
Excision and grafting: 3rd- burns and some deep dermal partial thickness burns
Grafts
Synthetic Skin
Definitive Burn Wound Closure
Autograft
Biosynthetic Skin Substitutes
Grafts
is a skin graft harvested from a healthy, uninjured donor site on the patient
Take skin off non burned and put on burned area - looks like webbing - not solid - tack on with sutures/staples on edges
Best - less chance rejection
Autograft
Cadaver skin
Homografts (allografts): Homograft skin can be obtained from living donors or deceased donors (cadaver skin)
Heterografts (xenografts): a graft transferred between two different species to provide temporary wound coverage. The most common and widely accepted xenograft is pigskin (porcine skin)
Biosynthetic Skin Substitutes
Diff types synthetic skin (skin substitutes)
Integra functions as a temporary skin replacement that attaches to the open wound until the skin tissue grows enough to be replaced by skin grafts. It is a two-layer sheet with the inner layer created from tendon material from cows and a substance called glycosaminoglycan made from shark cartilage. The outer layer is silicon-based with a clear and natural appearance to view the skin tissue reconstruction
Synthetic Skin
The rehabilitative phase of care of the patient with burns starts from the admission of the patient and may last years, depending on future surgical procedures, therapy needs, contracture prevention, and psychological or emotional needs of the patient.
Much later
Planning rehab early; can predict needs early based on surface area and types of wounds; actual rehab phase starts later
Moved from wounds, preventing infections to mental health issues and mobility issues
Impaired Physical Mobility
Scar Management
Rehabilitation phase
Contractures that develop after a burn injury
The affected body parts should be positioned to prevent long-term deformity.
Frequent change of position also is important and may need to be performed as often as every hour.
Splints used to prevent contractures must be checked daily for proper fit and effectiveness.
Impaired Physical Mobility
Scars - Contract and shrink
On face - Can have issues with dry eye; issues with eating
Multiple surgeries where debulk scar tissue
The goal of scar management is to minimize scarring, making the skin flat, elastic, and close to the original color
Areas of the skin that required skin grafting also have a visible scar.
Scar formation can be reduced with compression garments.
Scar massage stretches the scar and provides moisture
Surgical excision may be recommended
Scar Management
- debride, abx ointment, infection control big
Acute phase
fluid management; ABCs, prevent big comps
Resucitative phase -
Shock is a life-threatening manifestation of circulatory failure that leads to cellular and tissue hypoxia resulting in cellular death and dysfunction of vital organs.
Shock is characterized by decreased oxygen delivery and/or increased oxygen consumption or inadequate oxygen utilization leading to cellular and tissue hypoxia
Effects of shock are reversible in the early stages and a delay in diagnosis and/or timely initiation of treatment can lead to irreversible changes including multiorgan failure (MOF) and death
There are mainly 3 broad categories of shock
Shock
Life-threatening prob
Simplest terms - something affecting tissues from getting oxygenated
Shock is a life-threatening manifestation of circulatory failure that leads to cellular and tissue hypoxia resulting in cellular death and dysfunction of vital organs.
Septic, anaphylactic, or neurogenic
Hypovolemic:
Characterized by decreased intravascular volume and increased systemic venous assistance a.nd end‐organ hypoperfusion
Cardiogenic:
Characterized by severe impairment of myocardial performance that results in diminished cardiac output, poor end‐organ hypoperfusion, and hypoxia
There are mainly 3 broad categories of shock
Low volume
Just preload problem
Definition: Inadequate fluid volume in the intravascular space.
Causes: Hemorrhage from any source, intravascular volume to the interstitial space, severe vomiting or diarrhea, diuresis.
How does the decreased preload cause a decreased cardiac output?
Name compensatory mechanisms seen in hypovolemic shock
Assessment
Management
Hemodynamics of hypovolemic shock
Hypovolemic shock
↓ preload (CVP & POAP)
Something affect volume in vascular bed
Burn shock where not in vessels - in outlying tissues - bled out from big trauma - severely dehydrated - too aggressive in taking fluid off with dialysis
Something happening where not enough volume in vascular/blood vessels
↓ Cardiac output (CO)
Because not have adequate preload - CO low
Pump not primed - not enough volume in ventricle to squirt out
↑ Systematic Vascular Resistance (SVR)
Compensatory mechanism with arteries being constricted
Inadequate cellular oxygen supply and ineffective tissue perfusion
Definition: Inadequate fluid volume in the intravascular space.
