Chapter 66: Nursing Management Critical Care Critical Care Nursing Critical Care/Intensive Care Units PICU any

any type of pediatric intensive care patient except cardiac NICU infant that has to have never left the hospital Critical Care Nurse o Performs frequent assessments to monitor trends in patients physiologic parameters (BP, ECG, etc.) o Provides psychologic support to patient and caregiver(s) o Important to be skilled in palliative and end-of-life care o Certifications critical care nurses can get Critical Care Certification (CCRN) Progressive Care Certification (PCCN) Cardiac Medicine (CMC) Cardiac Surgery (CSC) o Nurses should be aware of the scope of practice provided by their state's Nurse Practice Act In general, nurses can provide Patient and caregiver teaching about an illness or disease The general course of illness What usual treatment entails Diagnosis and prognosis are outside the scope of practice for a registered nurse Critical Care Patient o Common Problems of Critical Care Patients Usually immobile and at high risk for thromboembolism and skin problems Use of multiple invasive devices predisposes patient to hospital-acquired infections Sepsis and multiple organ dysfunction (MODS) may follow Nutrition Must collaborate with physician and dietician to determine how to meet nutritional needs Primary goal is to prevent or correct nutritional deficiencies Usually accomplished with Enteral (calories via GI tract) and Parenteral (calories via IV) nutrition Enteral nutrition is usually encouraged Preserves the structure and function of the gut mucosa Prevents the movement of gut bacteria across the intestinal wall and into the bloodstream In addition, early enteral nutrition is associated with fewer complications and shorter hospital stays, and is less expensive than parenteral nutrition Parenteral nutrition is used when Enteral route is unsuccessful or contraindicated Paralytic ileus, diffuse peritonitis, intestinal obstruction, pancreatitis, GI ischemia, intractable vomiting, and severe diarrhea Anxiety

Encourage patients and caregivers to express concerns, ask questions, and state their needs Include patient & caregiver in all conversations and explain purpose of equipment & procedures Structure patient's surrounding environment in a way that decreases anxiety For example, encourage caregivers to bring in photographs and personal items Judicious use of antianxiety drugs (e.g., lorazepam [Ativan]) and complementary therapies (e.g., guided imagery, massage) may reduce stress response that can be triggered by anxiety Pain Control of pain is paramount as many as 70% in ICU have moderate to severe uncontrolled pain ICU patients at high risk for pain include patients who Have medical conditions that include ischemic, infectious, or inflammatory processes Are immobilized Have invasive monitoring devices, including endotracheal tubes Require invasive or noninvasive procedures If giving Propofol for sedation, a daily sedation vacation (interruption of sedation) should be conducted allows patient to wake so a neurological assessment can be done Patients who are intubated can feel pain (could be grimacing or show change in vitals) If doing a dressing change, should give them prophylactic pain meds Impaired communication Some patients may not be able to speak b/c of the use of sedative and paralyzing drugs or an endotracheal tube Always explain what will happen or is happening to the patient when doing any procedure Explore using picture boards, notepads, magic slates, or computer keyboards if they cant talk Look directly at patient when speaking to them and use gestures when appropriate Comfort touch is important to some patients Encourage caregivers to touch and talk with the patient even if patient is unresponsive or comatose Sensory-Perceptual Problems Estimated that the prevalence of delirium in ICU patients is as high as 80% Factors Predisposing Patient to Delirium Demographic factors advanced age, preexisting cognitive impairment, vision/hearing impairments, history of drug or alcohol abuse Environmental factors sleep deprivation, anxiety, sensory overload, immobilization

Physical conditions hemodynamic instability, hypoxemia, hypercarbia, electrolyte disturbances, severe infections Certain drugs sedatives, Lasix, antimicrobials Must address physiologic factors (e.g. correct O2 levels, perfusion, and electrolyte problems) Use of clocks and calendars can help orient patient Presence of caregiver may help orient patient and reduce agitation Neuroleptic drugs (Haldol) can be used if patient demonstrates hyperactivity, insomnia, delusions Limit noise and explain noises that cannot be prevented Have conversations out of patient area unless involving patient in conversation Silent unnecessary alarms while doing procedures then reactivate them when done Sleep Problems Nearly all patients in ICU experience sleep disturbances significant stressor in ICU Contributes to delirium and possibly affects recovery Structure environment to promote patients sleep-wake cycle Cluster activities Schedule rest periods Dim lights at nighttime Open curtains during the daytime Obtain physiologic measurements w/o disturbing patient Limit noise Provide comfort measures (e.g. back rubs) Many patients on sleep aids to induce/maintain sleep benzos (Restoril) & benzo-like (Ambien) Issues Related to Caregivers o To be effective in caring for their loved one, caregivers need your guidance and support o Caregivers experience anxiety regarding patients condition, prognosis, pain and other discomforts, and finances If anxious about finances, consulting with case manager or social worker is helpful o Nurses must provide family-centered care need skills in crisis intervention Interventions active listening, reduction of anxiety, support of those who become upset or angry, acknowledgment of caregivers feelings and acceptance of their decisions, meeting informational, reassurance, and convenience needs Note: patients often exhibit early and subtle signs of deterioration (e.g. mild confusion, tachycardia) 6-8 hours before cardiac and/or respiratory arrest

Drugs Related to Critical Care Dopamine o Increases contractility of the heart CO is increased o Renal dose will open up the kidney function and helps increase urine output o At higher levels, blood pressure is increased and renal perfusion is decreased

