CMS exam 1

testing on: concept, patient SE, treatment. all select-alls have at least 2 answers. often all 5.

pH

normal for humans: 7.35-7.45

acidosis: many H ions, <7,35

alkalosis: few H ions, >7.45

acid: compound that allows H ions to break free (low pH)

base: compound that binds w H ions (high pH)

• lungs control CO2 (acid potential). kidneys control bicarb by reabsorbing or not (alkalotic potential)

buffer systems

chemical buffer system keeps pH constant

phosphate buffer system

protein buffer system

chemical buffer system

carbonic acid - bicarbonate buffer system

carbonic acid (acid) - H2CO3 (CO2 + H2O).

bicarbonate (base) - HCO3

• increases w CO2. eating many carbs. high metabolic action (like fever)

resp control (CO2 changes)

• changes quickly, seconds-minutes

• if acidic (many H), resp rate and depth increase to release CO2

• if alkaline (few H), RR and depth decrease to hold onto CO2

renal control (metabolic HCO3 changes)

• slower

• if acidic, H+ excreted in urine

• if alkaline, HCO3 excreted in urine

if resp broken, renal compensates and vise versa

acid base disturbances

resp acidosis, metabolic acidosis, resp alkalosis, metabolic alkalosis

• resp have root cause in ventilation or alveoli gas exchange

• metabolic causes by metabolism issue (not resp), by acids other than CO2, like lactic acidosis (caused by anaerobic resp), DKA, sulfuric acid

acidosis: abnormal increase in H due to excess acid or loss of bicarbonate (thru diarrhea)

• metabolic: due to excess metabolic acids or lost bicarbonate

  • due to salicylate (aspirin) intoxication

  • hypoxia, shock, sepsis → lactic acid

  • DKA → ketoacidosis

  • kussmauls resps SE of prev 3

  • renal failure

  • loss of bicarbonate

  • SE: hyperkalemia, dysrhythmias, confusion

  • intervention: treat cause, O2, fluids, K, sodium bicarb (if IV, pH <7.1 or coding; PO), dialysis, antidiarrheal meds (stop bicarb loss), diuretics (increase H+ loss)

• respiratory: excess of carbonic acid due to low RR or alveoli gas exchange

  • due to shallow breathing (weak resp muscles), resp depress (brain issue or sedation), obstruction of resp, blocked alveoli gas exchange

  • SE: CO2 causes vasodilation → cerebral edema → visual disturbance, headache, restlessness, agitation, confusion, drowsiness, coma

  • intervention: fix cause, positioning, O2, meds, IS, mechanical ventilation (increase CO2 loss), ambulation

alkalosis: abnormal decrease in H ions, due to excess bicarb or loss of acid

• SE (same for both): hypokalemia, hypocalcemia (alkaolosis makes Ca bind to albumin, trousseaus + chvosteks signs +), anxiety, irritability, dizziness, hypotension, mental confusion, numbness and tingling of digits, muscle twitching, tetany, seizures

• metabolic: excess bicarb due to high PO or IV bicarb

  • due to ingesting lots of bicarb or antacids, excess bicarb admin, loss of hydrochloric acid from stomach, diuretics (H loss)

  • intervention: treat cause, stop bicarb intake, give antiemetic, stop loop or thiazide diuretic, E/F replacement

• resp: carbonic acid deficit due to high RR or alveoli gas exchange (releasing too much CO2)

  • due to anxiety, pain, fever

  • intervention: reduce CO2 loss

    • anxiety: meditation, benzo, propanolol

    • pain: meditation, positioning, tylenol, narcotic

    • fever: antipyretic

acid base imbalances

metabolic acidosis, resp acidosis, metabolic alkalosis, resp alkalosis

• resp have root cause in ventilation or alveoli gas exchange

• metabolic causes by metabolism issue (not resp), by acids other than CO2, like lactic acidosis (caused by anaerobic resp), DKA, sulfuric acid

table

blood gasses

arterial blood gas sample taken by resp therapist. results in 15 min. thru A-line if needed often.

ABG interpreted using pH, PaCO2, and HCO3, and optionally PaO2

PCO2: measurement of partial pressure of CO2 in blood, reflects resp component.

• normal 34-45 mm Hg.

• > 45, excess CO2, pH acidosis

• <35 less CO2, pH alkalosis

HCO3: bicarbonate. measurement of bicarb in blood. reflects metabolic component of kidneys

• normal 22-26 mm Hg.

• >26 excess bicarb, alkalosis

• <22 less bicarb, acidosis

math:

• see pH, identify if acidosis (<7.35) or alkalosis (>7,45)

• see PCO2 and HCO3, identify

example:

• pH 7.20, acidosis (result of imbalance)

• PCO2 56, acidosis

• HCO3 (bicarb) 25, normal

• resp acidosis (caused by PCO2) with no compensation bcos HCO3 is normal and kidneys haven’t reacted yet. acute because of short timing (kidneys havent responded yet)

• compensation only if normal pH

arterial blood gas (ABG) compensation

signs of compensation:

• pH normal but PCO2 and/or HCO3 are imbalanced

• if one is acidosis, the other is alkalosis to balance pH

• lungs compensate if issue is metabolic, and kidneys compensate if issue if resp.

metabolic acidosis:

• low pH and low HCO3

• SE kussmal resps (rapid, deep resps to blow off CO2)

resp acidosis:

• low pH and high PCO2

• SE kidneys absorb bicarb

metabolic alkalosis:

• high pH and high HCO3

• SE low RR to retain CO2

resp alkalosis:

• high pH and low PCO2

• SE kidneys excrete bicarb

math

• pH 7.38, PCO2 49, HCO3 30

• PCO2 high acidosis, HCO3 high alkalosis

• pH is normal but closer to acid (from 7.4), showing that the issue is acidosis.