Pump not primed - not enough volume in ventricle to squirt out
Volume in arteries and veins low
How does the decreased preload cause a decreased cardiac output?
Arteries constricting
Name compensatory mechanisms seen in hypovolemic shock
Decreased Perfusion: Respiratory
Decreased Perfusion: Renal
Decreased Perfusion: Neuro
↑ lactate, Lactic acidosis
Metabolic acidosis
Decreased Perfusion: integumentary
Decreased Perfusion: CV
Assessment
↑ RR
↑ Anxiety
↑ partial pressure of carbon dioxide (PaCO 2)
Decreased Perfusion: Respiratory
↓ urine output
Increased BUN & Creat levels
Decreased Perfusion: Renal
Dizzy
Confusion
Agitation
Coma
Restless
Anxious
Decreased Perfusion: Neuro
Not enough RBCs for whatever reason - move from aerobic to anaerobic respiration - Kreb cycle - 20 ATP - anaerobic: 2 and Lactate - get lactic acid
less than two mmol/L
↑ lactate, Lactic acidosis
Respirations up - acidotic
Metabolic acidosis
Pale, cool skin (Class I - III), cyanotic, mottled, and extremely diaphoretic (class IV)
Decreased Perfusion: integumentary
↓ Peripheral pulses
Flat JVD
Tachycardia
Postural hypotension
Dysrhythmias
Cool, pale skin
Vasoconstriction: develop cool extremities and increased capillary refill time
Decreased Perfusion: CV
Correct the underlying cause - trauma and lot blood: give blood; took off too much fluid, give fluid; burn shock: hypovolemic - adjust amount fluid getting
Administer fluids
Medical management
Minimizing fluid loss - limit blood draws, observe lines for accidental disconnection, and apply direct pressure to bleeding sites
Administer volume replacement - Insert large-bore peripheral IVs and rapid administration of prescribed fluids
Administer vasopressor agents (if needed)
Assess response to therapy
Aggressive enough/too aggressive - do anything
Provide comfort and emotional support
Stressful on them
Preventing and maintaining surveillance for complication
DVTs, pressure ulcer
Nursing Management
Know hypovolemic state - necessary get all blood draws; ask if can switch it up
Observe lines - always give back waste syringe
Minimizing fluid loss - limit blood draws, observe lines for accidental disconnection, and apply direct pressure to bleeding sites
Lot volume - blood, albumin, NS - give fast
No peripheral get central
Veins not pop up - feel valley - no squish
Administer volume replacement - Insert large-bore peripheral IVs and rapid administration of prescribed fluids
Need some preload
Nothing to squeeze - constrict nothing - need give volume
Administer vasopressor agents (if needed)
Low
Cardiac output/Cardiac index: high, normal, or low?
low
PAOP: high, normal, or low? - PA catheter
high
SVR: high, normal, or low?
low
SVO2: high, normal, or low?
Contractility part
Care about LV
Something wrong at myocardium, LV
Definition: Failure of the heart to effectively pump blood forward.
As a compensatory mechanism,
Assessment
Hemodynamics of cardiogenic shock
Medical management
Nursing management
Cardiogenic shock
↓ Stroke Volume (SV)
Not pumping blood out LV - SV decreased - contributes to CO - which will be lower
↓ Cardiac output (CO); CI < 2.2 L/min/m2
↑ Systemic Vascular Resistance (SVR)
Try compensate by elevated
Comp mech
↑ PAOP
Go up - not have forward flow with CO - starts to back up
Cause: not going forward so this is the effect
↓ LVSWI
Hallmark
Decreased cellular oxygen supply and ineffective tissue perfusion
Causes: MI, cardiomyopathy, valvular disease (acute papillary muscle, or septal rupture; cardiac tamponade), and massive pulmonary embolus
Definition: Failure of the heart to effectively pump blood forward.
High to compensate
How does the heart rate attempt to compensate?
Low BP - hypotensive
Restless, anxious
Trying help circ what got - decreases fill time - compound issue of decreased CO
Increased RR
What assessment findings are associated with increased HR?
Tachypneic
Is the cardiogenic shock patient eupnic, tachypneic, or bradypenic?