Dobutamine o Helps the heart pump efficiently o Use in cardiogenic shock Levophed o Vasoconstriction, which helps increase blood pressure o Long-term use can cause necrosis of the extremities fingers, toes, etc. Nitroglycerin o Vasodilation, which relieves chest pain o Can give the patient a severe headache usually will give them Tylenol as well Propofol o Sedation o Also helps for nausea leaves the body very quickly so it does not help the nausea for long o Can drop BP quickly o Two Types Regular Nut based watch for nut allergies to avoid anaphylaxis Prescedex o Sedation Epinephrine o Low BP, allergic reaction Norepenephrine/Levophed o Shunt the blood to vital organ extremities are effected the most Amiodorone o Antidysmic

Hemodynamic Monitoring Measurement of pressure, flow, and oxygenation within the cardiovascular system o Invasive monitoring internally placed devices o Noninvasive monitoring external devices Values Commonly Measured in the ICU o Systemic and pulmonary arterial pressures o Central venous pressure (CVP) o Pulmonary artery wedge pressure (PAWP) (also known as pulmonary artery occlusive pressure [PAOP]) o CO/CI o SV/SV index [SVI] o O2 saturation of the hemoglobin of arterial blood (SaO2) o Mixed venous oxygen saturation (SvO2) o These measurements allow you to calculate Resistance of the systemic and pulmonary arterial vasculature O2 content, delivery, and consumption Hemodynamic Terminology o Cardiac Output volume of blood in liters pumped by the heart in 1 minute o Cardiac Index measurement of CO adjusted for body surface area (BSA) More precise measurement of the efficiency of the pumping action of the heart o Preload volume in ventricle at the end of diastole o Afterload forces opposing ventricular ejection

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Systemic arterial pressure, resistance by aortic valve, and mass and density of the blood to be moved WANT TO LOOK AT SVR IN REGARDS TO AFTERLOAD (systemic vascular resistance) Systemic Vascular Resistance resistance of the systemic vascular bed Pulmonary Vascular Resistance resistance of the pulmonary vascular bed Contractility strength of the contraction If preload, heart rate, and afterload remain constant yet CO changes, contractility is changed Contractility is reduced in the failing heart

Principles of Invasive Pressure Monitoring o Invasive lines used in the ICU to measure systemic and pulmonary BPs o Pressure monitoring equipment is referenced and zero balanced to the environment Referencing positioning transducer so the zero reference point is at the level of the atria of the heart Stopcock nearest transducer usually the zero reference for the transducer To place this level with atria, need to find phlebostatic axis Transducers placed higher than the phlebostatic axis will produce falsely low readings Transducers placed lower than the phlebostatic axis will produce falsely high readings Zeroing confirms that when pressure within the system is zero, the monitor reads zero Open reference stopcock to room air (off the patient) and watch for a reading of zero

This allows use of atmospheric pressure as a reference for zero When to Zero? During the initial setup Immediately after insertion of arterial line when transducer has been disconnected from pressure cable or pressure cable has been disconnected from monitor When the accuracy of the measurements is questioned Types of Invasive Pressure Monitoring o Arterial Blood Pressure 20 gauge in the radial or femoral artery sutured in place Measurement of Blood Pressure with Invasive Lines Radial, brachial, or femoral Want to watch for infection red, swollen Should have good wave form and be zeroed (check zero to the transducer at the 4th intercostal space) Cuff pressure should be within 10 of arterial pressure Complications Hemorrhage use Luer-Lok connections, check arterial waveforms, and activate alarms If pressure in line falls (when line disconnects) an alarm will sound Infection inspect insertion site for inflammation/infection Change pressure tubing, flush bag, and transducer q96h When infection is suspected, remove catheter and replace equipment Thrombus formation To limit thrombus formation and maintain line patency, check continuous flush system q1-4h to make sure the pressure bag is inflated to 300 mm Hg, the flush bag contains fluid, and the system is delivering 3-6 mL/hour Should not be using heparin routinely for flush solution risk for thrombocytopenia Neurovascular impairment Loss of limb

Pulmonary Artery Flow-Directed Catheter Pulmonary Artery Catheter Insertion Note patients electrolyte, acid-base, oxygenation, and coagulation status Imbalances such as hypokalemia, hypomagnesemia, hypoxemia, or acidosis can make heart more irritable & increase risk of ventricular dysrhythmia during catheter insertion To maintain position, catheter is secured at point of entry on skin and length marked

Pulmonary Artery Pressure Measurements PAD (pulmonary artery diastolic pressure) & PAWP (pulmonary artery wedge pressure)

Both are sensitive indicators of cardiac function and fluid volume status Both increase in heart failure and fluid volume overload Both with volume depletion PAWP is pressure generated by left ventricle (left ventricle function) Basing fluid therapy on PA pressure can restore fluid balance w/o overcorrection or undercorrection of the problem (can avoid pulmonary edema) Complications with Pulmonary Artery Catheters Infection and Sepsis Must have careful surgical asepsis for insertion and maintenance of catheter & tubing Monitor patient for local and systemic changes redness, exudate at insertion site, fever, increased WBC count Must remove catheter if there are any signs of infection To reduce risk of infection change flush bag, pressure tubing, & stopcock q96h and remove hemodynamic monitoring once it is no longer needed Air Embolus Always check balloon integrity before insertion discard defective catheters After insertion, balloon rupture or injection of air into any lumen can cause air embolus To reduce risk of air embolus first aspirate blood to check for absence or presence of blood and only inject prescribed volume of air into balloon before obtaining PAWP o If blood is aspirated from balloon port or balloon air does not all come back into the syringe, label port do not use and contact physician Always use Luer-Loks on all pressure lines and activate low pressure alarms Pulmonary Infarction or PA Rupture Causes o Balloon may rupture, releasing air and fragments that could embolize o Prolonged balloon inflation may obstruct blood flow o Catheter may advance into a wedge position, obstructing blood flow o Thrombus could form and embolize To reduce risk of air embolus/pulmonary infarction never inflate balloon beyond capacity (1-1.5 mL of air), monitor PA pressure waveforms continuously for evidence of catheter occlusion, dislocation, or spontaneous wedging