• PCO2 is the acidosis one, so resp primary issue. renal compensated. compensated rep acidosis

math

• pH 7.44, PCO2 49, HCO3 33

• pH normal but on alkalosis side (from 7.4), showing alkalosis is the issue

• PCO2 normal, acidosis and HCO3 high, alkalosis.

• renal primary cause, resp compensation

• compensated metabolic alkalosis

• pH 7.51, PCO2 25, HCO3 24

• pH alkalosis, PCO2 alk, HCO3 normal

• pH is alk, showing alk problem. PCO2 is alk, showing that resp is cause

• uncompensated resp alkalosis

• pH 7.2 (acidosis), PCO2 40 (normal), HCO3 12 (acidosis)

• acidosis is the issue. HCO3 kidneys caused issue.

• uncompensated metabolic acidosis

• SE/cause of kussmauls, hypoxia, salicylate, sepsis, toxic, etc

acute respiratory failure

hypoxemic: PaO2 < 60 mm Hg

• low O2 in blood

hypercapnic: PaCO2 > 45 mm Hg, pH <7.35

• cannot remove CO2 from blood

• due to failure of oxygenation or failure of ventilation

initial SE: dyspnea, tachypnea, restlessness, confusion

progressive SE: worsening acidosis, cardiac dysrhythmias, increased ICP, coma, death

oxygenation failure (primary hypoxia cause):

• decreased or absent blood flow, decreased O2 exchange at alveoli, not enough O2

ventilatory failure (primary hypercapnia cause):

• extrapulmonary:

  • muscular disorder → diaphragm use issue

  • brain dysfunction, spinal cord injury

  • external pressure → hypoventilation

• intrapulmonary:

  • airway resistance or obstruction

  • lung compliance

treat: treat cause, support ventilation & gas exchange

• O2 therapy, minimize O2 demand, meds, positioning, mechanical ventilation

ventilation perfusion ratio

ventilation (V) / perfusion (Q)

physiologic shunting: area is ventilated but alveoli has limited gas exchange

non-invasive positive pressure ventilation

continuous positive airway pressure (CPAP):

• positive pressure during entire inspriation and expiration. must have spontaneous respirations and proper mask seal

bilevel positive airway pressure (BPAP):

• higher positive pressure during inspiration and lower positive pressure durign expiration. must have spontaneous respirations & proper mask seal

• IPAP - inspiratory PAP

• EPAP - expiratory PAP

indication:

• CPAP: sleep apnea

• BIPAP: resp exacerbations (COPD, CHF), palliative, post-extubation

contraindications:

• altered LOC, inability to protect airway, resp distress, need for PO access (meds, food), N/V, cannot control oral secretions, facial trauma, inability to establish mask seal

complications:

• gastric distension, aspiration, nasal/facial skin breakdown, nasal dryness/congestion, eye irritation, anxiety

endotracheal intubation & mechanical ventilator

indications:

• compromised airway, resp exacerbations, ABG imbalances, cardiac arrest, low LOC, resp support during & post surgery, life-long use for progressive neuromusc diseases

complications:

• anxiety, delirium, hypotension (due to less room for heart due to big lungs), barotrauma (too much air), ulcer, malnutrition, RF infection, muscle atrophy

nurse role: stabilize airway, gather equipment, inform patient, IV meds, monitoring + assessment, stabilize tube + suction PRN, verify placement, LF gastric distension

confirm placement:

• LF exhaled CO2 level

• auscultate bilateral breath sounds

• symmetry of chest expansion

• chest x-ray (2-3 cm above carina)

goal: short term (2-3 wks), patent airway, low WOB, remove secretions, provide ventilation + O2, prevent complications

ventilator-associated events (VAE):

• infectious lung injury: ventilator-associated pneumonia (VAP)

• non-infectious lung injury: ventilator-caused injury, atelectasis

  • VAP BUNDLE interventions:

    • HOB 30-45

    • oral care q2-4 hr (6x daily)

    • q12h CHG

    • sedation assessment (stop sedation daily, readiness to wean)

    • peptic ulcer disease prophylaxis (pepsid to stop malnourishment issues)

    • DVT prophylaxis (SCDs, heparin, PT)

    • turn q2

intubation pic

in-line suction (closed unit)

closed unit vs normal suctioning (see trach)

adaptor at the ETT-vent circuit interface that allows suctioning of airway without disconnecting ventilator

pros: stability of PEEP, lower RF infection

cons: hypoxia, trauma

ventilator alarms

high pressure: alarms when peak inspiratory pressure (PIP) is high. means that it requires too much pressure to oxygenate the patient. AMBU bag at bedside (for manual ventilation)

• nurse job: assess patient

• cause: coughing, gagging, tube biting

• anxious, fighting ventilator

• airway displaced or obstructed

• decreased compliance of lung or collapse

low pressure: alarms when PIP is too low.

