MS4 exam 2

Chapter 25
 We know heart anatomy, look up a picture if you want to refresh
 Primary pacemaker for myocardium: SA node

 Critical care nursing

o Address urgent, acute and life-threatening situations
o Critical care RN’s work autonomously while using high level critical
thinking and problem solving to assess, intervene, and evaluate pt.
outcome
o Common critical care pt. problems: nutrition, pain, anxiety, delirium,
sensory perception issues, impaired communication, confusion, sleep
problems, caregiver coping (educate/prep them)

 Hemodynamic monitoring
o Measurement of pressure, flow and oxygenation within the CV system
o Asses heart function, fluid balance, and effects of drugs on CO
o Continuous assessment**
o Contractility: strength of ventricular contraction. Positive inotropes (Epi,
NE, dopamine, isoproterenol, dobutamine, calcium, digitalis. Negative
inotropes (alcohol, CCB, BB, acidosis). Increased contractility increases SV
and myocardial o2 requirements
o Stroke volume SV: amount of blood ejected by heart w/ each beat. 60-
130 mL is average
o CO: amount of blood ejected by heart each min, normal 4-6L/min. HR x
SV.

 Cardiac output
o Decreased CO: dehydration, hemorrhage, GI bleed, burns, surgery, shock,
deficit/loss of cardiac function (MI, cardiomyopathy, CHF)
o Determinants: HR is it too fast/slow. Tachycardia shortens filling time
leading to dec volume= dec CO. Bradycardia decreases ejection= dec CO

 General principals
o Preload: L ven end-diastolic pressure. Stretch of the ven myocardium at
end diastole and ven are filled.
o Determined by volume left in the ven at the end of diastole= affects SV
o Pressures are used to evaluate volume at the end of diastole
o AKA: filling pressures, how full is the tank? Is there enough gas to do the
job.
o Pulmonary artery wedge pressure: measurement reflects L ven preload.
Best measurement to determine effectiveness of treatment for pt. with L
ven HF. Normal range 6-12
 o CVP: reflects R ven preload
 Increased preload
o Increased by increasing the return of circulating blood volume to ven
o Hypervolemia treatment: diuretics (lasik/furosemide,
bumex/bumetanide, metolazone/zaroxolyn) and vasodilators nitro
o Will improve CO

 Decreased preload
o Decreased by a reduction in the volume of blood returning to the ven
o Treat of hypovolemia: volume expanders (NS, LR (crystalloids) albumin,
hetastarch), if Hgb. Low provide PRBC (colloids)

 Afterload
o Resistance the blood in the ven must overcome to force the valves open
and eject contents to circulation. How hard the chambers of the heart
have to push to get blood out
o SVR: reflect L ven afterload, normal 800-1200 dynes/sec/cm-5. (more
direct measurement)
o PVR: reflects R afterload, normal <250 dynes/sec/cm-5
o Determined by: vascular resistance/pressure in the pipes are they dilated
or constricted, aortic compliance, inability of the heart muscle to contract,
thickness/viscosity of blood, hypoxemia causes vasoconstriction

SVR: systemic vascular resistance: reflects left sided afterload

More accurate measurement of afterload
Elevated: Hypertension, Vasopressor use, Aortic stenosis, Hypothermia
Decreased: Septic, anaphylactic, neurogenic shock, Vasodilators and hypovolemia,
Medication side effects

PVR: pulmonary vascular resistance: reflects right-sided afterload

Elevated: Pulmonary HTN, Hypoxia, PE, Pulmonary stenosis
Decreased: Vasodilator use and hypovolemia

Afterload
Elevated: MI, cardiomyopathy, polycythemia increased blood viscosity
Decreased: decreased volume, end stage cirrhosis, vascular resistance and
hypoxemia

 Treatment of increased afterload

o Vasodilators: nitroprusside, nitro, hydralazine
o ACE inhibitors: captopril, enalapril, enalaprilat. Dilate arteries/veins by
blocking ANG formation, promotes NA/water excretion
o CCB: diltazem, nifedipine, nicardipine. Blocks Ca, cause muscle
relaxation/dilation
 Treatment of decreased afterload
o Vasopressors/constrictors: dopamine, NE, epi, phenylephrine
o Caution w/ vasocon: they increase SVR, which will increase work of
heart and dec peripheral perfusion

 MAP
o Perfusion pressure seen by organs in the body
o MAP greater than 65 mmHg is enough to sustain organs of the average
person under most conditions
o If MAP falls significantly below this number for enough time, blood will
not perfuse organs and they will become ischemic. High MAP indicates
increased CO
o Normal: 70-105. SBP +2(DBP)/3
o Regulated by CO and SVR

 Invasive pressure monitoring

o CVP line: measure R ven preload obtained from PA cath using one of the
proximal lumina or central venous cath placed in jugular or subclavian
vein. High CVP shows R ven failure or volume overload, low CVP shows
hypovolemia
o PA catheter
o Art line
o Minimally invasive CO monitoring devices: Edwards life-sciences Vigileo