Systolic blood pressure <90 mm Hg
Acute drop in BP >30 mm Hg
Heart rate >100 beats/min
Weak, thready pulse
↓ Cardiac output
Cardiac index <2.2 L/min/m2
↑ PAOP
↑ CVP
↑ SVR
Dysrhythmias
Chest Pain
+ JVD
Diminished heart sounds
+ S3 & S4
Cool, pale, moist skin
Change in sensorium
Tachypnea
Urine output < 30 ml
Crackles
↑ BUN & Creat
↓ PaO 2 and ↓ SaO 2
↓ LOC
These clinical manifestations should remind you of right and left heart failure
Assessment
low
Cardiac output/Cardiac index: high, normal or low?
high
PAOP: high, normal, or low?
high
SVR: high, normal, or low?
low
SVO2: high, normal, or low?
low
LVSWI: high, normal, or low?
Driven by PCP
Identify and treat the underlying cause
Administer pharmacologic agents to maintain adequate BP & tissue perfusion
Intubation and mechanical ventilation are usually necessary to support oxygenation.
Mechanical devices to enhance CO - if really low
Medical management
MI – emergent PCI or CAB
End stage CHF – VAD
Papillary muscle rupture: IABP surgery
Balloon pump and impella
Focus on LV - with afterload reduction
Cardiogenic shock from chronic illness with CHF - Consider longterm - VADs
Acute illness - balloon pump then to OR suite if papillary muscle rupture very bad
Cardiogenic shock - OR suite available go to that; if not balloon pump or impella then to OR suite
Identify and treat the underlying cause
Inotropic (↑ contractility): Dobutamine, dopamine, milrinone - get LV to pump harder - myocardium dead/tapped out - cannot make it work harder - go back to balloon stuff
Vasopressor - Norepinephrine
Diuretics may be used for preload reduction.
Antidysrhythmics to suppress or control dysrhythmias
Administer pharmacologic agents to maintain adequate BP & tissue perfusion
With caution - BP up to perfuse organs - may work but sometimes not if LV done - see BP go down
Both medications increase myocardial oxygen demand - the lowest possible doses should be used.
Pressure with
Not work harder to get valve open
Aortic valve not open because resistance to high
Vasopressor - Norepinephrine
Less volume for LV too push around
Diuretics may be used for preload reduction.
Irritable LV = PVCs and runs - hopefully get out - vtach
Vdyrsrhythmias
Antidysrhythmics to suppress or control dysrhythmias
Intraaortic balloon pump (IABP)
Percutaneous ventricular assist device (VAD, Impella)
Extracorporeal membrane oxygenator (ECMO - first two in acute illness works) - CO really low - LV so damaged and needs lot time heal - need take all work load off so get into ECMO
Mechanical devices to enhance CO - if really low
Limit myocardial oxygen demand
Measures to enhance myocardial oxygen supply
Monitor and manage heart rate, preload, afterload, and contractility.
Nursing management
Administer analgesics, sedatives, and agents to control afterload and dysrhythmias
Sedation - continuous IV infusion
Manage it - limit myocardial demand
Position the patient for comfort
Limit activities
LV barely perfuse all organs while in bed so no laps around hospital
Provide a calm and quiet environment and offer support to reduce anxiety
Teach the patient about the condition
Not in acute phase - wait until later
Limit myocardial oxygen demand
Supplemental oxygen, Manage device therapy
Hemodynamics - LVSWI increase as get better and ischemic LV part perfused and starts functioning - does not always happen
Watch for affect when give vasodilators and + inotropes or diuretics - LV not working - may not respond
Measures to enhance myocardial oxygen supply
Measure and trend hemodynamic variables
Controlled administration of fluids and inotropic and vasoactive agents.
Close assessment and management of respiratory function is also essential to maintain adequate oxygenation.
Dysrhythmias are very common and require immediate recognition and treatment. - see if having more PVCs/longer runs; getting progressively worse/better; really big ant wall MIs take out septum - see AV blocks and other dysrhythmias
Mechanical device therapy: Assess for complications that include infection, bleeding, thrombocytopenia, hemolysis, embolus, stroke, device malfunction, circulatory compromise of a cannulated extremity, and sepsis.
Monitor and manage heart rate, preload, afterload, and contractility.