• cause: leak in circuit preventing breath from being delivered

• cuff leaks in ET or trach tube

• patient extubated self

ventilator settings

ventilator settings:

• FiO2 (fraction of inspired O2): O2 concentration. 21% (room air conc) to 100%

• rate: bpm

• tidal volume (VT): set of volume of air delivered on inspiration

• peak inspiratory pressure (PIP): pressure applied on inspiration to deliver set tidal volume.

• positive end expiratory pressure (PEEP; range of 5-20): air pressure maintained thru expiration. prevent alveoli collapse, good for if need more lung surface area to increase gas exchange.

  • goal: treat persistent hypoxemia. keep alveoli open longer. improve gas exchange. lower WOB

  • complications: hypotension, barotrauma, pneumothorax

modes:

pressure/volume modes:

• volume-targeted

• pressure-targeted (preset airway pressure)

ventilator trigger mode:

• assist control (AC mode; first choice)

  • controls breathing more than patient

  • vent assists with breath to the set tidal volume, ensures the breath occurs regardless of patient desire

  • pt can initiate breath, but the vent inserts exact volume of air into lungs

  • decreases patient WOB

  • cons: potential resp alkalosis. pt can breathe faster then set RR

• synchronized intermittent mandatory ventilation (SIMV)

  • used after AC. vent assists with set tidal volume on some programmed breaths.

  • increases patient WOB on unassisted breaths. pt can breathe faster than the set RR

  • cons: potential resp alkalosis

weaning: re-establish spontaneous independent breathing, minimize sedation

• AC → SIMV → positive pressure support

• extubation: O2, high fowlers, DB & C/suction, monitor

acute respiratory distress syndrome (ARDS)

caused by direct or indirect lung injury. 35-45% mortalityn

• injury → low bloodflow → RBC accumulation → inflammation → damage to alveolar membrane → increased capillary permeability → proteins + fluid leave into interstitial space → pulm edema

• fluid in alveoli + low blood flow → alveoli damage → difficulty to produce surfactant → alveolar collapse → impaired gas exchange

• RR raises but O2 can’t cross membrane. CO2 crosses easier → blood O2 and CO2 both drop

• pulm edema worsens → inflammation causes ambrosia → worsened gas exchange → hypoxemia → resp acidosis

SE:

• sudden and progressive pulm edema from inflammatory cascade (non-cardiac)

• severe hypoxemia that is unresponsive (refractory) to O2 therapy

• decreased lung compliance

• dense pulm infiltrates with ground-glass appearance on chest x-ray (turning to fibrosis

common comorbidities (don’t study)

• direct: severe thoracic trauma, diffuse pulm infection. toxic gas, aspiration, prolonged mech vent use

• indirect: severe sepsis, shock, or anaphylaxis. severe nonthoracic trauma, pulm emboli, metabolic disorders, hematologic disorders, drug overdose/ingestion

phases:

• Phase 0 Acute Lung Injury 3ish days

  • expected SE: initial sever dyspnea, labored WOB, low PaO2 + SpO2, tachycardia, disorientation, anxiety

  • possible SE: fever, diaphoresis, hypotension, crackles

• Phase 1 ARDS - Exudative, 7-10 days

  • SE: low surfactant, crackles,

  • diagnose:

    • chest x-ray → diffuse bilateral infiltrates

    • ABGs → resp acid

    • hypocapnea, PaO2 <60

    • cardiac tests to rule out cardiac origin

• Phase 2 - Fibroproliferative, weeks to months

  • repair: dead cells removed → fluids dissipate → alveoli repaired → surfactant produced

• Phase 3 - Fibrotic, weeks to months

  • 50% mortality

  • resolution

    • SE: ventilator, long-term care facility, barotrauma

  • fibrosis: irreversible, higher mortality

    • SE: multi-organ dysfunction, vent dependent, barotrauma,

mgmt:

• vent support - high peep/FiO2 (to keep lungs open), small tidal volumes (prevent barotrauma in alveoli)

• positioning - HOB elevated, or prone (allows the fluid to enter diff alveoli so the wet alveoli get a break, + taking heart weight off lungs helps w breathing)

• nutrition - enteral or TPN

• circ support - conservative fluids + monitor UOP

• drugs - diuretics, antibiotics

• sedation to help patient accept the high WOB from ventilator

• ECMO (extracorporeal membrane oxygenation; removes blood, adds O2 and removes CO2, puts it back in), oxygenation

critical care

environment: for life-threatening situations. supplies are highly sophisticated and readily accessible

patients: many complex + interrelated issues, frequent priority reorganization, time limits due to rapid condition changes. acquire complete and detailed history + physical exam

monitoring

• cardiac telemetry

• hemodynamic: arterial line + MAP, cardiac output + input, pre-load + CVP, swan Ganz (PA pressure + PCWP)

stressors: sleep cycle interruption, sleep deprivation, mental altering drugs, fear. new environment, new faces, noise, light levels, inaccessibility to friends and family, lack of privacy, lack of info, anticipation of pain, impaired communication, excess alarms

arterial line (A-line)

BP and blood samples can be taken. includes a fluid bag connection to ensure clots don’t form (clotted artery creates surgical emergency)

mean arterial pressure (MAP):

