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Test 1

Terms in this set (122)

pH
7.35-7.45
PaCO2
35-45
PaHCO3
22-26
PaO2
80-100
Noninvasive Positive-Pressure Ventilation (NPPV)
oPositive pressure ventilation without an artificial airway
•BIPAP (Pressure High/Pressure Low): 2 pressures at once- high on inspiration and low on exhalation
•CPAP (Pressure Low)

*High flow nasal canula pt needs to keep mouth closed
Mechanical Ventilation
oPurpose is to support the respiratory system until the underlying cause of respiratory failure can be corrected
oVentilator failure requires manual ventilation of the patient
Ventilator Indications
oFor patients in acute respiratory failure who are unable to maintain adequate gas exchange evidenced by ABG's
oClinical definition of respiratory failure is:
•PaO₂ ≤ 60 (50) mm Hg with FiO₂ > 50% (hypoxemia failure)
•PaCO₂ ≥ 50 mm Hg with pH of 7.25 or less (hypercapnic)
oRespirations <10 or GCS <8
Determining normal or compensation
7.4 is used as the middle marker for the pH and it's determined if it's acidotic or alkalosis depending on where it falls on the scale
Positive Pressure Ventilation
oPositive pressure forces air into the lungs
oOpposite of spontaneous breathing

-Breathing in: lungs expands which means the volume increased and leads to lower pressure
-breathing out: decrease in lung volume means higher pressure
Ventilator Variables
oMandatory vs demand breaths
-Min. number of breaths per minute vs any # of breaths the follows the min. breath

oPressure vs volume
-Giving O2 until certain limit is met vs specific amount of air is given (pressure pushes air in and volume is based on title volume)

oPressure regulated volume control (PRVC): dual control
-looks at the last breath to make adjustments to meet the pt needs
Ventilation Modes
oAssist/Control (A/C) - CMV
-volume or pressure can be used. Continual mechanical ventilation, every breath the ventilator will assist with the breath
-pt at risk for resp alkalosis and lazy diaphragm and vent dependence
-pressure and volume are set

oSynchronized Intermittent Mechanical Ventilation (SIMV) - IMV
-only helps with mandatory breaths, allows pt to exercise resp on own (min/vol =rrxV

oPressure ventilation - CPAP, BiPAP, and pressure support (inhalation only) need adequate spontaneous breathing
Ventilator Settings
oRespiratory rate (bpm Rate): mandatory breaths
oTidal volume (Vt)
oPEEP: positive end expiratory pressure, at the end of inhalation extra pressure is added to keep alveoli open and prevent collapse
•Increased PEEP causes decreased CO
•Can cause tension pneumothorax
•can increase shunting blood to the brain so it can increase ICP
oFIO2: fraction on inspired oxygen, over 60% RF O2 toxicity
oVentilator settings need to be order by the physician and documented
Ventilator Complications
oAirway - extubation, dislodged/moved ET tube, airway damage, mucosa damage
oPulmonary - barotrauma, O2 toxicity, resp. acidosis/alkalosis, VAP, dysphagia/aspiration
oCardiovascular - hypotension, ↓CO
oGastrointestinal - stress ulcers, GI bleed, nutrition, aspiration
oPsychosocial - anxiety/stress, sleep disturbances, communication
Alarms for ventilatory RN action
oNever silence an alarm and walk away
oHave an ambu bag at bedside at all times
oAlways assess your patient first
oManually bag ventilate patient if problem cannot be identified immediately
Troubleshooting a Ventilator
D - displaced or dislodged

O - obstruction (secretions, blood, mucus, emesis, biting)

P - pulmonary problems (pneumothorax or tension pneumothorax, patient coughing)

