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UTA NURS 4581 Exam 2

UTA NURS 4581 Critical Care Exam 2

Respiratory Acidosis Compensatory Response and Effect HCO3– retention and H+ excretion by kidney; HCO3– level should go up (> 26) and Urine pH should decrease (< 6) if compensated
Respiratory acidosis causes Chronic obstructive pulmonary disease, Barbiturate or sedative overdose, Chest wall abnormality (e.g., obesity), Severe pneumonia, Atelectasis, Respiratory muscle weakness (e.g., Guillain-Barré syndrome), Mechanical hypoventilation
Respiratory acidosis manifestations Drowsiness, Dizziness, Headache, Disorientation→ Stupor & coma; ↓ Blood pressure, Ventricular fibrillation (related to hyperkalemia from compensation), Warm, flushed skin (related to peripheral vasodilation); Seizures; Hypoventilation and hypoxia
Respiratory acidosis management identify/treat cause (do not give bicarbonate) by increasing ventilation and decreasing dead space (increase rate and volume of respiration); for COPD it is normal for them to be in fully compensated acidosis and no treatment is necessary
Respiratory Alkalosis Compensatory Response and Effect (rare, in chronic cases) HCO3– excretion by kidney or shifting of HCO3– into cells in exchange for Cl-; HCO3– level should decrease (< 22) and Urine pH should increase if renal involvement (> 6)
Respiratory alkalosis causes Hyperventilation (caused by hypoxia, pulmonary emboli, anxiety, fear, pain, exercise, fever); Stimulated respiratory center caused by septicemia, encephalitis, brain injury, salicylate poisoning; Mechanical hyperventilation
Respiratory alkalosis manifestations Lethargy, Light-headedness, Confusion; Tachycardia, Dysrhythmias (r/t hypokalemia); Nausea, Vomiting, Epigastric pain; hypocalcaemia manifestations (Tetany→ convulsions & unconsciousness) from increased binding of calcium to protein; hyperventilation
Respiratory alkalosis management slow ventilation, rebreather mask, increase dead space
Metabolic Acidosis Compensatory Response and Effect CO2 excretion by lungs; increased RR (Kussmaul respirations) and kidneys attempt to excrete additional acid; decreased PaCO2 (<35), decreased urine pH (<6)
Metabolic acidosis causes Diabetic ketoacidosis, Lactic acidosis, Starvation, Severe diarrhea, Renal tubular acidosis, Renal failure, Gastrointestinal fistulas, Shock, Poisoning
Metabolic acidosis manifestations Drowsiness, Headache, Disorientation→ coma; ↓ Blood pressure, Dysrhythmias (r/t hyperkalemia from compensation), Warm, flushed skin (related to peripheral vasodilation); Nausea, vomiting, diarrhea, abdominal pain; Kussmaul respirations (Deep, rapid)
Metabolic acidosis management indentify/treat underlying cause; sodium bicarbonate (NaHCO3) if severe
Metabolic Alkalosis Compensatory Response and Effect CO2 retention by lungs and HCO3– excretion by kidney; decreased RR, increased PaCO2 (> 45), increased urine pH (> 6)
Metabolic alkalosis causes Severe vomiting, Excess gastric suctioning, Diuretic therapy (increased excretion of H+), Potassium deficit, Excess NaHCO3 intake, Excessive mineralocorticoids
Metabolic alkalosis manifestations Dizziness, Irritability, Nervousness, confusion; Nausea, Vomiting, Anorexia; hypokalemia manifestations; hypocalcemia manifestations (r/t increased calcium binding to proteins); Hypoventilation
Metabolic alkalosis management treat underlying cause, Diamox (acetazolamide)
Diamox (acetazolamide) classification and use Diuretic, carbonic anhydrase inhibitor, antiglaucoma agent, antiepileptic; used to treat acute altitude sickness; glaucoma; seizures; and edema
Length of time for renal compensatory mechanisms to begin after acute onset of respiratory acidosis within 24 hours (up to 72 hours); bicarbonate normal until then (uncompensated)
Risk of acidosis compensatory mechanism of shifting H+ into cells from blood Hyperkalemia (from potassium shifting out of cells to replace H+) which can cause Dysrhythmias or Ventricular fibrillation
Risk of alkalosis compensatory mechanism of shifting H+ out of cells into blood stream Hypokalemia (from potassium shifting out of blood to replace H+) which can cause Dysrhythmias
PaCO2 Normal 35-45
HCO3- Normal 22-26
pH Normal 7.35-7.45
Base excess (B.E.) Normal +/-2.0
PaO2 Normal 80-100
O2 Sat Normal 96-100%
Hypoxemia low oxygen tension in the blood characterized by a variety of nonspecific clinical signs and symptoms
hypoxemic respiratory failure oxygenation failure; a condition in which the PaO2 is 60 mm Hg or less when the patient is receiving an inspired oxygen concentration of 60% or greater (normal PaO2 is 80-100)
hypoxemic respiratory failure causes V/Q mismatch; shunt; diffusion limitation; alveolar hypoventilation
Ventilation-Perfusion (V/Q) mismatch alveola receive too little blood flow (perfusion) in relation to air (ventilation) or too little air (ventilation) in relation to blood flow (perfusion)
V/Q mismatch causes ventilation issue: COPD, pneumonia, asthma, atelectasis; perfusion issue: PE
shunt blood exits the heart without having participated in gas exchange
shunt causes anatomic shunt (e.g., VSD) or intrapulmonary shunt (e.g., acute respiratory distress syndrome [ARDS], pneumonia, pulmonary edema)
Diffusion limitation when gas exchange across the alveolar-capillary membrane is compromised by a process that thickens, damages, or destroys the membrane
Diffusion limitation causes severe emphysema, PE, pulmonary fibrosis, interstitial lung disease, ARDS, exercise
Alveolar hypoventilation a generalized decrease in ventilation that results in an increase in the PaCO2 and a consequent decrease in PaO2.
