Critical_Care_Notes

Critical Care
Notes
Clinical Pocket Guide
Janice Jones, PHD, RN, CNS Brenda Fix, MS, RN, NP
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Jeanie Krause-Bachand, MSN, EdD, RN, BC
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BASICS CV RESP GU NEURO GI
HEMA/
ENDO
ONCO
MULTISYS CC MEDS TOOLS

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1
Physical Assessment
Reusable Assessment Form
Name: Room: Age:
Diagnosis:
Surgeries/Past Hx:
Activ ity: Diet: DNR/DNI:
Allergies:
Neurological/MS:
ICP:
Cardiac:
VS/A-line:
ECG:
Hemodynamics: PAD PAS PCWP CVP
IABP:
Respiratory:
Ventilator:
ABGs/SpO2:
GI:
GU:

Wounds/Incisions:
Drainage Tubes:
Treatments:
Special Needs:
Other:
BASICS
BASICS
Normal Arterial and Venous Blood Gases
Blood Gas
Components Arterial Venous
pH 7.35–7.45 7.31–7.41
PO2 80–100 mm Hg 35–40 mm Hg
PCO2 35–45 mm Hg 41–51 mm Hg
HCO3 22–26 mEq/L or mmol/L 22–26 mEq/L or mmol/L
Base Excess (BE) –2 to +2 mEq/L or mmol/L –2 to +2 mEq/L or mmol/L
O2 saturation 95%–100% 68%–77%
Blood Gas Results
Arterial Venous
pH
PO2
PCO2
HCO3
Base Excess (BE)
O2 saturation
Quick Blood Gas Interpretation
Acid-Base Disorder pH PCO2 HCO3
Respiratory acidosis if compensating
Respiratory alkalosis
Metabolic acidosis

Metabolic alkalosis
Full or total compensation: pHwill be within normal limits
2
3
Compensation:
• 3
• 2
Also look f or mixed respiratory and metabolic problems.
PaCO2 or HCO3 in a direction opposite its predicted direction or not close to predictiv e v alue.
Common Causes of Acid-Base Imbalances
Respiratory acidosis COPD, asthma, headinjury, pulmonary
edema, aspiration, pneumonia, ARDS, pneu-
mothorax, cardiac arrest, respiratory depres-
sion, CNS depression, or head injury
Respiratory alkalosis Hy perventilation, anxiety, fear, pain,
f ev er, sepsis, brain tumor, mechanical
ov erventilation
Metabolic acidosis Diabetes mellitus, acute and chronic renal
f ailure, severediarrhea, alcoholism, starva-
tion, salicylateoverdose, pancreatic
f istulas
Metabolic alkalosis Loss of gastric acid (vomiting, gastric
suction), long-term diuretic therapy
(thiazides, furosemide), excessive NaHCO3
administration, hypercalcemia
BASICS
BASICS

Pulse Oximetry
SpO2 monitoring: Monitoring saturation of peripheral O2
SpO2 Level Indication
>95% Normal
91%–94% May be acceptable, provide O2 as necessary, encourage C&DBor suctionprn
85%–90% Prov ide O2 as necessary, encourage C&DB or suction prn, may be normal forCOPD patient
<85% Prepare f or possible intubation
False readings may occur because of anemia, CO poisoning, hypothermia, hypovolemia, peripheral vasoconstriction caused by disease or medications.
Lactic Acidosis
Lactic acid is a by product of anaerobic metabolism. Increased lev els indi-cate inadequate perf usion of v ital organs with resultant tissue hy poxia. May
result f rom inadequate perf usion and oxy genation of v ital organs; post cardiac or respiratory arrest; cardiogenic, ischemic, or septic shock; drug
ov erdoses, seizures, cancers, or diabetes mellitus.
Critical v alues: Blood pH, <7.35, and lactate >5–6 mEq/L or >45 mg/dL.
Treat with sodium bicarbonate IV if acidosis is readily ev ident.
Capnography
Capnography is the measurement, display , and monitoring of the concen-tration or partial pressure of CO2 (PETCO2) in the respiratory gases at the
end of expiration. The capnogram display s the maximum inspirato-ry and expiratory CO2 concentrations during a respiratory cycle, which indirectly
ref lect the production of CO2 by the tissues and the transport of CO2 to the lungs. Sudden changes in CO2 elimination should be moni-tored in
selected cardiorespiratory patients and postoperativ ely af ter major cardiothoracic surgeries. Capnography can also be used to v erify ETT position and
monitor the ef f ectiveness of CPR.
4
5
Causes of PETCO2 Causes of PETCO2
Fev er Hy pothermia
Hy pertension Hy potension
Increased cardiac output Decreased cardiac output
Hy poventilation Hy perventilation
Hy povolemia Hy pervolemia
Airway obstruction Airway obstruction
Bronchial intubation Accidental extubation
Pulmonary embolus

Cardiac arrest
Apnea
Normal range of ETCO2 is 35–45 mm Hg
• 2ETCO2 < 35 = respiratory alkalosis
• 2ETCO2 > 45 = respiratory acidosis There are f iv e characteristics of the capnogram that should be ev aluated: f requency , rhy thm, height , baseline,
and shape.
Normal Capnogram
m m H
g
Expiration Inspiration
III
II
I
Time
Phases I, II, and III represent expiration, the bolded lines represent inspira-tion. Long periods of a flat wav e f orm indicate apnea, dislodged endotra-
cheal tube, esophageal intubation, or patient disconnect f rom v entilator.
BASICS
BASICS
Artifical Airways and Mechanical Ventilation
Artifical Airways
Endotracheal Tube
• Adult oral tube sizes: Males 8.0–8.5, I.D. (mm); f emales 7.0–8.0. I.D. (mm) (internal diameter).

• Placement is 2 cm abov e the carina. Verify by auscultating f or breath sounds bilaterally , unif orm up-and-down chest mov ement, CXR, and
checking end-tidal CO2 immediately af ter intubation.
• Cuf f pressure: 20–25 mm Hg.
Tracheostomy Tube
• Size will v ary .
• Cuf f pressure: 20–25 mm Hg.
Minimal leak technique or minimal occluding v olume v erif ies that an ETT or tracheostomy tube is at its lowest inf lation point. Attach a 10-mL sy ringe to
the balloon of the inf lated cuff. Position y our stethoscope on the patient’s neck at the area of the carotid pulse. Inf late balloon cuff to a point where no
leak is heard. Slowly remov e air f rom the inf lated cuf f until y ou hear a slight leak at the height of inspiration. Then add 1 mL of air back into the cuf f .
Cuff pressure can also be monitored v ia a calibrated aneroid manome-ter dev ice. Connect manometer to cuff. Def late cuff. Reinf late cuff in 0.5 mL
increments until desired cuf f pressure is achiev ed. Check cuf f pressure ev ery 8–12 hrs or per agency protocol.
Mechanical Ventilation
Classificationof Ventilators
Positive Pressure Ventilation
• Volume-Cycled Ventilator: Deliv ers a preset constant v olume of air and preset O2.
• Pressure-Cycled Ventilator: Produces a f low of gas that inf lates the lung until the preset airway pressure is reached.
• Time-Cycled Ventilator: Programmed to deliv er a v olume of gas ov er a specif ic time period through adjustments in inspiratory -to-expiratory ratio.
6
7
• High-Frequency Jet Ventilator (HFJV): Deliv ers 60–100 bpm with low tidal v olumes under considerable pressures.
Negative PressureVentilation
Uses the old iron lung principle by exerting a negativ e pressure on the chest wall to cause inspiration. No intubation required. Custom fitted “cuirass” or
“turtle” shell unit that f its ov er the chest wall. May be utilized at night f or patients who require assistance during sleep.
Modes of Ventilation
• Controlled Mechanical Ventilation (CMV): Machine controls rate of breathing. Deliv ery of preset v olume (TV) and rate regardless of patient’s
breathing pattern. Sedation or paraly zing agent (e.g., Pav ulon) usually required.
• Assist Controlled Ventilation (ACV): Patient controls rate of breathing. Inspiratory ef f ort triggers deliv ery of preset v olume.
• Intermittent Mandatory Ventilation (IMV): Patient breathes sponta-neously (own tidal v olume) between v entilator breaths of a preset v olume
and rate.
• Synchronized Intermittent Mandatory Ventilation (SIMV): A f orm of pressure support v entilation. Administers mandatory v entilator breath at a
preset lev el of positiv e airway pressure. Monitors negativ e inspira-tory ef f ort and augments patient’s spontaneous tidal v olume or inspira-tory ef f ort.
Sy nchronized with patient’s breathing pattern.
• Positive End-Expiratory Pressure (PEEP): Increases oxy genation by increasing f unctional residual capacity (FRC). Keeps alv eoli inf lated af ter
expiration. Can use lower O2 concentrations with PEEP; decreas-es risk of O2 toxicity . Ordered as 5–10 cm H2O.
• Continuous Positive Airway Pressure (CPAP): Maintains positiv e pressure throughout the respiratory cy cle of a spontaneously breath-ing
patient. Increases the amount of air remaining in the lungs at the end of expiration. Less complications than PEEP. Ordered as 5–10 cm H2O.
• Bilevel Positive Airway Pressure (BiPAP): Same as CPAP but settings can be adjusted f or both inspiration and expiration.
• Pressure Support Ventilation (PSV): Patient’s inspiratory ef f ort is assisted by the v entilator to a certain lev el of pressure. Patient initiates all
breaths and controls f low rate and tidal v olume. Decreases work of breathing.
BASICS

BASICS
• Inverse Ratio Ventilation (IRV): All breaths are pressure limited and time cy cled. Inspiratory time usually set longer than expiratory time.
IMV, SIMV, CPAP, BiPAP and PSV can all be used in the weaning process.
Weaning
Sample Criteria for Weaning: Readiness
• Alert and cooperativ e
• FIO2 < 40%–50% and PEEP <5–8 cm H2O
• Hemody namically stable
• pH >7.34
• PaO2 >80 mm Hg
• PaCO2 <45 mm Hg
• PaO2/FIO2 ratio >200
• Vital capacity 15 mL/kg and minute v entilation <10
• Hemoglobin >7–9 g/dL and serum electroly tes within normal limits
• Spontaneous respirations >6 b/min. or <35 b/min.
• Negativ e inspiratory pressure –30 cm H2O
• Relativ ely af ebrile with limited respiratory secretions
• Inotropes reduced or unchanged within prev ious 24 hrs
• Sedation discontinued
Weaning Methods
• T-tube weaning: Place patient on T-tube circuit on same FIO2 as on v entilatory assistance. Monitor ABGs af ter 30 min. Prov ide a brief rest period
on the v entilator as needed and continue to monitor ABGs until satisf actory. Extubate when patient is rested, good spontaneous respiratory ef f ort,
and ABGs within acceptable parameters.
• IMV/SIMV weaning: Decrease IMV rate ev ery 1–4 hrs. Monitor spon-taneous breaths. Obtain ABGs within 30 min. of v entilator change. Allows f or
gradual change f rom positiv e-pressure v entilation to spon-taneous-pressure v entilation.
• PSV: Use low lev els of PSV (5–10 cm H2O). Decrease in 3–6 cm of H2O increments. Usef ul in retraining respiratory muscles due to long-term
v entilation.
8
9
• CPAP/BiPAP: Prov ides expiratory support, maintains positiv e intratho-racic pressure. BiPAP adds inspiratory support to CPAP. Prev ents res-
piratory muscle f atigue.
Nursing assessment during weaning
• Vital signs and hemody namics (PAS, PAD, PCWP, CO, CI)
• Dy srhy thmias or ECG changes
• Oxy genation/Ef ficiency of gas exchange
• CO2 production and elimination
• pH lev el
• Bedside pulmonary f unction tests
• Work of breathing including use of accessory muscles
• Lev el of f atigue
• Patient discomf ort
• Adequate nutrition

Ventilator Alarms
Ventilator alarms should nev er be ignored or turned of f . They may be muted or silenced temporarily until problem is resolv ed.
Checklist of Common Causes of Ventilator Alarms
Patient causes:
• Biting down on endotracheal tube
• Patient needs suctioning
• Coughing
• Gagging on endotracheal tube
• Patient “bucking” or not sy nchronous with the v entilator
• Patient attempting to talk
• Patient experiences period of apnea
Mechanical causes:
• Kinking of v entilator tubing
• Endotracheal tube cuf f may need more air
• Leak in endotracheal tube cuf f
• Excess water in v entilator tubing
• Leak or disconnect in the sy stem
• Air leak f rom chest tube if present
• Malf unctioning of oxy gen sy stem
• Loss of power to v entilator
BASICS
BASICS
Pathophysiological causes:
• Increased lung noncompliance, such as in ARDS
• Increased airway resistance, such as in bronchospasm
• Pulmonary edema
• Pneumothorax or hemothorax
Nursing Interventions
• Check v entilator disconnects and tubing.
• Assess breath sounds, suction as needed.
• Remov e excess water f rom v entilator tubing.
• Check endotracheal cuf f pressure.
• Insert bite block or oral airway .