E - equipment issues (kinks in tubing, fluid in tubing, malfunction, connection to O2)
Inline Suctioning
1.Check breath sounds
2.Hyperoxygenate patient
3.Use 5-10 mL saline (maybe?)
4.Insert catheter until patient coughs or you meet resistance
5.Suction and withdraw catheter
6.Reassess patient and suction again if needed
7.Document procedure
vWatch for PVCs
IHI VAP Bundle
oElevate HOB to 30-45°
oSedation interruptions and assess readiness to wean
oPeptic ulcer prophylaxis
oDVT prophylaxis
oMouth care Q4 - chlorhexidine
Readiness to Wean
oTeam effort
oEBP: weaning protocols managed by nurses and RTs' produce a reduction in ventilator days and shorter hospital stays
oAssessment for readiness to wean
oExtubation
Acute Respiratory Failure
oRespiratory system either fails in oxygenation or carbon dioxide elimination
o2 categories
-Type 1: hypoxemic or oxygenation failure: PaO2 <50/60 and FiO2 >50%

oType 2: hypercapnic or ventilatory failure: PaCO2 >50 with pH <7.25
Hypoxemic or Oxygenation Failure
oPresent when PaO₂ is not adequately maintained

7 mechanisms:
oHypoventilation
oIntrapulmonary shunting
oVentilation-perfusion mismatch
oDiffusion defects
oLow cardiac output
oLow hemoglobin level
oTissue hypoxia
Hypoventilation
oAlveolar ventilation refers to the amount of gas that enter the alveoli per minute
oIf alveolar ventilation is reduced due to hypoventilation the PAO₂ and PaO₂ will fall
oAlso causes an increase in alveolar CO₂
oPrecipitating factors are drug overdose causing CNS depression, neurological disorders, abdominal or thoracic surgeries
oTreatment aimed at increasing O₂ delivery and blowing off CO₂ - ↑ PEEP, FIO₂, or I:E ratio
Intrapulmonary Shunting
oNormally a small amount of unoxygenated blood returns to the left ventricle; this is a physiological shunt
oIf a larger amount of blood that is not oxygenated enters the left ventricle this is a pathological shunt and PaO₂ decreases - enters directly or not enough time for diffusion to take place
oCauses are ASD, VSD, atelectasis, pneumonia, pulmonary edema, and mucous plugs
oTreatment is directed toward the opening of the alveoli and improving ventilation
Ventilation Perfusion Mismatch
oNormally ventilation equals perfusion ventilation to perfusion (V/Q) ratio ≈ 1.0
oIf ventilation is less than perfusion the V/Q ratio is < 1.0 (e.g., atelectasis, tumor, mucus plug, pneumonia, pulm. edema)
oIf perfusion is less than ventilation the V/Q ratio is > 1.0 ( e.g., PE, pulm. infarct, cardiogenic shock)
oBoth are examples of V/Q mismatch
oIn respiratory failure the most common cause of the mismatch is hypoxemia
oV/Q mismatch not mutually exclusive of other mechanisms - can happen simultaneously
Diffusion Defects
oAffects movement of gas from an area of high concentration to low concentration across the aveolar-capillary membrane
oDecreased surface area, inflammation, or fibrosis of tissue inhibits gas exchange - structural issue with the lung
oCommon causes include pulmonary fibrosis, pleural mesothelioma, granuloma, interstitial edema, etc.
oHypercapnia is a late sign
Low Cardiac Output
oThe mechanism of delivering oxygen to the tissues is cardiac output
oIf the cardiac output decreases less oxygen is delivered to the tissues
oLactic acidosis occurs when the body can no longer compensate for the low cardiac output and the cells convert to anaerobic metabolism
oTissue hypoxia can result in cellular death and organ failure
Low Hemoglobin Level
oOxygen binds to the hemoglobin and is delivered to tissues
oIf not enough Hgb is available, oxygen cannot be delivered to the tissues
oAlterations in Hgb include carbon monoxide poisoning, sickle cell anemia, chemotherapy, kidney failure, bone marrow issues, and nutritional deficits (folate, B12, & iron)
Tissue Hypoxia
oBody switches to anaerobic metabolism when oxygen is inadequate for needs
oAnaerobic metabolism is not as efficient as aerobic and organ hypoxia occurs
oLactic acid is created as a byproduct
Failure of Ventilation
oWhen ventilation is decreased hypercapnea results
oHypoventilation: CO2 accumulates in the alveoli and is not blown off causing respiratory acidosis
oVentilation perfusion mismatch: dead space occurs when an area is well ventilated but reduced perfusion and there is no gas exchange
oCommon causes same as failure of oxygenation - hypoventilation and V:Q mismatch