Pressure tracing will be blunted with occlusion and will appear wedged if PA catheter advances and becomes wedged o Physician must reposition catheter immediately o ALWAYS CLOSE LINE WITH CLAMP OR STOPCOCK WHEN LINE IS DISCONNECTED o NEVER LEAVE BALLOON INFLATED FOR MORE THAN 4 BREATHS (8-15 SECONDS) EXCEPT DURING INSERTION To reduce risk of thrombus/embolus formation PA catheter needs to be continuously flushed with a slow infusion of normal saline Ventricular Dysrhythmias Can occur during PA catheter insertion or removal or if tip moves from PA to R ventricle and irritates ventricular wall (PA catheter would not be able to be wedged) Needs to be repositioned by physician and chest x-ray done to confirm location Central Venous or Right Atrial Pressure Measurement (CVP) Measurement of right ventricular preload Measured with PA catheter using the proximal lumen located in the right atrium or with a central venous catheter placed in the internal jugular or subclavian vein Also reflects fluid volume problems, but PA diastolic pressure & PAWP are better indicators of it Increase in CVP reflects heart failure or volume overload WANT TO CVP TO CARDIAC OUPUT!!! Decrease in CVP reflects volume depletion CVP Waveform Interpretation a wave represents atrial contraction x descent represents atrial relaxation c wave represents the bulging of the closed tricuspid valve into the right atrium during ventricular systole v wave represents atrial filling y descent represents opening of the tricuspid valve and filling of the ventricle

Invasive Cardiac Output Measurement Techniques Normal resting cardiac output is 4-8L per minute CO & CI are in shock states (e.g. cardiogenic, hypovolemic) and heart failure CO with exercise and at rest with fever or early sepsis TDCO (intermittent bolus thermodilution CO) CO is calculated from temperature change in pulmonary artery when a fixed volume and known temperature of a solution is injected into proximal port in right atrium CO measured by computer from area under the temp curve Want curve to be smooth Larger area under curve = lower CO Smaller area under curve = higher CO Repeat 3x with each measurement 1-2 minutes apart to determine CO Must have three normal curves to be valid throw out any abnormal curves CCO (continuous cardiac output method) CO measured with a PA catheter (placed in the right atrium) that has a heat-exchange CO catheter attached to detect changes in temp when blood passes through R ventricle Every 30-60 seconds, a bedside computer displays average CO for the past 3-6 minutes Eliminates need for fluid boluses, decreases contamination, permits ongoing evaluation MORE RELIABLE THAN TDCO METHOD Minimally Invasive Cardiac Output Monitoring Techniques Use of a specialized sensor that attaches to a standard arterial pressure line and a monitor Measures CCO/CCI, SV/SVI, and stroke volume variation q20secs More research needed to find if this approach can replace hemodynamic monitoring with PA catheter Venous Oxygen Saturation Both CVP (central venous pressure) and PA (pulmonary artery) catheters can include sensors to measure O2 saturation of hemoglobin in venous blood O2 saturation of blood from PA catheter = mixed venous oxygen saturation (SvO) O2 saturation of blood from CVP catheter = central venous oxygen saturation (ScvO) Both are adequate for the measurement of adequate tissue oxygenation Normal SvO/ScvO at rest is 60-80% SvO/ScvO arterial oxygenation, low CO, low hemoglobin, consumption or extraction of O If below 60%, observe for changes in arterial oxygenation

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Monitor pulse oximetry or ABGs Indirectly assess CO and tissue perfusion changes in mental status, strength or quality of peripheral pulses, capillary refill, urine output, skin color & temp If arterial oxygenation, CO, and hemoglobin are unchanged, the in SvO/ScvO is from O consumption or extraction could be metabolic rate, pain, movement, or fever

SvO/ScvO Could be from an improvement (e.g. O saturation, improved perfusion, metabolic rate) or from a problem (e.g. sepsis) o In sepsis there is a ability of tissues to use O at the cellular level

Noninvasive Hemodynamic Monitoring Impedance Cardiography (ICG) o Method of obtaining CO and assessing thoracic fluid status continuous or intermittent o Uses four external electrodes that deliver a high frequency, low amplitude current to measure the change in impedance in the ascending aorta and left ventricle over time Impedance the resistance to the flow of electric current o Cannot use in patients with generalized edema or third spacing excess volume interferes with accuracy Noninvasive Arterial Oxygenation Monitoring Pulse Oximetry o Monitoring SpO may reduce frequency of ABG sampling o o o SpO is normally 95%-100% Can put pulse ox probe on forehead, earlobe, etc. if cannot get good reading on fingers Normally used to evaluate effectiveness of oxygen therapy and how patient tolerates position changes or decreases in fraction of inspired air (FIO)

Nursing Management of a Patient on Hemodynamic Monitoring Obtain Baseline Data o General appearance Does the patient appear tired, weak, exhausted? o Level of consciousness Cardiac reserve may be insufficient to sustain even minimum activity Changes in mental clarity may reflect problems with cerebral perfusion or oxygenation o Skin color/temperature Pallor, cool skin, and diminished pulses may indicate decreased CO If patient is bleeding and developing shock, BP might initially be stable, yet patient may become increasingly pale and cool from peripheral vasoconstriction Conversely, patient with septic shock may remain warm/pink yet develops tachycardia and BP instability o Vital signs o Peripheral pulses o Capillary Refill o Urine output Monitoring urine output reflects the adequacy of perfusion to the kidneys Patient with diminished perfusion to GI tract may have hypoactive or absent bowel sounds Correlate baseline data with data obtained from biotechnology o e.g., ECG; arterial, CVP, PA, and PAWP pressures; SvO2/ScvO2 o Single hemodynamic values are rarely significant o Monitor the whole clinical picture Circulatory Assist Devices (CADs) Used to decrease cardiac work & improve organ perfusion in patients with heart failure when drugs are no longer adequate All CADs decrease ventricular workload, increase myocardial perfusion, and augment circulation Provide Interim Support in Three Types of Situations o Left, right, or both ventricles require support while recovering from acute injury (e.g., postcardiotomy) o Patient must be stabilized before surgical repair of the heart (e.g., a ruptured septum) o Heart has failed, and the patient is awaiting cardiac transplantation Intraaortic Balloon Pump (IABP) most commonly used CAD o Provides temporary circulatory assistance (improving coronary blood flow) to compromised heart by Reducing afterload (reducing systolic pressure) Enhancing the aortic diastolic pressure