 CVP and PAWP

o CVP: assess R ven preload or R ven end-diastolic pressure. Measured in R
atrium or in vena cava close to heart at end of diastole
o Reflects fluid volume status. Low= hypovolemia, high= R ven failure or
volume overload
o PAWP: L ven failure, used to assess L ven function and pressures
generated by L ven. Measurement of pulmonary capillary pressure

 CV pressure monitoring systems complications

o Pneumo/hemo, air embolism, laceration of major vessels, catheter
malabsorption leading to dysrhythmia, thrombus formation occurring at
tip of catheter
o NSG management: record CVP hourly or more often to trend data. Daily
assess need for line to reduce blood stream infections
 • Illustrated catheter has five lumina.
When properly positioned, the
distal lumen exit port is in the PA
and the proximal lumen ports are in
the right atrium and right ventricle.
• The distal and one of the proximal
ports are used to measure PA and
central venous pressures,
respectively. A balloon surrounds
the catheter near the distal end. The
balloon inflation valve is used to
inflate the balloon with air to allow
reading of the pulmonary artery
wedge pressure. A thermistor
located near the distal tip senses PA
temperature and is used to measure
thermodilution cardiac output
when solution cooler than body
temperature is injected into a
proximal port.

 Function of PA catheter
o Allows for continuous bedside monitoring and assessment of: vascular
tone, myocardial contractility, fluid balance.
o Measures pulmonary artery pressure, CVP, and hemodynamic calculated
values

 Indications for PA catheter

o Pulmonary artery catheter is indicated in pt. whose cardiopulmonary
pressures, flows and circulating volume require precise, intensive
management. Any decreased CO
o MI, cardiogenic shock, CHF, shock all types, valvular dysfunction, pre-op,
intra-op and post-op monitoring, ARDS, burns, trauma and renal failure
 Balloon if inflated once
inside R atrium

Watch continuously as PA
cath is inserted

Once PAWP waveform is

observed, placement is
correct and balloon may
be deflated

o Perform cardiac XR to confirm placement

 Wedging
o When the distal balloon is inflated the catheter is wedged in a small
pulmonary capillary stopping forward flow
o The opening at the distal tip (see insert) looks forward through thr
pulmonary circulation and the pulmonary veins and into the L atrium
o If the mitral valve is normal, L ven end diastolic pressures can be obtained

 PAWP pressure safety points

o Watch monitor during inflation and stop when you see PAWP waveform
o Never inject more than 1.5mL of air or any fluid into PA port
o Don’t keep balloon inflated longer than 15 seconds or 4 respiratory cycles
o When completes, allow air to passively exit balloon

 Intra-arterial pressure monitoring

o A-line or art line, arterial line
o Indications: acute HTN/hypoT, respiratory failure, shock, frequent ABGs,
coronary interventional procedures, ARDS, renal failure and burns
o Perform Allen test to assess patency of radial/ulnar arteries
 o Asses site distal to arterial line hourly: assess if limb is cool, pale, cap
refill >3 seconds, neurological impairment

 Arterial pressure monitoring

o Complications: hemorrhage, infection, thrombus, neuro impairment, loss
of limb is impairment is not identified/treated, dysrhythmias

 Arterial line alarms

o High pressure alarms: may indicate occlusion (thrombus), assess pt. hand
for pallor, pulses, cap refill. Call provider is s/s evident, check for
kinking/occlusion in tube
o Low pressure alarm: assess pt. BP, hypotension may be caused by cardiac
dysrhythmia. Check for disconnection in tubing, risk for hemorrhage

 Pressure line tubing set

o Continuous flush irrigation system
o Delivers 3-6mL of NS per hour, document in pt. hourly intake
o Maintain line patency, limit thrombus formation

 Principals of invasive pressure monitoring

o Equipment must be referenced and zero balanced to environment and
dynamic response characteristics optimized
o Referencing: position transducer so zero reference point is at the leel of
atria of heart or phlebostatic axis = 4th intercostal space at mid-axillary
point

Mark this location with a

marker on the pt. skin

Leveling procedure: the air

fluid interface on the
pressure monitoring
system is at the level of the
stopcock closest to the
transducer

 Zero the system

o Zeroing: confirms that when pressure within system is zero, monitor
reads zero
o Done after transducer is leveled
 o Done with initial setup, beginning of shift, and when values don’t fit
clinical picture
o Always follow manufacture’s guidelines
o Procedure: to zero the system the stopcock is turned off to the pt. and
open to air by removing the stopcock cap. The nurse then activates the
zero button on the monitor