Acute Respiratory Distress Syndrome
oacute onset within one week of clinical insult
odiffuse, bilateral pulmonary opacities not explained by other conditions
oaltered oxygenation and PEEP or CPAP requirements ≥ 5cm H2O
oMost common risk factors: sepsis, pneumonia, trauma, and aspiration
*around a 50% in-hospital mortality rate
Acute Exudation Response Phase
oUncontrolled, systemic inflammatory reaction secondary to a lung injury
oRelease of inflammatory mediators cause damage to the alveolar-capillary membrane which leads to increase in permeability
oFluid leak from the capillaries into the alveoli resulting in pulmonary edema (intrapulmonary shunting)
oDecreased lung compliance reduces ventilation (V/Q mismatch)
oResults in decreased oxygenation
Proliferative Phase
oOccurs 4-21 days after the insult
oPulmonary edema ceases
oFibrin starts to form and leads to hypoxemia (beginning of diffusion defects)
oOverlaps fibrotic phase
Fibrotic Phase
oOccurs 14-21 days after insult
oFibrosis destroys the lung tissue and lungs become thickened, stiff, and noncompliant (diffusion defect)
oInflammation and pulmonary edema begin again and white out on chest x-ray (intrapulmonary shunting)
Nursing Interventions for ARDS
oMaintain oxygenation and eliminate underlying cause
oProtective strategies: low tidal volume and low end peak inspiratory pressure; FiO2 and PEEP; adjusted according to the patient's condition; low volumes and increased respirations
oVentilator changes based on ABGs
oPaCO2 within a permissive hypercapnea range 50 to 70 and pH 7.30 to 7.45 (for COPD)
oCorticosteroids use still highly debated
RN care ARDS
oSedation and comfort measures
oNeuromuscular blocking
oProne positioning (refer to lab video)
oFluid and electrolytes
oLasix and Albumin
oAntibiotics and bronchodilators
oPsychosocial
Pulmonary Embolus
oDyspnea, tachycardia, rapid decrease in oxygen saturation, feeling of impending doom, syncope
oRequires immediate diagnosis and intervention
oThrombolytic therapy or embolectomy
Evolution of Critical Care Nursing
●Critical care nursing is specifically concerned with patient and family responses to life-threatening problems, the prevention as well as cure of problems such as trauma, major surgery, or complications of illness.
●Patients have become increasingly complex and encompass both acute and critically ill patients.
2022 National Patient Safety Goals
❑Identify patients correctly
❑Improve staff communication
❑Use medicines safely
❑Use alarms safely
❑Prevent infection
❑Identify patient safety risks
❑Prevent mistakes in surgery
Identify patients correctly
1.Use at least two ways to identify patients. For example, use the patient's name and date of birth. This is done to make sure that each patient gets the correct medicine and treatment.
Improve staff communication
2. Get important test results to the right staff person on time.
Use medicines safely
3. Before a procedure, label medicines that are not labeled. For example, medicines in syringes, cups and basins. Do this in the area where medicines and supplies are set up. Take extra care with patients who take medicines to thin their blood. Record and pass along correct information about a patient's medicines. Find out what medicines the patient is taking. Compare those medicines to new medicines given to the patient. Give the patient written information about the medicines they need to take. Tell the patient it is important to bring their up-to-date list of medicines every time they visit a doctor.
❑Use alarms safely
4. Make improvements to ensure that alarms on medical equipment are heard and responded to on time.
❑Prevent infection
5. Use the hand cleaning guidelines from the Centers for Disease Control and Prevention or the World Health Organization. Set goals for improving hand cleaning. Use the goals to improve hand
cleaning.
❑Identify patient safety risks
6. Reduce the risk for suicide.
❑Prevent mistakes in surgery
7. Make sure that the correct surgery is done on the correct patient and at the correct place on the patient's body. Mark the correct place on the patient's body where the surgery is to be done. Pause before the surgery to make sure that a mistake is not being made.
AACN: HEALTHY WORK ENVIRONMENT
●Communication
●Collaboration
●Culture of Safety

