Multisystem (Burns & shock) Flashcards by Kelsey Klipfel

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

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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:

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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

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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

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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

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Airway and Breathing
Have to have both to have adequate oxygenation and ventilation

What are we assessing? - Oxygenation Alterations

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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

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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

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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

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Deficient fluid volume
Fluid shifts - intracellular to extracelluar

Circulation: - Fluid Resuscitation

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Hypovolemic shock - hypovolemia relative because fluid not where supposed to be

Burn shock - Fluid Resuscitation

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hyperkalemia, hypokalemia, hyponatremia
Leaked out
Electrolytes in fluid that is being leaked out

Electrolyte imbalance: - Fluid Resuscitation

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Very high risk
What is the most common source of infection?
What are some infection control measures?

Risk for Infection

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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?

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Wash hands

What are some infection control measures?

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Causes:
release of potassium from damaged cells
metabolic acidosis
impaired kidney function caused by hemoglobinuria, myoglobinuria, or decreased renal perfusion.

Hyperkalemia:

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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

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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

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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

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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

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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

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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

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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

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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

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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