 NSG management
o Obtain baseline data
o Thorough assessment, general appearance
o LOC, skin color/temp
o VS, peripheral pulses, UO
o Monitor trends and evaluate whole clinical picture
o Ensure post-procedure chest XR is obtained
o Inspect for bleeding at site
o Tissue ischemia
o Neurov injury, assess
o S/s of infection
o Dampened waveform may indicate thrombus on catheter (occluded
catheter)
o Check connections in tubing
o Sterile non-vented caps only
o Pressure bag is at 300 mmHg
o Adequate fluid volume in system and bag
o Keep alarms on at all times
o Change tubing/flush system per policy
o Use only 0.9% saline for pressure tubing fluid
 Additional critical care concepts
o Rothman index: software tool for mapping a pt. overall health over time.
Generates “health score” based on factors such as VS, labs, nursing
assessments and lab results
o Circulatory assist devices: intra-aortic balloon pump, LVAD, RVAD<
BVAD, impella
o ECMO

 Rothman
o Need cardiac assessment and temp (may sub respiratory assessment) to
calculate RI
o Discharge without concern: RI over 65
o Continuing monitoring: RI 40-65
o Transport to ICU or higher level of care such as rapid: RI below 40
o How often to assess RI: at bedside handoff, throughout shift w/ each
assessment, always at the end of shift w/ handoff
 Circulatory assist devices
o Decrease cardiac work and improve organ perfusion when drug therapy
fails
o Provide interim support when L/R or both ven require support while
recovering from injury (MI)
o Decrease ven workload and increase myocardial perfusion
o Examples: intraaortic balloon pump, ventricular assist device
IABP machine
Provides temporary
circulatory assistance
Benefit: dec ven
workload, inc
myocardial perfusion,
augment circulation

Improved coronary
blood flow, inc. CO.
Improved perfusion to
organs

 IABP: NSG management

o Use aseptic technique for insertion and dressing changes, monitor for s/s
of infection
o Monitor hourly: UO, pulses, LOC
o Check circulation, sensation, movement in both legs at least every hour
o Complications: vascular injury, thrombus, embolism, thrombocytopenia,
peripheral nerve damage, ischemia to periphery/kidneys/bowels,
infection

 VADs
o Short/long term
o Allows for more mobility than IABP
o Insertion into path of flowing blood to augment or replace action of ven
o Internal/external
o L/R or bi
o Typical VAD shunts blood from L atrium or ven to the device and then to
aorta
 Indications for use: failure to
wean from bypass, failure
after MI, bridge-awaiting
transplant

Cannula sites depend on

type of device used

 NSG Management
o Similar to care for pt. w/ IABP
o Frequent assessment, observe for complications
o Pt. may be mobile and require activity plan
o Observe pt. for bleeding, cardiac tamp, ven failure and thromboembolism
o In-depth teaching if discharged to home, pt. must have a competent
caregiver present at all times
o Goals: recovery through ven improvement, heart transplant, artificial
heart implantation
o Many pt. will die or choose to terminate device-causing death.
Psychological support to pt. and family

 Extracorporeal membrane oxygenation

Used w/ covid pts.

Chapter 14
 Burns injuries
o 486,000 require medical attention yearly
o Most occur in homes, young children and elderly highest risk
o Nurses must educate on prevention
o Very expensive and complicated injury
 Gero considerations
o Normal aging puts pt. at risk for burns due to age related changes
o Unsteady gait, limited eyesight, diminished hearing, thinning/less
elasticity in skin, delayed wound healing, longer rehab, pneumonia often
results
o Dermal layer thins, loss of elastic fibers, reduced subcu tissue, decreased
vascularity
o Poor healing, more severe injuries, often have other comorbidities

 Classification of burns
o Severity of injury is determined by: depth of burn, TBSA, presence of
inhalation injury, location of burn, risks including age/comorbid
conditions
o 40% TBSA burns are high risk for morbidity and mortality

 Types
o Thermal: Caused by flame, hot liquid, scald, steam or contact with hot
objects. Most common. Severity depends on burning agent and duration
of contact time

o Chemical: Contact w/ acids, alkalis, or organic compounds. Alkalis are

hard to manage, causes protein hydrolysis and liquefaction. Turns into
liquid deepening burns. Damages continue until neutralized. Chemical
should be quickly removed from skin, clothing removed. Tissue
destruction may continue for 72h. Common acids: household cleaners.
Alkalis: oven/drain cleaners, fertilizers, heavy industrial cleaners.
Organic compounds: phenols (chemical disinfectant) petroleum (gas and
creosote), produce burns and systemic toxicity.

o Electrical: deceiving, not able to follow its path. Severity of injury

difficult to assess due to “iceberg” effect. May cause muscle spasms strong
enough to break long bones, or may fall and then break bones. Pt. at risk
for: dysrhythmia (may be immediate or within 24h) cardiac arrest,
metabolic acidosis, myoglobinuria. Monitor EKG, c-sine maintenance

o Radiation: risk due to terrorism, depends on dose

o Smoke inhalation may occur w/ exposure to flames. Inhalation of hot

air/noxious chemicals, damage to respiratory tract. Upper airway injury,
will see: facial burns, singed nasal hair, hoarseness, painful swallowing,
darkened oral/nasal membranes, carbonaceous sputum (black), hx of
being burned in enclosed space, clothing burns around chest/neck.
Airway edema
 o CO poisoning. Inhaled CO displaced oxygen, resulting in hypoxia.
Hypoxia/death at CO levels 20%+. Treat w/ 100% humidified oxygen.