-ex: SBAR
Quality and Safety Education for Nurses (QSEN)
QSEN EXEMPLAR page 7
a. Concise (over the phone to MD or MLP) or b. Report format RN to RN
SBAR for Teamwork and Collaboration
Situation: State what is happening at the present time that has warranted the SBAR communication.
Background: Explain circumstances leading up to this situation. Put the situation in context for the reader or listener (MD, MLP).
Assessment: State what you think is the problem.
Recommendation: State your recommendation to correct the problem.
SupportFamily of Critically Ill Patients
●Decision Making
●Family Coping
●Staff Stress
●Cultural Support of Family
●Spiritual & Religious Support
●Family Visitation
●Family Environment of Care
●Family Presence During Rounds
●Family Presence During Resuscitation
●Palliative Care
Primary obligation of professional nurses:
●Protect the patient
●Protect the patients' basic rights.
Ethics & Nursing requirement
●Recognize ethical dilemma(s) threatening patient rights
●Participate in the resolution
Advanced directive
●Instructions for expressing desires related to healthcare decisions should incapacitation occur (ex. Designation of a healthcare surrogate, living wills)
Living Will
●Instructions for withholding specific treatments if incapacitation occurs (ex. Do not intubate, no ventilator) not legally binding in some states

*think end of life
Durable Power of Attorney
●Legally designated agent to make medical decisions if incapacitation occurs (recommended)

*legal document
Consent- 3 elements
process that entails the exchange of information between the healthcare provider and patient or patient's proxy.

3 elements required:
1.Competence - understand information (i.e., Oriented [free from pain, depression, sedation], Mental Capacity intact)
2.Voluntariness - without Coercion or fraud
3.Disclosure of Information (MD duty) - sufficient (i.e., Diagnosis, Condition, Prognosis & Risks)

NOTE: RN is patient advocate. Ensures informed consent process completed per legal standards & institutional policy.
End of Life Issues
▪Culturally Competent EOL Care
▪Withholding, Limiting or withdrawing life support
-Ventilator
-Medical Treatments (i.e. vasopressors, nutrition, dialysis)
▪Pharmacological Management of Life Support Withdrawal
▪Emotional & Psychological Care of Patient and Family
▪Organ Donation
Living Donor and Kidney Paired Exchange Donation
●18 yo & willing to donate
●Good physical & mental health
●Well informed of risks
●Good support system
●Able to take off work
●BMI <35
●No DM, CA, kidney/heart dx, normal/controlled BP, No Hep C or HIV
●No drug or ETOH problems
Brain Dead Donor
If brain dead pt is considered dead. Pt has complete irreversible cessation of function of the brain and brain stem

-irreversible cause of coma
-get them to normal core temperature and stay alive
-normal systolic BP
-Able to perform a neuro exam
Organ Donation After Circulatory Death
-donation that does not meet brain death criteria
-depends on medical or mechanical life sustaining methods
-depends on vent or vasoactive/inotropic meds (pt permanently on this and relies on them to live)
Focus of Donor Management
●Maintain BP
●Maintain normal serum glucose
●Maintain normothermia
●Treat anemia
●Treat coagulopathy/thrombocytopenia
●Provide mechanical ventilation
●Maintain optimal fluid/electrolyte
●Treat polyuria
●Maintain normal acid-base
End of Life Care Guidelines
▪Present clear consistent message: med/care team need to have a clear communication
▪Allow ample time
▪Patient will not be abandoned: aggressive care and comfort care
▪Facilitate continuity of care: in the case pt is transferred to another unit
Palliation
care interventions designed to relieve symptoms of illness or injury that negatively affect the quality of life of the patient or family
Hospice
associated with palliative care delivered at the home or in special hospice facility to patients approaching the end of life
Post Mortem Care
▪Remove lines & Foley
▪Bathe patient, attach toe tag
▪Place patient in body bag
▪Transfer to Morgue
Management of Pain & Anxiety
●Nonpharmacological Management (Early Strategies)
-Environmental Manipulation
-Complementary and Alternate Therapy
●Pharmacological Management