All highlight
Lot in CV
Look in the story
Non-stemi not ok - MI evolved - not any less sick - past acute phase where can get myocardium back
Pt. A was admitted with a non-STEMI. He stated his chest pain started about 12 hours prior, but he delayed going to the ED until after his daughter’s graduation. History: dyslipidemia, appy, broken rt tibia, MI x 2, Rt. SFA stent. Admission Assessment
Neuro: A & O x 4, Nervous about being in the hospital again
Pulm: SOA with minimal exertion, anterior rales, bibasilar crackles
GI/GU: Urine Output: Scant
CV: S1, +holosystolic (pansystolic) murmur, heard best at the fifth intercostal space, midclavicular line, 1+ radial, doppled post tib pulses. Cap refill > 3 sec, Orthostatic hypotension
Integ: Cool
Anything concerning?
Need increase CO - all sort CO issues
Get another 12-lead
Compare to other MIs to see if same as when left the hospital
Give meds to decrease SVR
Murmur is normal - figure out what murmur is from - fifth intercostal space, midclavicular line: mitral valve
New murmur not good
Increase and optimize oxygenation - not good CO - optimize what circulated - not good output - upper 90s-100s
Look at response to therapies
What should the nurse anticipate doing next?
All Vs are anterior
Septal 1 and 2
5 and 6 = lateral
Vs = pumping chamber
Completed MI - new Q wave - Q negative deflection - whatever is dead is dead - not coming back - see if anything salvagable - once Q wave done with process
Cath in femoral vein
The assessment findings are concerning. The nurse assesses the patient’s pain and notifies the primary provider. The primary provider orders a 12 lead ECG. IV access is obtained. 12 lead ECG: Shows a previous Inferior MI and new Q waves in V2 – V6. The patient was taken to the CV lab and a stent was placed in the proximal LAD. The patient continued to decompensate. A PA catheter was placed.
What is wrong with this patient?
Cardiogenic shock
All matches what said earlier
Wrong
Pain management by careful morphine titration
↑ Contractility
↓ Preload
↓ Afterload
Treatment priorities - Start by analyzing each hemodynamic value.
Decrease preload via venous dilation, decrease heart rate and afterload by decreasing sympathetic nervous system stimulation, and decrease anxiety.
Control cardiac pain
M morphine - cognizant of BP - dilate all arteries, including coronary arteries - having chest pain; give with fluid see if LV handle fluid to maintain BP
O oxygen
N nitrates
A aspirin
Pain management by careful morphine titration
Dopamine, dobut
↑ Contractility
Diuretics - with little fluid to maintain preload - balancing it out when giving pressure - not dump out BP
Looks high on numbers because backward flow - more space to go
↓ Preload
Not mess with venous dilators - go to balloon pump or impella device - cardiogenic shock - afterload has to be mechanical
↓ Afterload
Definition:
Causes: a hypersensitivity reaction.
Assessment
Medical management
Nursing management
Anaphylactic shock
Difference between rxn and shock - is severity
Shock - rxn; Is vascular tone - SVR
Severe hypersensitivity reaction with peripheral vasodilation and increased capillary permeability
Severe allergic rxn
Massive global vasodilation
↓ Preload (CVP & POAP)
Because all arteries dilated out - preload down - not have it to get to LV down CO low
↓ Cardiac output (CO); ↓ CO
↓ SVR
Very prompt
Inadequate cellular oxygen supply and ineffective tissue perfusion
Definition:
Classic anaphylactic rxn with wheezing and airway
Will be hypotensive and tachycardiac
Cardiovascular
Cutaneous
Respiratory
Neurologic
Gastrointestinal
Genitourinary
Assessment
Hypotension
Tachycardia
Bradycardia
Chest pain
Cardiovascular
Allergic rxn part
s&s of allergic rxn
Pruritus
Erythema
Urticaria
Angioedema
Sense of warmth
Cutaneous
First time have drug - be aware at risk; NKDA - may not have had it
Anaphylactic part
Lump in throat - glottis level
Cough
Dyspnea
Dysphagia
Hoarseness
Stridor
Wheezing
Rhinitis
Chest tightness
Snoring respirations
Tongue fill oral space where drooling
Respiratory
Not perfusing head
Restlessness
Uneasiness
Apprehension
Anxiety
Dizziness
Headache
Sense of impending doom
Confusion
Syncope or near syncope
Unresponsiveness
Neurologic
Nausea
Vomiting
Diarrhea
Cramping/abdominal pain
Back burner
Gastrointestinal
Incontinence
Back burner
Genitourinary
The goals of therapy are to remove the offending antigen.