 Classification of burns according to depth of tissue destruction

o 1st degree: superficial. Involves outermost layer of skin, sunburn
o 2nd degree: partial thickness. Involves entire epidermis and varying
portions of dermis. Painful w/ blisters
o 3rd degree: full thickness. Total destruction of epidermis, dermis and
underlying tissue. Lack of sensation, may involve connective tissue and
muscle. Leathery appearance
o 4th degree: full thickness. Extends into deep tissue, muscle or bone.
Charred appearance, no sensation (thick about what a dead burned body
looks like)

 Rule of nines
o Most common method for adults
o Based on anatomic regions
o Each area representing approx. 9% of the TBSA

o If ½ of 1 arm were burned (aka

anterior or posterior) TBSA is
4.5%

 Patho of burn injury: CV system

o Dysrhythmia and hypovolemic shock
o Impaired circulation to extremities
o Tissue ischemia: paraesthesia, tingling, poor circulation, necrosis
 o W/ burn injury, immediate decrease in CO that precedes loss of plasma
volume
o Vaso-constrictive compensatory mechanism to loss of plasma volume.
Workload of the heart/o2 demand increases. Hypovolemia is the
immediate consequence of the plasma volume loss and results in
decreased perfusion and oxygen delivery. As fluid loss continues due to
capillary leakage, and vascular volume decreases, cardiac output
continues to decrease and the blood pressure drops. This is the onset of
burn shock. Burn shock is initially a type of hypovolemic shock. The
systemic inflammation causes the release of free oxygen radicals that
increase capillary permeability, causing increased plasma loss and
subsequent peripheral edema. As a compensatory response to
intravascular fluid loss, the SNS releases catecholamines, resulting in an
increase in peripheral resistance (vasoconstriction) and an increase in
pulse rate that further decreases tissue perfusion.
o Circulation to extremities can be severely impaired by deep
circumferential burns and subsequent edema

 Patho: F/E shifts

o More fluid shifting out of the vascular space into interstitial spaces
o Edema increase causing pressure on the small blood vessels in distal
extremities. Obstructing blood flow and causing tissue ischemia
o As the capillary walls become more permeable, water, sodium, and later
plasma proteins (especially albumin) move into interstitial spaces and
other surrounding tissue. The colloidal osmotic pressure decreases with
progressive loss of protein from the vascular space. This results in more
fluid shifting out of the vascular space into the interstitial spaces. (Fluid
accumulation in the interstitium is termed second spacing.)
o Fluid also moves to areas that normally have minimal to no fluid, a
phenomenon termed third spacing. Examples of third spacing in burn
injury are exudate and blister formation, as well as edema in non burned
areas.
o Hyperkalemia at first due to cell destruction. K moves out of cells into
vascular space
o Hypokalemia occurs later after fluid resuscitation and K moves back into
cells
o Hyponatremia: Na rapidly moves into interstitial spaces and remains
until edema formation ceases. Na levels vary in response to fluid
resuscitation
o RBCs are hemolyzed by a circulating factor released at time of burns
o Elevated hematocrit, due to hemoconcentration
o The circulatory status is also affected by hemolysis of RBCs from
circulating factors (e.g., oxygen free radicals) released at the time of the
burn, as well as by the direct insult of the burn injury.
 o Thrombosis in the capillaries of burned tissue causes an additional loss of
circulating RBCs.
o An elevated hematocrit is commonly caused by hemoconcentration
resulting from fluid loss. After fluid balance has been restored, dilution
causes the hematocrit levels to drop. Hemoconcentration leads to a
thickening of the blood, which can contribute to renal damage, lead to
clots, and stroke.

 Parkland formula to determine IVF needs

o Prevent shock
o Guideline for initial IVF rate and requires continuous monitoring of status
o Colloid sol like albumin is given after 12-24h
o Based on pt. body weight and TBSA
o UO is most commonly used parameter for assessment of adequacy
o EX: Parkland Formula for Adults: (day 1)
Total during 1st 24 hours from time of injury:
  4mL x kg x TBSA burn
First half given in the 1st 8 hours
Second half given in the next 16 hours
EXAMPLE: pt weight: 70 kg; TBSA: 60%
4mL x 70 kg x 60% TBSA
16,800ml for the 1st 24 hours
8,400ml in the 1st 8 hours
Rate: 8400mL/8 hrs=1,050ml/hr
The next 16 hours
  Rate: 8400mL/16hrs = 525 mL/hr

 Kidney
o Decrease blood flow
o Myoglobin (from muscles) and hgb. From damaged RBCs travel to
kidneys= red urine
o Acute tubular necrosis (ATN). Eventual acute kidney injury