s/sx of anxiety or pain
●Constipation
●Cool Extremities
●Diaphoresis
●Hypertension
●Increased Cardiac Output ●Increased Glucose production
●Mydriasis (pupillary dilation) ●Nausea
●Pallor and Flushing
●Sleep disturbance
●Tachycardia Tachypnea
●Urinary retention
DELIRIUM IN THE ICU
Risk Factors
1.Coma
2.Pre-existing dementia - Non-Modifiable
3.History of hypertension
4.Alcohol or Narcotic dependence
5.High illness severity at admission (i.e., hypoxemia, head trauma)
6.Advanced age (>70) - Non-Modifiable
7.Psychotropic medications (i.e., benzos, opioids)
8.Uncontrolled pain
9.Cigarette smoking
10.Sleep deprivation
Hemodynamic Monitoring
•Goal: accurately assess the patient and optimize oxygen delivery and tissue perfusion
•Monitor physiologic relationships to assess if oxygen delivery is sufficient
•Data needs to be accurate and assessed correctly
Arteries
•high pressure, low volume, high-resistance; able to dilate and constrict in response to metabolic demand
Capillaries
•low-pressure, thin-walled vessels; pt can appear edemas bc of leaks in the capillaries
Veins
•high-capacity, low-resistance, less elastic; able to dilate and constrict in response to metabolic demands
-we manipulate veins for therapeutic reaction
Blood
more viscous the blood, greater the turbulence/resistance
Physics of Blood
•Rate of flow
•Resistance is the ease fluid flows: BP measures the amount of resistance of systole and diastole
•Friction: more friction -> more resistance (plaque build up)
•Increased resistance decreases compliance
•Increased metabolic demands results in increased blood volume; If we need more O2 we need an increase in volume, not just O2 but any form of metabolic needs
•Smooth vessel walls have faster flow bc of the less resistance
CO=SVxHR
•Stroke Volume: Preload (volume into the heart), After load (volume out of the heart), Contractility (strength of the heart)

•Heart Rate: Slow HR decreases CO ( decrease BP)
•Increased HR decreases filling time, which may decrease CO
Physiological changes through the lifespan
•Elasticity and compliance decrease (increased resistance)
•HTN develops
•Resistance leads to hypertrophy
•Stiffening of ventricle leads to heart failure
•Decreased intrinsic and maximal heart rate
•Heart block and valvular dysfunction
Noninvasive Hemodynamic Modalities
-BP
-Jugular venous distension (JVD)
-Lactic acid blood test: it can show injury to the cell
Invasive Hemodynamic Monitoring
•Used when noninvasive measures are not accurate or provide enough data to adequately care for the patient
•Frequently seen with shock, cardiac tamponade, ruptured ventricular septum, heart failure, right ventricular infarct, complex surgical patients
•Need to determine adequacy of tissue perfusion, preload, afterload and contractility

*if pt needs constant monitoring or data doesn't appear to be accurate
Arterial Lines
•Continuous BP
•Assess efficacy of vasoactive medications: bc they may need to be titrated
•Frequent labs/ABGs: bc of the limited number of art sticks that are possible
•Do not administer medications: not even in emergencies
-flush with normal saline to keep line clear
-RF: clots
Central Venous Catheters
•May or may not be used for hemodynamic monitoring
•Estimate fluid status
•Can give large quantity of medications
•Some vasoactive medications must be given via CVC
•Can transduce a central venous pressure (CVP): helps determine fluid pressure
Pulmonary Artery Catheters
•Most invasive
•Assess left heart function
•Measures CO, PAP, SvO2
•May have an injection port: for a vasoactive drip
•Can transduce a central venous pressure
-RN: can't put it in or take it out
-Venous blood gas measure when ABG
Equipment for Pulmonary Artery Catheters
1. Invasive Catheter
2. Noncompliant pressure tubing
3. Transducer with stopcock
4. Flush system
5. Bedside monitoring system
RN assessment Pulmonary Artery Catheters
•Insertion site: should have a biopatch
•Waveforms
•Vitals
•Ensure that PAC is not wedged
•Ensure pressure bag is inflated correctly
•Check for air in tubing: RF air emboli
•Ensure that transducer is level: •phlebostatic axis
•Monitor for complications
•Depth of PA catheter
Nursing Interventions Pulmonary Artery Catheters
•Position the patient
•Zero the line to phlebostatic axis: 4th intercostal space and mid (axillary line) AP diameter
•Dynamic response testing (Square wave test)
•Dressing change
•Address abnormals found in assessment
•Ensure PAC is not wedged: not too far in
•Check CO: flush dextrose to check CO
Mean Arterial Pressure (MAP)
MAP is a indicator of perfusion