If cause of the alarm cannot be f ound immediately or cause cannot be readily resolv ed, remov e patient f rom v entilator and manually v entilate patient
using a resuscitation bag.
Call respiratory therapy stat.
Continue to assess patient’s respiratory status until mechanical v entila-tion is resumed.
Ventilator Complications
Complication Signs & Symptoms/Interventions
Barotrauma or • High peak inspiratory and mean airway
v olutrauma—acute lung pressures
injury , may result in pneu-
• Diminished breathsounds
mothorax or tension pneu-
• Tracheal shif t
mothorax, pneumomedi-
• Subcutaneous crepitus
astinum, pneumoperi-
toneum, subcutaneous • Hy poxemia
crepitus
Insert chest tube or needle thoracostomy.
Intubation of right main- • Absent or diminishedbreathsounds in
stem bronchus lef t lung
• Unilateral chest excursion
Reposition ETT.
Continued
10
11
Ventilator Complications—Cont’d
Endotracheal tubeout of • Absent or diminishedbreathsounds
position or unplanned extu- Note location of tube at the lip (21–22 cm).
bation Reposition ETT or reintubate.

Restrain only when necessary.
Tracheal damage due to • Blood in sputum when suctioning
excessive cuff pressure
• Frequent v entilator alarm
(>30 cm H2O) Monitor ETT cuf f pressure every 4–8 hrs.
Perf orm minimal leak technique.
Ensure minimal occluding volume.
Damage to oral or nasal • Skin breakdown or necrosis to lips,
mucosa nares, or oral mucous membranes
Reposition tube side-sideof mouth every
day .
Apply petroleum jelly to nares.
Prov ide oral care withtoothbrush every
2 hrs.
Aspiration • Feeding v iewed when suctioning
Tracheo-esophageal • If blue dy eis used, sputum is blue in color
f istulas Use blue dy e withenteral feedings if
aspiration suspected.
Keep head of bed 30–45 degrees.
Administer proton pump inhibitors or his-
tamine H2-receptor antagonists.
Ventilator-assisted • Ref er to section on VAP
pneumonia Assess color and odor of sputum.
Respiratory infection Monitor temperature, WBC count, ESR.
Increased risk of sinusitis
Decreased venous return • Hy potension
decreased cardiac out-
• Decreased CVP, RAP, and preload
put due to increased
Monitor v ital signs and hemodynamics.
intrathoracic pressure
Continued
BASICS
BASICS
Stress ulcer and • Blood in nasogastric drainage
GI bleeding
• Hematemesis and/ormelena
Hematest nasogastric drainage, emesis,

f eces.
Administer proton pump inhibitors or his-
tamine H2-receptor antagonists.
Paraly tic ileus • Absence of diminished bowel sounds
Prov ide nasogastric drainage with
intermittent suction.
Turn and position patient frequently.
Inadequate nutrition, loss • Ref er to section on nutrition.
of protein
Start enteral feedings if appropriate.
Start total parenteral nutrition if GI tract
nonf unctional or contraindicated.
Increased intracranial • Changes in lev el of consciousness
pressure
• Unable to f ollow commands
Assess neurological status frequently.
Fluid retention due to Assess foredema.
increased humidification
Administer diuretics.
f rom ventilator, increased
Drain v entilator tubingfrequently.
pressure to baroreceptors
causing a release of ADH
Immobility Turn and position patient frequently.
Skin breakdown Assess skin for breakdown.
Assist patient out of bed to chairunless
contraindicated.
Keep skin clean and dry, sheets wrinkle-
f ree.
Communication difficulties Keep communication simple.
Obtain slate or writing board.
Use letter/picture chart.
Communicateusing sign language.
Continued
12
13
Urinary tract infection • Urine becomes cloudy, concentrated,
odorous
Change/remove Foley catheter.
Ensure adequate hydration.

Administer antiinfectives.
Deep v ein thrombosis • Painf ul, swollen leg; pain may increase
on dorsif lexion
Assess forpulmonary embolism. See
respiratory section.
Administer heparin or enoxaparin.
Psy chosocial concerns: • Anxious
f ear, loss, powerlessness,
• Dif ficulty sleeping
pain, anxiety, sleep distur-
• Poor pain control
bances, nightmares, loneli-
Administer anxiolytics, sedatives,
ness
analgesics.
Cluster activities to promote periods of
sleep.
Allow patient to makechoices when
appropriate.
Allow f or f requent family visits.
Keep patient and family informed.
Hemodynamic Monitoring
Hemodynamic Parameters
Arteriov enous oxy gen dif f erence . . . . . . . . . . . 3.5–5.5 v ol% or 4–8 L/min Aortic pressure:
■ Systolic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .100-140 mm Hg ■Diastolic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .60–80mm Hg ■ Mean .
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .70–90 mm Hg

BASICS
BASICS
Cardiac output (CO = HR X SV) . . . . . . . . . . .
. . . . . . . . . . . . . . . .4–8
L/min
Cardiac index (CO/BSA) . . . . . . . . . . . . . . . . .
. . . . . . . . . . . . . .2.5–4
L/min
Central v enous pressure (CVP) . . . . . . . . . . . . . . . . . . . . . . . . .2–8 mm Hg
** Same as right atrial pressure (RAP)
Cerebral perf usion pressure (CPP) . . . . . . . . .
2–6 mm Hg or 5–12 cm
H2O
Coronary artery perf usion pressure (CAPP) . . . . . . . . . . . . .60–80 mm Hg
Ejection f raction (Ej Fx or EF) . . . . . . . . . . . . ................60%–75%
Lef t arterial mean pressure . . . . . . . . . . . . . . . . . . . . . . . . . . .4–12 mm Hg
Lef t v entricular sy stolic pressure . . . . . . . . . . . . . . . . . . . .100–140 mm Hg
Lef t v entricular diastolic pressure . . . . . . . . . . . . . . . . . . . . . . .0–5 mm Hg
Lef t v entricular stroke work index (LSWI) . . . . . . . . . . . .30–50 g/beats/m2
Mean arterial pressure (MAP) . . . . . . . . . . . . . . . . . . . . . . .70–100 mm Hg
Oxy gen consumption (VO2) . . . . . . . . . . . . . .
. . . . . . . . . .200–250
mL/min
Oxy gen delivery (Do2) . . . . . . . . . . . . . . . . . . .
. . . . . . . . .900–1100
mL/min
Pulmonary artery pressure (PAP):
■ Systolic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .20–30 mm Hg ■Diastolic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .10–20mm Hg ■ Mean .
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .10–15 mm Hg
Pulmonary capillary wedge pressure (PCWP) . . . . . . . . . . . . .4–12 mm Hg Right arterial mean pressure . . . . . . . . . . . . . . . . . . . . . . . . . . .2–6 mm Hg
Right v entricular pressure:
■ Sy stolic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20–30 mm Hg
■ Diastolic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .0–8 mm Hg
■ End Diastolic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2–6 mm Hg
Right v entricular stroke work index (RSWI) . . . . . . . . . . . . .7–12 g/m2/beat
Pulmonary vascular resistance (PVR) . . . . . . . . . . .20–130 dynes/sec/cm
-5
Pulmonary v ascular resistance index (PVRI) . . . . . . . .200–400 dy nes/sec/
cm5/m2
Pulmonary ventricular stroke index . . . . . . . . . . . . . . . . . . .5–10 g/beat/m
2
Right atrial pressure (RAP) . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2–6 mm Hg Stroke
index (SI) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .30–650 mL/beat/m
2
Stroke volume (SV = CO/HR) . . . . . . . . . . . . . . . . . . . . . . . . .60–100 mL/beat Systemic
vascular resistance (SVR) . . . . . . . . . .900–1,600 dynes/sec/cm
-5
Systemic vascular resistance index . . . . . .1,360–2,200 dynes/sec/cm
-5
/m
2
Systemic venous
oxy gen saturation(SvO2) . . . . . . . . . . . . . . . . .60%–80%
14
15
Cardiac Output Components
Preload Contractility Afterload
PaO2 SaO2 Hemoglobin (Hgb)
Right atrial pressure Stroke v olume Pulmonary vascular resistance
Central v enous Cardiac output Sy stemic vascular resistance
pressure
Lef t ventricular Tissue perf usion Blood pressure
end diastolic

pressureP
Pulmonary Artery Catheter
The purpose of the pulmonary artery catheter, also known as the Swan-Ganz catheter, is to assess and monitor lef t v entricular f unction and can
determine preload, assess contractility , and approximate af terload.
PCWP approximates lef t atrial pressure and lef t v entricular end diastolic pressure.
Increases in PCWP, LAP, or LVEDP indicates heart f ailure, hy perv olemia, shock, mitral v alv e insuff iciency , or stenosis. Decreases in PCWP, LAP, or
LVEDP indicate hy pov olemia.
PA Catheter Waveforms
The pulmonary artery catheter is threaded through the right atrium and right v entricle and into the pulmonary artery. Insertion is done v ia f luo-roscopy
or monitoring wav ef orm changes.
Catheter advanced
to right atrium,
balloon is 40
inf lated. Pressure
30
is low, usually Hg
20
2–5 mm Hg. mm Balloon catheter
10 Right atrium
0
Time
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BASICS

Catheter is floatedto right ventricle with the balloon inflated. Wave-forms indicate a systolic pressure of 25–30 mm Hg anda diastolic pressure of 0–5 mm Hg.
40
30
Hg
20
mm
Balloon catheter
10
Right ventricle 0
Time
As the catheter moves into the pulmonary artery, thesystolic pres-sureremains the same but the dia-stolic pressureele-vates to 10–15 mm Hg.
mm
Hg
40
30
20

10
0
Time
Pulmonary
artery
Balloon
catheter
The catheter is moved until it can be wedged in a smaller vessel. When the balloon is inflated, the pressure recorded is that pressurein front of thecatheter. It is
an approximate measure of the left ventricularend diastolic pressure.
Pulmonary
artery wedge
40
30
Hg
20
mm
Balloon
catheter 10
0
Time
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Problems with Pulmonary Artery Catheters
Problem Check For/Action
No wav eform • Loose connections
• Tubing kinked or compressed
• Air in transducer
• Loose/cracked transducer
• Stopcock mispositioned
• Occlusion by clot: Aspirate as per policy
Ov erdamping (smaller • Air bubble or clot in the system
wav ef orm withslow • Catheter position: Reposition patient or
rise, diminished or hav e patient cough
absent dicrotic notch) • Kinks or knotting
• Clot: Aspirateas per policy
Catheter whip (erratic • Catheter position: Reposition patient or
wav ef orm, variable catheter; obtain chest x-ray
and inaccurate
pressure)
Inability to wedge • Balloon rupture: Turn patient on left side;
catheter (no wedge check catheterposition for retrograde
wav ef orm after slippage
inf lating balloon)
Complications of Pulmonary Artery Catheters
• Risk f or inf ection
• Altered skin integrity
• Air embolism
• Pulmonary thromboembolism
• Cardiac tamponade
• Dy srhy thmias