alveolar hypoventilation causes restrictive lung disease, CNS disease, chest wall dysfunction, acute asthma, neuromuscular disease
hypoxemia manifestations Dyspnea, Tachypnea, Prolonged expiration (I:E
hypoxemia LATE manifestation Paradoxic chest/abdominal wall movement with respiratory cycle, Cyanosis, Coma, Dysrhythmias, Hypotension
hypoxemia management increase oxygenation
Hypercapnia greater than normal amounts of carbon dioxide in the blood; also called hypercarbia
hypercapnic respiratory failure ventilatory failure; a condition in which the PaCO2 is above normal (> 45) in combination with acidemia (arterial pH < 7.35)
hypercapnic respiratory failure causes airflow obstruction and air trapping; CNS conditions that suppress drive to breath; conditions that prevent normal movement of chest wall; neuromuscular conditions causing respiratory muscle weakness or paralysis
airflow obstruction and air trapping conditions can cause hypercapnic respiratory failure; includes asthma, COPD, cystic fibrosis
CNS conditions that suppress drive to breath can cause hypercapnic respiratory failure; includes opioid or other respiratory depressant drug overdoses
conditions that prevent normal movement of chest wall can cause hypercapnic respiratory failure; includes flail chest, kyphoscoliosis, morbid obesity
neuromuscular conditions causing respiratory muscle weakness or paralysis Guillain-Barré syndrome, muscular dystrophy, myasthenia gravis (acute exacerbation), or multiple sclerosis
hypercapnia manifestations Dyspnea, rapid/shallow RR, ↓ Tidal volume, ↓ Minute ventilation, Morning headache, Disorientation, Progressive somnolence, Elevated ICP, Dysrhythmias, HTN, Tachycardia, Bounding pulse, Muscle weakness, ↓ Deep tendon reflexes, Pursed-lip, tripod position
hypercapnia LATE manifestations ↓ RR, Tremors, seizures; Coma
acute respiratory failure management identify/treat cause; O2 therapy, mobilization of secretions (hydration/humidification, CPT, airway suctioning), positive pressure ventilation; goal: PaO2 55-60 with least amount of O2 admin
acute respiratory distress syndrome (ARDS) a sudden and progressive form of acute respiratory failure in which the alveolar-capillary membrane becomes damaged and more permeable to intravascular fluid; when a patient's PaO2/FIO2 ratio is less than 200 (e.g., 80/0.8
acute lung injury (ALI) a condition that occurs when the patient's PaO2/FIO2 ratio is 200-300 (e.g., 86/0.4
ARDS common causes Aspiration of gastric contents, Viral/bacterial pneumonia, Sepsis, Severe massive trauma, Transfusion-related acute lung injury (e.g., multiple blood transfusions), Shock states, Cardiopulmonary bypass, Near-drowning, Acute pancreatitis
ARDS three phases (1) injury or exudative phase, (2) reparative or proliferative phase, and (3) fibrotic phase
ARDS manifestations asymptotic at first or dyspnea, tachypnea, cough, restlessness, fine crackles, hypoxemia and respiratory alkalosis, edema, diaphoresis, changes in sensorium with decreased mentation, cyanosis, pallor, pleural effusions
ARDS complications Ventilator-Associated Pneumonia, Barotrauma, Volutrauma, Stress Ulcers, Acute kidney injury
Barotrauma rupture of alveoli during mechanical vent, causing presence of air in locations not usually found, leading to pulmonary interstitial emphysema, pneumothorax, SQ emphysema, pneumoperitoneum, pneumomediastinum, pneumopericardium, and tension pneumothorax
Volutrauma alveolar fractures (damage or tears in the alveoli) and movement of fluids and proteins into the alveolar spaces when large tidal volumes are used.
ARDS management Respiratory therapy (O2, Lateral rotation, PEEP, prone positioning, mechanical ventilation); supportive therapy (identify/treat cause, hemodynamic monitoring, inotropic/vasopressor meds, diuretics, IVF, sedation/analgesia, neuromuscular blockade)
ARDS Diagnostic findings Refractory Hypoxemia (Acute lung injury: PaO2/FIO2 ratio between 200-300 OR Acute respiratory distress syndrome: PaO2/FIO2 ratio <200); Chest X-Ray shows white space; PAWP ≤18 mm Hg and no evidence of HF
Mechanical ventilation the process by which the FIO2 is at 21% (room air) or greater and is moved in and out of the lungs by a mechanical ventilator.