Normal cardiac cycle is one third systole and two thirds diastole. These components are divided by 3 to obtain average perfusion pressure
"Normal" Range: 65-105mm HG

MAP = SBP + (DBP X 2) 3
120 + (80 X 2) = 93 MAP

Assess for perfusion to determine individual parameters!!!! (urine, cap and neuro)
MAP normal
65-105

*but can also be pt specific
Central Venous Pressure: CVP
•Central Venous Pressure (CVP) or Right Atrial Pressure (RAP)
•Assess preload of the right side of the heart
•Rudimentary (rough indicator) indicator for volume (more specific than BP & HR)
•Normal is 2-6 mm HG (but some disease processes may require different ranges)
•Helps determine volume (preload) vs. vasopressors (afterload)
-CVP low: volume issue
-volume needs to be adequate for vasopressor to be effective
CVP normal
2-6

-CVP low: volume issue
Cardiac Output
•Stroke volume x heart rate
•Amount of blood pumped out by the ventricle every minute
•4-8 L/min
Cardiac index
CO individualized to BSA
Normal: 2.5-4.2 L/min/m2
Stroke Volume
•Amount of blood ejected per heartbeat
•Average resting stroke volume is about 70 mL and heart rate is 60-130beats per minute
•SV determined by three factors: preload, afterload and contractility

*to increase CO: increase stroke volume or heart rate or both
Preload
•Degree of ventricular stretch before the next contraction: amount of volume coming in
•Impacted by length of diastole and venous return
•Frank-Starling mechanism: maximal ventricular stretch=maximal CO
•Passive Leg Raise test used to assess preload responsiveness to volume
-BP is taken, pt lays down and both legs are raised 30 degrees for a minute, BP is taken and if BP is increased the pt needs more volume. If BP stays the same volume isn't the issue
Afterload
•Amount of resistance the ventricles must overcome to pump blood out of the ventricle into the vasculature
•Impacted by arterial tone, blood viscosity, turbulence in vessels and valve capacity
•Resistance of systemic BP to left ventricular ejection is called systemic vascular resistance: normal is 770-1500 dynes/sec/cm
•Resistance of the pulmonary BP to right ventricular ejection is called pulmonary vascular resistance - less than 250 dynes/sec/cm

-SVR: low -> not enough resistance -> pt needs vasopressors
-SVR: high -> pt may be already on vasopressors OR -> may be compensatory mechanism bc body doesn't have enough volume
Contractility
•Strength of the heart muscle
•Impacted by preload- optimal preload ensures maximal stretch, leading to maximal CO (Frank-Starling law)
-looks at ejection fraction
-Fraction low: contractility is low
Pulmonary Artery Pressure
•Pressure in the pulmonary artery
•Pulmonary artery systole (PAS): 15-25 mm HG
•Pulmonary artery diastole (PAD): 8-15 mm HG

*sildenafil to treat pulmonary HTN
Pulmonary capillary wedge pressure/Pulmonary artery occlusion pressure
•Reliable indicator of left ventricle function
•Nurses do not wedge PAC!!
•Complications include pulmonary infarct and PA rupture
•Use PAD for similar measurement
•Normal 8-12mm Hg
Ejection Fraction
•Percentage of end-diastole volume ejected with each stroke
•Normal 55%-65%
•Indicator of contractility
-can help determine if pt is in HF or if an inotrope is needed
Tissue Perfusion
•Measure ABG and VBG simultaneously: 2 RNs needed
•Compare results
•Indicates if hypoxia is a supply or absorption issue (PVA2 is high)
•Absorption issues include:
•Shunting oxygen away from the tissue (i.e. a thrombus blocks an artery, shunting blood supply)
•Increased affinity of hemoglobin for oxygen (i.e. CO2 concentration, temperature, or PH)
•Interstitial edema leads to increased diffusion distance between capillaries and cells
•Cells are unable to use the oxygen being delivered