Reverse the effects of the biochemical mediators
Medical management
IMMEDIATELY DISCONTINUE whatever is being administered that caused the reaction.
Getting medication - stop immediately
Less dose get hopefully less severe sx - little shock as bad as wors shock
The goals of therapy are to remove the offending antigen.
Address anaphylactic part - Administer Epinephrine - bronchodilation, vasoconstriction, and increased myocardial contractility and inhibits further release of biochemical mediators; constrict arteries; help with bronchospasms and swelling
Intravenous glucagon administered to treat bronchospasm and hypotension in these patients
Diphenhydramine (Benadryl)
Oxygen
Intubation & mechanical ventilation - little lip swelling - intubate because downhill fast
Administer fluids - fill vascular bed; just because epi not back to normal vascular tone; IV epi not long half life; dump pressure after IV bolus off do epi drip until over the rxn
Reverse the effects of the biochemical mediators
Prevention
Nursing interventions
Nursing management
Check allergies - not always guarantee; desensititiations
Monitor pt. response when administering blood & blood products.
Monitor pt. response when administering medication for the first time
Prevention
Administer epinephrine - first - addresses the airway; help make bronchus less irritable to dilate bronchial tree
Facilitate ventilation - Positioning the patient to assist with breathing and instructing the patient to breathe slowly and deeply; Try get up - tongue fill up and to back of throat - sit up
Protect Airway – Administer prescribed medications - benadryl, steroids, epi drip
Administer volume replacement - Insert large-bore peripheral IV - still dilated out give lot of fluids; 5-10L if persistently dilated
Provide comfort and emotional support - Medications to relieve itching and applying warm soaks to skin
Maintain surveillance for recurrent reactions - as epi wears off same back to rxns
Prevent and maintain surveillance for complications.
DVTs, bed sores
Nursing interventions
starts coughing and has a stridor
hoarse
short of air and chest tightness, and that their tongue feels big
restless
BP 81/38 HR 120, RR 24, SaO2 90%.
The nurse is caring for a patient who is having a head CT with and without contrast. After receiving the contrast bolus the patient starts coughing and has a stridor, his voice is hoarse when he reports they are short of air and chest tightness, and that their tongue feels big. The pt is restless and is attempting to get from the CT table unassisted. The vital signs are as follows: BP 81/38 HR 120, RR 24, SaO2 90%.
Focus in on
Anaphylactic rxn - usually hypertensive
In anaphylactic shock because of BP - really low
What is happening to this patient?
Vascular tone - too dilated - sudden dilation or decrease SVR
Not progressive
What caused the drop in blood pressure?
Call a code, administer epinephrine, prepare for intubation
Epinephrine to stop the rxn from getting worse so can intubate - both airway
Interventions:
Not seen a lot
Definition:
Causes: Anything that disrupts the sympathetic nervous system: Interrupted impulse transmission or blockage of sympathetic outflow from the vasomotor center in the brain
Most common is Spinal cord injury
Assessment
Management
Neurogenic shock
The loss or suppression of sympathetic tone causing massive peripheral vasodilation, inhibition of the baroreceptor response, and impaired thermoregulation
SCI
Lose Vascular tone - arteries too dilated - SVR way too low
↓ Preload (CVP & POAP)
Too much space and not filled decreases this
↓ Cardiac output (CO); ↓CI
↓ Afterload (SVR)
Inadequate cellular oxygen supply and ineffective tissue perfusion
CNS
Definition:
Hypotension
Cause: vasodilation
Bradycardia
Cause: inhibition of the baroreceptor response
Warm dry skin
Cause: pooling of blood in the extremities and loss of vasomotor control in surface vessels of the skin that control heat loss
Tachypnea
Cause: Compensatory mechanism
Hypothermia
Cause: loss of vasomotor tone in the cutaneous blood vessels that dilate and constrict to maintain body temperature
↓ Peripheral pulses
Cause: SVR low - not have nice bounding pulse - fluids not filling it - extra space with nothing in there
Anxiety
Cause: HR too fast as laying there; not perfusing head; emotions in frontal lobe - goes first
ABG: Resp Alkalosis
Cause: beginning stages; do have increased RR
Flat jugular veins
Cause: no preload
↓ urine output
Cause: no preload; CO - not perfusing
Assessment
Correct the underlying cause - dealing with somebody who had complete transection of SC - wait it out
Administer fluids to fill vascular bed
Vasopressors are used as necessary to maintain blood pressure and organ perfusion
If can give vasopressors - mechanism vasopressors to constrict - may not work and sometimes does but can try
Symptomatic bradycardia: Atropine, epinephrine IV infusion, isoproterenol IV infusion, or temporary pacing
Hypothermia: Warming measures and environmental temperature regulation.