 GI assessment
o N/V, distention, paralytic ileus, decreased BS
o Decreased blood flow and sympathetic stimulating during early phase
causes reduced GI motility and promotes dev of paralytic ileus
o Place NGT
o Curling’s ulcer: stress ulcer, erosion of duodenal mucosa from
regurgitation and increased secretion of gastric acid. Blood in the stool,
coffee ground emesis, frank blood

 Skin changes
 o Anatomic changes: skin may regrow as along as part of the dermis is
present
o Functional changes: high risk for infection
o Temp: skin tissue necessary to maintain normal temp. Loss of
thermoregulation

 Phases of burn injury

o Emergent or resuscitative phase: onset of injury to completion of fluid res
o Acute/intermediate stage: from beginning of diuresis to wound closure
o Rehab: from wound closure to return to optimal physical and
psychosocial adjustment

 Emergent phase
o Primary survey, establish airway, supply 02
o F/E shifts, risk is hypovolemic shock
o RBCs are hemolyzed
o Thrombosis, elevated Hct. Due to hemo-concentration
o On scene care: safety #1, prevent injury to rescuer
o Stop injury, extinguish flames, cool burn, irrigate, chemical burns
o Primary survey: ABCDE, airway, breathing, circulation. VS, Start
humidified oxygen and large bore IVs. Remove restrictive clothing, cover
wounds
o Secondary survey: all body systems and obtain history of incident and
pertinent history. Monitor for fluid volume deficit
o Assess extent of burn, observe for erythema, blistering of lips, buccal
mucosa and singed nasal hair
o Burns on face, neck and chest, hoarseness, respiratory secretions,
monitor ABGs, pulse ox and prep to intubate
o Goals (48-72h in this stage)
1. Secure airway 2. Support circulation (fluid replacement) 3. Prevent
infection (careful wound care) 4. Maintain body temp (hypothermia may
cause shivering and inc 02 demand and vasoconstriction leading to tissue
ischemia and necrosis) 5. Provide emotional support and assess anxiety

 Acute/intermediate phase
o Continue assessment and maintain respiratory and circulatory support.
F/E balance, GI and renal function
o Prevent infection, burn wound care (wound cleaning, debridement,
topical AB, dressings, wound grafting) pain management
o Early positioning/mobility
o Nutritional support
o 12-14 days long
o Restore fluid balance, monitor DW, UO, I/O
o Prevent infection
 o Modulate hyper metabolism: body in overdrive, increased demands, high
calorie, high protein diet

 Complications r/t burn injury

o Acute respiratory failure (ARF)
o Acute respiratory distress syndrome (ARDS)
o Heart failure and pulmonary edema
o Sepsi
 Rehab phase
o Begins w/ wound closure, ends w/ pt. return to highest possible level of
functioning
o Emphasis on psychosocial adjustment, prevention of scars and
contractures, resumption of preborn activity
o Psychosocial counseling
o This phase may last years or even a lifetime if pt. needs to adjust to
permanent limitations

 Burn wound care

o Wound cleaning
o Remove loose dead tissue prior to cleansing
o Gently w/ mild soap/water. Give pain meds prior
o Use topical agents. Antimicrobial, silvadene
o Debridement: remove necrotic tissue that contains bacterial or foreign
bodies
o Natural D: spontaneous
o Mechanical D: use of surgical tools to remove eschar
o Surgical D: surgical excision of devitalized tissue done before natural
separation of eschar occurs
o Chemical: topical agents used to promote removal of eschar
A.
Escharotomy
For full
thickness
B.
Fasciotomy
Incision is
deeper, into
fascia to
relieve
constriction

 Surgical management
o Surgical excision, wound covering, skin graft
o Autograft is from self. Allograft is from donor
 Typical graft donation site
At risk for infection and
rejection

 Pain management
o Burn pain has been described as one of the most severe forms of pain
o Pain accompanies care and treatments such as a wound cleaning and
dressing changes
o Types of burn pain: background or resting (inactive pt.), procedural (OT,
PT, procedures) breakthrough (usually w/ activity, episodic and intense)
o With 4th degree there is no pain, when healing areas around burn have
pain

 Pain meds
o Analgesics: IV route due to abnormal absorption of muscles in stomach
o Morphine, hydromorphone (dilaudid), fentanyl
o Ice not used, decreases blood flow
o RN interventions: continually assess pain, use in combo w/ non-pharm
methods
Nutrition
o Consult dietician
o Large burn areas may require
5000+ kcal/day
o High calorie, high protein intake
o NGT
o TPN if GI tract is not functioning.
Last resort due to inc. risk for
infection
o Let them each WHATEVER they
want, encourage family to bring
food

 Scar treatment/prevention
o Pressure garments used to prevent hypertrophic scarring and
contractures
o Scars will be present but not as severe, may be used up to 1y after injury
 o Elastic bandages used initially to promote circulation
o Hypertrophic scars form within initial wound injury and push outward
around wound
o Keloid scars extend beyond the margins of original wound
o Early ambulation is needed to promote respiratory function and promote
mobility. Even BEFORE extubation