• Altered cardiopulmonary tissue perf usion due to thrombus f ormation; catheter in wedged position leading to pulmonary inf arction
• Catheter displacement/dislodgement
• Loss of balloon integrity or balloon rupture
• Pneumothorax
• Hemothorax
BASICS
BASICS
• Frank hemorrhage
• Pulmonary artery extrav asation
• Pulmonary artery rupture
Intra-Arterial Monitoring
An arterial line (A-line) is used if f requent blood pressure and arterial blood gas determinations are needed. It is especially usef ul
• Af ter surgery .
• For patients with unstable v ital signs.
• For patients experiencing hy poxemia.
Perf orm Allen’s test prior to insertion. Elev ate the patient’s hand with his or her f ists clenched. Release pressure ov er only the ulnar artery. Color
returns to the hand within 6 seconds if the ulnar artery is patent and ade-quate collateral blood f low present.
Compressing the radi- Observ ing f or pallor Releasing pressure
al and ulnar arteries and observ ing f or
return of normal color

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Intra-Arterial Waveform
100
mm
Hg
0
Time
Components of Waveform
• Systolic peak: Ventricular ejection and stroke v olume. Sharp rise and rounded top.
• Dicrotic notch:
Tapering of down stroke f ollowing dicrotic notch
Important assessments: changes in capillary ref ill/blanching, sensation, motion, or color that may indicate lack of perf usion to the extremity
MAP sy stolic BP (diastolic BP 2) = 70–100 mm Hg 3
Decreased tissue perf usion—decreasing urine output, elev ation in BUN:Creatinine ratio, altered mental status with decreasing lev el of consciousness,
restlessness, dy spnea, cy anosis, dysrhy thmias, abnor-mal ABGs, weak or absent peripheral pulses, increased capillary ref ill time (>3 sec), diminished
arterial pulsations, bruits.
BASICS
BASICS
Potential Complications of Intra-Arterial Monitoring
• Hemorrhage
• Air emboli

• Equipment malf unction/inaccurate pressure
• Dy srhy thmias
• Inf ection
• Altered skin integrity
• Impaired circulation to extremities
Nutrition Issues in Critical Care
Primary Concerns
• Starv ation and catabolism
• Stress hy permetabolism
• Fluid v olume def icit
• Fluid v olume excess
Stress and Nutrition
Metabolic rate increases with the release of catecholamines + glucagon
•
(albumin).
Nitrogen excretion increases.
Body weight decreases.
1 kg body weight = 1 liter of f luid retained or lost.
Body Mass Index
BMI is a simple means of classifying sedentary (physically inactiv e) indiv id-uals of av erage body composition and may indicate obesity . It is calculated
by the f ollowing: Body mass index (BMI) = weight (kg) ÷ height (meters)2
1 kg = 2.2 lbs Normal BMI = 20–25 kg/m2
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A BMI >30 kg/m2 indicates obesity , >40 kg/m2 indicates morbid obesity . An increase in BMI has been associated with heart disease and diabetes.
A BMI <18.5 kg/m2 suggests a person is underweight. A BMI <17.5 may indicate the person has anorexia or a related disorder.
BMI does not take into account f actors such as f rame size and muscularity .

Signs and Symptoms of Fluid Volume Deficit:
Hypovolemia
• Dry mucous membranes; dry cracked tongue
• Thirst
• Poor skin turgor
• Sunken ey eballs
• Subnormal temperature
• Decreased or orthostatic blood pressure
• Weak, rapid heart rate and increased respiratory rate
• Decreased capillary ref ill
• Urine output decreased (<30 mL/hr)
• Increased specif ic grav ity of urine (<1.030)
• Decreased central v enous pressure
• Increased hemoglobin and hematocrit
• Increased BUN and serum osmolarity
• Increased BUN:creatinine ratio
• Lethargy , mental conf usion
Signs and Symptoms of Fluid Volume Excess:
Hypervolemia
• Crackles in lungs; dy spnea, shortness of breath
• Decreased hemoglobin and hematocrit
• Decreased specif ic grav ity of urine
• Distended neck v eins and jugular v enous pressure
• Edema and decreased serum osmolarity
• Full, bounding pulse; tachy cardia
• Increased BP, CVP, and PAP
BASICS
BASICS
• Mental conf usion, restlessness
• Moist mucous membranes
• Pulmonary congestion or pleural ef f usion
• Weight gain
Enteral Tube Feedings

Gastric Access
• Nasogastric tube (NGT)
• Oral
• Percutaneous endoscopic gastrostomy (PEG)
• Nasoduodenal tube (NDT)
• Low-prof ile gastrostomy dev ice (LPGD)
Small Bowel Access
• Nasal-jejunal tube (NJT)
• Percutaneous endoscopic jejunostomy (PEJ)
Types of Tube Feedings
• Intermittent or bolus feedings: A set v olume of f ormula is deliv ered at specif ied times.
• Continuous feedings: A set rate of f ormula is deliv ered ov er a period of time.
• Cyclic feedings: Similar to a continuous f eeding but the inf usion is stopped f or a specif ied time within a 24-hour period, usually 6–10 hours.
Checking Tube Placement
• Aspirate gastric contents and check pH.
• Gastric aspirate pH 1–4 but may be as high as 6 if patient is on med-ication to reduce gastric acid (f amotidine, ranitidine, pantoprazole).
• Small intestine aspirate pH >6.
• Obtain chest x-ray .
• Inject 20–30 mL of air into the tube while auscultating ov er the epi-gastrium. Air in the stomach can be heard v ia a swooshing sound.
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Tube-Feeding Formulas
Standard Very High-Protein/Wound-Healing
Pediatric Fiber-Containing
Diabetic Elemental and Semi-Elemental
Pulmonary Immune-Enhancing or Stress Formulas
Renal Concentrated
Feeding Tube Complications
Mechanical Complications Interventions
Nasopharyngeal discomfort • Reposition tube.
Esophageal ulceration or bleeding • Consider PEG or PEJ tube.
esophageal v arices
Clogged tube • Flush with lukewarm water after
ev ery f eeding.
Hosp. Protocol:

Tube displacement • Reposition tube.
Extubation • Insert new tube.
• Consider PEG or PEJ tube.
Stomal leak or infection • Keep area around stoma clean
and dry .
Nonmechanical
Complications Interventions
Nausea, vomiting, cramps, • Withhold or decrease
bloating, abdominal distention amount, rate, and frequency
of f eedings.
• Change to low-f at formula.
Diarrhea • Withhold or decreaseamount,
rate, and f requency of feedings.
Aspiration • Hold f eedings. Check
residuals.
• Keep HOB elev ated 30°–45°
during f eedings and 1 hr. after
bolus f eedings.
Continued
BASICS
BASICS
Feeding Tube Complications—Cont’d
Nonmechanical Complications Interventions
Gastric reflux • Hold f eedings. Check residuals.
• Keep HOB elev ated 30°–45°.
Dumping syndrome: nausea, • Withhold or decrease
v omiting, diarrhea, cramps, amount, rate, and
f requency of feedings.
Checking for Residuals
• Assess ev ery 4–6 hrs f or continuous f eeding and prior to bolus f eeding.

• Using a 30- to 60-mL sy ringe, withdraw gastric contents f rom the f eeding tube. Note v olume of f ormula.
Volume Indication
<50 mL Normal residual.
50-100 mL Repeat measurement of residual every 1–2 hrs.
>100 mL Stop f eeding. Check residual after 3–4hrs. When
residual is <100 mL, resume feeding at slower rate,
amount, or frequency.
Total Parenteral Nutrition (TPN)
TPN is an IV solution of 10%–50% dextrose in water (CHO), amino acids (protein), electroly tes, and additiv es (vitamins, minerals, trace elements of
insulin, v itamin K, zinc, f amotidine). Fat emulsions prov ide f atty acids and calories. Solutions >10% dextrose must be inf used v ia a central line.
• 1000 mL 5% D/W contains 50 g sugar = <200 calories
• 1000 mL 25% dextrose contains 250 g sugar = 1000 calories
Indications
• Sev ere malnutrition
• Burns
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• Bowel disorders (inf lammatory disorders, total bowel obstruction, short bowel sy ndrome)
• Sev ere acute pancreatitis
• Acute renal f ailure
• Hepatic f ailure
• Metastatic cancer
• Postoperativ e major surgery if NPO >5 day s
Nursing Care
• Each bag of TPN should be changed at least ev ery 24 hrs with tubing change.
• Monitor intake and output and weigh the patient daily .
• Monitor glucose lev els, including f inger stick blood sugars ev ery 4 to
6 hours. Cover with regular insulin as necessary. If poor control of serum glucose, consider adding insulin to TPN and continue rainbow coverage.
• Monitor serum electroly tes including magnesium, phosphate, trigly c-erides, prealbumin, CBC, PT/PTT, and urine urea nitrogen.
• Assess IV site f or redness, swelling, and drainage.
• Change gauze dressing around IV site ev ery 48 to 72 hours, as per protocol. Transparent dressings may be changed ev ery 7 day s.
• If TPN is temporarily unav ailable, hang 10% D/W at the same rate as TPN. Monitor f or hy pogly cemia.
• Place TPN on inf usion pump. Monitor hourly rate. Nev er attempt to “catch up” if inf usion not accurate.
• Patients generally are taken of f of TPN prior to surgery .
Complications
Complications from TPN may be catheter-related, mechanical, or metabolic.
Complications of TPN Signs and Symptoms

Inf ection, catheter-related Leukocytosis; fever; glucose intolerance;
sepsis, septicemia, catheter site red, swollen, tender; drainage
septic shock
Hy poglycemia Shaking, tachycardia, sweating, anxious,
Blood glucose dizziness, hunger, impaired vision,
<70 mg/dL weakness, fatigue, headache, irritability
Continued
BASICS
BASICS
Complications of TPN Signs and Symptoms
Hy perglycemia Extreme thirst, frequent urination,
Blood glucose dry skin, hunger, blurred vision,
>200 mg/dL drowsiness, nausea
Prerenal azotemia +
, signs of dehydra-
tion, lethargy, coma
Hepatic dysfunction
alkaline phosphatase)
Pneumothorax, SOB, restlessness, dyspnea, signs
hy drothorax of hy poxia, chest pain radiating
Subclav ian/carotid to back, arterial blood in syringe,
artery puncture tachy cardia, pulsatile blood flow, bleeding
f rom catheter site
Air embolus Respiratory distress, dyspnea, SOB, tachy-
arrest
Dy srhythmias Atrial, junctional, andventricular arrhyth-
Hy po-/hypernatremia Normal v alues: 135–145 mEq/L or 135–145
mmol/L
Hy po-/hyperkalemia Normal v alues: 3.5–5.0 mEq/L or 3.5–5.0
mmol/L
Hy po-/hyperphosphatemia Normal v alues: 3.0–4.5 mg/100 mL or
1.0–1.5 mmol/L
Hy po-/hypermagnesemia Normal v alues: 1.5–2.0 mEq/L or 0.8–1.3
mmol/L
Hy po-/hypercalcemia Normal v alues: 8.5–10.5 mg/100 mLor
2.1–2.6 mmol/L
Infectious Diseases
Critical Care Risk Factors
• Inv asiv e dev ices
• Immunocompromising conditions
• Serious underly ing illness

• Prolonged stay in critical care unit
• Colonization and cross-inf ection
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• Ov eruse of antibiotics
• Elderly
Methicillin-Resistant Staphylococcus aureus (MRSA)
Etiology
Health-care associated bloodstream and catheter-related inf ections. Transmitted by close contact with inf ected person. Health-care worker may be
colonized with MRSA strain with absence of symptoms. The Staph. aureus bacterium is resistant to methicillin, amoxicillin, penicillin, oxacillin, and
other antibiotics.
Signs and Symptoms
• Skin infection: Boil or abscess
• Surgical wound: Swollen, red, painf ul, exudate (pus)
• Bloodstream: Fev er, chills
• Lung infection/pneumonia: Shortness of breath, f ever, chills
• Urinary tract: Cloudy urine, strong odor
Diagnosis
• Culture of inf ected area
Treatment
• Vancomy cin (Vanocin, Vancoled)
• Linezolid (Zy v ox)
• Daptomy cin (Cubicin)
Clostridium Difficile (C-diff)
Etiology
C. difficile is a common cause of antibiotic-associated diarrhea (AAD) and is transmitted through the f eces or any surf ace, dev ice, or material that has
become contaminated with f eces.
BASICS
BASICS
Signs and Symptoms