• (SBP + [2 x DBP]) / 3

• if >65, organs are perfused. 65-110 good

• always calculate MAP

hemodynamics

cardiac output: amount of blood ejected by heart in 60 seconds, average 4-8L

preload: volume of blood

afterload (systemic vascular resistance SVR): how much resistance heart is beating against

contractility: how strong each contraction is

control of peripheral circ: dilation/constriction of vesselscentr

central venous pressure (CVP) line

measurement of the right atrium, the blood returning the preload

can be measured with regular centra line cath or PIC line, or with Swan Ganz

normal: CVP 2-6 mm Hg

• if high, too much preload, fluid overload, probs heart failure

• if low, fluid deficit, small preload, hypovolemia

Swan Ganz catheter

put into right IJ, goes thru right atrium, right ventricle, ends in pulm artery

also measures pressure in blood flow

normal: 15-26 mm Hg / 5-15 mm Hg

if high: heart failure

if low: hypovolemia

• pulm capillary wedge pressure (PCWP): estimates pressure of left atria

  • can’t inflate balloon more than 1.5mL

  • normal: 6-12 mm Hg

  • if high: heart failure

  • if low: hypovolemia

intracranial pressure monitoring

normal: 10-15 mm Hg

neuron death: sustained >20

shock

widespread abnormal cellular metabolism that occurs when oxygenation and tissue perfusion needs are not met to the necessary level to maintain cell function. identified thru perfusion and oxygenation.

aerobic metabolisms turn anaerobic → increased lactic acid → metabolic acidosis

types:

• hypovolemic: inadequate volume

• cardiogenic: inadequate pump

• distributive: ineffective vasculature

  • neurogenic, chemical (anaphylaxis, sepsis, capillary leak), obstructive

stages (need to know all info):

• initial: box 31.3 pg 764

  • MAP drops 5-10 mm Hg from baseline; vasoconstriction

  • raise in HR or tachycardia for no reason

  • slight raise in RR

  • slight vasoconstriction, paler skin

  • normal UOP

  • sense of impending doom

  • normal acid base

• nonprogressive/compensatory

  • MAP drops 10-15 mm Hg from baseline

  • raise in HR, possibly tachycardic, continued sympathetic stimulation

  • raise in RR, SpO2 drops 2-5% from baseline

  • skin is pale and cool, blood shunts away from extremities and more toward organs

  • UOP decreases slightly, increased thirst

  • anxiety, fear, sense of urgency

  • mild metabolic acidosis

• progressive

  • MAP >20 mm Hg from baseline

  • HR tachycardic but pulses weak due to shunting

  • tachypneic, resp distress

  • O2 drops 5-20% from baseline

  • skin is pale, cool, and diaphoretic (anoxia to non-essential organs, no skin perfusion). possible cyanosis in nail beds and oral mucosa

  • UOP little to none. dark and concentrated. increased BUN/Cr

  • confusion, agitation, brain is less perfused

  • metabolic acidosis + hyperkalemia

• refractory (irreversible)

  • MAP <65 mm Hg. cannot be maintained via fluids, vasopressors, etc.

  • HR is messed up. tachy, brady, dysrhythmia, vtach, etc. severe hyperkalemia. acidic blood.

  • resp failure, intubated.

  • no peripheral pulses, maybe carotids. SpO2 not measurable due to constriction + coldness. skin is mottled, dusky, grey, cold.

  • no UOP

  • unresponsive, coma, seizure activity

  • resp (due to no CO2 release) and metabolic (mixed) acidosis. severe hyperkalemia.

cellular (pic):

• walls more permeable, efflux of K, influx of Na and H2O, cell membrane + organelles swell

• blood hyperkalemia and blood hyponatremia

perfusion

working pump, working vessels that dilate and constrict, plasma with appropriate mobility and nutrients

needs:

• adequate volume of blood (preload)

• effective pumping by heart (CO)

• constriction and dilation of vasculature SVR)

• unobstructed pathway for blood flow

oxygenation

needs:

• blood flow (CO)

• amount of hemoglobin to carry O2

• % of arterial O2 hemoglobin saturation

O2 consumption (not tested):

• body’s demand for O2, reflecting body’s metabolism

• magnitude of O2 consumption deficit correlated with mortality rates

• low O2 consumption is common in shock

  • due to reduction in blood flow

    • hypovolemic: not enough blood flow

    • cardiogenic: not pumping 4-8L/min

    • obstructive: clots

  • uneven distribution of blood

    • septic

    • anaphylactic

    • neurogenic: spinal, brain

O2 delivery wiggle room (not tested): body normally provides 3-4x more O2 than needed for the metabolism

causes of hypoperfusion and hypoxia

volume: not enough volume, wrong type of volume

pump ineffective

vasculature ineffective: volume isn’t where it needs to be

obstruction in pathway

hypovolemic shock

loss of whole blood, plasma, or interstitial fluids in quantities that the body’s metabolic needs are not met. not enough volume or wrong volume perfusion (saline vs blood)

decrease in blood volume or plasma → decrease in venous return (preload) → low SV → low CO → low tissue perfusion → anaerobic metabolism → lactic acid production → myocardial depression

low CO → low coronary artery perfusion + inadequate cellular perfusion → RF infection + hemorrhage → organ damage

causes: GI bleed, GSW, hemorrhage, bowel perforation, dehydration, MVA, trauma, diabetes insipidus (too much diuresis)

SE:

• skin: longer cap refill time. cool, pale skin due to vasoconstriction. clammy moist skin due to epinephrine + norepinephrine