 Prevent contractures
o Maintain neutral body position
o Use splints to maintain position of hands, elbows, knees and neck
o Perform ROM 3x daily minimum, ambulate as early as possible after fluid
shifts resolve
o Compression dressings used after graft heals

 Positioning
Home care
o Psychological support
o Skin/wound care
o Exercise and activity
o Nutrition
o Pain management
o Support for all above

Chapter 62
 Shock
o Life threatening condition w/ dec tissue perfusion and impaired cellular
metabolism
o Leads to poor gas/nutrient exchange
o Demand for o2/nutrients exceeds supply
o Affects all body systems
o May develop slow or rapid, pt. with any disease state may be at risk for
developing shock
o Hypoperfusion of tissue causes: dec o2/nutrients (energy)
o Hypermetabolism: cell membranes become permeable, allows fluid and
electrolyte shifts, cells swell
o Activation of inflammatory response

 Cellular effects of shock

 o Cell swells and membranes become more permeable, allowing
electrolytes and fluids to seep out of and into the cells
o Na/K pump becomes impaired, cell structures, primarily the
mitochondria are damaged. Cell death occurs

 Shock stages
o Stage 1: compensatory
o Stage 2: progressive
o Stage 3: irreversible
o Aggressive therapy should begin w/in 6h, especially in septic shock

 Compensatory/stage 1
o SNS causes vaso-con, increased heart contractility
o This maintains BP/CO
o Fight or flight response
o Catecholamines, hormone and/or NT release
o Body shunts blood from skin, kidneys, GI tract to brain, heart, lungs to
ensure vital organ blood supply
o S/S: cool/clammy skin, low OU, dec BS, normal BP, increased HR/PR,
confusion, agitation
o Will see lactic acid accumulation

 Progressive/stage 2
o Mechanisms that regulate BP can no longer compensate
o Decreased BP/MAP
o ALL organs suffer from hypoperfusion
o Vaso-con continues, further compromising cellular perfusion
o Mental status continues to deteriorate from dec cerebral perfusion,
hypoxia, results in lethargy
o Lungs begin to fail, dec pulmonary blood flow causes further hypoxia,
CO2 levels inc, alveoli collapse, leaking pulmonary capillaries (pulmonary
edema)
o Inadequate perfusion of the heart: dysrhythmias, ischemia
o When MAP falls below 70 GFR cant be maintains: results in AKI and dec
OU
o Liver function: dec blood flow, build up of meds/waste products such as
ammonia and lactic acid
o GI function: ischemia, ulcer formation, inability to process nutrients
o Hematologic function: inflammatory response, deposits of micro-thrombi
and consumption of clotting factors
o DIC may occur as cause/complication of shock
o S/S: dec BP/MAP, HR >150, crackles, rapid/shallow respirations,
mottled/petechiae on skin
 Irreversible/stage 3
o Organ damage is so severe that pt. doesn’t respond to treatment and cant
survive
o BP low, renal/liver functions fail, anaerobic metabolism worsens acidosis,
multiple organ dysfunction progresses to complete organ failure
o S/S: HR irregular, resp/circulatory requires mechanical vent, skin is
jaundiced, OU anuric, need dialysis
o NSG management: monitor pt., prevent complications, provide comfort,
prevent injury, support, update family

 Shock in older pt.

o Older adults can recover from shock if detected/treated appropriately
o Meds such as BB used to treat HTN may mask tachycardia a primary
compensatory mechanism to inc CO during hypovolemic states
o Aging immune system may not mount a true febrile state (+101) lack of
febrile response or inc. trend in temp should be addressed. Pt. may report
fatigue
o Heart doesn’t function well in hypoxemic state, aging heart may respond
to dec in myocardial oxygenation w/ dysrhythmias that may be
misinterpreted as normal part of aging
o Progressive decline in resp muscle strength, max ventilation, response to
hypoxia. Older pt. may have dec resp reserve and decompensate quickly
o Changes in mentation may be misinterpreted as dementia. Sudden change
in mentation should be aggressively assessed for acute delirium and
treated for presence of infection and organ hypoperfusion

 Classifications
o Hypovolemic, cardiogenic, obstructive, distributive (neurogenic, septic,
anaphylactic)

 Lab studies
o H/H: dec w/ fluid resuscitation. May inc w/
hypovolemia/hemoconcentration
o BUN/CR: inc d/t renal hypoperfusion
o Glc: inc early in shock due to release of glycogen by liver. Dec as shock
progresses
o Serum electrolytes Na/K: Na inc in early shock, K dec in early shock
o Lactic acid: builds up later on, metabolic acidosis
o ABGs: resp alkalosis hyperventilation early shock. Metabolic acidosis
later in shock when lactic acid accumulates in blood

 Hypovolemic shock
o Most common
 o S/S: AMS, restless, disoriented, hypotension, low BP, cool and clammy
skin, dyspnea, tachy, obvious bleeding, dec OU
o Inadequate fluid volume in intravascular space
o Volume loss may be absolute (external) or relative (internal)
o Physiologic response is similar in both External: fluid loss
Trauma, surgery, vomit,
diarrhea, diuresis, DI