Indications for mechanical ventilation (1) apnea or impending inability to breathe, (2) acute respiratory failure, (3) severe hypoxia, and (4) respiratory muscle fatique.
Negative pressure ventilation the use of chambers that encase the chest or body and surround it with intermittent subatmospheric or negative pressure.
Positive pressure ventilation (PPV) the primary method used with acutely ill patients; During inspiration the ventilator pushes air into the lungs under positive pressure.
volume ventilation a predetermined tidal volume (VT) is delivered with each inspiration, and the amount of pressure needed to deliver the breath varies based on the compliance and resistance factors of the patient-ventilator system.
pressure ventilation the peak inspiratory pressure is predetermined and the VT delivered to the patient varies based on the selected pressure and the compliance and resistance factors of the patient-ventilator system.
Mechanical Ventilator Setting: Respiratory rate (f) Number of breaths the ventilator delivers per minute; usual setting is 6-20 breaths/min
Mechanical Ventilator Setting: Tidal volume (VT) Volume of gas delivered to patient during each ventilator breath; usual volume is 6-10 mL/kg
Mechanical Ventilator Setting: Oxygen concentration (FIO2) Fraction of inspired oxygen (FIO2) delivered to patient; may be set between 21% (essentially room air) and 100%; usually adjusted to maintain PaO2 level >60 mm Hg or SpO2 level >90%
Mechanical Ventilator Setting: Positive end-expiratory pressure (PEEP) Positive pressure applied at the end of expiration of ventilator breaths; usual setting is 5 cm H2O
Mechanical Ventilator Setting: Pressure support Positive pressure used to augment patient's inspiratory pressure; usual setting is 6-18 cm H2O
Mechanical Ventilator Setting: I:E ratio Duration of inspiration (I) to duration of expiration (E); usual setting is 1:2 to 1:1.5 unless IRV is desired
Mechanical Ventilator Setting: Inspiratory flow rate and time Speed with which the VT is delivered; usual setting is 40-80 L/min and time is 0.8-1.2 sec
Mechanical Ventilator Setting: Sensitivity the amount of effort the patient must generate to initiate a ventilator breath; it may be set for pressure triggering or flow triggering; usual setting for a pressure trigger is 0.5-1.5 cm H2O below baseline pressure and for a flow trigger is 1-3 L/min be
Mechanical Ventilator Setting: High-pressure limit Regulates the maximal pressure the ventilator can generate to deliver the VT; when the pressure limit is reached, the ventilator terminates the breath and spills the undelivered volume into the atmosphere; usual setting is 10-20 cm H2O above peak inspirat
controlled ventilatory support the ventilator does all of the work of breathing
assisted ventilatory support the ventilator and the patient share the WOB
Assist-Control (AC) or Assisted Mandatory Ventilation (AMV) Requires that rate, VT, inspiratory time, and PEEP be set for the patient. The ventilator sensitivity is also set, and when the patient initiates a spontaneous breath, a full-volume breath is delivered.
Intermittent Mandatory Ventilation (IMV) and Synchronized Intermittent Mandatory Ventilation (SIMV) Requires that rate, VT, inspiratory time, sensitivity, and PEEP are set for the patient. In between “mandatory breaths,” patients can spontaneously breathe at their own rates and VT. With SIMV, the ventilator synchronizes the mandatory breaths with the pa
Pressure Support Ventilation (PSV) Provides an augmented inspiration to a spontaneously breathing patient. When the patient initiates a breath, a high flow of gas is delivered to the preselected pressure level and pressure is maintained throughout inspiration.
Pressure-Control Inverse Ratio Ventilation (PC-IRV) Combines pressure-limited ventilation with an inverse ratio of inspiration to expiration.
Positive End-Expiratory Pressure (PEEP) Creates positive pressure at end exhalation and restores functional residual capacity (FRC). The term PEEP is used when end-expiratory pressure is provided during ventilator positive pressure breaths.
Continuous Positive Airway Pressure (CPAP) Similar to PEEP, CPAP restores FRC. This pressure is continuous during spontaneous breathing; no positive pressure breaths are present.
High-frequency ventilation (HFV) used mostly in pediatrics; delivery of a small VT (usually 1 to 5 mL/kg of body weight) at rapid respiratory rates (100 to 300 breaths/min) in an effort to recruit and maintain lung volume and reduce intrapulmonary shunting.
Positioning r/t ARDS the repositioning of a patient from a supine or lateral position to a prone (on the stomach with face down) position to improve lung recruitment through various mechanisms.
Extracorporeal membrane oxygenation (ECMO) used mostly in pediatrics; a modification of cardiac bypass (only bypassing lungs) and involves partially removing blood from a patient with large-bore catheters, infusing O2, removing CO2, and returning the blood back to the patient.
Positive Pressure Ventilation (PPV) complications cardiovascular (decreased circulation, preload, CO, and hypotension); pulmonary (barotrauma, volutrauma, Alveolar hypoventilation, Alveolar hyperventilation, VAP); sodium and water imbalances; neurologic (increased ICP); GI (stress ulcers, GI bleeding); m
Train-of-four assessment used for administration of paralytics; the use of a peripheral nerve stimulator to deliver four successive stimulating currents to elicit muscle twitches. The number of twitches will vary with the percentage of neuromuscular blockade. The usual goal is on
Mechanical ventilator weaning phases the preweaning phase, the weaning process, and the outcome phase.