Dilated out - blood next to the dermis
Medical management
Mobilization
Elevate HOB
VTE prophylaxis measures
Implement and assess response to medical management
Nursing Management
BP 81/40, HR 36, RR 28
Anxious
pulses are doppled, JVD flat
The nurse is caring for a patient admitted with multiple fractures including the C4 vertebra fracture. The admission vitals are BP 81/40, HR 36, RR 28, T 96.4 F, SpO2 97%. The patient is anxious, alert and oriented. Resp assessment WDL, CV assessment: S1, S2, pulses are doppled, JVD flat, skin is warm and dry.
Does anything in this assessment pique your interest?
Low BP - not cool clammy skin - dilated out - not last long
Hypotension
Cause: vasodilation
Bradycardia
Cause: inhibition of the baroreceptor response - not enough pressure on baroreceptors kick in
Carotid massages work - extra pressure on baroreceptor to drop BP and HR
Not enough pressure or volume to put pressure this kicks in as comp mechanism on them to drop HR and BP
Warm dry skin
Cause: pooling of blood in the extremities and loss of vasomotor control in surface vessels of the skin that control heat loss
Tachypnea
Cause: Compensatory mechanism
↓ Peripheral pulses
Cause: SVR low - not have nice bounding pulse - fluids not filling it - extra space with nothing in there
Anxiety
Cause: HR too fast as laying there; not perfusing head; emotions in frontal lobe - goes first
Flat jugular veins
Cause: no preload
List the causes of the abnormal assessment.
Neurogenic shock
C4 vertebra fracture
Which shock state is this patient in? What is the key fact that led you to this answer?
Sepsis:
Septic shock:
Infection:
Bacteremia:
Organ dysfunction:
Sepsis - CM
Septic shock
Assessment
Management
Sepsis and septic shock
Life-threatening organ dysfunction related to a dysregulated host response to infection (gram-negative and gram-positive aerobes, anaerobes, fungi, and viruses)
Deadly
Sepsis:
A subset of sepsis in which extreme circulatory, cellular, and etabolic abnormalities significantly increase mortality.
Septic shock differs from sepsis in that the complications are more severe, and the risk of patient mortality is greater.
Have to have sepsis to be in septic shock
Systemic infection and now progressed not perfusing organs
Septic shock:
A pathologic process that results from an invasion of a normal part of the body by pathogenic or potentially pathogenic microorganisms
Infection:
Presence of viable bacteria in the blood
Bacteria in the blood - looking for it when draw blood cultures
Bacteremia:
Abnormality or impairment of normal organ function, with or without direct insult or damage to the organ
Organ dysfunction:
Depends on underlying cause (where primary source, how big bacterial load on system)
General Variables
Inflammatory variables
Tissue perfusion variables
Hemodynamic variables
Organ dysfunction variables
Sepsis - CM
Fever >38° C (100.4° F) or hypothermia <36° C (96.8° F) - either extreme
Tachycardia, heart rate >90 beats/min
Tachypnea
Altered mental status
Significant edema or positive fluid balance
Hyperglycemia (blood glucose >140 mg/dL) in the absence of diabetes
General Variables
Leukocytosis or leukopenia (WBC >12,000/mm3, <4000/mm3)
Have elevated WBC or severely low
Inflammatory variables
Hyperlactatemia (>1 mmol/L)
Decreased capillary refill or mottling
Tissue perfusion variables
Arterial hypotension (SBP <90 mm Hg; MAP <70 mm Hg, or an SBP decrease >40 mm Hg)
SvO2 >70% - higher at the beginning
Vascular tone fine - bacteria/defensive line not letting O2 offload causing high SvO2
Cardiac index > 3.5 L/min
Hemodynamic variables
Arterial hypoxemia (Pao2/Fio2 <300 mm Hg)
Acute oliguria (urine output <0.5 mL/kg/h or 45 mL for at least 2 hr)
Creatinine increase >0.5 mg/dL - not perfusing kidneys
Coagulation abnormalities (INR >1.5 or PTT >60 seconds) - liver not perfused
Ileus - gut not perfused
Thrombocytopenia (platelet count <100,000/m3)
Hyperbilirubinemia (plasma total bilirubin >4 mg/dL or 70 mmol/L) - liver
