Summary

This document introduces critical care nursing, focusing on the care of critically ill patients post-injury, surgery, or life-threatening illness. It outlines the scope of practice, competencies for critical care nurses, and the nursing process.

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Medical surgical 3 MODULE 1: NURSING CARE OF CLIENTS WITH LIFE THREATENING CONDITIONS, ACUTELY ILL/MULTI ORGAN PROBLEMS INTRODUCTION TO CRITICAL CARE 7. Clinical Inquiry or innovator/evaluator:...

Medical surgical 3 MODULE 1: NURSING CARE OF CLIENTS WITH LIFE THREATENING CONDITIONS, ACUTELY ILL/MULTI ORGAN PROBLEMS INTRODUCTION TO CRITICAL CARE 7. Clinical Inquiry or innovator/evaluator:  the ongoing process of questioning and CRITICAL CARE NURSING: evaluating practice, providing informed  is the field of nursing with a focus on the utmost practice and innovating through research care of the critically ill or unstable patients and experiential learning following extensive injury, surgery or life 8. Facilitator of learning: threatening diseases  the ability to facilitate learning for patients,  Goal: of critical care nursing is to provide nursing staff, physicians and members of essential individualized care directed toward the other health care disciplines; include both survival of the person and the achievement of formal and informal facilitation of learning. optimal physiologic, psychologic, emotional and social potential. PROFESSIONAL ORGANIZATIONS: SCOPE OF CRITICAL CARE PRACTICE: 1. American Association of Critical Care Nurses (AACN)  The critical care nursing practice is based on a scientific body of knowledge and incorporates  was established in 1969 to help educate the professional competencies specific to critical nurses working in the ICU. care nursing practice and is focused on  It is committed to provide the highest quality restorative, curative, rehabilitative, maintainable, resources to maximize the nurses contribution to or palliative care, based on identified patient caring and improving the health of critically ill need. patients and their families. https://www.aacn.org/ NURSE COMPETENCIES FOR CRITICAL CARE NURSES 2. Critical Care Nurses Association of the 1. Clinical Judgment: Philippines, Inc (CCNAPI)-  includes clinical decision making, critical  is a specialty Nursing Organization that caters thinking and a global grasp of the situation, and continuing uplifting the standards of coupled with nursing skills Filipino Critical Care Nurses by providing 2. Advocacy/ Moral agency: updated and Evidence-Based training,  working on another’s behalf and workshops, and seminars. representing the concerns of the patient, family and community; serving as a moral https://www.ccnapi.org/ agent 3. Caring practices:  The constellation of nursing activities that are responsive to the uniqueness of the NURSING PROCESS IN CRITICAL CARE: patient and the family and that create a  It is the same in critical care situations as it is in compassionate and therapeutic environment any other patient setting` 4. Collaboration:  ASSESSMENT: for critically ill differs from the  working with others in a way that promotes assessment of other clients only in reference to and encourages each person’s contributions the type of technical devices, these are adjuncts toward achieving optimal and realistic to the direct observational data which the nurse patient goals. gathers through a careful history taking and 5. Systems thinking: physical examination.  the body of knowledge and tools that allows  NURSING INTERVENTION: the ultimate goal is the nurse to appreciate the care to promote, sustain and restore optimal levels of environment that recognizes the holistic physiologic, psychological and social interrelationship that exists within and functioning. across health care system.  