Mechanical ventilator preweaning phase assessment phase; determines ability to breath spontaneously by assessing muscle strength and endurance, minute ventilation, breathing pattern, lungs are clear
Indicators for Weaning from mechanical ventilator reversal of underlying cause; adequate oxygenation; hemodynamic stability (absence of myocardial ischemia or clinically significant hypotension); and ability to initiate an inspiratory effort
Mechanical ventilator weaning parameters maximum inspiratory pressure -20 to -30; minute ventilation <10 L/min; PaCO2 normal for patient (e.g., elevated for COPD); PaO2 ≥ 60; FIO2 ≤ 50%; PEEP ≤ 5 cm; and PSV ≤ 10
Minute ventilation (VE) Tidal volume multiplied by respiratory rate over 1 min; normal 5-10 L/min; indices for weaning ≤ 10 L/min
TLC Total Lung Capacity
VC Vital Capacity
IC Inspiratory Capacity
MIF Maximum Inspiratory Force.
FRC Functional Residual Capacity
VT Tidal Volume
MV Minute Volume
Rate (number of ventilator breaths delivered per minute) X VT
IRV Inspiratory Reserve Volume
ERV Expiratory Reserve Volume
RV Residual Volume
VD Dead space
FIO2 Fraction of inspired oxygen, or oxygen concentration delivered by ventilator (21%- 100%).
ACV Assist Control Ventilation
SIMV Synchronized Intermittent Mandatory Ventilation.
PEEP Positive End Expiratory Pressure.
CPAP Continuous Positive Airway Pressure.
PSV Pressure Support Ventilation
IRV Inverse Ratio Ventilation
PCV Pressure Controlled Ventilation
BiLevel Bilevel ventilation; allows spontaneous breaths along with PSV/PCV
Ramsay scale or Bispectral Index Monitor Scale used to assess sedation level in patients on mechanical ventilation; ranges from 1 (anxious, agitated, restless, or all three) to 5 (does not respond to painful stimulus)
Neuromuscular blocking agents suffix “URIUM” or “ONIUM” (e.g., Atracurium besylate, Cisatracurium besylate, Doxacurium chloride, Pancuronium bromide, Vecuronium bromide)
factor commonly responsible for sodium and fluid retention in the patient on mechanical ventilation decreased renal perfusion with increased release of renin
Oropharyngeal airway purpose Maintain airway in unconscious patients and used as a bite block for patients with endotracheal tubes
Oropharyngeal airway sizing place the airway on the patient’s cheek with the flat plate at the lips. The end of the airway should hit the jaw.
Oropharyngeal airway insertion invert the airway so the tip is facing upward. Slide the airway in and rotate so the tip is toward the oropharynx.
Oropharyngeal airway maintenance remove when mouth care is performed and clean with toothbrush and water or a mixture of hydrogen peroxide and mouthwash. If patient’s condition does not permit airway removal, perform mouth care with airway in place.
Nasopharyngeal airway purpose Facilitates suctioning in semi-conscious/conscious patient
Nasopharyngeal airway sizing place the airway on the patient’s cheek with the flange at the nares. The end of the airway should hit below the mandible.
Nasopharyngeal airway maintenance Change from side-to-side every 72 hours. Clean airway and re-lubricate prior to reinsertion
Endotracheal Tube airway purpose Provide stabilization of airway; Ensure proper ventilation via mechanical ventilator; Facilitate removal of secretions
Oral ET tube advantages Can be rapidly inserted in an emergency situation; A larger diameter tube can be used, resulting in reduced work of breathing because there is less airway resistance; do not kink as much as nasal tubes; suctioning and secretion removal is easier; no risk
Nasal ET tube advantages More stable than oral tubes; more difficult to dislodge; Can be placed “blindly”, without visualization of the larynx; Mouth care can be easily performed; a bite block is not needed; less risk of laryngeal trauma from larger tubes
Tracheostomy purpose Bypass an upper airway obstruction; Facilitate removal of secretions; Permit long-term mechanical ventilation; Permit oral intake and speech in the patient who requires long-term mechanical ventilation
Cuffed tracheostomy tube When properly inflated, low-pressure, high-volume cuff distributes cuff pressure over large area, minimizing pressure on tracheal wall.
Cuffed tracheostomy tube indication used with patients at risk of aspiration or in need of mechanical ventilation
Fenestrated tracheostomy tube When inner cannula is removed, cuff deflated, and decannulation plug inserted, air flows around tube, through fenestration in outer cannula, and up over vocal cords. Patient can then speak.