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Balloon inserted percutaneously or surgically into the femoral artery, advanced toward the heart, and positioned in the descending thoracic aorta just below the left subclavian artery and above the renal arteries During systole balloon is deflated (on R wave), which facilitates ejection of the blood into the periphery In early diastole, balloon begins to inflate (on T wave) In late diastole, balloon is totally inflated Increases aortic pressure and increases coronary perfusion pressure with the end result of increased coronary and cerebral blood flow X-ray is used to verify location after placement IABP therapy is called Counterpulsation balloon inflation is opposite to ventricular contraction 1:1 ratio in acute phase of treatment one IABP cycle of inflation and deflation for every heartbeat

Complications with IABP Therapy Signs of a leak include Less effective augmentation Repeated alarms for gas loss Blood backing up into the catheter Patient is relatively immobile, limited to side-lying or supine positions with HOB <45 degrees May be difficult to find comfortable position Patient may experience sleeplessness and anxiety Adequate sedation, pain relief, skin care, and comfort measures are essential Nursing Considerations for Patient with IABP Therapy Must perform frequent and thorough cardiovascular assessments that include o Measurement of hemodynamic parameters (e.g., PA and arterial pressures, CO, CI, SVR, SV) o Auscultation of the heart and lungs o Evaluation of the ECG (e.g., rate, rhythm) o Assess adequate tissue perfusion (e.g., skin color and temperature, mental status, capillary refill, peripheral pulses, urine output, bowel sounds) at regular intervals o It is expected that IABP therapy will improve these parameters IABP therapy is weaned as patient improves 1:1 to 1:2 to 1:3, etc. until line is removed/patient is stable Pumping is continued until line is removed, even if patient is stable, to avoid thrombus formation around catheter

Ventricular Assist Devices (VADs) o Short and long-term support for the failing heart increase or replace action of the ventricle Temporary device with capability to partially or totally support circulation until the heart recovers or a donor heart can be obtained o Allows more mobility than the IABP o Can be internal (e.g. peritoneum) or external o Typically, shunts blood from left atrium or ventricle to the device, then to the aorta some right or biventricular o Indications for VAD

Failure to wean from CPB (cardiopulmonary bypass) or postcardiotomy cardiogenic shock CPB technique that temporarily takes over the function of the heart and lungs during surgery, maintaining the circulation of blood and the oxygen content of the body Cardiotomy cardiogenic shock heart has been damaged by an incision made in the heart (sometimes used for suction during heart surgery) and cannot supply enough blood to the body Bridge to recovery or cardiac transplantation Patients with New York Heart Association Classification IV who have failed medical therapy o Contraindications for VAD BSA less than manufacturer's limit (e.g., 1.3 m2) Renal or liver failure unrelated to a cardiac event Co-morbidities that would limit life expectancy to less than 3 years o Nursing Considerations for Patient with a VAD Similar to that of the patient with an IABP Observe the patient for bleeding, cardiac tamponade, ventricular failure, infection, dysrhythmias, renal failure, hemolysis, and thromboembolism Unlike patient with an IABP, who must remain in bed with limited position change, patient with VAD may be mobile and requires an activity plan In some cases, patients with VADs may go home Preparation for discharge is complex and requires in-depth teaching about the device and support equipment (e.g., battery chargers) Patients must have a competent caregiver present at all times Implantable Artificial Heart o Used to replace the heart of patients who are not eligible for a transplant and have no other treatment alternative o Less expensive implantation and drug therapies than an organ transplant Patients do not require immunosuppression therapy & dont experience long-term effects of this therapy o PATIENTS REQUIRE LIFELONG ANTICOAGULATION THERAPY Nursing Management for All Circulatory Assist Devices (IABP & VAD) Goal is recovery through o Ventricular improvement o Heart transplantation o Artificial heart implantation Many patients will die or choose to terminate device, causing death Psychologic support for patient and caregiver is essential Artificial Airways Endotracheal Tube Intubation o Tube is placed into the trachea via the mouth or nose past the larynx o Performed quickly and safely at the bedside o Oral Intubation ET tube passed through mouth and vocal cords into trachea with aid of a laryngoscope or bronchoscope

Oral intubation preferred for most emergencies b/c airway can be secured rapidly Uses a larger-diameter tube than nasal route, which reduces the work of breathing (WOB) due to less airway resistance Risks of Oral Intubation May be difficult to place if head and neck mobility is limited (e.g. suspected spinal cord injury) Teeth can be chipped or dislodged during procedure Salivation is increased and swallowing is difficult Patient may obstruct ET tube by biting down on it o Can use sedation along with bite block or oropharnygeal airway to avoid this Mouth care is a challenge due to limited space in oral cavity o Can use smaller/pediatric-sized oral products for tooth brushing, cleaning, & suctioning Nasal Intubation ET tube is placed blindly (without seeing larynx) through the nose, nasopharynx, and vocal cords Nasal intubation used when head and neck manipulation is risky