in the critical care setting the immediate 6. Response to diversity: goal is to: ensure client’s survival by  the sensitivity to recognize, appreciate and determining priority intervention incorporate differences in the provision of  Physiologic problem - addressed first. care  Once life-threatening stressors have been alleviated, priorities are reorganized Abigail marie Prelims | Medical Surgical 3 1  Awareness and acceptance are the  The HIGHEST PRIORITY in caring for critically heart of cultural competence. ill patient is the maintenance of a patent 6. Presencing and reassurance: AIRWAY and adequate VENTILATION – ABC  Presence or “just being there” can be a meaningful strategy to alleviate distress or anxiety. CRITICAL CARE UNIT/ INTENSIVE CARE UNIT  a unique environment in which the most II. Epidemiologic Profile of mortality/morbidity: sophisticated medical, nursing and technical interventions can be integrated to combat life- Global: Leading cause of death: threatening illness. 1. Ischemic heart disease  Patients experience stress, anxiety most 2. Stroke often caused by sense of isolation 3. COPD because of separation from family, 4. Lower Respiratory Infections threat of helplessness, loss of control, 5. Neonatal conditions sense of loss of function and self- esteem and fear of death. 6. Trachea, bronchus, lung cancer  The critical care nurse can demystify the 7. Alzheimers ICU for the patient and family by 8. Diarrheal disease assessing their needs and concerns 9. Diabetes Mellitus regarding the ICU environment and by 10. Kidney Disorders assessing how well the patient and family are coping with the situation. National Level:  COVID-19 ranks among leading causes of death ASSESSMENT OF CRITICALLY ILL CLIENTS: in 2020 — PSA 1) Subjective Data  Other leading causes of death include:  Before starting assessment and getting the 1. Ischaemic heart diseases nursing history, perform an initial 2. Neoplasms/cancer assessment of the client’s ABCs - known as 3. Cerebrosvascular diseases the primary survey of the client with a life- 4. Diabetes threatening condition. 5. Pneumonia  It is important to note the client’s initial level 6. Hypertensive diseases of consciousness and monitor the client for any subsequent changes.  Begin by asking the patient’s main concern – focus on the client’s reason for seeking health care and further questions to illicit more pertinent information 2) Objective Data – gathered thru a physical exam using the IPPA  In going through the assessment phase sometimes before the process is done, interventions maybe given INTERVENTIONS:  Interventions for a client in critical care unit to reduce anxiety and stress thereby promoting adaptation in critically ill patients includes: 1. Create a healing environment 2. Fostering trust 3. Provide information 4. Allowing control: help a patient increase autonomy and reduce over powering sense of loss of control. 5. Cultural sensitivity  Cultural assessment includes patients response to illness, cultural norms, beliefs and world views Abigail marie Prelims | Medical Surgical 3 2 UNIT 1: RESPONSES TO ALTERED VENTILATORY FUNCTION FOCUS TOPICS: Classification of asthma severity (NAEPP - National Asthma and Prevention Program) A1. Acute Asthma A2. Acute Respiratory Distress Syndrome/ IRDS SYMPTOMS NIGHT LUNG SYMPTOMS FUNCTIONS A3. Acute Respiratory Failure Symptoms Symptoms (Forced A4. Respiratory Pandemics 2x a month FEv1 or PERSISTENT eek but 80% Airway obstruction can occur in two ways: day predited MILD 1. Inflammation Exacerbations PEF 2. Airway hyperresponsiveness may affect variability 20-  Severe airway obstruction can be fatal. activity 30% Predisposing factor: Allergy Daily symptoms > 1 time a FEV 1 or  Chronic exposure to airway irritants or allergens Daly use of week PEF 60% TO inhaled short- < 80% PERSISTENT also increases the risk of asthma. MODERATE acting beta2 predicted Common allergens: agonist PEF A. Seasonal Exacerbations