Tracheostomy advantages Less risk of long-term damage to the airway; Patient comfort may be increased because no tube is present in the mouth; Patient can eat; The patient can speak, if the cuff can be deflated, or a speaking tube is used; Mobility may be increased
Tracheostomy dislodgement management immediately attempt to replace it; if cannot be replaced, raise to semi-fowlers to alleviate dyspnea; if severe dyspnea causes a respiratory arrest, cover stoma with a sterile dressing and ventilate patient with bag-mask ventilation until help arrives
Tracheostomy emergent replacement spread stoma in cleanest manner possible, insert obturator into replacement tube, and apply water-soluble lubricant to tip of tube, and insert tube into stoma at a 45 degree angle, remove obturator immediately after successful insertion
Indications that patient needs suctioning Coarse crackles or rhonchi over large airways; moist cough; Increase in peak inspiratory pressure on mechanical ventilation; Restlessness or agitation if accompanied by a decrease in SpO2
Chest tube purpose To remove air and/or fluid from the pleural cavity or mediastinal area; To prevent air and/or fluid from re-accumulating in the pleural cavity or mediastinal area; To re-expand the lung and restore and maintain normal negative intrapleural pressure
Chest tube placement indications pneumothorax, hemothorax, pleural effusion, empyema, and prevention of cardiac tamponade post-heart surgery
Visceral pleura membrane lining the lungs which does NOT have any sensory pain fibers or nerve endings
Parietal pleura membrane lining the chest cavity which does have sensory pain fibers and therefore irritation of the parietal pleura causes pain with each breath.
Pleural space The space between the visceral pleura and parietal pleura; a closed, double-walled sac which contains 20-25 mL of fluid
Pleural fluid purpose (1) it provides lubrication, allowing the pleural layers to slide over each other during breathing; and (2) it increases cohesion between the pleural layers, thereby facilitating expansion of the pleura and lung during inspiration.
Mediastinum the space above the diaphragm and between the lungs which contains the heart, great vessels, and esophagus
Current research related to stripping chest tubes Avoid aggressive chest-tube manipulation, including stripping or milking, because this can generate extreme negative pressures in the tube and does little to maintain chest-tube patency.
Current research related to clamping chest tubes Clamping prevents the escape of air or fluid, increasing the risk of tension pneumothorax. Never clamp it when transporting the patient or for an extended period, unless ordered by the physician (such as for a trial before chest-tube removal).
Pneumothorax a collection of air or gas in the pleural space causing the lung to collapse; a collapse greater than 15% can cause respiratory compromise, necessitating insertion of a chest tube.
Tension pneumothorax life-threatening emergency; rapid accumulation of air in the pleural space causing severely high intrapleural pressures with resultant tension on the heart and great vessels; causes a mediastinal shift pushing the heart, great vessels, trachea, and lungs
Hemothorax accumulation of blood in the pleural space (e.g., due to surgery or trauma)
Pleural effusion an abnormal accumulation of fluid in the intrapleural spaces of the lungs (usually serous, perhaps CHF, or from tumor process)
Chylothorax the presence of lymphatic fluid in the pleural space due to a leak in the throacic duct (trauma, surgical procedures, malignancies)
Empyema an accumulation of purulent exudates in a body cavity, especially the pleural space, as a result of bacterial infection, such as pleurisy or tuberculosis
Positioning of pt with Chest Tube position patient on operative side to facilitate expansion of remaining lung
Chest Tube removal removed at end of expiration and close with dressing (Vaseline gause) ASAP; chest x-ray
Chest tube complications site infection, malposition, pneumonia, vasovagal response from rapid removal of fluid, Re-expansion pulmonary edema following rapid expansion of a collapsed lung or evacuation of large amounts of fluid (generally > 1.5 liters), Shoulder disuse atrophy wh
Mediastinal Chest Tube indication Following heart surgery mediastinal chest tubes are placed in the mediastinal area, most commonly directly under the sternum.
Mediastinal Chest Tube purpose To prevent accumulation of fluid around the heart which could lead to a cardiac tamponade, a potentially lethal complication.
EKG grid paper small squares width 0.04 seconds
EKG grid paper small squares height 0.1mV
EKG grid paper large squares width 0.2 seconds
EKG grid paper large squares height 0.5mV
Length of strip needed to determine rate/min 6 seconds (multiply number by 10)
Grid method large squares between two cardiac cycles divided by 300
P wave represents depolarization of the atria.
QRS complex indicates depolarization of the ventricles.
T wave represents repolarization of the ventricles.