Contraindications for Nasal Intubation Patients with facial fractures Suspected fractures at the base of the skull Postoperatively after cranial surgeries Downfalls of Nasal Intubation Nasal tube uncomfortable for some because it presses on the septum

Some do prefer nasal though b/c no need for bite block and mouth care is easier More subject to kinking than oral tubes WOB is greater due to longer, narrower tubes that have more airflow resistance Suctioning and secretion removal are more difficult Linked with sinus infection and ventilator-associated pneumonia o Indications for Endotracheal Intubation Upper airway obstruction (e.g., secondary to burns, tumor, bleeding) Apnea High risk of aspiration Ineffective clearance of secretions Respiratory distress Tracheostomy o Surgical procedure that is performed when the need for an artificial airway is expected to be long term o Early tracheostomy (2-10 days) may have advantages over delayed, particularly when need for mechanical ventilation is predicted to be longer than 10-14 days Endotracheal Intubation Procedure o Unless emergent, consent for procedure is needed o Important to tell patient they will not be able to speak during intubation but you will provide other means of communication their hands may be restrained for safety purposes o Required for Intubation/Mechanical Ventilation Self-inflating bag-valve-mask (BVM) available & attached to O Ambu bag The slower the bag is deflated/inflated, the higher the O concentration (90-95% from reservoir) Suctioning equipment ready at bedside IV access Before Intubation Assemble and check the equipment to be used Remove patients dentures and/or partial plates (for oral intubation) Administer drugs as ordered Preoxygenate the patient using Ambu bag and 100% O for 3-5 minutes Ventilate b/w each attempt using Ambu bag and 100% O EACH ATTEMPT IS LIMITED TO < 30 SECONDS For oral intubation, place patient supine with the head extended and neck flexed (sniffing position) Allows visualization of vocal cords by aligning axes of mouth, pharynx, and trachea After Intubation Inflate the cuff and confirm placement of ET tube while patient is manually ventilated Use an end-tidal CO detector to measure the amount of exhaled CO from lungs

 Place detector b/w Ambu bag and ET tube if there is a color change, CO is present If no CO detected, tube is in esophagus and needs to be reinserted CO Detector is MOST ACCURATE way to determine if tube is in lungs Auscultate lung apices/bases for bilateral breath sounds Listen for lung sounds if CO detector is not available Auscultate epigastrium to check for absence of air insufflations Observe chest for symmetric chest wall movement SpO should be stable or improved look at patients color as well After all evidence above shows proper placement, connect tube to O source and secure ET tube connected to either humidified air, O, or a mechanical ventilator Suction ET tube and pharynx Insert bite block as needed Arrange for portable chest x-ray immediately to confirm tube location (35 cm above carina in adult) Allows patient to move neck w/o dislodging tube or causing it to enter right primary bronchus

Once x-ray confirms proper placement, mark position of tube at lip, teeth or nose Obtain ABGs within 25 minutes after intubation to get oxygenation and ventilation status Continue pulse ox monitoring to estimate arterial oxygenation IF PATIENT PULLS TUBE OUT, BAG THEM IMMEDIATELY Rapid-sequence intubation (RSI) Rapid, concurrent administration of both a paralytic and a sedative agent during emergency airway management to decrease risk of aspiration, combativeness, and injury to patient NOT INDICATED IN PATIENTS WHO ARE COMATOSE OR IN CARDIAC ARREST Must monitor patients O status during procedure with pulse ox Medications Often Used

 Sedative-hypnotic amnesic (midazolam [Versed]) if agitated, disoriented, combative Rapid-onset opioid (fentanyl [Sublimaze]) to blunt pain of laryngoscopy and intubation Paralytic drug (succinylcholine [Anectine]) to produce skeletal muscle paralysis Atropine to limit secretions Nursing Management for Artificial Airways Maintaining Correct Tube Placement o Monitor ET tube placement every 2-4 hours o Confirm exit mark on ET tube remains constant while At rest Providing patient care Repositioning Transporting o Incorrect tube placement is an emergency Stay with patient and maintain airway Support ventilation Secure help immediately If necessary, ventilate with BVM and 100% O o If dislodged tube isnt repositioned, minimal or no O2 is delivered to lungs or entire tidal volume is delivered to one lung places the patient at risk for pneumothorax Maintaining Proper Cuff Inflation o Cuff is an inflatable, pliable sleeve encircling outer wall of ET tube o Stabilizes and seals ET tube within trachea and prevents escape of ventilating gases o Cuff can cause tracheal damage o Measures to Avoid Tracheal Damage by Cuff Inflate the cuff with air measure & monitor cuff pressure Normal arterial tracheal perfusion is estimated at 30 mm Hg Cuff pressure should be maintained at 20 to 25 mm Hg Cuff pressure is measured and recorded after intubation and on a routine basis (q8h) using Minimal occluding volume technique (MOV) Mechanically Ventilated Patients o Place stethoscope over trachea o Inflate cuff to MOV by adding air until no air leak heard at peak inspiratory pressure Spontaneously Breathing Patients o Inflate cuff until no sound heard after deep breath or after inhalation w/ a BVM o Use manometer to verify cuff pressure is between 20 and 25 mm Hg o Record cuff pressure in chart If adequate cuff pressure cannot be maintained, or larger volumes of air are needed to keep the cuff inflated, the cuff could be leaking, or tracheal dilation could occur at the cuff site