variability > B. Perennial affect activity 30% Exacerbations >2 Common triggers for asthma symptoms and x/ week; may exacerbations include: lasts for days Continual Frequent FEV 1 or 1. airway irritants (e.g., air pollutants, cold, heat, PERSISTENT symptoms PEF 3. Exercise (inhale and exhale) exacerbations 30% 4. Stress (intense emotions) 5. hormonal factors 6. Medications (NSAIDS) 7. Viral respiratory tract infections Signs and symptoms of acute asthma varies with 8. Gastroesophageal reflux bronchospasm: 1. Dyspnea or SOB associated with wheezing Eosinophils and Basophils → lead to allergic 2. Wheezing - generalized reactions Additional Assessment findings:  Tachycardia  Retractions  Restlessness  Anxiety  Inspiratory(stridor) /expiratory (wheezing)  Hypoxemia  Hypercapnea  Cough  Sputum production Abigail marie Prelims | Medical Surgical 3 3  Expiratory prolongation Peak Flow Monitoring  Cyanosis  Peak flow meters - measure the highest  Elevated Pulsus paradoxus (systolic blood volume of airflow during a forced expiration pressure in expiration exceeds that on Volume may be measured in color-coded zones: inspiration by more than 10mmhg)  GREEN ZONE - signifies 80% to 100% of DIAGNOSTIC STUDIES: personal best  YELLOW - 60% to 80% A. Laboratory Assessment:  RED - less than 60%. A.1. ABG If peak flow falls below the red zone, the patient  The arterial oxygen level (PaO2) – may should take the appropriate actions prescribed by decrease during an asthma attack. their primary provider.  Early: the arterial carbon dioxide level (PaCO2) may be decreased STATUS ASTHMATICUS:  Later in an asthma episode - PaCO2 rises A.2. Allergy testing - to ascertain precipitating STATUS ASTHMATICUS allergens  rapid onset, severe, and persistent asthma that does not respond to conventional therapy. A.3. Pulmonary Function Tests  The attacks can occur with little or no  Pulmonary function tests (PFTs) – the warning and can progress rapidly to most accurate tests for asthma, measured asphyxiation. using spirometry.  FEV1(Forced Expiratory Volume) and FVC PATHOPHYSIOLOGY: (Forced Vital Capacity) and FEV1:FVC  severe bronchospasm, with mucus plugging ratio leading to asphyxia.  An increase of a least 12% and 200mL  A ventilation–perfusion abnormality results in in FEV1 after inhaling a short-acting hypoxemia. bronchodilator indicates significant  There is a reduced PaO2 and initial respiratory reversibility and confirms the presence alkalosis, with a decreased PaCO2 and an of asthma. increased pH.  As status asthmaticus worsens, the PaCO2 MEDICAL MANAGEMENT: increases and the pH decreases, reflecting respiratory acidosis. I. Drug Therapy:  Quick-Relief Medications: Clinical manifestations:  Beta-agonist - bronchodilators- increase  Extremely labored breathing , tachycardia, bronchiolar smooth muscle relaxation. diaphoresis, acute anxiety  Wheezing 1. Short-acting inhaled beta2-adrenergic  Use of accessory muscles for breathing agonists (SABA) (e.g., albuterol  Distention (ENGORGED) of neck veins [Proventil, Ventolin], levalbuterol  As obstruction worsens - wheezing disappear - [Xopenex HFA], and pirbuterol [Maxair]) - impending respiratory failure medications of choice for quick relief of If the condition is not reversed, the patient may acute symptoms and relax smooth develop pneumothorax and cardiac or muscle. pulmonary arrest. 2. Anticholinergics (e.g. Ipratropium [Atrovent]) inhibit muscarinic cholinergic Nursing Alert!!! Increasing PaCO2 - the first objective receptors and reduce intrinsic indication of status asthmaticus vagal tone of the airway. 3. Corticosteroids are the most potent and effective anti-inflammatory medications Medical Management: II. Oxygen Therapy  Close monitoring of the patient and objective  Supplemental oxygen – is often used during reevaluation for response to therapy are key in an acute asthma attack. status asthmaticus.  