• thirst: thirsty due to increased serum osmolality

• UOP: low due to vasoconstriction, low GFR, and ADH release

• LOC: hyper-alert then decreases

• HR: tachycardia. SV decreases → HR increases to maintain CO

• RR: high RR and depth to improve O2, blow off Co2, compensate for impending acidosis, increase right heart filling volume

• hyperkalemia, hyponatremia

diagnosis: H/H, electrolytes

hemodynamics:

• CVP (central venous pressure) preload 2-6 mm Hg

• MAP 65-110 mm Hg

• (SBP + 2DBP) / 3

treat:

• airway: O2, HOB up

• breathing

• circulation: stop blood loss, restore lost volume, add fluids to improve UOP

• crystalloid solutions (LR, .9% NS): to provide intravasc expansion

• albumin: effective volume expander, may increase mortality sometimes. (also used in ascites)

• hetastarch: plasma volume expander. no danger of hepatitis. cheaper than blood. doesnt replace hemoglobin

• FFP: give if fluid loss is due to plasma loss (burns). also for clotting disorders

• blood: for major blood loss (whole blood, packed RBCs, etc)

• raise foot of bed to push blood to core, helps with oxygenation and increases CO

• dobutamine, milrinone, digoxin: inotropic agents to improve left ventricular function and give cardio support

• norepinephrine and neo-synephrine: improve preload by giving fluids or vasoconstrictors after volume has been replaced

• dopamine

secondary treat (fix stuff caused by our meds)

• correct acid-base issues

• monitor fluid overload rebound

• meet nutritional needs. thru guts if bowel sounds. thru TPN if no bowel sounds

cardiogenic shock

caused when the heart’s pumping ability becomes impaired → low cardiac output (CO). 40% mortality

cause: conditions that cause dysfunction of left ventricular, right ventricle, or both due to ischemia, structural issues, or ischemia

• low cardiac contractility → low SV and CO → pulm congestion + low tissue perfusion + low coronary artery perfusion

• low coronary artery perfusion → low cardiac contractility again

SE: very similar to HF but patient also can’t perfuse or oxygenate

• crackles, fluid overload, pulm edema, JVD, pitting edema, peripheral edema, scrotal edema (this is the diff between cardio shock and hypovol shock)

• low BP

• weak pulses

• cool and clammy skin

• low UOP, low bowel sounds, low everything

• altered LOC

• HF

treat:

• give inotrope, diuretic, vasopressor, vasodilator

  • norepinephrine: vasopressor to fix low BP

  • inotrope: to increase heart contractility and improve organ perfusion

  • diuretic: allows body to pee off extra fluid overload

  • dobutamine, milrinone: increase CO

  • nitroglycerin, nitroprusside: vasodilator to decrease afterload and lower left ventricular workload. hypothetically lowers BP but reduces resistance.

    • only if systolic BP > 110

    • if <110, vasoconstrictor instead

• O2, raise HOB

• increase CO by fixing dysrhythmias, hypo or hypervolemia

distributive/circulatory shock finish anaphylactic patho

heart works, volume is fine. problem is vasculature

anaphylactic: hypersensitivity allergic reaction to antigen → massive vasodilation → low CO + increased capillary permeability → bronchoconstriction → inflammation → increased coronary permeability → misdistribution of blood → blood doesn’t return to heart → low preload → low CO → bad perfusion

SE: hives, angioedema, stridor, periorbital edema, flushed skin, rash

• goes from anaphylaxis to anaphylactic shock due to low O2 and perfusion

• low BP

• low CO

• high HR (compensation)

• low UOP

• skin is rashed, flushed and warm → cold and cool

treat: epinephrine, vasoconstrictor, fluids, O2, raise HOB, diphenhydramine (benadryl), steroids

neurogenic:

• cause: spinal cord injury (T6 and up), spinal anesthesia, brain medulla damage, drugs (ganglionic blocking agents, barbiturates), etc.

• SE: massive vasodilation → low vascular tone → low systemic vascular resistance → low CO → low perfusion → impaired cell metabolism

  • massive BP + MAP drop (normal good MAP: 65) (for neuro: MAP >85-90 to improve spinal cord perfusion)

  • HR decreases (no more sympathetic NS stimulation to compensate bcos sympathetic NS is the issue)

  • initial pink, warm, flushed skin (blood pooling in extremities). then quickly becomes cold due to lack of circulation

  • neuro patients have very poor temp reg

• treat: O2 + raise HOB for oxygenation.

  • fluids to replace the fluids that are in the wrong place

  • vasoconstrictors (norep, epine) to fix the massive vasodilation and get blood back to heart

septic: chemically induced → triggered sepsis → anaphylaxis → capillary leak

shock complications: (don’t memorize)

• brain: low O2, hypoxia, seizures, LOC, lethargy, coma, etc

• kidneys: vasoconstriction, necrosis, oliguria, high BUN/Cr

• myocardium: low CO and low coronary perfusion, myocardial failure, increases dysrhythmias, low CO

• fluid shifts: water moves into cells w Na, lowering blood volume, cellular edema, lower metabolic activity

• peripheral circ: vasoconstriction to increase blood volume, fluid moves from interstitial to intravascular to increase BV, compensation fails and blood shunts away from organs and to brain and heart

• bowels: vasoconstriction, ischemia, ulcers, death

• liver: low blood flow, hypoxia, infection, met acidosis, DIC, hard to get rid of toxins

• glucose: hyperglycemia due to needing more energy

• ARDS: low lung bloodflow → low surfactant → atelectasis. high cap permeability → fluid leaks from capillaries into lung → pulm edema

disseminated intravascular coagulation (DIC)

global inappropriate microcirculation clotting.