PR interval normal duration 0.12-0.2 seconds (or three to five tiny boxes)
QT interval normal duration 0.34-0.43 seconds and may vary by gender
QRS interval normal duration 0.06-0.1 seconds (or 1.5 to 2.5 tiny boxes)
Sinus bradycardia management Ensure IV in place; O2; cardiac monitoring; identify cause; atropine (if symptomatic or unstable); TCP or dopamine/epinephrine drip if atropine is ineffective
Sinus tachycardia management Ensure IV in place; O2; cardiac monitoring; identify and treat cause; beta blocker or calcium channel blocker if medication is needed
Supraventricular Tachycardia/Paroxymal Supraventricular Tachycardia management Ensure IV in place, O2; cardiac monitoring; 12 Lead EKG; Vagal maneuvers; Adenosine (6mg rapid IV push); amiodarone, beta blockers, digoxin, or calcium channel blockers (when Vagal maneuvers and Adenosine fail); cardioversion (if unstable)
Atrial flutter management ensure IV is in place; O2; cardiac monitoring; obtain 12 Lead EKG; calcium channel blockers, amiodarone, beta blockers, digoxin, and anti-coagulation; cardioversion
Atrial fibrillation management ensure IV in place; O2; cardiac monitoring; 12 Lead EKG; calcium channel blockers (e.g., Cardizem), amiodarone, beta blockers, digoxin, and anti-coagulation; cardioversion
Junctional rhythm management ensure IV in place; O2; cardiac monitoring; identify cause and treat; Atropine (if unstable); TCP or dopamine/epinephrine drip (if atropine is ineffective)
First Degree AV Block causes Ischemia of SA node; Digitalis Toxicity; Acute MI; Beta Blocker overdose
First Degree AV Block management ensure IV in place; O2; cardiac monitoring; identify and treat cause
Second Degree AV Block, Type I management Ensure IV in place; O2; cardiac monitoring; identify and treat cause
Second Degree AV Block, Type 2 management Ensure IV in place, O2; cardiac monitoring; identify/treat cause; Atropine (if symptomatic or unstable); TCP
Third Degree AV Block management Ensure IV in place; O2; cardiac monitoring; identify and treat cause; TCP; pacemaker (temporary transvenous or permanent)
Premature Ventricular Contractions (PVC) causes myocardial ischemia, injury and infarction; electrolyte imbalance; hypothermia, hypoxia, acidosis
Premature Ventricular Contractions (PVC) management ensure IV line; O2; cardiac monitoring; identify and treat cause
Ventricular Tachycardia causes myocardial ischemia, injury and infarction; electrolyte imbalance; hypothermia, hypoxia, acidosis
Ventricular Tachycardia management (with a pulse) ensure IV in place; O2; cardiac monitoring; 12 Lead; cardioversion or antiarrhythmic medication (amiodarone or lidocaine); identify and treat cause
Ventricular Tachycardia management (without a pulse) ensure unresponsive and call for help; initiate chest compressions; defibrillation; ensure IV in place; cardiac monitoring; ventilate with bag-valve-mask; if persists, epinephrine (or Vasopressin) and antiarrhythmic (amiodarone or lidocaine); ACLS as need
Ventricular Fibrillation causes myocardial ischemia, injury and infarction; electrolyte imbalance; hypothermia, hypoxia, acidosis
Ventricular Fibrillation management ensure unresponsive and call for help; initiate chest compressions; defibrillation; ensure IV in place; cardiac monitoring; ventilate with bag-valve-mask; if persists, epinephrine (or Vasopressin) and antiarrhythmic (amiodarone or lidocaine); ACLS as need
Asystole management ensure unresponsive and call for help; initiate chest compressions; defibrillation; ensure IV in place; cardiac monitoring; ventilate with bag-valve-mask; epinephrine (or Vasopressin) and atropine; re-check EKG every 2 min; ACLS as needed
Pulseless Electrical Activity (PEA) management ensure unresponsive and call for help; initiate chest compressions; ensure IV in place; cardiac monitoring; verify PEA; ventilate with bag-valve-mask; epinephrine (or Vasopressin) and atropine; re-check EKG every 2 min; ACLS as needed
Defibrillation the treatment of choice to terminate VF and pulseless VT; passage of a DC electric shock through the heart that is sufficient to depolarize the cells of the myocardium, subsequently repolarizing myocardial cells which allows the SA node to resume the role
Monphasic vs. biphasic defibrillators Monophasic defibrillators deliver energy in one direction and biphasic defibrillators deliver energy in two directions (Fig. 36-20). Biphasic defibrillators deliver successful shocks at lower energies and with fewer postshock ECG abnormalities than monoph
Defibrillator electrical voltage Biphasic defibrillators deliver the first and any successive shocks using 120 to 200 joules. Recommendations for monophasic defibrillators include an initial shock at 360 joules.
automatic external defibrillator (AED) a defibrillator that has rhythm detection capability and the ability to advise the operator to deliver a shock using hands-free defibrillator pads.
Synchronized cardioversion synchronized circuit in the defibrillator delivers a countershock that is programmed to occur on the R wave of the QRS complex of the ECG.
Synchronized cardioversion indications the therapy of choice for the patient with hemodynamically unstable ventricular (e.g., VT with a pulse) or supraventricular tachydysrhythmias (e.g., atrial fibrillation with a rapid ventricular response).
Synchronized cardioversion electrical voltage Start energy levels at 50 to 100 joules and increase if needed.
implantable cardioverter-defibrillator (ICD) lead system placed via a subclavian vein to the endocardium with battery-powered pulse generator implanted SQ. monitors HR and rhythm, identifies VT or VF and delivers a 25-joule or less shock to the patient’s heart.
implantable cardioverter-defibrillator (ICD) indications patients who (1) have survived SCD, (2) have spontaneous sustained VT, (3) have syncope with inducible ventricular tachycardia/fibrillation during EPS, and (4) are at high risk for future life-threatening dysrhythmias (e.g., have cardiomyopathy).
transvenous pacemaker a lead or leads that are threaded transvenously to the right atrium and/or right ventricle and attached to the external power source
Epicardial pacemaker Often used with cardiac surgery; Temporary electrodes are sutured to epicardium and brought out through chest wall. If it is necessary to pace, terminals can be connected to power source. When pacing is no longer necessary, a pull on the wires will break
transcutaneous pacemaker (TCP) used to provide adequate HR and rhythm to the patient in an emergency situation; electrodes are placed on the patient’s anterior and posterior chest walls and attached to an external pacing unit.