Oxygen is delivered by mask, nasal cannula, or  Initially: Short-acting beta2-adrenergic agonist endotracheal tube. and subsequently a short course of systemic corticosteroids Abigail marie Prelims | Medical Surgical 3 4  Refractory hypoxaemia (hypoxaemia 1. Short- acting inhaled beta2-adrenergic that does not improve with oxygen agonists administration) is the hallmark of  pMDI (Pressured Metered Dose Inhaler) ARDS. with or without a spacer may be used for nebulization of the medications. Risk Factors are associated with the development of  Methylxanthines ARDS  Drug Classification - Bronchodilators A. Indirect Pulmonary Injury- insult would occur from  The classic drug in this class is the other parts of the body where in the mediators is theophylline (Theo-Dur). transported to the lungs via the circulation  Drug ingestion and overdose 2. Supplemental oxygen and IV fluids for  Hematologic disorders (disseminated hydration. intravascular coagulopathy (DIC), massive  Oxygen therapy transfusions, cardiopulmonary bypass)  High-flow supplemental oxygen is  Metabolic disorders (pancreatitis, uremia) best delivered using a partial or  Fat or air embolism complete non rebreathing mask.  Shock (any cause)  Trauma (pulmonary contusion, multiple 3. Magnesium sulfate, a calcium antagonist, may fractures, head injury) be given to induce smooth muscle relaxation  Major surgery  Maybe given as a single 2 g infusion  Sepsis- most common cause over 20 minutes - it may be helpful in treating patients who present with B. Direct Pulmonary Injury- insult would be in the lung severely compromised pulmonary epithelium itself there by destroying the lung epithelium function, who have not responded to including that of the pulmonary vasculator. initial therapy, and with persistent  Aspiration (gastric secretions, drowning, hypoxemia (GINA, 2015). hydrocarbons)  Adverse effects of magnesium  Prolonged inhalation of high concentrations of sulfate may include facial warmth, oxygen, smoke, or corrosive substances flushing, tingling, nausea, central  Blunt trauma (pulmonary contusion) nervous system depression, respiratory  Localized infection (bacterial, fungal, viral depression, and hypotension. pneumonia) NURSING MANAGEMENT: PATHOPHYSIOLOGY  main focus of nursing management is to actively assess the airway and the patient’s response to treatment.  The nurse should be prepared for the next intervention if the patient does not respond to treatment. A2. ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS): Acute Respiratory Distress Syndrome (ARDS):  can be thought of as a spectrum of disease, from its milder form (acute lung injury) to its most severe form of fulminate, life-threatening ARDS.  This clinical syndrome is characterized by a severe inflammatory process causing diffuse alveolar damage that results in sudden and progressive pulmonary edema, increasing bilateral infiltrates on chest x- ray, hypoxemia unresponsive to oxygen supplementation regardless of the amount of PEEP, and the absence of an elevated left atrial pressure (Siegel, 2015a) Abigail marie Prelims | Medical Surgical 3 5  If the is alveolar hypoventilation → decrease STAGE IV Multiple organ Type II cell amount of oxygen (>10 days) involvement, hyperplasia,  Intrapulmonary shunting- severe form of Persistent difficulty thickening of ventilation, perfusion mismatch wherein there infiltrates, new maintaining interstitial wall would be a mixing of unoxygenated and pneumonic adequate fibrosis, oxygenated blood → decrease amount of infiltrates, oxygenation, macrophages, oxygen in the blood causing hypoxemia to recurrent sepsis, fibroblasts, occur pneumothorax pneumonia remodeling of arterioles Hallmarks of ARDS: 1. Pathological changes in lung vascular tissue ASSESSMENT FINDINGS: (microvascular permeability, pulmonary Dyspnea, tachypnea, anxiety- early manifestation hypertension, pulmonary