o In this situation, notify physician to reposition or change the ET tube Minimal leak technique (MLT) Similar to MOV, except you remove small amount of air from cuff until a slight air leak is auscultated at peak inflation Both techniques aim to prevent risks of tracheal damage due to high cuff pressures Monitoring Oxygenation and Ventilation o Auscultate to confirm bilateral breath sounds o Monitor patient for adequate oxygenation by assessing clinical findings ABGs, SpO2, and SvO2/ScvO2 o Assess for signs of hypoxemia change in mental status (e.g., confusion), anxiety, dusky skin & dysrhythmias Maintaining Tube Patency o You should NOT routinely suction a patient must assess first to determine need for suctioning o Indications for Suctioning Visible secretions in the ET tube Sudden onset of respiratory distress Suspected aspiration of secretions Increase in peak airway pressures Auscultation of adventitious breath sounds over the trachea and/or bronchi Increase in respiratory rate and/or sustained coughing Sudden or gradual decrease in PaO and/or SpO o Open Suction Technique (OST) or Closed Suction Technique (CST) CST maintains oxygenation and ventilation during suction and reduces exposure to patients secretions o Prevent hypoxemia by hyperventilating patient before beginning & between each pass with Ambu bag & 100% O and limiting each pass to 10 seconds or less o Keep suction pressure under 120 mmHg to avoid damage to the tracheal mucosa increases risk of infection o Make sure to adequately hydrate patient and humidify inspired gases to thin secretions if too thick to suction o Try postural drainage, percussion and turning patient q2h to help move secretions into larger airways Providing Oral Care and Maintaining Skin Integrity o Use saline or water swabs to prevent mucosal drying (lips, tongue, gums) o Reposition and retape ET tube q24h and as needed to avoid skin breakdown from pressure of tubing

Fostering Comfort and Communication o Patients may experience anxiety related to inability to communicate well and not knowing what to expect o ET tube often requires sedating the patient until it is no longer required to blunt anxiety and discomfort Complications of Endotracheal Intubation o Unplanned (inadvertent) Extubation Unplanned removal of the ET tube from the trachea can be catastrophic & usually complicates recovery Can be due to patient removal or accidental removal from movement or procedures Can be obvious (patient holding tube) or not so obvious (tip of tube in hypopharynx or esophagus) Signs of Unplanned Extubation Patient speaking Activation of the low-pressure ventilator alarm Diminished or absent breath sounds Respiratory distress Gastric distention Should this occur, remain with patient, call for help, and manually o ventilate with Ambu bag at 100% O Aspiration Airway not protected from aspiration due to tube splinting epiglottis in open position Cuff cannot totally prevent trickle or oral/gastric secretions from entering trachea Secretions accumulate above the cuff and when it is deflated, those secretions can move into the lungs Some ET tubes provide continuous suctioning of secretions above the cuff

Oral intubation causes an increase in salivation and difficulty swallowing must suction when needed All intubated patients receiving enteral feedings must have HOB elevated a minimum of 30-35 degrees unless medically contraindicated Mechanical Ventilation FIO is at 21% (room air) or greater and is moved in and out of lungs by a mechanical ventilator Mechanical ventilation is NOT curative o Supports patients until able to independently breath or until a decision is made to withdraw mechanical ventilation Negative Pressure Ventilation o Encases the chest and uses negative pressure to pull the chest outward reduces intrathoracic pressure o Air rushes into the upper airway, which is outside the sealed chamber o Expiration is passive machine cycles off to allow chest to retract o Noninvasive does not require artificial airway Positive Pressure Ventilation o Volume ventilation predetermined tidal volume is delivered with each inspiration o Pressure ventilation peak inspiratory volume is predetermined Settings of Mechanical Ventilation

Mechanical Ventilation Alarms and What Causes and Activation

Complications of Positive Pressure Ventilation o Cardiovascular System o Pulmonary system Barotrauma Volutrauma Alveolar hypoventilation Alveolar hyperventilation Ventilator-associated pneumonia o Sodium and water imbalance o Neurologic system o Gastrointestinal system o Musculoskeletal system o Psychosocial needs o Machine disconnection or malfunction

Chapter 67: Shock/SIRS/MODS (10 questions) What is Shock?

Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism Imbalance in supply/demand for O2 and nutrients

Types of Shock Cardiogenic Shock o Systolic or diastolic dysfunction o Compromised cardiac output (CO) o Precipitating Causes Myocardial infarction Cardiomyopathy Blunt cardiac injury Severe systemic or pulmonary hypertension Cardiac tamponade Myocardial depression from metabolic problems o Decreased filling of the ventricle will result in decreased stroke volume. o Despite treatment, mortality rates for patients with cardiogenic shock range from 50% to 85%. o Early manifestations Tachycardia Hypotension Narrowed pulse pressure myocardial O2 consumption o Physical Examination Tachypnea, pulmonary congestion (crackles, wheezes, course breathe sounds) Will give Lasix (push over 2 minutes), Albuterol with Atrovent for pulmonary congestion Want to monitor output and blood pressure after giving Lasix Pallor; cool, clammy skin Decreased capillary refill time cyanosis in fingertips (if fingertips are cool, pulse ox will not be right should be within 10 of the heart rate) Anxiety, confusion, agitation in pulmonary artery wedge pressure Will have arterial line for pressures and frequent blood gases Decreased renal perfusion and UO o The early clinical presentation of a patient with cardiogenic shock is similar to that of a patient with acute decompensated heart failure o The hearts inability to pump blood forward will result in a low CO (<4 L/min) and cardiac index (<2.5 L/min/m2) o Tables 67-3 and 67-4 further describe the clinical presentation of a patient with cardiogenic shock. o Increase in PAWP heart not pumping ventricle filling LVEDP. o Studies that are helpful in diagnosing cardiogenic shock include laboratory studies (e.g., cardiac enzymes, troponin levels, b-type natriuretic peptide [BNP]), electrocardiogram (ECG), chest x-ray, and echocardiogram. o Will give Dobutamine