RF: pregnant people, amniotic embolus, abrupto placentae, trauma, any shock, septic shock, cancer, toxins

cause: infllammatory response → coagulation activation → clots capillaries → clotting factors run out → paradoxical bleeding.

SE:

treat: O2 for hypoxemia, fluid for volume, RBC, FFP, clotting factors

• if caught during clotting phase (before bleeding), give heparin to break down clots to stop using all clotting factors

multiple organ dysfunction syndrome (MODS)

multiple (more than 2) organs affected by shock

signs of organ dysfunction: bad LOC, no bowel sounds, low UOP, etc

sepsis thinking

low UOP due to low perfusion to kidneys

drop in O2 due to global response to infection → low perfusion to all organs

sepsis

#1 cause of death

infection → overwhelming inflammatory process → systemic response → coagulation → impairment of fibrinolysis → RF DIC → bad blood flow → low perfusion → cells shut down → organs fail → death

#1: systemic inflammatory response syndrome (SIRS) signs

• temp > 100.4 or <96.8

• HR >90

• RR >20

• WBC >12 or <4

• 10% increase in neutrophil bands

#2: sepsis (>2 SIRS criteria + suspected or confirmed infection

#3: severe sepsis (organ dysfunction)

• SE: infection, organ dysfunction, hypotension, hypoperfusion, SBP <90 or MAP <65

  • hypoperfusion: tachypnea, oliguria, alteration in LOC, lactate > 4 mmol/L (shows lactic acid in blood due to anaerobic due to bad perfusion; normal 2.2 or less)

#4: septic shock + multiple organ dysfunction syndrome (MODS)

• RF: age <1 or >65, malnutrition, hypothermia, central venous catheters, endotracheal intubation or ventilation, aspiration, infection with resistant microorganisms, any chronic illnesses, immunodeficiency (HIV, alcoholism, chemo, transplant), invasive procedures

• SE: fluids + treatments not working. severe sepsis + hypotension

  • MODS:>2 organ dysfunctions without homeostasis even if treatment

  • hypotension: SBP <90 or reduction of 44 mm Hg from baseline or MAP <65

  • WBC changes

  • increased % of neutrophil bands

  • temp changes, chills

  • low skin perfusion, low cap refill

  • low UOP

  • low PLT, skin mottling

  • hyperglycemia

  • petechiae or purpura

  • tachypnea, tachycardia, LOC

• labs:

  • cultures of urine, blood, sputum, wounds

  • polymerase chain reaction system (PCRS) to LF what type of infection

  • WBC left shift, PLT

  • lactate > 4 mmol/L (norm 2.2 or less)

  • procalcitonin >2 mcg/L (norm <0.5)

  • coag profile PT/INR & PTT

  • d-dimer

  • activated protein C

  • cytokines

• treat: vasopressor (norepinephrine + levo??)

  • 1 hr sepsis bundle:

    • measure lactate level

    • give fluids at 30mL/kg for hypotension or for lactate > 4 mmol/L (give first if unstable/hypotensive)

    • get cultures before giving antibiotics (do first if stable)

    • give broad-spectrum antibiotics within 1 hr of sepsis

  • volume replacement (fix)

    • fluid intervention: crystalloids (NS or LR) 30mL/kg or low volume. colloids or albumin. blood replacement if HGB <7

    • antimicrobial: early therapy + eliminate source of infection

    • glucose:

      • hyperglycemia: pro-inflammatory, pro-coagulant, interferes with immune by impairing neutrophils + wound healing and increasing RF infection.

      • keep BG 140-180 to reduce mortality

    • vasopressor: hypotensive → add fluids + norep. A-line. dobutamine if myocardium depressed. no dopamine bcos it can promote tachydysrhythmias

    • lung ventilation:if ventilation, prevent barotrauma, avoid high pressures to tidal volume, use low tidal volume, use PEEP, HOB 30-45

    • antibiotics

prevention: handwashing, infection control, oral care, turn patients, catheter care, wound care, identify RF, get quick cultures if febrile, assess well

nursing (do not study):

• fix fever/hypothermia, tachycardia, tachypnea, hypotension

• monitor heart (rhythm, CO, SVR)

• monitor ventilation (ABGs, pulse ox, lung sounds, RR)

• renal: UOP <5 mL/kg/hr, BUN/Cr, Na

• hemat: bruising, bleeding, PLT, PT/INR, aPTT, fibrin

• nutrition: feed bowels if they are on, maintain protein, normalize glucose

• GI: N/V, abd distention, bowel sounds, high enteral residuals >200mL (not digesting food), hyperbilirubinemia, high liver enzymes

• neuro: restlessness, LOC, GCS

• skin: temp, color

skin function

protective barrier, thermoreg, fluid retention, sensation, vitamin D absorption,

burns

SE: loss of skin function caused by source, heat intensity, exposure duration, skin thickness, plasma loss (55% of blood volume, 90% water)

major burns (>20% total body surface area TBSA):

• fluid imbalance: inflammation, edema, redness, turns systemic ASAP, vasodilation, capillary permeability, fluid loss

• hemodynamic changes: cardiac output decreases, SNS response (stress) → hypermetabolism (up to 1 yr) + hyperglycemia

types:

thermal (common): contact, steam, flame, scalding liquids

chemical: contact, fumes, ingestion, injection. depends on chemical concentration + volume

• household cleaners

electrical (high vs low volt): entry + exit points, cardiac + renal concerns. dysrhythmias due to electricity.