Permanent pacemaker Implanted in chest via pouch and powered by batteries that last 10 or more years; Can be externally programmed with signals from a specially programmed unit.
Indications for pacemaker insertion bradydysrhythmias (symptomatic sinus bradycardia, sinus arrest, slow ventricular rhythm); heart blocks (2nd degree A-V block with slow V response, 3rd degree block, Bundle branch block in anterior MI); Sick-Sinus-Syndrome (Brady-Tachy Syndrome)
Indication for atropine use vs. pacemaker insertion atropine only affects ventricles and is used for 1st degree AV heart block; pacemakers used for 2nd and 3rd degree heart blocks
Asynchronous (fixed-rate) pacing mode Delivers a stimulus regardless of patient's spontaneous cardiac activity. Used only with no spontaneous beats - asystole.
Synchronous (demand) pacing mode Initiates a beat only when a preset interval has passed without spontaneous activity. Allows spontaneous beats to occur without competition from the pacemaker.
Pacemaker failure to sense pacemaker fails to recognize spontaneous atrial or ventricular activity, and it fires inappropriately, potentially causing ventricular tachcardia (VT)
Pacemaker failure to capture the electrical charge to the myocardium is insufficient to produce atrial or ventricular contraction, resulting in serious bradycardia or asystole.
Phlebostatic axis an external landmark used to identify the level of the atria in the supine patient.
Phlebostatic axis location The intersection of two imaginary lines: one drawn vertically through the fourth intercostal space at the sternum, and another drawn horizontally through the midchest, halfway between the outermost anterior and outermost posterior points of the chest.
Zeroing confirms that when pressure within the system is zero, the monitor reads zero.
Referencing positioning the transducer so that the zero reference point is at the level of the atria of the heart (phlebostatic axis).
Allen test Apply pressure to the radial and ulnar arteries simultaneously. open and close the hand repeatedly. The hand should blanch. Release pressure on the ulnar artery. If pinkness fails to return within 6 seconds, the ulnar artery is inadequate and the radial a
Normal capacity of PA catheter balloon 1 to 1.5 mL of air
PA catheter exit port locations distal lumen is in the pulmonary artery and proximal lumen ports are in the right atrium and right ventricle.
PA catheter complications infection and sepsis, air embolus, ventricular dysrhythmias, PA catheter cannot be wedged, pulmonary infarction or PA rupture
Universal Donor Blood Type O- (no antibodies and Rh is negative)
Blood administration catheter size 19 gauge or larger needle for adults, 23 gauge or larger, thin-walled scalp vein needle for pediatrics or adults whose large veins are inaccessible.
Blood administration tubing Y-type administration set with filter
Blood y-site compatibility NS IV solution ONLY. Use of any other solution with blood product is totally inappropriate.
Blood infusion time constraints Do not keep blood out of monitored refrigerator >30 min. before starting transfusion; Do not use same blood filter for > 4 hours or 2 units; Do not allow unit of blood to “hang” for > 4 hours.
Blood transfusion reactions occur most often first 15 minutes of administration
Blood transfusion reactions febrile, non-hemolytic; mild allergic; anaphylactic; acute hemolytic; sepsis
Acute hemolytic blood transfusion reaction ABO incompatibility, causes RBC destruction, can cause acute renal failure, shock, cardiac arrest, death.
Acute hemolytic blood transfusion reaction manifestations chills, fever, low back pain, increased heart rate, increased respiratory rate, decreased blood pressure then shock, possible arrest.
Febrile, non-hemolytic blood transfusion reaction most common type; sensitive to donor WBC’s, platelets, or plasma proteins.
Febrile, non-hemolytic blood transfusion reaction manifestations chills, fever, HA, flushing, muscle pain.
Mild allergic blood transfusion reaction sensitivity to foreign plasma proteins.
Mild allergic blood transfusion reaction manifestations flushing, itching, urticaria.
Anaphylactic blood transfusion reaction infusion of IgA proteins to IgA-deficient pt. that has IgA antibody.
Anaphylactic blood transfusion reaction manifestations anxiety, wheezing, then cyanosis, shock, possible arrest.
Circulatory overload blood transfusion reaction fluid administered faster than circulation can accommodate. Lasix given in between to prevent.
Circulatory overload blood transfusion reaction manifestations cough, dyspnea, HA, increased blood pressure, increased heart rate, JVD.
Sepsis blood transfusion reaction transfusion of contaminated blood components.
Sepsis blood transfusion reaction manifestations rapid chills, high fever, vomiting, diarrhea, decreased blood pressure, shock.