endothelial damage) 2. Increased lung edema STAGE I: - restlessness, dyspnea, tachypnea, 3. Impaired gas exchange (1st 12H) moderate to extensive use of accessory muscles The pulmonary surfactant is produced by the alveolar STAGE II severe dyspnea, Coarse bilateral ( 24H): crackles, decreased air entry to type-II (AT-II) cells of the lungs. dependent lung fields, increased agitation and restless (Cerebral hypoxia) Clinical Presentation and Pathological Changes STAGE III decreased air entry bilaterally, during ARDS: ( 2-10 days): impaired responsiveness (maybe R/T sedation necessary to maintain STAGE CLINICAL PATHOLOGICAL mechanical ventilation) , decreased PRESENTATION CHANGES gut motility, generalized edema. Poor STAGE I Dyspnea, Neutrophil skin integrity and breakdown (1st 12 H) tachypnea sequestration, no STAGE IV symptoms of MODS including CXR - normal evidence of ( >10 days): decreased urine output, poor gastric cellular damage motility, symptoms of impaired STAGE II Dyspnea, Neutrophil coagulation or system involvement of (24H) tachypnea, infiltration, respiratory system with gradual Patchy cyanosis, vascular improvement overtime. alveolar tachycardia. congestion, fibrin infiltrates , Coarse bilateral strands, increased normal heart crackles interstitial and DIAGNOSTIC STUDIES: size alveolar edema 1. ABG - hallmark of ARDS - deterioration of ABG STAGE III Hyperdynamic Type II cell – hypoxemia PaO2 38 C or < inflammatory appearance of the lungs lung volume, 36C exudate  Presence of air → bronchograms (bronchi is normal heart HR > 90BPM filled with air) size RR > 20BPM or 3. PFT (Pulmonary function test): shows Paco2 < decreased lung compliance with reduced vital 32mmHg capacity, minute volume and functional vital WBC > 12,000 capacity cells/mm3 or <  Vital capacity- maximum amount of air 4,000 cells/mm3 expelled from the lungs after maximum or > 10% inhalation immature band  Minute volume (minute ventilation)- volume of gas inhaled or exhaled per minute  Functional vital capacity- maximum Abigail marie Prelims | Medical Surgical 3 6 amount of air exhaled during forced INVASIVE MECHANICAL VENTILATION expiratory volume 4. Pulmonary artery pressure monitoring shows MECHANICAL VENTILATION normal pressures in ARDS, helping distinguish  Is indicated when NIV management modalities ARDS from cardiogenic pulmonary edema- fail to adequately support oxygenation and/or cardiac origin ventilation 5. WBC – increase  Life saving intervention 6. Platelet, Hgb – decrease 7. Clotting factor - decrease/ abnormal  Fewer deaths with controlled hypoventilation  Historical cohorts and case series have reported MEDICAL MANAGEMENT mortality rates of 7.5-23% (critical care medicine, 2012) I. Pharmacologic Therapy- no definitive drug therapy  To facilitate the transport of oxygen and CO2 1. Antibiotic therapy- prescribed after the source between the atmosphere and the alveoli to of infection is identified enhance pulmonary gas exchange 2. Bronchodilators (relaxation and dilate) and  Adverse effects reported in one retrospective Mucolytics (liquefy)- help maintain the patency study of 88 episodes of mechanical ventilation of airway and reduce inflammatory reaction and were hypoventilation (20%), barotrauma (14%) accumulation of secretions in the airways and arrhythmias (10%), (Critical Care Nursing 3. Exogenous surfactant replacement therapy - Journal, 2016) increase compliance and prevent atelectasis  is the process of using an apparatus to facilitate 4. Inhaled nitric oxide (an endogenous the transport of oxygen and CO2 between the vasodilator) – help reduce the ventilation atmosphere and the alveoli for the purpose of perfusion mismatch and improve oxygenation enhancing pulmonary gas exchange 5. Corticosteroids- may be used late in the course of ARDS when pneumonic change Clinical objectives occurs  include reversing hypoxemia and acute II. Nutritional