• electrical wires, poles, lightning

inhalation: from thermal or chemical agents

• environment, work

radiation:

burn depth: (11th, p 467 table 21.8)

superficial thickness (1st degree): thru epidermis.

• SE: nerve damage, feels pain when burnt, redness, blanchable

partial thickness (2nd degree): past epidermis and into dermis.

• superficial partial thickness: halfway thru dermis

• deep partial thickness: fully thru dermis

• SE: nerve damage, feels pain when burnt, blistered, moist

full thickness (3rd degree): thru epidermis, dermis, and SQ tissue. difficulty healing, needs grafts.

• SE: pain cannot be felt in this layer because nerves are not in SQ. pain only felt in less burnt areas, dry, discolored. leathery or charred.

deep full-thickness (4th degree): thru epidermis, dermis, SQ, and muscle, sometimes to bone. cannot heal, grafts don’t help, needs amputation

• SE: same as full thickness

burn care

total body surface area (TBSA)

decided by TBSA, type of burn, depth, what body parts (if dependent or independent), age, and past medical history

circumferential: all the way around. circumferential burns on a leg would be 18

RF: diabetes, cardiac issues, renal function + liver function (for meds), pulm function, mobility

TBSA determines how much fluid is needed to fix the patient.

• rule of nines (pic): estimates TBSA in 9% increments. does not measure 1st degree. done before hospital/ED. even if only half of a part is burnt, count the whole part.

  • 18%: front abd, back abd

  • 9%: front L leg, front R leg, back L leg, back R leg

  • 4.5%: front R arm, front L arm, back R arm, back L arm, face, back of head

  • 1%: groin

phases of burn care

#1 resuscitative: hemodynamic stabilization thru fluid status + UOP (foley)

• onset of injury → 48 hrs

• SE before treatment: high serum K (burnt out of cells), high BG (stress), low Na (fluids gone), high HGB/HCT (lost plasma dehydrated), possible metabolic acidosis (due to hypovolemia). RF hypovolemic + distributive shock (capillary leak)

• primary survey:

  • airway/breathing: patent, LF inhalation injury. give bronchodilators or O2. intubate if too edematous

  • circulation: replace fluids using resuscitative formula

  • disability: stabilize injuries

  • expose + examine: temp reg

  • NG tube for nutrition if poor gut perfusion. burns gotta be washed + debrided. give tetanus shot.

• inhalation injury: RF smoke heat or toxic chemicals in smoke

  • in upper airway (above glottis) or lower airway (below glottis; alveoli damage, RF ARDS)

  • SE: edema in airway, LOC, facial burns, sooty sputum, singed face nose hairs, blistered mucosa + lips, vocal hoarseness, stridor, wheezing, dyspnea, tachypnea

  • treat: if suspected, intubate. baseline chest x-ray, 100% O2 w tight-fitting mask, raise HOB, ABGs + carboxyhemoglobin levels, bronchodilators

• carbon monoxide poisoning:

  • tasteless, odorless gas due to incomplete combustion of carbon-containing fuels.

  • binds to O2 receptors on HCG molecules → low O2 carrying capacity

  • affects cardiac muscle

  • makes SpO2 unreliable due to being unable to properly sense O2 in skin

  • normal carboxyhemoglobin: <10%

  • coma + death carboxyhemoglobin: >60%

• cardio issues: plasma shifts from intravasc to interstitial within 30 min, lasting 48 hrs.

  • SE low CO due to hypovolemia → vasoconstriction → tachycardia, cardiac dysrhythmias

• GI: low gut perfusion → peristalsis → RF duodenal ulcer (Curling’s ulcer) + RF translocation of intestinal bacteria (if gut is hungry and can’t eat, it finds bacteria to eat)

• renal: low kidney perfusion → RAAS triggers → oliguria → rhabdomyolysis → RF acute tubular necrosis

#2 acute: prevent infection + UOP

• 48 hrs → wound closure

• survey:

  • lung sounds (LF fluid overload)

  • GI + renal function (UOP)

  • address hypermetabolism + nutritional needs

  • wound + infection care

  • pain mgmt

  • positioning + mobility

• pulm: RF pulm edema RF fluid resus, RF bronchial pneumonia, RF ARDS, RF infection with intubation

• cardio: fix capillary leakage (fluids), maintain UOP, titrate IV fluids (no more huge boluses), strict I/O, E/F balance

• GI + renal: RF gastric ulcer, paralytic ileus RF narcotics, AKI. increased metabolic rate. (NG tube, high protein)

• nutrition: high calorie + protein diet needed. hypermetabolism 100-200% above baseline. manage stress (from fluid loss), inflammation, heat loss, muscle atrophy, daily weights, vitamins

• pain + mobility: hella pain + anxiety meds. account for drug tolerance. medicate before dressing change. early ambulation. specialty beds + positioning (prevent hands + feet contracting and getting stuck).

• immune: wound closure. early surgical debridement. infection control (PPE, cultures asap, barrier techniques for changes)

  • primary bacteria source is hair

  • no fresh flowers or plants

#3 rehabilitative: increase mobility and reduce contractures. most wounds closed → closest to baseline. may take 2-5 yrs.