Hypovolemic Shock could be loss of blood or dehydration o LOW BLOOD VOLUME o Absolute hypovolemia loss of intravascular fluid volume Hemorrhage, GI loss (e.g., vomiting, diarrhea), Fistula drainage, Diabetes insipidus, Hyperglycemia, Diuresis o Relative hypovolemia Results when fluid volume moves out of the vascular space into extravascular space (e.g., interstitial or intracavitary space) Termed third spacing One example of relative volume loss is leakage of fluid from the vascular space to the interstitial space from increased capillary permeability, as seen in sepsis and burns. o Response to acute volume loss depends on Extent of injury or insult, Age, General state of health o Clinical Manifestations Anxiety Tachypnea Increase heart rate Decrease in stroke volume PAWP urinary output If loss is >30%, blood volume is replaced o Overall assessment of physiologic reserves may indicate the patients ability to compensate. A patient may compensate for a loss of up to 15% of the total blood volume (approximately 750 mL). Further loss of volume (15% to 30%) will result in a sympathetic nervous system (SNS)-mediated response. This response

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results in an increase in heart rate, CO, and respiratory rate and depth. Stroke volume, central venous pressure (CVP), and PAWP are decreased because of the decreased circulating blood volume. Loss of autoregulation in the microcirculation and irreversible tissue destruction occur with loss of more than 40% of total blood volume. Common laboratory studies and assessments that are done include serial measurements of hemoglobin and hematocrit levels, electrolytes, lactate, blood gases, and central venous oxygenation (ScvO2), and hourly urine outputs

Neurogenic Shock o DISTRIBUTIVE SHOCK o Hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and can last up to 6 weeks. o Can occur in response to spinal anesthesia o Results in massive vasodilation, leading to pooling of blood in vessels o The injury results in massive vasodilation without compensation due to the loss of SNS vasoconstrictor tone. o Depression of the vasomotor center of the medulla from drugs (e.g., opioids, benzodiazepines) also can lead to decreased vasoconstrictor tone of the peripheral blood vessels, resulting in neurogenic shock. o o Initially, the patients skin will be warm owing to the massive dilation. o As the heat disperses, the patient is at risk for hypothermia. o Later, the patients skin may be cool or warm, depending on the ambient temperature. o Bradycardia instead of tachycardia..loss of SNS, and PS response o Clinical Manifestations Hypotension Bradycardia is huge in neurogenic shock Temperature dysregulation (resulting in heat loss) Dry skin Poikilothermia (taking on the temperature of the environment o

Anaphylactic Shock o Acute, life-threatening hypersensitivity reaction Massive vasodilation Release of mediators capillary permeability o Clinical Manifestations sudden onset of symptoms Anxiety Confusion Dizziness Sense of impending doom Chest pain Incontinence Swelling of the lips and tongue, angioedema Wheezing, stridor Flushing, pruritus, urticaria Respiratory distress and circulatory failure o As capillary permeability increases, fluid leaks from the vascular space into the interstitial space o Anaphylactic shock can lead to respiratory distress Caused by laryngeal edema or severe bronchospasm, and circulatory failure, due to massive vasodilation Septic Shock o Septic shock has three major pathophysiologic effects Vasodilation

Maldistribution of blood flow Myocardial depression Clinical Manifestations coagulation and inflammation fibrinolysis Formation of microthrombi Obstruction of microvasculature Hyperdynamic state Increased CO and decreased SVR Tachypnea/hyperventilation Temperature dysregulation urine output Altered neurologic status GI dysfunction Respiratory failure is common

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Sepsis Systemic inflammatory response to documented or suspected infection Severe sepsis Sepsis + Organ dysfunction Septic shock = Presence of sepsis with hypotension despite fluid resuscitation Presence of tissue perfusion abnormalities The main organisms that cause sepsis are gram-negative and gram-positive bacteria. Parasites, fungi, and viruses can also cause the development of sepsis and septic shock. In as many as 10% to 30% of patients with sepsis, the causative organism is not identified MUST DO BLOOD CULTURE RIGHT AWAY TO ISOLATE ORGANISM

Obstructive Shock o Develops when physical obstruction to blood flow occurs with decreased CO From restriction to diastolic filling of the right ventricle due to compression Abdominal compartment syndrome o Patient will experience: Decreased CO Increased afterload Variable left ventricular filling pressures o Rapid assessment and immediate treatment are important. o Pulmonary embolism and left ventricular thrombi cause an outflow obstruction as blood leaves the right ventricle through the pulmonary artery. o Other clinical signs include jugular vein distention and pulsus paradoxus.

Clinical Presentation of Major Types of Shock

Emergency Management

Stages of Shock Usually not clinically apparent Metabolism changes from aerobic to anaerobic. Lactic acid build-up. ( LA is a waste product that requires oxygen for removal from the body by the liver) Not enough oxygen due to decreased tissue perfusion Compensatory stage: reversible stage during which compensatory mechanisms are effective and homeostasis is maintained.

STAGES OF SHOCK: PROGRESSIVE STAGE OF SHOCK

STAGES OF SHOCK: IRREVERSIBLE STAGE

Irreversible or refractory stage: compensatory mechanisms are not functioning or are totally ineffective, leading to multiple organ dysfunction syndrome.