Organ dysfunction variables
Definition:
Common sources: the respiratory, GU, and GI systems; the skin; and the soft tissues; from anywhere
Patho:
Septic shock
A dysregulated systemic inflammatory and immune response to microbial invasion that produces organ injury
Something wrong and systemic inflammatory response - bacterial - nasty viral/fungal based infections - hard treat fungal infections from blood stream
↓ Preload (CVP & POAP)
↑ Cardiac output (CO) & CI
High to compensate - not getting O2 - circulate more - not working because bacteria preventing to get taken up by the tissues
↓ Afterload (SVR):
Dilated out
↓ LVSWI:
Eventually
Inadequate cellular oxygen supply and ineffective tissue perfusion
Definition:
Microorganism enters the body and stimulates the inflammatory/immune system
anywhere get infection; hospital: VAP progresses, confused pts incontinent - paints bedrail poo and goes to mouth or open wound
Containment failure, Endothelial damage (see lot with this), and coagulation dysfunction
Systemic/metabolic alterations
Apoptosis
Patho:
Diagnostic criteria for Sepsis
Inflammatory variables
Assessment
Fever (> 38oC)
Tachycardia ( > 90 bpm)
Altered mental status
Generalized edema/ +fluid balance
Diagnostic criteria for Sepsis
WBC > 12,000 mcL or < 4,000 mcL
↑ C-reactive protein
ABG: ↓ PaO2, ↓ HCO3,
↑ PaCO 2
Hypotension
Wide pulse pressure
Full, bounding pulse
Pink, warm, flushed skin
decreased respiratory rate
Crackles
Change in sensorium
Decreased urine output
Serum lactate > 2 mmol/L
Anaerobic type respiration to get ATP to generate fuel - gets lactic acidosis
Progresses to MODS
Septic shock people - progress to MODS - someone in MODS - likely have septic shock is high
Inflammatory response - septic shock and so is MODS
MODS - in septic - start with pneumonia - septic shock - then kidneys down because inflammation took them down or other organ sys
Issues with perfusion
Inflammatory variables
Hour 1 Bundle
Broad spectrum abx - when cultures back: abx specific to bacteria; if abx started first - use diff blood containers so know after abx
Intubation and mechanical ventilator: Oxygenation goal PaO2 greater than 70 mm Hg
Cultures: At least two blood cultures plus urine, sputum, and wound cultures should be obtained to find the location of the infection.
Intravascular devices (peripheral IV, PICC, Central venous access, art line) that may be the source of the infection should be removed after the establishment of alternative vascular access
Nutrition: Enteral nutrition
Medical management
Hand culture - want everything cultured - every wound cultured, sputum culture; two sets blood cultures - two diff sites 10 mins aparts
Central line or PICC line - pull it - maintain sterile field and cut tip off and get that sent off to get cultured
Put in PIV after pull central
Measure lactate level
Remeasure lactate if initial lactate is elevated (>2 mmol/L)
Obtain blood cultures BEFORE administering antibiotics
Administer broad-spectrum antibiotics
Begin rapid administration of 30 mL/kg crystalloid for hypotension or lactate level ≥4 mmol/L
Apply vasopressors (Norepinephrine) if hypotensive during or after fluid resuscitation to maintain MAP ≥65 mm Hg
Hour 1 Bundle
Identify pts at risk for developing septic shock
Nosocomial type infection - do everything to prevent them - do not want to cause harm to pt
Prevention - Nursing management
Early identification of sepsis syndrome - identify source and treat
Administer prescribed fluids, medications, and nutrition
Provide comfort and emotional support
Preventing and maintaining surveillance for complications.
Obtain cultures before starting IV antibiotics: two blood cultures plus urine, sputum, and wound cultures
PICC, Central lines, Art line: Remove using sterile technique. With sterile scissors, cut about 2 inches off the tip and put it in a sterile specimen container, and send it to the lab for culture.
Identify bug
Taking everything out and culturing everything
Management - Nursing management