• Watery diarrhea (at least 3 BMs/day f or 2 or more day s)
• Fev er
• Loss of appetite
• Nausea
• Abdominal pain and tenderness
Diagnosis
• Stool culture
Treatment
• Discontinue antibiotics. May giv e metronidazole (Flagy l) to treat diarrhea
Revised CDC Guidelines 2007
• Perf orm hand hy giene af ter touching blood, body f luids, secretions, excretions, and contaminated items immediately af ter rem ov ing glov es and
between patient contacts.
• Alcohol-based hand gels are the pref erred method f or hand decon-tamination between patients. Decontamination should be perf ormed af ter
contact with a patient and/or medical equipment.
• Glov es and gown should be worn when in contact with clothing or exposed skin with blood or body f luids, secretions, and excretions.
• Mask, ey e protection (goggles), and f ace shield should be worn dur-ing procedures such as suctioning or endotracheal intubation if splashes or
spray s of body f luids or blood may occur. For patients with suspected or prov en inf ections transmitted by respiratory aerosols, such as SARS, a
f it-tested N95 or higher respirator should also be worn.
• For injected medications, single-dose v ials are pref erred to multiple-dose v ials.
During patient transport, masks are not necessary if the patient is wearing a mask. Health-care workers should continue to wear masks when caring f or
patients with droplet precautions. For more inf ormation: http://www. cdc.gov /ncidod/dhqp/pdf /guidelines/Isolation2007. pdf
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Psychosocial Issues in Critical Care
Sensory Overload and Deprivation
• Sensory Overload: A condition in which sensory stimuli are receiv ed at a rate and intensity bey ond the lev el that the patient can accommodate.
• Sensory Deprivation: A condition in which the patient experiences a lack of v ariety and/or intensity of sensory stimuli.
Types of Sensory Stimuli
• Visual
• Auditory
• Kinesthetic
• Gustatory
• Tactile
• Olf actory
Signs and Symptoms of Sensory Problems

• Conf usion
• Hallucinations
• Lethargy
• Behav ioral changes (combativ eness)
• Increased startle response
• Disorientation
• Anxiety
• Restlessness
• Panic
• Withdrawal
• Mood swings
• Withdrawal
Near-Death Experience
The experience of patients that they hav e glimpsed the af terlif e when coming close to death. These perceptions may include:
• Seeing an intense light
• Seeing angels or departed lov ed ones
• Trav eling through a tunnel
BASICS
BASICS
Out-of-Body Experience
The experience of being away f rom and ov erlooking one’s body . The patient f eels that the mind has separated f rom the body .
Family Needs of the Critical Care Patient
• Relief of anxiety .
• Assurance of competent care.
• Timely access to the patient.
• Accurate and timely inf ormation about the patient’s condition and prognosis in easily understandable terms.
• Early notif ication of changes in the patient’s condition.
• Explanations regarding the env ironment, machinery , and monitoring equipment.
• Honest answers to questions.
• Emotional support.
• Regard f or the spiritual needs of the f amily and patient.

Organ Donation
Transplantable organs include:
• Kidney s
• Heart
• Lungs
• Liv er
• Pancreas
• Intestines
Corneas, the middle ear, skin, heart v alv es, bone, v eins, cartilage, ten-dons, and ligaments can be stored in tissue banks and used to restore sight,
cov er burns, repair hearts, replace v eins, and mend damaged con-nectiv e tissue and cartilage in recipients.
Healthy adults between the ages of 18 and 60 can donate blood stem cells: marrow, peripheral blood stem cells, and cored blood stem cells.
Nursing Role in Organ Donation
• Prov ide accurate inf ormation regarding donation.
• Identif y possible donors early .
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• Work closely with the organ procurement organization and members of the health team to illicit donations.
• Prov ide emotional support to f amilies considering donation, making sure to respect their cultural and religious belief s.
• Become a donor adv ocate among colleagues and f or patients and their f amilies.
General Criteria for Brain Death
• Absence of purposiv e mov ement
• Flaccid tone and absence of spontaneous or induced mov ements
• Persistent deep coma
• Absence of spontaneous respiration
• Absence of brainstem ref lexes:
• Midposition or pupils f ixed and dilated
• No corneal, gag, or cough ref lexes
• Absence of spontaneous oculocephalic (doll’s eye phenomenon) reflex
• No v estibular response to caloric stimulation
• Isoelectric or f lat electroencephalogram (EEG)
• Absent cerebral blood f low
These criteria v ary f rom state to state.
Hemodynamic management of potential brain-dead organ donors: ensure adequate intrav ascular v olume and adequate cardiac output to ensure
consistent perf usion to v ital organs.
• MAP >60 mm Hg
• Urine output >1.0 mL/kg/hr
• Lef t v entricular ejection f raction >45%

Nursing care
• Fluid management—f luids or diuretics
• Inotropic agents to correct low cardiac output
• Vasopressors to correct v asodilatation
• Thy roid hormone
• Corticosteroids to reduce inf lammation
• Vasopressin to support renal f unction
• Insulin to control glucose lev els
BASICS
BASICS
• Regulate v entilator settings including use of PEEP
• Suction f requently to promote adequate oxy genation
Specif ic organ donation protocols:
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Sedation, Agitation, and Delirium Management
Sedativ es should be titrated without impairing neurological assessment. Analgesics should be titrated to keep pain lev el <3 on 0–10 scale.
Assessment
Prior to sedation, exclude and treat possible causes of agitation and conf usion:

• Cerebral hy poperf usion
• Cardiac ischemia
• Hy potension
• Hy poxemia or hy percarbia (elev ated blood CO2)
• Fluid and electroly te imbalance: acidosis, hy ponatremia, hy po-gly cemia, hy percalcemia, hepatic or renal insuf f iciency
• Inf ection
• Drug-induced
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33
Use nonpharmacologic therapies such as massage, distraction, minimize noise. Cluster activ ities to allow f or uninterrupted periods of sleep. Assess
pain on 0–10 scale or f aces scale and look f or nonv erbal cues.
Medications for Sedation, Pain, and Delirium
Benzodiazepines
• Diazepam (Valium)
• Lorazepam (Ativ an)
• Midazolam (Versed)
Keep antidote f lumazenil (Romazicon) av ailable.
Narcotics
■ Morphine sulf ate ■ Hy dromorphone (Dilaudid)
■ Codeine ■ Oxy codone (OxyContin)
■ Fentanyl ■ Remif entanil (Ultiva)
Alpha-adrenergic Receptor Agonists
• Clonidine (Catapres)
• Dexmedetomidine (Precedex)
Neuroleptics/Antipsychotics/Butyrophenones
• Haloperidol (Haldol)
• Droperidol (Inapsine)
Sedatives/Hypnotics
• Propof ol (Dipriv an)
Physiological Responses to Pain and Anxiety
■ Tachy cardia ■ Hy pertension
■ Diaphoresis ■ Tachy pnea
■ Sleep disturbance ■ Nausea

Signs of Sedative or Analgesic Withdrawal
• Nausea, v omiting, diarrhea
• Cramps, muscle aches
• Increased sensitiv ity to pain
BASICS
BASICS
•
• Delirium, tremors, seizures, agitation
Medication Management
• Monitor body and limb mov ements, f acial expression, posturing, muscle tension f or signs of pain.
• Monitor f or acute changes or f luctuations in mental status, LOC, disorientation, hallucinations, delusions.
• Ev aluate arousability .
• Monitor neurological status including pupillary response, response to v erbal commands and pain.
• Monitor respiratory rate and respiratory ef f ort, respiratory depression, BP, HR.
Sedation Assessment Scales
Sedation-Agitation Scale (SAS)
Score Level of Sedation-Agitation Response
7 Dangerous agitation Pulling at endotracheal tube,
thrashing, climbing over bed
rails
6 Very agitated Does not calm, requires
restraints, bites endotracheal
tube
5 Agitated Attempts to sit up but calms to
v erbal instructions
4 Calm and cooperative Obey s commands
3 Sedated Dif ficult to rouse, obeys simple
commands
2 Very sedated Rouses to stimuli; does not
obey commands
1 Unarousable Minimal or no response to
noxious stimuli
Reprinted with permission from Riker, R. et al. Critical Care Medicine, 1994,22(3), 433-440.
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Bispectral IndexMonitoring (BSI)

Phy siological assessment of sedation: Examines the EEG and monitors states of increased and diminished cortical arousal. Scoring:
0 Isoelectric brain activity (flat EEG)
40–60 General anesthesia
60–70 Deep sedation
70–80 Moderate (conscious) sedation
90–100 Awake state
Pain Visual Analog Scale (VAS)
no pain 0 _____________________________________________ worst pain 10
no anxiety 5 sev ere anxiety
Delirium Assessment
Delirium has been associated with poor patient outcomes. Patients with delirium hav e higher ICU and hospital stay s along with a higher risk of death.
It is characterized by an acute onset of mental status changes that dev elop ov er a short period of time, usually hours to days. It may fluctu-ate ov er
the course of a day . It may be combined with inattention and dis-organized thinking or altered lev el of consciousness. The DSM IV describes three
clinical subty pes: hy peractive, hypoactive, and mixed. Hy peractive delirium may be conf used with anxiety and agitation.
Benzodiazepines may cause or worsen delirium.
Haloperidol (Haldol) is the drug of choice to treat delirium in the ICU patient.
The Conf usion Assessment Method f or the Intensiv e Care Unit (CAM-ICU) score has been used to screen f or delirium in the ICU population.
BASICS
BASICS
Complications of Sedation, Agitation, and Delirium Therapy
• Hy potension
• Patient unresponsiv eness
• Respiratory depression
• Delay ed weaning f rom mechanical v entilator
• Complications associated with immobility : pressure ulcers, throm-boembolism, gastric ileus, hospital-acquired pneumonia

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Acute Coronary Syndrome (ACS)
ACS is the term used to denote any one of three clinical manif estations of coronary artery disease:
• Unstable angina
• Non-ST elev ation MI
• ST elev ation MI
Pathophysiology
Unstable angina represents the progression of stable coronary artery dis-ease to unstable disease. Rupture of atherosclerotic plaque causes throm-
bus f ormation and partial occlusion in coronary arteries.
Clinical Presentation
ACS presents with chest pain, diaphoresis, SOB, nausea and v omiting, dyspnea, weakness, and f atigue. Look for sy mptoms of MI —midsternal chest
pain, may be described as pressure, squeezing, f ullness, or pain. May radiate to jaw, neck, arms, or back and usually lasts more than 15 minutes.
Assessment f or chest pain and associated sy mptoms of ACS include: Use of PQRST method when assessing pain, phy sical exam, v it al signs,
auscultate f or S3 or S4 gallop, auscultate lungs f or crackles, and assess peripheral v essels f or pulse def icits or bruits .
Diagnostic Tests
• ECG
• Echocardiogram
• Cy cle cardiac markers (troponin I, CK, CK MB, my oglobin, C-reactiv e protein)

Management
• Administer oxy gen to maintain SaO2 >90%.
• Establish IV access.
CV
CV
• Perf orm cardiac monitoring.
• Administer SL nitrogly cerin tablets or oral spray , ev ery 5 minutes x 3 doses. If pain persists, IV nitrogly cerin may be start ed.
• Monitor f or hy potension and headaches f rom v asodilatation.
• Administer aspirin and hav e patient chew it, if not already on daily dose.
• Administer IV morphine, 2–4 mg ev ery 15 minutes until pain is controlled.
• Monitor f or hy potension and respiratory depression.
• Unless contraindicated, administer a beta blocker.
Unstable Angina
Unstable angina is the sudden onset of chest pain, pressure, or tightness due to insuf f icient blood f low through coronary art eries.
Pathophysiology
2
Chest pain presents as substernal pain, tightness, dullness, f ullness, heav -iness or pressure, dyspnea, sy ncope, pain radiating to arms, epigastrium,
shoulder, neck, or jaw.
Women may experience more aty pical sy mptoms such as back pain; GI sy mptoms, such as indigestion, nausea and v omiting, and abdominal f ull-
ness; whereas men may experience ty pical sy mptoms such as midsternal chest pain radiating into the lef t arm.
Diagnostic Tests
• 12-lead ECG
• Lab work: cardiac markers: creatine kinase (CK), creatine kinase-my ocardial band (CK-MB), troponin I (TnI), and my oglobin
• Exercise or pharmacological stress test
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39
• Echocardiogram
• Nuclear scan
• Cardiac catheterization and coronary artery angiography