Therapy respiratory acidosis, relieving respiratory  Patients with ARDS require 35 to 45 distress, preventing or reversing atelectasis and kcal/kg/day to meet metabolic requirements. respiratory muscle fatigue, permitting sedation  Enteral feeding – first consideration and neuromuscular blockade, decreasing  Parenteral nutrition oxygen consumption, reducing intracranial pressure, and stabilizing the chest wall. III. Mechanical ventilation- supporting respiratory Other indicators:  Mechanical ventilation- mainstay of ARDS management  Inadequate alveolar ventilation  FiO2 (Fraction of inspired oxygen) is set at  Abnormal ABG values (progressive respiratory the lowest possible level to maintain a PaO2 acidosis) higher than 60 mmHg and oxygen saturation of  Physical assessment (declining mental status) approximately 90%.  Providing ventilatory PEEP support is a critical INTUBATION: part of the treatment of ARDS. Easier for lungs  Passing an endotracheal tube through the nose to oxygenate again. or mouth into the trachea  Improve oxygenation, help increase  Provides a patent airway functional residual capacity, reverse alveolar collapse  Prone position- improve perfusion to less damage parts of the lungs and would improve ventilation perfusion mismatch and decrease the intrapulmonary shunting  Rapid sequence intubation- method of choice in ED  Crucial objective: to prevent any further increase lung hyperinflation and refractory hypoxemia  Prevent worsening of respiratory failure. Abigail marie Prelims | Medical Surgical 3 7  Rapid sequence intubation (RSI) is a seven- MODES OF VENTILATION: step process that is often used to intubate the critically ill patient. 1. Assist-control (A/C) mode  the ventilator is able to sense when patient 7 P’s of rapid sequence intubation initiates inspiration, at which point the 1. Preparation- prepare necessary equipments ventilator “assists” by delivering a special (emergency cart) tidal volume to the patient. 2. Pre-oxygenation- with 100% oxygen for 3-5  This mode of ventilation is indicated for mins via tight fitting mask patients who are apneic. 3. Pre-treatment- administration of medication to  In A/C ventilation, more commonly decrease the physiologic response to intubation called continuous mandatory (volume (lidocaine, fentanyl, atropine sulfate, low dose or pressure) ventilation (CMV), the paralytic agent or neuromuscular blocker)- given ventilator delivers a preset tidal volume 3 mins before the next step or pressure at a preset rate of 4. Paralysis with induction – administration of respirations sedative and paralytic agent in rapid sequence intubation to achieve induction and paralysis 2. SIMV (Synchronized Intermittent Mandatory  midazolam, ketamine, propofol → to Vent) facilitate rapid loss unconsciousness  This mode allows the patient to breathe  Vecuronium or Succinylcholine → to spontaneously through the ventricular circuit induce paralysis without increased resistance, while at the 5. Protection and positioning of patient predetermined intervals, the next  Place in supine position – before spontaneous breath is assisted by the intubation machine.  head tilt technique  also delivers a preset tidal volume and  Cricoid pressure- to protect airway number of breaths per minute. 6. Placement of ET tube  Between ventilator-delivered breaths,  Each intubation attempt → limited only the patient can breathe spontaneously to 30 seconds = to prevent hypoxemia with no assistance from the ventilator on  Assess the presence of breath those extra breaths. sounds(bilaterally) and chest movement  Absence of breath sounds = esophageal Common Ventilator Settings: intubation  Tidal volume set depends on lung status  Breath sounds (1 side only) = mainstem  Normal= 12 mL/kg ideal body weight intubation  COPD= 10 mL/kg ideal body weight 7. Post-intubation management  ARDS= 6-8 mL/kg ideal body weight  Rate