Blood transfusion reaction management Stop the transfusion. Keep IV open with NS. Report to MD and blood bank immediately. Re-check ID tags and numbers. Treat sx per MD and monitor V/S. Send to blood bank. Collect blood and urine samples and send to lab. Document thoroughly. Pt/family teachin
Whole Blood RBCs, plasma, and clotting factors given for massive blood loss; 450+/-45ml given rapidly to stabilize patient
PRBC RBCs with preservative given to increase O2 carrying capacity in anemic patients; 250-300ml given at a rate of 2-3 hrs/unit
LP iiRAD RBC RBCs with reduced leukocytes (to prevent reactions done by filtration, washing or freezing) that has been exposed to radiation (to render the donor lymphocytes incapable of replication, preventing graft versus host reaction); 250-300ml given over 2-3 hrs
Pooled Platelets 5 to 6 units of pooled random donor units given to control or prevent bleeding with thrombocytopenia; 50-70ml/unit given at a rate determined by volume tolerance
Single Donor Platelets Platelet rich plasma collected by apheresis given to control or prevent bleeding with thrombocytopenia; 200-400ml given at a rate determined by volume tolerance
Fresh Frozen Plasma (FFP) H2O, albumin, globulins, antibodies, and clotting factors given to increase clotting factors in patients with a demonstrated coagulation deficiency; 200-250ml given at 200ml/hr depending on volume tolerance
Cryoprecipitate Factor VIII, Willebrand’s factor, fibrinogen & Factor XII given to correct Factor VIII, Factor XIII and fibrinogen deficiencies, hemophilia A; 10-20ml/unit given at 1-2ml/minute
Immune Serum Globulin (IgG) Gamma Globulin given to provide passive immune protection, treat hypogammaglobulinemia; volume and rate varies by manufacturer
Albumin; Plasma Protein Fraction (PPF) Albumin & globulin given to provide volume expansion when crystalloid solutions are not adequate; 50-100ml albumin and 250ml PPF given at 0.2-0.4ml/minute
CO normal 2-8 L/min
CI normal 2.2-4 L/min
Decreased CO and CI indicates shock states (e.g., cardiogenic, hypovolemic) and heart failure
Increased CO and CI during exercise (normal), hyperdynamic state often seen with fever or early sepsis
Central venous pressure (CVP) right ventricular preload or right ventricular end diastolic pressure under normal conditions, measured in right atrium or in vena cava close to heart
Steady CVP WNL indicates right heart is still adequately handling venous return
Normal CVP 2-8 mm Hg
Decreased CVP indicates hypovolemia
Increased CVP indicates right ventricular failure or volume overload
Pulmonary artery wedge pressure (PAWP) left ventricular preload; a measurement of pulmonary capillary pressure which reflects left ventricular end-diastolic pressure under normal conditions
Normal PAWP 6-12 mm Hg
Decreased PAWP hypovolemia
Increased PAWP left ventricular heart failure and fluid volume overload
Systemic vascular resistance (SVR) (MAP-CVP) x 80/CO; measure that reflects afterload; opposition encountered by the left ventricle
SVR normal 800-1200 dynes/sec/cm-5/m2
Decreased SVR indicates vasodilation, which may occur in shock states (e.g., septic, neurogenic) or with drugs that reduce afterload
Increased SVR indicates vasoconstriction from shock, hypertension, increased release or administration of epinephrine and other vasoactive agents, or left ventricular failure
Pulmonary vascular resistance (PVR) (PAMP–PAWP) × 80/CO; measure that reflects afterload; opposition encountered by the right ventricle
PVR normal <250 dynes/sec/cm-5
Drug given for Torsades de Pointes Magnesium sulfate
Drug that provides rapid BP reduction in HTN crisis Sodium Nitroprusside (Nipride)
Drug that dilates coronary and peripheral blood vessels, causing reduced BP Nicardipine (Cardene)
First drug given for SVT Adenosine (Adenocard)
Drug given to help raise BP and increase myocardial contractility Dobutamine (Dobutrex)
First drug given for pulseless rhythms Epinephrine
First drug given for Vtach with a pulse Amiodarone (Cordarone)
Drug given for acute angina Nitroglycerin (Tridil)
Drug given for bradycardia Atropine
Drugs used to treat tachycardia Beta blockers
Beta blockers suffix "OLOL"
ACE inhibitor suffix "PRIL"
Shockable rhythms VF and pulseless VT
Pacemaker failure to capture management check connections; increase output or mAs; turn on left side; CPR or TCP as needed.
Synchronized cardioversion steps place pads on pt; sedate pt; set to 50-100 joules; push synchronize button –confirm synch; “clear” and push shock button
VAP prevention elevate HOB 45 degrees, maintain ET cuff pressure at 20 cm H2O, good handwashing, and meticulous oral care
Endotracheal Tube placement confirmation listen for breath sounds bilaterally (if on one side, too far); use CO2 detector (if not detecting CO2, not far enough); chest x-ray
PEEP cardiovascular response decreased CO; increased HR; and decreased BP
Refractory Hypoxemia seen in ARDS; hypoxemia unresponsive to increasing concentrations of O2, includes Acute lung injury (PaO2/FIO2 ratio between 200-300) OR Acute respiratory distress syndrome (PaO2/FIO2 ratio <200)
Pneumothorax manifestations O2 sats drop, restlessness, and no breath sounds on affected side
Created by: camellia