Management
• Bedrest.
• Obtain ECG and lab work.
• Assess chest pain f or f requency , duration, cause that triggered pain, radiation of pain, and intensity based on pain scale f rom 1 to 10, with 1 being
no pain and 10 being worst pain.
• Supply O2.
• Pharmacological treatment:
• Early conserv ativ e, for low-risk patient: Anti-ischemic, antiplatelet, and antithrombotic drug therapy ; stress and treadmill tests.
• Early inv asiv e: Same drug therapy as early conserv ativ e but f ol-lowed by diagnostic catheterization and rev ascularization.
•
• Administer morphine sulfate IV if symptoms persist after receiving NTG or in patients who have pulmonary congestion or severe agitation.
• Administer beta blocker: metoprolol.
• Administer ACE inhibitors in patients with LV dy sf unction or CHF with HTN, not recommended in patients with renal f ailure.
• Administer calcium channel blockers: Verapamil (Calan, Isoptin) or diltiazem (Cardizem) if patient not responding f rom beta blocker or nitrates.
*Use sev ere caution when combining blocking agents*
• Administer antiplatelet: Aspirin 160–325 mg, chewed.
• Administer GP IIb- IIIa inhibitor: Eptif ibatide (Integrilin) or tirof iban (Aggrastat) if no contraindications (i.e., bleeding, stroke in past month, sev ere
HTN, renal dialy sis, major surgery within the past 6 weeks, or platelet count <100,000 mm3 ).
• Administer antithrombotic: Heparin.
• Administer anticoagulant: Enoxaparin (Lov enox).
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Acute Myocardial Infarction (AMI)
AMI is the acute death of my ocardial cells due to lack of oxy genated blood f low in the coronary arteries. It is also known as a heart attack.
Pathophysiology
AMI presents with chest pain or discomf ort lasting 20 minutes or longer. Pain can be described as pressure, tightness, heav iness, burning, or a
squeezing or crushing sensation, located ty pically in the central chest or epigastrium; it may radiate to the arms, shoulders, neck, jaw, or back.
Discomf ort may be accompanied by weakness, dy spnea, diaphoresis, or anxiety, not reliev ed by NTG. Women may experience aty pic al discom-f ort,
SOB, or f atigue. Diabetic patients may not display classic signs & sy mptoms of AMI. Elderly may experience SOB, pulmonary edema, dizzi-ness,
altered mental status.
ST-segment elev ation MI: Look f or tall positiv e T wav es and ST-segment elev ation of 1 mm or more abov e baseline.
Non-ST segment elev ation MI: May include ST-segment depression and T-wav e inv ersion.

Diagnostic Tests
• ECG f indings
• Cardiac markers (CK, my oglobin, and troponins)
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Management
• Focus on pain radiation, SOB, and diaphoresis.
• Obtain a 12-lead ECG and lab draw f or cardiac markers.
• MONA: morphine, O2, NTG, and 160–325 mg aspirin, po. If allergic to aspirin, giv e ticlopidine (Ticlid) or clopidogrel (Plav ix).
• Administer supplemental O2 to maintain SpO2 >90%.
• Administer SL NTG tablets or spray .
• Administer IV morphine 2–4 mg ev ery 15 minutes until pain is con-trolled. (Monitor f or hy potension and respiratory depression.)
Hypertensive Crisis
Hy pertensiv e crisis is def ined as a sev ere elev ation in blood pressure (sy s-tolic BP >179 mm Hg, diastolic BP >109 mm Hg), which may or may not
lead to organ damage. There are two ty pes of hy pertensive crisis:
• Hypertensive emergency: Rapid (hours to day s) marked elev ation in
• Hypertensive urgency: Slow (day s to weeks) elev ation in BP that usu-ally does not lead to organ tissue damage.
Pathophysiology
Hy pertensiv e crisis presents with
• Chest pain
• Dy spnea
• Neurological def icits
• Occipital headache
• Visual disturbance
• Vomiting
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Diagnostic Tests
• CT scan of chest, abdomen, and brain
• 2-D echocardiogram or transesophageal echocardiogram
• ECG
• Lab draws: CBC, cardiac markers, BUN, creatinine, UA, urine toxicology
Management
• Administer O2 to maintain PaO2 >92%.
• Obtain VS-orthostatic BP ev ery 5 min, then longer interv als.
• First-line medical therapy : Labetalol (Trandate) and adrenergic-receptor blocker with both selectiv e alpha-adrenergic and nonselec-tiv e beta-
adrenergic receptor blocking actions.
• Administer v asodilator: Nitroprusside (Nipride) and NTG.
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•
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agents: captopril (Capoten) or clonidine (Catapres).
Congestive Heart Failure (CHF)
CHF, which is sometimes ref erred to as “pump f ailure,” is a general term for the inadequacy of the heart to pump blood throughout the body . This
def icit causes insuf ficient perf usion to body tissues with v ital nutrients and oxy gen.
Pathophysiology
There are two ty pes of CHF failure: Lef t-sided f ailure and right-sided f ailure. Both may be acute or chronic and mild to sev ere, caused by HTN, CAD, or
v alv ular disease, inv olv ing the mitral or aortic v alv e. CHF can also be div id-ed into two subty pes: systolic heart f unction and diastolic heart f unction.
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• Sy stolic heart f unction results when the heart is unable to contract f orcef ully enough, during sy stole, to eject adequate amounts of blood into the
circulation. Preload increases with decreased contractility and af terload increases as a result of increased peripheral resistance.
• Diastolic heart f ailure occurs when the lef t v entricle is unable to relax adequately during diastole. Inadequate relaxation prev ents the v entri-cle f rom
f illing with suf f icient blood to ensure adequate cardiac output.
Lef t-sided CHF presents as:
• Dy spnea
• Diaphoresis
• Orthopnea
• Tachy cardia
• Tachy pnea
• Paroxy smal nocturnal dy spnea

• Fatigue
• Pulmonary crackles
• Wheezes
• S3 gallop
• Frothy pink-tinged sputum
• Weakness
• Conf usion
• Restlessness
Right-sided CHF presents as:
• Right upper quadrant pain
• Peripheral edema
• JVD
• Hepatomegaly
• Hepatojugular ref lux and edema
• HTN
• Anorexia
• Nausea
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Diagnostic Tests
• B-ty pe natriuretic peptide (BNP) lev el
• Chest x-ray
• Echocardiogram
• Pulmonary artery pressure catheterization
Management
• Primary goal in managing heart f ailure is to maintain cardiac output.
• Secondary goal is to decrease v enous (capillary ) pressure to limit edema.
• Diuretics (f urosemide): Aimed at controlling f luid retention.
• Beta blockers (metoprolol): Aimed at reducing cardiac workload.
• Nitrates (NTG, nitroprusside): Aimed at enhancing my ocardial con-tractility .
• Inotropes (dobutamine): Aimed at enhancing my ocardial contractility .
Abdominal Aortic Aneurysm (AAA)

• is a localized, chronic abnormal dilation of an artery located between the renal and iliac arteries, hav ing a diameter at least 1.5 times that of the
expected diameter with a natural history toward enlargement and rupture.
Pathophysiology
There are just theories about the pathology of AAA because the etiology is not completely understood. Theories suggest that atherosclerosis and
destruction of elastin and collagen f ibers in the v essel walls contribute to the dev elopment.
Pathophysiology for Atherosclerosis
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Pathophysiology Involvementwith Elastinand Collagen
• may present as asymptomatic or symptomatic. When asymptomatic, look for a pulsatile, periumbilical mass with or without a bruit. When
sy mptomatic, symptoms include:
• Early satiety
• Nausea
• Vomiting
• Gastrointestinal bleeding
• Back pain
• Lower extremity ischemia
• Venous thrombosis
• Flank/groin pain
AAA can also mimic:
• UTI inf ection
• Renal obstruction
• Ruptured disc
• Div erticulitis
• Pancreatitis
• Upper gastrointestinal hemorrhage
• Abdominal neoplasm
• Peptic ulcer perf oration
Diagnostic Tests
• Abdominal ultrasound (f irst line of diagnostic testing)
• CT scan of the abdomen
• Abdominal x-ray
• Aortogram

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Management
• Administer beta blocker to lower arterial pressure to the lowest SBP (120 mm Hg or less).
• May use newer alpha-beta-blocker labetalol (Trandate) in place of nitroprusside and a beta blocker; do not giv e direct v asodilators such as
hy dralazine.
Postoperative Management
• Goal of postoperativ e care is to reduce af terload and pressure at the repair site.
• Administer IV nitroprusside with esmolol (Brev ibloc) or labetalol (Trandate) and titrate the dosage to keep sy stolic BP below 120 mm Hg as
ordered.
• Starting immediately af ter surgery , continuously monitor the patient’s neurological status, cardiac rhy thm, RR, hemody namics, urine output, core
body temperature, f luid and electroly te imbalance.
• Prov ide analgesia.
• Monitor f or acute renal f ailure, ischemic colitis, spinal cord ischemia, and aorto-enteric f istula.
• Assess patient’s gastrointestinal f unction.
• Report urine output less than 0.5 mL/kg/hr, which indicates dehy dra-tion, v olume def icit, or decreased renal f unction.
Aortic Dissection
Aortic dissection is a tear (without hematoma or an intramural hematoma) in the aortic wall, causing a longitudinal separation between the intima and
adv entitia lay ers resulting in a div ersion of blood f low f rom its normal arterial pathway . Aortic dissection requires emergent surgery .
Pathophysiology
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Consider acute phase if diagnosed within f irst 2 weeks of onset of pain.
PresentingSymptoms
• Mimics inf erior wall MI
• CHF

• CVAP
• Standard ty pe A aortic dissection: Sev ere chest pain, sometimes sharp
• Standard ty pe B dissection: Sev ere chest pain radiating to the back; described as “ripping or tearing” pain
• Pain can shif t to the abdomen
• Increasing restlessness (sign of extending dissection)
• Decrease in urine output
Diagnostic Tests
• Chest x-ray : Shows widening mediastinum
• ECG
• Transthoracic echocardiogram
• Transesophageal echocardiogram
• CT scan
• Aortography
• MRI
Management
• Measure BP in both arms. Monitor HR, RR, and pain lev el.
• Perf orm f requent peripheral pulse checks, ankle brachial index mea-surements, and neurological assessments.
•
• Plan f or emergency surgery .
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Pericardial Effusion
Pericardial eff usion is the abnormal accumulation of more than 50 mL of fluid (normal: 15–50 mL to serv e as lubricant f or the v isceral and parietal
lay ers of pericardium) in the pericardial sac, which may lead to noncom-pression of the heart, which interf eres with heart f unction.
Pathophysiology
Clinical Manifestations
Pericardial ef f usion can be asy mptomatic with up to 2 L accumulated f luid in the pericardial sac.
• Complaints of dull, constant ache in the lef t side of the chest with sy mptoms of cardiac compression.
• Muf f led heart sounds.