*Hypoxia: low ABG
*Absorption: high VBG
Noninvasive Cardiac Monitors
Safer for patients
May not be as accurate
Can trend values: over time
Can be expensive
Vasoactive Medication
•Increase BP through vasoconstriction
•Need to be given in a central line
•Rate, dose and concentration patient specific
•Titrate to a MAP or SBP goal
-Increase SVR and increase afterload
Epinephrine
•Vasoconstrictor
•Delays absorption of local anesthetic
•Controls superficial bleeding
•Elevate blood pressure
•Overcome heart block
•Restore cardiac function in cardiac arrest (code)
•Bronchodilation
•Treats anaphylactic shock
•Adverse reactions: HTN, dysrhythmias (especially tachycardia), angina, necrosis, hyperglycemia
Norepinephrine
•Vasoconstrictor
•Similar actions to epi: but not during anaphylaxis
•Doesn't act on beta2
•Adverse effects include tachydysrhythmias, angina, hypertension & local necrosis
•Only given IV
•Used for hypotension and cardiac arrest
•Used after pt returns from a code
•assess fingers and toes: peripheral vasoconstrictor
Vasopressin
•Vasoconstrictor
•Increases water reabsorption
•Concentrated urine
•Stimulate contraction of vascular and GI smooth muscle
•Plasma levels for muscle contraction are higher than what occurs physiologically
•"Systemic pressor"
Phenylephrine
•Vasoconstrictor
•Increases BP IV
•Reduces nasal congestion locally
•Usually not first choice vasoconstrictor
•May be used with other vasoconstrictors
Dobutamine
•Increases contractility (Inotrope)
•Continuous IV infusion
•Monitor BP, EKG, I&O
•Can cause tachycardia
•Increases BP
•Dobutamine > Dopamine in heart failure bc it doesn't increase BP resistance

*HF doesn't increase systemic vascular resistance
Dopamine
•Inotrope
•Low doses: increased renal perfusion
•Increases myocardial contractility
•Increase cardiac output
•Adverse effects: tachycardia, dysrhythmias, angina, necrosis
•Monitor urine output
•Low ejection fraction an inotrope is going to help

*For kidney pt bc better for increasing renal perfusion
Albumin
•Blood product
•Shifts fluid into the vasculature
•Ideal for patients who are inter-vascularly dry, but have interstitial edema
•Use new tubing with every bottle
•Vent the bottle
•Glass bottle
•Viscous, sticky

*give to pt that: low CVP, low CVP with crackles in the lungs
Central venous pressure (CVP)
2-6
Cardiac Output value
4-8
Cardiac Index
2.5-4
Stroke Volume value
70
Pulmonary artery pressure
25/10
PAOP/PAWP (pulmonary artery occlusion/wedge pressure)
8-12
Ejection Fraction value
55-65%
Systemic vascular resistance (SVR)
770-1500
pulmonary vascular resistance
under 250
Lungs (overventilation vs underventilation)
-Over: Resp. Alk

-Under: resp. acid
Not lungs (prolonged suction/vomiting vs other)
-Prolong suction: met alk

-Other: met acid
CAM ICU
1. acute change in mental status

2. Inattention (more than 2 errors)

3. Altered level of consciousness (RASS other than 0 -> delirium)

4. Disorganized thinking (>1 error yes)
Preventing Delirium in ICU
-change pt room or position of the bed
-open window or shades to differentiate between day and night
-regular updates/plan for the day. Fill in dry erase board every day
Lactic acid
0.5-1.6

-If elevated want to decrease the value by 20% every 2hrs
-Labs in green vile, put on ice and goes to the lab within 15 minutes of being drawn
Beta blockers
-pt must have normal volume and hemodynamically stable before admin
-never give with vasopressors: bc meds cancel each other out
What does my pt need? Volume
-trauma
-surgery
-dialysis
-positive passive leg raise test
-low CVP
-High SVR
What does my pt need? Vasopressors
-S/sx of FVO
-High CVP
-Low SVR
What does my pt need? Albumin
-no volume in vasculature
What does my pt need? Inotropes
-HF
-Low ejection fraction
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