• maintain or improve mobility: positioning, specialty beds, splinting to prevent contractures, PT, OT

• cosmetics: minimize scarring, protect skin integrity, sunscreen, compression garments 23 hrs/day 6-24 mo.

• give resources + support for discharge: grief, PTSD, chronic pain

IV fluid resuscitation formula

during phase 1 resuscitative burn phase

done in 1st 24 hrs, for major burns (>20% TBSA). LR because it is isotonic and also has electrolytes + lactate, making it similar to plasma. warm the fluids to maintain temp reg.

IV LR (Parkland formula; for all burn types)

• 4 mL x TBSA (whole number) x kg

• calculates for 24 hrs of fluid

• first 50% of fluids given within first 8 hrs of injury (not arrival)

• second 50% over next 16 hrs

• successful if UOP > 30mL/hr

• injury 5:30pm, TBSA 30%, weight 100kg

• 4 mL x 30 × 100 → 120 × 100 → 12,000mL LR

• 1st 6,000mL ends by 1:30am

• 2nd 6,000mL ends by 5:30pm

working if:

• fixed LOC

• HR <120

• SBP >100, MAP >65

• UOP >30mL/hr

• blood pH 7.35-7.45

wound care

for phase 2 acute burn phase

• PPE + remove dressings as often as ordered

• gentle cleaning + debridement. encourage granulation

• maintain room temp, pain control, communication

• monitor sedation, airway, + VS

• prevent cross-contamination (change gloves between wounds)

non-surg debridement: mechanical, enzymatic, wound vac

surgical excision: wound grafting, escharotomy (to remove eschar; incision down to superfiical fat)

compartment syndrome: occurs in burns of chest or limbs.

• SE: pulse, paresthesia, palor, paralysis, pain

• treat:

  • escharotomy: cutting in and allowing expansion of skin to accommodate for edema and bloodflow

  • fasciotomy: deep incision thru fascia (above muscle)

grafts

autograft/allograft: taking patient’s own skin from an unburnt area to cover granulated wound. best option

• split thickness wound (epidermis + half wound at donor site. sheet or meshed graft.

• aftercare: no debridement or cleaning. only change dressings if ordered (surgeons picky)

• donor site heals within 1-2 wks. graft adherence within a few days.

biological skin substitutes: from allograft or xenograft. temporary. removed or rejected by body before a more perm solution.

• allograft: living related donor or cadaver

• xenograft: animal skin donor

donor site: often anterior thigh. less painful than og site. multiple dressing options like polyurethane, hydrocolloids, hydrogel.

shock and sepsis jeopardy notes

stages of shock

initial shock: patient HR increased from baseline, mild vasoconstriction, compensates UOP (WDL)

refractory shock: HR tachy, brady, complete heart block, or dysrhythmia

progressive shock: HR rapid but weak, UOP anuric, tachypneic

non-progressive shock: MAP decrease of 10-15 from baseline + O2 decreases 2-5%

progressive shock: MAP decreased > 20 from baseline

type of shock

septic shock: severe sepsis w hypotension despite fluid replacement. needs vasopressor support

anaphylactic shock: sudden life-threatening hypersensitive reaction to antigen

hypovolemic shock? caused by loss of whole blood, plasma, or interstitial fluids in high quantities and metabolic needs cant be met

neurogenic shock: caused by spinal cord injury or spinal anesthesia

cardiogenic shock: dysfunction of L ventricle, R ventricle or both due to ischemia, structure, or dysrhythmias

signs of shock

septic shock: fever, bounding pulse, high lactate

hypovolemic shock: hypotension, low UOP, flat neck veins

neurogenic shock: bradycardia, poor temp reg

cardiogenic shock: crackles, HTN, JVD

anaphylactic shock: flushed skin, angioedema, hives

concepts

multiple organ dysfunction syndrome: high liver enzymes, neuro change, low UOP, hypotension

treat underlying cause: how to fix any shock

tachycardia: first signs of shock requiring investigation

what are the 2 core concepts of shock: oxygenation and perfusion

3 Ps of perfusion: pipes, pumps, plasma

treatments:

inotropes: increases cardiac contractility

epinephrine: med IV, SQ, nasally, and ET

.9% NS, LR: isotonic fluids for volume replacement

norep: most commonly used vasopressor for all shocks

nitroglycerin: low afterload/SVR during cardiogenic shock

sepsis:

sepsis: SIRS criteria + infection

septic shock: in severe sepsis, fluids arent effective for MAP, vasopressors must be added

SIRS criteria: tachycardia, increased RR, 10% increase in bands, fever, or hypothermia

lactate: 2.2 normal, >4 mmol is concerning

sepsis bundle: IV fluids, lactate level, blood cultures, antibiotics

q&a

ABGs: SE, body’s compensation, treatment

know lab values + SE, Na, K, Ca

resp failure: indications, complications, contraindications, vent settings, pH, hypercapnia, PO2. bipap vs cpap indications, complications. ARDS SE, RF. ARF RF. AC vs SIMV. confirmation of ET tube: chest xray, bilat lung rise, bilat lung sounds, exhaled CO2. VAP bundle: CHG oral care 2/day, HOB up, sedation vacation, DVT, PUD prophylaxis. high vs low vent alarms.

pulm artery pressure high vs low, MAP, CVP?,