• May or may not present with pericardial f riction.
• Dullness of percussion of the lef t lung ov er the angle of scapula (Ewart’s sign).
•
Diagnostic Tests
• Echocardiogram
Management
• Pain management.
• Pericardiocentesis perf ormed by a phy sician.
• Position changes decrease SOB.
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• Wound care af ter pericardiocentesis, care of pericardial catheters.
• Frequent assessments of VS, pulses, LOC, respiratory status, skin and temperature changes, intake and output.
• Prev ent cardiac tamponade.
Cardiac Surgeries
Coronary Artery Bypass Graft (CABG)
CABG is an open-heart surgical procedure i n which a blood vessel from another part of the body, usually the saphenous vein from the leg, is g rafted below the occluded
coronary artery so that blood can bypass the blockage.
Pathophysiology
Surgery is perf ormed on those patients with coronary artery disease, causing blockage to the coronary arteries. Fatty streaks deposited in arterial
intima stimulates an inf lammatory response that causes prolif er-ation. Prolif eration causes blood v essels to f orm f ibrous caps, and deposits build up as
atheromas or plaques. Plaques pile up obstructing the blood f low.
Diagnostic Tests
• Health history
• Exercise treadmill testing
• Gated SPECT imaging
• Echocardiography
• Electron Beam Computed Tomography (EBCT)
• Lab work: lipid prof ile
Postoperative Care

• Common postop care includes maintaining airway patency and moni-toring the patient’s pulmonary status, v ital signs, intake and output.
• Perf orm peripheral and neurov ascular assessments hourly f or f irst 8 hours.
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• Monitor neurological status.
• Titrate drugs: v asopressor and inotropes to optimize cardiac f unction and BP.
• Monitor chest tube drainage and record amount.
• Watch f or signs of bleeding and monitor hemoglobin and hematocrit ev ery 4 hours.
• Monitor patient’s pain and medicate as needed.
Coronary Stenting/Percutaneous Coronary Intervention
Percutaneous coronary interv ention (PCI) is a common interv ention f or angina. In a catheterization lab, a catheter equipped with an inf latable bal-loon
tip is inserted into the appropriate coronary artery. When the lesion is located, the catheter is passed through the lesion, the balloon is inf lated, and the
atherosclerotic plaque is compressed, resulting in v essel dilata-tion. Intracoronary stents are usually inserted during PCI. Stents are used to treat
abrupt or threatened abrupt closure or restenosis f ollowing PCI.
Procedure
Stents are expandable meshlike structures designed to maintain v essel patency by compressing the arterial walls and resisting v asoconstric-tion.
Stents are caref ully placed ov er the angioplasty site to hold the v essel open.
• Aty pical or ty pical chest pain
• SOB
• Dy spnea
• Sy mptoms of angina
Diagnostic Tests
• ECG
• Echocardiogram
• Chest x-ray
• Lab tests: cardiac markers
Managementof Clinical Condition
• Administer antiplatelet agents (aspirin, ticlopidine, clopidogrel).
• Administer IV inf usion of gly coprotein IIb IIIa inhibitors (eptif ibatide).
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• Monitor f or signs and sy mptoms of bleeding at catheter site.
• Monitor f or chest pain.

Stent Insertion
Stent Inflation and Expansion
Balloon Removal and Stent Implantation
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Cardiac Valve Replacement
Clinical conditions that require a surgical procedure to replace the v alv e with either a mechanical v alv e or a porcine v alv e include:

• Acquired v alv ular dy sfunction
• Mitral v alv e stenosis
• Mitral v alv e regurgitation
• Mitral v alv e prolapse
• Aortic stenosis
• Aortic regurgitation
The surgical procedure is the same as open-heart surgery except the heart is not by passed, only the v alv e is replaced.
Pathophysiology
• Mitral v alv e regurgitation: Fibrotic and calcif ic changes prev ent mitral
• Mitral v alv e prolapse: The v alv ular leaf lets enlarge and prolapse into
• Aortic stenosis:
• Aortic regurgitation: Aortic v alv e leaf lets do not close properly
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• Mitral stenosis: Fatigue, dy spnea on exertion, orthopnea, paroxy smal nocturnal dy spnea, hemopty sis, hepatomegaly , JVD, pitting edema, atrial
f ibrillation, apical diastolic murmur.
• Mitral valve regurgitation: Fatigue, dy spnea on exertion, orthopnea, palpitations, atrial f ibrillation, JVD, pitting edema, high-pitched holosy stolic
murmur.
• Mitral valve prolapse: Aty pical chest pain, dizziness, sy ncope, palpita-tions, atrial tachy cardia, v entricular tachy cardia, systolic click.
• Aortic stenosis: Dy spnea on exertion, angina, sy ncope on exertion, f atigue, orthopnea, paroxy smal nocturnal dy spnea, harsh sy stolic
crescendo-decrescendo murmur.
• Aortic insufficiency: Palpitations, dy spnea, orthopnea, paroxy smal nocturnal dy spnea, f atigue, angina, sinus tachy cardia, blowing
decrescendo diastolic murmur.
Diagnostic Tests
• Echocardiogram
• ECG
• Cardiac angiogram
• Exercise tolerance test
Management
• Routine postoperativ e care: maintain airway patency , monitor pul-monary status.
• Monitor v ital signs and intake and output.
• Perf orm peripheral and neurov ascular assessments hourly f or f irst 8 hours af ter surgery .
• Monitor neurological status f or f irst 8 hours postoperativ ely .
• Titrate medications, pressors and inotropes to optimize cardiac f unc-tion and BP.

• Monitor chest tube drainage.
• Watch f or signs of bleeding by monitoring hgb and hct ev ery 4 hours.
• Monitor f or pain.
• Start on anticoagulation therapy when approv ed by cardiac surgeon.
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Cardiac Transplant
Cardiac transplant is a surgical procedure to remov e a diseased heart and replace it with a healthy donor heart.
Causes That Lead to Cardiac Transplant
End-stage heart disease includes congenital heart disease (single v entri-cle phy siology , coronary sinusoids), cardiomy opathy (primary : idiopathic,
f amilial, secondary pregnancy , drug-induced), and acquired heart disease (v alv ular disease).
Criteria for Heart Transplant
• CHF
• CAD with intractable angina sy mptoms,
• Ventricular dy srhy thmias unresponsiv e to medical/surgery therapy
• Primary cardiac tumors with no ev idence of spread to other body sy stems
Diagnostic Tests Prior to Transplantation
• Echocardiogram
• Right heart catheterization
• Pulmonary f unction tests
• Exercise treadmill test
• Abdominal ultrasound
• Chest x-ray s
• Coronary angiogram
• Cardiac biopsy
• Chromosome testing
• Lab tests: chemistries, CBC, human leukocy te antigens (HLA) anti-body screening, v iral antibody screening (HIV, cy tomegalov irus, herpes
v irus, v aricella, Epstein- Barr)
Postoperative Care
• Admit to Cardio Thoracic ICU, 24–48 hours on v entilator until anesthesia cleared f rom sy stem.
• Foley catheter to grav ity , monitor output closely .
• Daily chest x-ray .
• Monitor chest tube sites and drainage (generally will hav e 2–3 chest tubes in place).

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• Pulmonary toilet measures hourly , once extubated.
• Perf orm and document complete nursing assessments f requently during f irst 12–24 hours af ter surgery .
• Watch f or signs and sy mptoms of bleeding.
• Treat dy srhy thmias.
• Prev ention of right-sided heart f ailure.
• Watch f or early signs of rejection, inf ection, immunosuppressiv e issues.
• Monitor f or signs of drug toxicity .
• ICU care f or about 3–5 day s post-op.
• Treatment of rejection: treated with increased doses of cy closporine, azathioprine, high-dose corticosteroids, prednisone, monoclonal anti-bodies or
poly clonal antibodies.
• Highest risk f or inf ection: 1 week post-op.
Signs and Symptoms of Rejection
• Low-grade f ev er
• Fatigue
• SOB
• Peripheral edema
• Pulmonary crackles
• Pericardial f riction rub
• Arrhy thmias
• Decreased ECG v oltage
• Increased JVD
• Hy potension
• Cardiac enlargement on x-ray
• Vascular degeneration
• Tachy cardia
• Fatigue
• Palpitations
• Nausea and v omiting
Other Complications
• Inf ection
• CAD
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Carotid Endarterectomy (CE)
CE is a surgical procedure to remov e plaque material f rom inside the carotid artery , improv ing the carotid luminal diameter, allowing adequate blood
f low, theref ore prev enting stroke. The procedure is indicated in symptomatic patients with carotid-territory TIA or minor strokes who hav e carotid artery
stenosis of 70%–99%.
Pathophysiology of the Disease Process Leading to CE
• Signs and sy mptoms of TIA or stroke
• Dizziness
• Lightheadedness
Diagnostic Tests
• Ultrasound of carotid artery
• Magnetic resonance angiography (MRA)
• Contrast enhanced MRA (CEMRA)
• Intra-arterial angiography (IAA)
Managementof Clinical Condition
• Assess surgical site f or bleeding.
• Perf orm f requent neurological checks.
• Administer antihy pertensiv e medications.
• Administer statins.
• Administer antiplatelet agents.
• Administer aspirin (81–325 mg) bef ore and af ter surgery .
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Infections of the Heart
Endocarditis
Endocarditis is the inf lammation of the inner most lay er of the heart. It can include the heart v alv es, chordae tendinea, cardiac septum or the lining of
the chambers. It is caused ty pically by bacterial inf ections (Streptococcus viridans or Staphylococcus aureus).
Pathophysiology

Endocarditis presents as:
• Acute onset of f ev er
• Chills
• Night sweats
• Anorexia
• My algia
• Arthralgia
• Extreme f atigue and malaise
• Nausea and v omiting
• Headache
• Weight loss
• SOB
• Chest pain
• Abdominal pain
• Conf usion
• Pain in the muscles, joints, and back
Be suspicious if petechiae appears on the conjunctiv a, neck, anterior chest, abdomen, or oral mucosa. Look for Janeway lesions (nontender macule)
on patient’s palms and soles, Osler’s nodes (tender, ery thema-tous, raised nodules) on f ingers and toe pads, and splinter hemorrhages under
f ingernails.
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Diagnostic Tests
• Transthoracic echocardiogram
• Abdominal computed tomography (CT) or MRI
• Positiv e blood cultures
Management
• Antibiotic prophy laxis bef ore certain inv asiv e procedures.
• Priorities include supporting cardiac function, eradicating the inf ec-tion, and prev enting complications, such as systemic embolization and heart
f ailure.
• Do not giv e anticoagulants because of risk of intracerebral hemorrhage.
Pericarditis
Pericarditis is inf lammation of pericardium that can cause f luid to accu-mulate in the pericardial space due to idiopathic causes, inf ection, cardiac
complications, autoimmune reactions, certain drugs, or trauma.

Pathophysiology
Sharp, constant chest pain that is located in the midchest (retrosternal) is the most common sy mptom. A hallmark sign of pericarditis is if the patient
leans f orward while sitting to reliev e chest pain. Pain may radiate to the neck, shoulders, and back; radiation to the ridge of the lef t trapez-ius muscle is
specif ic f or pericarditis.
Depending on the cause, patient may also hav e f ev er, malaise, tachy -pnea, and tachycardia. Pericardial friction rub, heard in the lower sternal
border, is the most important physical sign.
Diagnostic Tests
• ECG
• Echocardiogram
• Chest x-ray
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• Lab work: cardiac markers
• Complete blood count
• Urinaly sis
• Transesophageal echocardiogram (TEE)
Management
• NSAIDs may be used f or up to 2 weeks.
• Monitor f or cardiac tamponade.
• More sev ere pain can be controlled with morphine.
• If cause is inf ectious, antibiotics or antif ungal drugs may be adminis-tered.
• Treatment: Antibiotics specif ic to the pathogen f or at least 6 weeks.
• If a pericardiectomy is perf ormed, continue assessments of VS, lab work, and the appearance of wounds and insertion sites of inv asiv e lines.
• Monitor temperature and cardiac rhy thm, assess f or heart murmurs.
• Perf orm neurological assessments, inspect skin surf aces, and monitor drug peaks and troughs, and urine output.
Pacemakers/AICD
There are three ty pes of pacemakers:
• Transcutaneous (external)
• Percutaneous
• Permanent
Transcutaneous Pacemakers
Transcutaneous pacemakers are used f or noninv asiv e temporary pacing, accomplished through the application of two large external electrodes. The
electrodes are attached to an external pulse generator, which can operate on alternating current or battery . The generator emits electrical pulses,
which are transmitted through the electrodes and then transcuta-neously to stimulate v entricular depolarization when the patient’s heart rate is slower

than the rate set on the pacemaker. Used as an emergency measure, a transcutaneous pacemaker should be used f or 48–72 hours only . Electrodes
should be changed ev ery 24 hours minimally .
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Percutaneous Pacemakers
Percutaneous pacemakers are f or inv asiv e temporary pacing. An inv asiv e temporary pacemaker sy stem consists of an external battery pulse gener-
ator and pacing electrodes, or lead wires. These wires attach to the gen-erator on one end and are in contact with the heart on the other end. Electrical
pulses, or stimuli, are emitted f rom the negativ e terminal or the generator, f low through a lead wire and stimulate the cardiac cells to depolarize.
Permanent Pacemakers
Permanent pacing is perf ormed f or the resolution of nontemporary con-duction disorders, including complete heart block and sick sinus sy n-drome.
Permanent pacemakers are usually powered by a lithium battery and hav e an av erage lif e span of 10 y ears.
Automatic Implantable Cardioverter Device (AICD)
AICD is indicated f or the patient who has experienced one or more episodes of spontaneous sustained v entricular tachy cardia (VT) or v en-tricular
f ibrillation (VF) unrelated to MI or other causes amendable to correction.
Cardiac Tamponade
Cardiac tamponade is excessiv e f luid or blood f rom the heart in the peri-cardial space that accumulates pressure in the pericardial sac and aff ects the
heart’s f unction.
Pathophysiology
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•
First Signs
• Anxiety and restlessness
• Cool, diaphoretic skin
Classic Signs
• Beck’s triad: muf f led heart sounds, increased JVD, and hy potension