Internal: fluid shift

Hemorrhage, burns, ascites,
peritonitis, dehydration

 Hypovolemic shock management

o Stop loss, fluid/blood replacement, pharm therapy w/ vaso-con drugs if
NO response to IVF
o Administer blood fluids safely, redistribute fluid w/ modified
trendelenburg w/ FOB elevated
o Recognize complications and report ASAP

 Hypovolemic shock IVF

o Insert 2 large bore IVs
o Crystalloids NS/LR
o 3:1 rule, 3 mL of solution for each mL of blood lost
o Caution in use of LR, liver failure therefore cant convert lactate iron to
bicarb
o Colloids: blood products, albumin used if primary cause if hemorrhage
and pt. not responding to crystalloids. Most common colloid solution used
for hypovolemic shock is 5% albumin

o Evaluation: best indicator to evaluate effectiveness of fluid resuscitation:

inc in UO 0.5mL/kg/hr or >30mL/hr
o Labs: evaluate renal status, BUN/CR, CR is better indicator
o Monitor skin, mental status

 Cardiogenic shock
o Systolic or diastolic dysfunction of the pumping action of the heart results
in dec CO
o Impaired tissue perfusion and cellular metabolism
 o Causes: systolic dysfunction is
the hearts inability to pump
blood forward
o Affects L ven: MI,
cardiomyopathy, bunt cardiac
injury, severe
systemic/pulmonary HTN,
myocardial depression from
metabolic problems
o Dysrhythmias: brady and tachy
o Diastolic dysfunction: inability
of heart to fill during diastole
(impaired filling)
o Pericardial tamponade,
ventricular hypertrophy,
cardiomyopathy, dysrhythmia,
structural (stenosis,
regurgitation, septal rupture,
tension pneumo)

o Will see low CO an cardiac index

S/S: chest pain, tachy, hypotension,

dysrhythmias, fatigue, feeling of doom,
tachypnea, pulmonary congestion, crackles,
dyspnea, pallor, cool/clammy skin,
prolonged cap refill time, weak pulses,
 Cardiogenic shock care
anxiety, confusion, agitation, dec renal
perfusion results in dec UOP o First line: o2, pain
control
o IVF cautiously, flash pulmonary edema may result w/ rapid fluid bolus
 o Restore blood flow to the myocardium by restoring balance between o2
supply and demand (use thrombolytic therapy, angioplasty w/ stenting,
emergency revascularization, valve replacement)
o Drug therapy: vasoactive agents
1. Vasodilators reduce preload and afterload. Exp. Nitroprusside/nipride,
NTG.
2. Inotropes improve contractility, strengthens the heart muscle, and
increases SV/CO. Exp. Dopamine, dobutamine
3. Diuretics to reduce fluid accumulation. Exp. Lasix
4. Nitrates dilate coronary arteries and increase blood flow. Exp.
NTG/nitro

 Evaluation of cardiogenic shock

o Did CO improves?
o Skin should be warm and pink
o Resp should be clear, no crackles, normal RR and sats and decreased
pulmonary edema
o Urinary output increased
o Neuro: alert, oriented and decreased confusion

 Distributive, neurogenic
o Results from disruption of the SNS control of vessel tone
o Vasodilation and misdistribution of blood volume and blood flow,
decreased intravascular tone
Acute spinal cord injury causes
o Categories: neurogenic, septic, anaphylactic
1. Loss of sympathetic
innervation below level of injury.
Will see vasodilation-
hypotension, warm/dry skin, loss
of urinary bladder tone, paralytic
ileus, loss of perspiration, loss of
cutaneous/deep tendon reflexes
Or
2. Parasympathetic innervation
continues unopposed. Will see
bradycardia

Vasodilation: dec BP, inc HR

1. Manifestations of neurogenic shock: hypotension, bradycardia, temp

dysregulation (heat loss, risk for hypothermia), dry skin, initially warm,
 poikilothermia (take on temp of environment)

o Drug therapy: vasopressors to treat hypotension (phenylephrine, NE,

vasopressin)
o Need a central venous line for vasoactive meds, monitor IV site for tissue
sloughing. Atropine for bradycardia
o Caution in IVF because this isn’t a fluid volume loss issue

 Evaluation
o Monitor temp, HR, BP (might go dec)
o Give supplemental o2, monitor and prepare for possible intubation and
mechanically vent if necessary