Diagnostic Studies

Specific Strategies for the Treatment of Shock

Fluid Therapy in Shock

Nursing Assessment ABCs: airway, breathing, and circulation Focused assessment of tissue perfusion Vital signs, Peripheral pulses, Level of consciousness, Capillary refill Skin (e.g., temperature, color, moisture), Urine output Brief history Events leading to shock, Onset and duration of symptoms Details of care received before hospitalization Allergies Vaccinations Nursing Process Nursing Diagnosis or Priorities Planning Implementation Evaluation

Shock to SIRS to MODS If in Multisystem failure feet turn cyanotic (necrotic) and it starts to go up (will damage GI, liver, kidneys) Body is trying to save heart and brain

Diagnostic Studies for Shock Thorough history and physical examination No single study to determine shock Blood studies o Elevation of lactate o Base deficit 12-lead ECG Chest x-ray Hemodynamic monitoring Collaborative Care Successful management includes o Identification of patients at risk for shock o Integration of the patients history, physical examination, and clinical findings to establish a diagnosis o Interventions to control or eliminate the cause of decreased perfusion o Protection of target and distal organs from dysfunction o Provision of multisystem supportive care

General management strategies o Ensure patent airway. o Maximize oxygen delivery. Cornerstone of therapy for septic, hypovolemic, and anaphylactic shock = Volume expansion o Isotonic crystalloids (e.g., normal saline) for initial resuscitation of shock Colloids are effective volume expanders because the size of their molecules keeps them in the vascular space for a longer period of time. Despite this fact, colloids are costly, and no definitive studies demonstrate that using colloids for resuscitation improves patient outcomes. o Volume expansion If the patient does not respond to 2 to 3 L of crystalloids, blood administration and central venous monitoring may be instituted. Complications of fluid resuscitation Hypothermia Coagulopathy Primary goal of drug therapy = Correction of decreased tissue perfusion o Vasopressor drugs (e.g., norepinephrine) If the patient has persistent hypotension after fluid resuscitation and normalized CVP (8 to 12 mm Hg), a vasopressor (e.g., norepinephrine [Levophed], dopamine [Intropin]) and/or an inotrope (e.g., dobutamine [Dobutrex]) may be added. o Achieve/maintain MAP >60 to 65 mm Hg. o Reserved for patients unresponsive to fluid resuscitation o Medications used to improve perfusion in shock are administered intravenously via an infusion pump and a central venous line Fluid replacement is calculated using a 3:1 rule (3 mL of isotonic crystalloid for every 1 mL of estimated blood loss).

SIRS

Systemic inflammatory response syndrome (SIRS) is a systemic inflammatory response to a variety of insults. Generalized inflammation in organs remote from the initial insult Triggers o Mechanical tissue trauma: burns, crush injuries, surgical procedures o Abscess formation: intraabdominal, extremities o Ischemic or necrotic tissue: pancreatitis, vascular disease, myocardial infarction o Microbial invasion: bacteria, viruses, fungi o Endotoxin release: gram-negative bacteria o Global perfusion deficits: postcardiac resuscitation, shock states o Regional perfusion deficits: distal perfusion deficits

SIRS is manifested by two or more of the following conditions: Temperature >38 degrees Celsius or <36 degrees Celsius. Heart rate>90 beats per minute. Respiratory rate>20 breaths per minute or PaCO2<32mmHg. White blood cell count > 12,000/cu mm, <4,000/ cu mm, or >10% band forms. MODS Multiple organ dysfunction syndrome (MODS) is the failure of two or more organ systems. o Homeostasis cannot be maintained without intervention. o Results from SIRS SIRS and MODS Pathophysiology Consequences of inflammatory response o Release of mediators o Direct damage to the endothelium o Hypermetabolism o Vasodilation leading to decreased SVR o Increase in vascular permeability o Activation of coagulation cascade

Last two systems to go down is brain and heart

Organ and metabolic dysfunction o Hypotension o Decreased perfusion o Formation of microemboli o Redistribution or shunting of blood o Respiratory system o Alveolar edema o Decrease in surfactant o Increase in shunt o V/Q mismatch o End result: ARDS o Cardiovascular system o Myocardial depression and massive vasodilation o Neurologic system o Mental status changes due to hypoxemia, inflammatory mediators, or impaired perfusion o Often early sign of MODS*** o Renal system o Acute renal failure if they survive they will need dialysis Hypoperfusion Release of mediators Activation of renin-angiotensin- aldosterone system Nephrotoxic drugs, especially antibiotics GI system o o o Motility decreased: abdominal distention and paralytic ileus Decreased perfusion: risk for ulceration and GI bleeding Potential for bacterial translocation

Signs of deteriation start from legs (modeling, color of skin, decrease pulseabdomen (kidneys, colon will see sore in colon, decrease UO and increase creatinine heart and lungs (with ventilator the lungs still pumping

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Hypermetabolic state o Hyperglycemia-hypoglycemia o Insulin resistance o Catabolic state o Liver dysfunction o Lactic acidosis Will increase Hematologic system o DIC Electrolyte imbalances Metabolic acidosis

SIRS and MODS Collaborative Care Prognosis for MODS is poor. Goal: prevent the progression of SIRS to MODS Vigilant assessment and ongoing monitoring to detect early signs of deterioration or organ dysfunction are critical. Prevention and treatment of infection Aggressive infection control strategies to decrease risk for nosocomial infection Once an infection is suspected, institute interventions to control the source. Maintenance of tissue oxygenation Decreased O2 demand Sedation Mechanical ventilation Paralysis Analgesia They still feel pain, indication, increase BP, HR and grimaces, need to give them med

Nutritional and metabolic needs Goal of nutritional support: preserve organ function o TPN, PPN Total energy expenditure is often increased 1.5 to 2.0 times. Use of the enteral route is preferred to parenteral nutrition. Monitor plasma transferrin and prealbumin levels to assess hepatic protein synthesis Support of failing organs ARDS: aggressive O2 therapy and mechanical ventilation DIC: appropriate blood products Renal failure: continuous renal replacement therapy or dialysis Know for test!! o 10-15 question on shock and critical care SIRs effect berating first o CP reading, art line reading MODs effect from ground up o 2 med questions o 10-HIV o HIV screening and testing on HIV o Know ventilators for test - know setting up and helping with ventilation o If high? If low?, Complication?