• Narrow pulse pressure (SBP and DBP)
• Tachy cardia
• Weak, thready pulse
Late Signs
•
• Electrical alternans (alternating lev els of v oltage in the P wav es and QRS complexes in all leads and may occur in T wav es)
Diagnostic Tests
• Chest x-ray
• Echocardiogram
Management
• Call MD stat.
• Obtain Stat 2-D echocardiogram.
• Obtain Stat chest x-ray .
• Obtain Stat lab work.
• MD to place PA catheter.
• Place patient in supine position, HOB elev ated 30°–60°.
• Administer O2.
• Giv e sedativ es, morphine f or chest pain.
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• Obtain ECG.
• If on mechanical v entilation: No positiv e pressure used.
• Inotropic drugs on standby .
• Blood, plasma, v olume expander on hand.
ACLS Algorithms: Cardiac/Respiratory Arrest
Ventricular Fibrillation (VF) or Pulseless Ventricular Tachycardia (VT)
• Shock: Biphasic: 200 J; monophasic: 360 J. Reassess rhy thm.
• CPR: Immediately perf orm 5 cy cles of CPR (should last about 2 min).
• Epinephrine: 1 mg IV or IO (2 to 2.5 mg, endotracheal tube) every 3–5 min
or Vasopressin: 40 units IV or IO, one time only . May use to replace 1st or 2nd dose of epinephrine (giv en without interrupting CPR).
• Shock: Biphasic: 200 J; monophasic: 360 J. Reassess rhy thm.
• Consider antiarrhythmics (giv en without interrupting CPR):
• Amiodarone: 300 mg IV or IO, may repeat 150 mg in 3–5 min.

• Lidocaine: 1.0–1.5 mg/kg IV or IO, may repeat 0.5 to 0.75 mg/kg q5–10 min, max 3 mg/kg.
• Magnesium: 1–2 g IV or IO f or Torsade de Pointes.
Asystole or PEA (Pulseless Electrical Activity)
• Resume CPR f or 5 cy cles (should last about 2 minutes).
• Epinephrine: 1 mg IV or IO (2 to 2.5 mg ET) ev ery 3–5 min or
Vasopressin: 40 units IV or IO, one time only . May use to replace 1st or 2nd dose of epinephrine (giv en without interrupting CPR).
• Atropine: 1 mg IV (2 to 3 mg endotracheal tube ev ery 3–5 min) (maxi-mum 3 mg) f or asy stole or brady cardic PEA.
Intra-Aortic Balloon Pump (IABP)
An IABP consists of a 30-cm poly urethane balloon attached to one end of a large bore catheter. The dev ice is inserted into the f emoral artery at the
groin, either percutaneously or v ia arteriotomy , with the balloon wrapped
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tightly around the catheter. Once inserted, the catheter is adv anced up the aorta until the tip lies just bey ond the origin of the L subclav ian artery. When
in place, the balloon wrapping is released to allow periodic balloon inf lations.
Effects
The intra-aortic balloon is inf lated with helium at the onset of each dia-stolic period, when the aortic v alv e closes. The balloon is def lated at the onset of
v entricular sy stole, just bef ore aortic v alv e opens. Inf lation of the balloon increases the peak diastolic pressure and displaces blood toward the
periphery . Def lation of the balloon decreases the end-diastolic pressure, which reduces impedance to f low when aortic v alv e opens at onset of sy stole.
This decreases v entricular af terload and pro-motes stroke v olume.
Diastole Systole
Aorta
Heart
Balloon
catheter
Descending
aorta
Renal
artery

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IABP waveforms
mm
Hg
Systole Diastolic augmentation
Time
Indications
• Cardiopulmonary by pass
• Cardiac transplant
• AMI with cardiogenic shock
• Acute mitral v alv e insuf ficiency
• Unstable angina
Contraindications
• Aortic regurgitation

• Aortic dissection
• Recently placed (within 12 months) prosthetic graf t in thoracic aorta
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ECGs
12-Lead ECG
I
II
III
aVR
aVL
aVF
V1

V2
V
3
V4
V5
V
6
Lead Placement
Midclavicular
line
Anterior
axillary line
Midaxillary
line

V6
V5
V1
V2
V3 V4
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Hemodynamics of Dysrhythmias
Atrial Dysrhythmias
Causes
• Amphetamines
• Cocaine
• Decongestants
• Hy pokalemia
• Hy perthy roidism
• COPD
• Pericarditis
• Digoxin toxicity
• Hy pothermia
• Alcohol intoxication
• Pulmonary edema
Ventricular Dysrhythmias
Bradycardia
•
Causes
• Vomiting
• Gagging
• Valsalv a maneuv er
• ETT suctioning

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O2 consumption.
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Symptoms
• Chest pain
• SOB
• Altered mental status
Treatment Considerations
• Atropine
• Epinephrine
• Isoproterenol (Isuprel)
• Pacemaker
• Dopamine if hy potensiv e
Tachycardia
Tachy cardia is def ined as a heart rate greater than 100 bpm.
Causes
• Caf f eine
• Nicotine
• Pain
• Fev er
• Stress
• Anxiety
Symptoms
• Altered LOC
• Chest pain or discomf ort
• Palpitations
• SOB
• Diaphoresis
• Hy potension
• Jugular v enous distention
Treatment Considerations
• Carotid massage
• Valsalv a maneuv er
• Cardiov ert at 100 J–360 J
• Radiof requency ablation
• Pacemaker
CV
CV
•
• Implantable cardiov erter def ibrillator (ICD), if indicated

Determining Rate and Measurement
To figure out rate (regular rhythms only), you can do one of the following:
Count the number of QRS complexes (regular rhythms only) in a 6-sec strip and multiply by 10.
Divide the number of large boxes between two R waves into 300.
Irregular rhythms should be counted for an entire minute.
Remember the number sequence below and find an R wave that falls on a heavy line. Starting from the next heavy line, count 30 0, 150, 100, and so forth, and whatever
line the next R wave falls on is the heart rate (see below for example).
1st R wav e 300 150 100 75 60 50 43
Next R wave here
would be 150 bpm.
Next R wave here would be 60 bpm.
Inherent rates of different cardiac regions:
SA Node .....................
60– 100
bpm
AV Node ....................... 40– 60 bpm
Ventricles..................... 20– 40 bpm

One big box represents
0.20 sec and is 5 mm
2
.
One small box
represents
0.04 sec and
is 1 mm
2
.
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Normal Cardiac Cycle and Measurements
QRS
P
T
R
P
Q S
P-R interval
0.04
sec
0.20
sec
P wave atrial depolarization; QRS v entricular depolarization;
• wave v entricular repolarization
Quick Guide to Analyzing the ECG
• Determine the ov erall rate:
• Determine the regularity : Regular or irregular.
• If irregular, is there any pattern?
• Examine the P wav es.
• Is there a P wav e bef ore each QRS? Is there more than 1 P wav e?
• Are P wav es absent?
• What is the conf iguration of the P wav e? Round? Saw toothed?
• Do they look the same?
• Do any occur earlier or later than expected?

• Are any P wav es located within the QRS or T wav e?
• Determine the PR interv al.
• Is it normal, prolonged, or shortened?
• Can it be measured?
• Is it the same f or each beat? Any pattern?
CV
CV
• Examine the QRS complex.
• Is there a QRS af ter each P wav e?
• Do they look the same?
• Do any occur earlier than expected?
• Is there a pattern to QRS complexes occurring early ?
Normal Cardiac Rhythm Parameters
NSR • 60 bpm–100 bpm
Bradycardia
• <60 bpm; consider sinus
brady cardia, AV block
Tachycardia
• >100 bpm; consider
atrial f ibrillation, atrial
f lutter,
suprav entricular
tachy cardia, ventricular
tachy cardia
PR interval • 0.12–0.20 sec
• >0.20 sec; consider AV
block
• <0.12 sec; consider
junctional rhythm
• Unable to determine;
consider atrial arrhythmia,
junc-
tional arrhy thmia;
examine QRS to
determine if
v entricular arrhythmia
P wave • Generally round
• Spiked, nonrounded;
consider atrial fibrillation
or PACs
QRS • 0.06–0.10 sec
• Wide, bizarre; consider
PVC, VT
Baseline is grossly irregular with no discernible P wav es; consider VT Flat baseline, asy stole; begin CPR f or either dy srhy thmia.

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Supraventricular Tachycardia (SVT)
P w ave buried in T w ave
• ■ Rate: 150–250 bpm
• Rhythm: Usually regular Unable
to■determinePRinterval:
Usually ■hiddenPwaves:inpreceding T wav e
• QRS: 0.06–0.10 sec, >0.10 sec if conducted through the v entricles
• Causes: Nicotine, stress, anxiety , caffeine
•Vagal maneuv er,■Managementadenosine (Adenocard, Adenoscan), amiodarone (Cordarone,
Pacerone), diltiazem (Cardizem), cardiov ersion, propaf enone (Ry thmol), f lecainide (Tambocor)
CV
Atrial Flutter
Flutter w aves

CV
• Atrial rate: 250–400 bpm
• PR interval: Unable to determine
• Rhythm: Regular or irregular depending if combination of degrees of block (e.g., 2:1 + 4:1)
• P waves: Saw-toothed f lutter wav es
• Ventricular rate: Slow or f ast depending on degree of block
• QRS: Normal or narrow
• Management: Diltiazem; sotalol, propranolol or other beta blockers, digoxin, amiodarone, propaf enone, f lecainide, magnesium, electrical
cardiov ersion, radiof requency ablation; anticoagulate
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Atrial Fibrillation
Irregular R-R intervals

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Atrium quiv ers instead of contracting, loss of atrial kick. Mural thrombi can lead to pulmonary
embolism or stroke. Sy mptoms include palpitations, f atigue, malaise, pulse def icit. risk of my ocar-
dial ischemia.
• Atrial rate: 400–600 bpm
• PR interval: Unable to determine
• Rhythm: Irregularly irregular
• P waves: None; f ibrillatory wav es
• Ventricular rate: Normal or f ast
• QRS: Usually narrow
• Management: Same as atrial f lutter; ibutilide (Corv ert) af ter cardiov ersion; anticoagulate
CV
Premature
Ventricular Contractions (PVC)

PVC
CV
May be unif orm (one ectopic f ocus or unif ocal) or dif f erent f oci (multifocal).
Patient may complain of lightheadedness, palpitations, heart skipping a beat.
• P wave: Absent bef ore PVC
• Rhythm: Irregular where PVC occurs
• QRS: Wide, bizarre, >0.10 sec; may be f ollowed by compensatory pause
• Causes: Healthy persons, caf f eine, nicotine, stress, cardiac ischemia or inf arction, digoxin toxicity , electroly te imbalances, hy povolemia, f ever,
hy pokalemia, hy poxia, hy permagnesemia, acid-base imbalance
• Management: Correct the cause, amiodarone, lidocaine