 Distributive, anaphylactic
o Acute, life threatening hypersensitivity reaction
o Profound hypersensitivity w/ systemic antigen-antibody response
o Massive vasodilation, release of mediators causing increased
inflammation in response to antigen, inc capillary permeability
o EPI is used first before IVF, causes peripheral vasoconstriction and
bronchodilation and blocks the effects of histamine. Also give
antihistamine Benadryl
o Care: Epi, bendryl, maintain patent airway (nebulized bronchodilators,
aerosolized epi, endotracheal intubation may be necessary)
o Bronchoconstriction and laryngeal edema occurs due to release of
chemical mediators.
o Maintain patent airway, monitor oxygenation, monitor response to IVF
(vitals, skin, OU)
o S/S: anxiety, confusion, dizziness, impending doom, chest pain,
incontinence, sudden onset of symptoms, swelling of lips/tongue,
angioedema, wheezing, stridor, flushing, pruritus, urticarial, resp distress
 \

 Distributive, septic shock

o Sepsis: systemic inflammatory response to documented or suspected
infection
o Severe sepsis: sepsis and organ dysfunction
o Presence of sepsis w/ hypotension despite fluid resuscitation. Presence of
tissue perfusion abnormalities hypoxia seen
o Main organism that cause sepsis are gram-/gram+ bacteria
o ***Septic shock has 3 major pathophysiologic effects: vasodilation,
maldistribution of blood flow and myocardial depression (dec EF,
ventricular dilation)
o S/S: inc coagulation and inflammation, dec fibrinolysis, formation of
micro-thombi, obstruction of microvasculature. Hyper-dynamic state, CO
may inc as body tries to correct dec tissue oxygenation. Tachypnea,
hyperventilation, temp dysregulation, dec UO, altered neuro status, GI
dysfunction (risk for GI bleed and paralytic ileus), resp failure is common
87% of pt. 40% develop ARDS. Often are intubated and vented
 o The body’s response to this organism is exaggerated

 Collaborative care for septic shock

o Fluid replacement to restore perfusion, hemodynamic monitoring w/ A-
line
o Vasopressor drug therapy
o IVF first
o Drugs: NE (levophed) 1st drug of choice, dopamine, vasopressin added is
no response to others, don’t titrate
o Goal: restore CO, monitor MAP >65 and OU >30 mL/hr
o Antibiotics after cultures obtained (exp. Blood, wound exudate, urine,
stool, sputum) Give within 1st hour if sepsis is suspected
o Broad spectrum AB given first, more specific AB given based on MO

 Obstructive shock
o Develops when physical obstruction to blood flow occurs, decreased CO
o Exp: hemothorax, pneumo, toamponade
o Prevents adequate circulating volume, from restriction to diastolic filling
of the R ven due to compression. Abdominal compartment syndrome
 o Rapid assessment and immediate treatment are important
Goal: remove obstruction ASAP
For cardiac tamponade:
pericardiocentesis to remove
accumulated fluid around the heart

 Collaborative care
o Successful management
o Interventions to control or eliminate the cause of dec perfusion
o Protection of target and distal organs from dysfunction
o Provision of multisystem supportive care
o ABCs, maintain airway and apply 02
o Monitor vitals
o Nutrition is vital to dec morbidity from shock
o Energy requirements are inc. pt. may need 3000 c/day
o Initiate TPN if eternal feedings contraindicated or fail to meet 80%of
daily caloric requirements
o Monitor protein, BUN, glucose and electrolytes

 Vasoactive meds
o Used when fluid therapy alone doesn’t maintain MAP
o Support hemodynamic status, stimulate SNS
o Check VS Q15min
o Give through central line if possible, extravasation may cause extensive
tissue damage
o Dosage usually titrated to pt. response

 Evaluation
o Normal or baseline ECG, BP, CVP and PAWP
o Normal temp, warm dry skin
o UO >0.5 mL/kg/hr, or >30mL/hr
o Normal RR and Sa02 >90%
o Verbalization of fears and anxiety

 SIRS
 o Systemic inflammatory response syndrome. Response to sepsis, MI,
trauma
o S/S: temp 101+ or less than 96.8, WBC >12,000 cell/mm
 MODS
o Multiple organ dysfunction syndrome, failure of 2+ organ systems
o Homeostasis cant be maintained without intervention
o Results from SIRS
o Uncontrolled inflammation, cell damage, inc. vascular permeability,
release of cell mediators, inc WBC, inc coagulation, dec BP, dec perfusion,
clots

 Collaborative care
o Prognosis for MODS is poor
o Goal: prevent progression of SIRS to MODS
o Vigilant assessment, ongoing monitoring to detect early signs of
deterioration or organ dysfunction
o MODS mortality rate is 70-80% when 3+ organ systems fail
o MODs care: provide info and support for family, prevent/treat infection,
maintain tissue oxygenation, nutritional/metabolic support, appropriate
support of individual failing organs
o Support failing organs: 02, vents, dialysis, IVF, blood
o Prevent/treat infection w/ aggressive control strategies: strict asepsis,
assess need for invasive lines
o Once an infection is suspected, institute interventions to control source
o Proper PPE and isolation precautions needed
o Nutritional/metabolic needs: use of enteral route is preferred to PN
promote GI motility
o Initiate PPI, to dec gastric ulcer formation
Nurses are often first to identify
change in pt. status
Onging communication is
necessary