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Ventricular Tachycardia (VT)
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Three or more PVCs together with the same shape and amplitude.
Unstable rhy thm. Easily progresses to VF if VT sustained & untreated.
Patient may or may not hav e a pulse, no BP.
• Atrial rate: Unable to determine; no P wav es; no PR interv al
• Ventricular rate: 100–250 bpm
• Rhythm: Usually regular
• QRS: Wide & bizarre, >0.10 sec
• Management: Amiodarone, procainamide, lidocaine, sotalol, immediate sy nchronized cardiov er-sion; pulseless VT is treated the same as VF

CV
Ventricular Fibrillation (VF)
Chaotic pattern. No ef f ective ventricular contraction. No C.O., no pulse, no BP. Brain death occurs with-in 4–6 min, if untreated.
• Atrial rate: Unable to determine; no P wav es; no PR interv al
• Ventricular rate: Fibrillatory wav es with no pattern
• Rhythm: Irregular
• Management: Amiodarone, procainamide, lidocaine, magnesium sulf ate, immediate def ibrillation at 200 J–360 J; CPR with epinephrine,
v asopressin & sodium bicarbonate; intubate, IV access if none present, induce mild hy pothermia 32°C–34°C (89.6°F–93.2°F)

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CV
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First-Degree AV Block
Problem in the conduction sy stem. May progress to more sev ere block.
Patient usually has no sy mptoms & no hemody namic changes.
• P wave: Present, bef ore each QRS
• Rhythm: Regular
• PR interval: >0.12 sec
• QRS: Normal
• Management: Correct the cause, close monitoring, usually benign

CV
Second-Degree AV Block—Mobitz I or
Wenckebach Phenomenon
Blocked beat
X
• P wave: Present until one P wav e is blocked with no resultant QRS
• Rhythm: Irregular
• PR interval: Gets progressiv ely longer until a QRS is dropped
• QRS: Normal
• Management: Correct the underly ing cause, atropine, temporary pacemaker
78

CV
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Second-Degree AV Block—Mobitz II
Problem with bundle of His or bundle branches.
May progress to more serious block.
• P wave: Present but atrial rate > v entricular rate
■ Conduction of P waves:QRS complexes in 2:1, 3:1 or 4:1 manner
• Rhythm: Regular
• PR interval: Normal if P wav e f ollowed by QRS
• QRS: Normal but QRS periodically missing, sometimes wide
• M anagement : At r opi
ne f or br adycar di
a, i
sopr ot er enol i
f ver y sl
ow r at e, pacem aker
CV

Third-Degree AV Block—
Complete Heart Block
Loss of sy nchrony between atrial and v entricular contractions.
Potentially lif e-threatening.
Digoxin toxicity a f requent cause.
■ P wave: Present but atrial rate> v entricular rate
■ Conduction of P waves in no relation to QRScomplexes
■ Rhythm: Regular atrial rateand ventricular rate
CV
■ PR interval: No relationof P waves to QRS complexes
■ QRS: Usually wide
■ Management: Atropinefor bradycardia, isoproterenol, pacemaker
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Respiratory Disorders

Adult Respiratory Distress Syndrome (ARDS)
ARDS is def ined as noncardiogenic pulmonary edema characterized by sev ere ref ractory hy poxemic respiratory failure and decreased pulmonary
compliance.
Pathophysiology
•
Sy mptoms of ARDS occur within 24 to 48 hours of cause and include:
• Increased respiratory rate, increased work of breathing, dy spnea, cy anosis
• Crackles, rhonchi or wheezes, dry cough
• Intercostal and suprasternal retraction, retrosternal discomf ort
• Agitation, restlessness, anxiety , confusion
• Diaphoresis
• Abdominal paradox
• Increased pressure to v entilate
• Hy poxemia ref ractory to increased f ractional concentration of oxy gen in inspired gas (FIO2)
• Increased peak inspiratory pressure
• Decreased lung v olume, decreased f unctional residual capacity , low v entilation/perf usion (V/Q) ratio
• Pulmonary capillary wedge pressure (PCWP) <18 mm Hg and/or no ev idence of CHF or lef t atrial hy pertension
• Acute respiratory alkalosis initially , which may progress to respiratory acidosis
• Worsening arterial blood gases (ABGs) with increased FIO2,, increased crackles
• Worsening partial pressure of arterial oxy gen (PaO2)/FIO2 (P/F) ratio
• Dif f use bilateral pulmonary inf iltrates on chest x-ray (CXR) indicates “whiteout”
• Fluid and electroly te problems
RESP
RESP
Diagnostic Tests
• Arterial and v enous blood gases
• Mixed v enous oxy gen saturation
• Continuous oxy genation monitoring v ia pulse oximetry
• Pulmonary f unction tests
• Pulmonary artery catheter
• Serial CXRs
• Chest computed tomography (CT)
• CBC, metabolic panel, serum lactate (lactic acid)

Management
• Treat underly ing cause.
• Administer O2 mask or mechanical ventilation withpositive end-expiratory pressure (PEEP)and high FIO2. Consider oscillator ventilator— used when difficulty
oxy genating a patient on conventional setting because of poor lung compliance (required neuromuscular blockade).
• Ref er to basics: mechanical v entilation, blood gases p. 6 and p. 2.
• Prov ide continuous arteriov enous hemof iltration (CAVH).
• Maintain hemody namic stability .
• Administer glucocorticosteroids.
• Administer surf actant therapy .
• Place patient in prone position.
• Administer diuretic; f luid management.
• Prov ide sedation or therapeutic paraly sis if necessary .
• Prov ide pain control.
• Prov ide nutritional support.
• Cluster activ ities to decrease f atigue.
• Inv estigational management of ARDS includes inhaled nitrous oxide, liquid v entilation, ECMO, alv eolar surf actant, and v asodilators.
Extracorporeal MembraneOxygenation (ECMO)
ECMO is a modif ied f orm of cardiorespiratory by pass. It prov ides oxy -genation and pulmonary support f or patients in sev ere respiratory f ailure,
particularly ARDS. Its purpose is to av oid high oxy gen concentrations and high peak inspiratory pressures, PEEP, and tidal v olume, while allowing the
lung to rest and heal.
Venovenous (VV) ECMO
The right internal jugular, saphenous, common iliac, or f emoral v eins are cannulated. The patient’s blood is circulated through a membrane
82
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oxy genator in which O2 is inf used and CO2 remov ed. ECMO can compensate f or approximately 70% of the patient’s gas exchange requirements.
Functional oxy gen saturation (SpO2) and CO2 are monitored continu-ously to maintain v alues of 50%–80% and 35–45 mm Hg, respectiv ely .
Complications include inf ections and sepsis, bleeding, disseminated intrav ascular coagulation (DIC) and intracranial bleeding, air emboli, renal
f ailure, decubitus ulcers, and heparin-induced thrombocy topenia. Nursing care is aimed toward prev enting complications.
Shunting
Anatomic shunt is def ined as the div ersion of blood f low f rom the right side of the heart directly into the lef t side of the heart without coming into contact
with the alv eoli.
Phy siologic shunt (capillary shunt; or right-to-left shunt) is def ined as the f low of blood f rom the right side of the heart, through the lungs, and into the
lef t side of the heart without taking part in alv eolar and capillary dif f usion. Pulmonary blood perf uses completely unv entilated alv eoli.
Absolute shunt (true shunt) is def ined as a combination of the anatom-ic and capillary shunt, and is generally ref ractory to oxy gen therapy . The V/Q
ratio expresses the relationship of alv eolar v entilation to pulmonary capillary perf usion:
• Decreased v entilation plus increased perf usion represents a low V/Q ratio.
• Increased v entilation plus decreased perf usion represents a high V/Q ratio.
Diagnostic Tests
• Alv eolar-arterial (A-a) gradient (PAO2/PaO2)
• PAO2 represents the partial pressureof alveolar O2 (mm Hg).

• PaO2 represents the partial pressure of arterial O2 (mm Hg).
• Value is used to calculate the percentage of the estimated shunt.
• Value represents the dif f erence between the alv eolar and arterial oxy gen tension.
• Normal A-a gradient v alue <15 mm Hg.
• Value is increased in atrial or v entricular septal def ects, pulmonary edema, ARDS, pneumothorax, and V/Q mismatch.
RESP
RESP
• a/A ratio (PaO2/PAO2).
• If ratio <0.60, shunt is worsening.
• Estimation of shunt using PaO2/FIO2 (P/F) ratio:
• P/F ratio 500 indicates a 5% shunt.
Ventilator-Assisted Pneumonia (VAP)
VAP is an airway inf ection that dev elops more than 48 hours af ter the patient is intubated. It is associated with increased m ortality, prolonged time
spent on a v entilator, and increased length of ICU/hospital stay .
Pathophysiology
VAP is usually caused by gram-negativ e bacilli or Staphylococcus aureus v ia microaspiration of bacteria that colonize the orophary nx and upper
airway s or bacteria that f orm a biof ilm on or within an endotracheal tube (ETT). The presence of an ETT also impairs cough and mucociliary clear-
ance. Suctioning also contributes to VAP.
VAP presents with:
• Increased RR, HR, and temperature (>38.3°C or 101°F)
• Increased WBC (>10,000/mm3)
• Increased purulent tracheal secretions
• Crackles
• Worsening oxy genation, hy poxemia, PaO2/FIO2 changes
Diagnostic Tests
• CXR shows new or persistent inf iltrate
• Tracheal aspirate and blood cultures
• Clinical Pulmonary Inf ection Score (CPIS) >6
• Bronchoscopy or bronchoalv eolar lav age
Management
• Monitor CXR and amount and color of tracheal secretions.
• Giv e IV antibacterials to which the known causativ e bacteria are sensitiv e. Consider:
• Piperacillin/tazobactam (Zosy n)
• Gentamicin (Garamy cin)
84

85
• Tobramy cin (Nebcin)
• Vancomy cin (Vancocin)
• Cef tazidime (Fortax, Ceptaz)
• Lev of loxacin (Lev aquin)
• Imipenem/cilastatin (Primaxin)
• Linezolid (Zy v ox)
• Ticarcillin (Ticar)
• Daptomy cin (Cubicin)
• Ticarcillin (Ticar)
• Ciprof loxacin (Cipro)
• Amikacin (Amikin)
• Aztreonam (Azactam)
Evidence-Based Practice Guidelines to Prevent VAP (Ventilator Bundle):
• Elev ate head of bed 30–45 degrees.
• Prov ide “sedation v acations”: Decrease amount and f requency of sedation.
• Assess readiness to extubate and extubate as soon as possible.
• Prov ide peptic ulcer disease prophy laxis with H2-receptor inhibitors.
• Prov ide deep v enous thrombosis prophy laxis.
• Use meticulous hand hy giene, use glov es appropriately .
• Use meticulous sterile technique when appropriate.
• Use a continuous aspiration of subglottic secretion (CASS) ETT.
• Prov ide meticulous oral care ev ery 12 hours, including brushing the teeth with a sof t toothbrush, tap water, and toothpaste f or 1–2 minutes; brushing
the tongue; and apply ing lip balm and moisturizing swabs. Follow with 0.5 oz of 0.12% chlorhexidine gluconate rinse to tooth enamel, gums, and
posterior orophary nx.
• Eliminate routine saline bronchial lav age during ETT suctioning.
• Use continuous lateral rotation therapy (CLRT).
• Drain condensation in v entilator tubing down and away f rom patient.
• Suction ev ery 4 hours and prn. Replace all suction equipment ev ery 24 hours.
• Feeding tubes should be placed bey ond the py lorus of the stomach.
• Discontinue mechanical v entilation as soon as possible. Consider bilev el positiv e airway pressure (BiPAP) and continuous positiv e airway
pressure (CPAP).
RESP
RESP

Hospital-Acquired Pneumonia Risk Index †
Factor Points Patient Patient
A B
Temperature (°C) >36.5 and <38.4 0
>38.5 and <8.9 1
>9 and <36 2
Blood leukocytes, μL >4,000 and <11,000 0
<4,000 or >11,000 1
Band forms >50% 1
Tracheal secretions None 0
Nonpurulent 1
Purulent 2
Oxygenation:
PaO2/FIO2, mm Hg >240 or ARDS 0
<240 and no ARDS 2
Pulmonary

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