of 10=12 breaths per minute Indications for Mechanical Ventilation (Brunner)  FiO2 of 100%= range is 21-100%  PEEP only as indicated after first arterial blood Laboratory Values gas determination  PaO2 50 mm Hg and pH 50mmHg  Headache  Conditions leading to acute respiratory  Dyspnea- hallmark of respiratory failure include impaired function of the: failure  CNS e.g drug overdose, head  air hunger trauma, infection, haemorrhage,  tachycardia  increased BP sleep apnea  Neuromuscular dysfunction 2. As hypoxemia progresses:  Musculoskeletal dysfunction  Confusion  Pulmonary dysfunction (COPD,  Lethargy * on physical assessment – use asthma, cystic fibrosis) of accessory muscles, decreased breath sound III. Combined ventilatory and oxygen failure Hypoventilation because of poor respiratory  Tachycardia movement  Tachypnea- severely ill  Impaired gas exchange at the alveolar  Central cyanosis- late sign of RD capillary membrane → Poor perfusion of  Diaphoresis oxygen in the arterial blood and carbon  Respiratory arrest dioxide retention  When lung perfusion is not adequate = With Severe hypercapnia- asterexis- involuntary ventilation perfusion mismatch jerking movement, flapping tremor, decrease level of  Both ventilation and perfusion is adequate = consciousness, headache, drowsiness, lethargy, more profound hypoxemia seizure, bradycardia, hypotension  Common in patients with:  Bronchitis Orthopneic position – place pillows on bedside table  Emphysema and rest their head over the pillow  Cystic fibrosis  Acute asthma attack 3. ABG findings: Oxygen failure – Metabolic acidosis (pH ,Decrease HCO3, Decrease or VENTILATION normal PaCO2) PERFUSION IMPAIRED GAS HYPOVENTILATION Ventilatory failure – Respiratory EXCHANGE MISMATCH acidosis – ( Decrease pH ,Increase or Normal HCO3, Increase PaCO2) (increased work of breathing) LABORATORY FINDINGS:  ABG HYPOXEMIA  EtCO2- End tidal carbon dioxide HYPERCAPNEA MEDICAL MANAGEMENT:  The objectives of the treatment is to: RESPIRATORY FAILURE  Correct the underlying cause  To restore adequate gas exchange in the lungs Dyspnea, Tachypnea Dyspnea Cyanosis Headache A. PHARMACOLOGIC MANAGEMENT: Restlessness Papilledema 1. Bronchodilators Confusion Tachypnea a. Beta-Adrenergic or Sympathomimetic Impaired Judgment HPN agents and Anticholinergics – Tachycardia Drowsiness administered in aerosol form (inhaler) HPN Systemic Vasodilation  For clients in mechanical Metabolic Acidosis HF intubation this drugs are Respi. Acidosis administered via in line nebulization  Example:  Beta-Adrenergic or Sympathomimetic agents: Abigail marie Prelims | Medical Surgical 3 13 Isoproterenol (Isuprel), B. OXYGEN THERAPY: Metaproterenol (Alupent),  VITAL: reverse the hypoxemia of ARF Albuterol, Salmeterol  GOAL: Achieve an O2 saturation of 85-90%  Anticholinergic – without oxygen toxicity Ipratropium Bromide  Higher levels DO NOT significantly increase (Atrovent) oxygen sat and may lead to hypoventilation in clients with chronic hypercapnia 2. Antibiotic therapy  In clients with COPD: Give 1-3L/minute of  Treat infection, identification of the oxygen through nasal cannula or 28% per source of infection is important venture mask to correct hypoxemia  For clients with Pneumonia – higher 3. Neuromuscular blocker concentration is necessary since gas  Induce paralysis of the voluntary diffusion is affected – 40-60% maybe muscles and to allow the ventilator to required. control respiration fully for its maximum  Must be used for short period of time to effectiveness avoid oxygen toxicity → impaired surfactant  Example: Pancuronium bromide synthesis→ lungs is less compliant→ ARDS (Pavulon). Atracium Besylate (Tracrium) or ATELECTASIS  Complete muscle paralysis is achieved within minutes of administration C. AIRWAY MANAGEMENT  After medication is DISCONTINUED –  indicated for clients who do not respond to or antagonist (Acetylcholinesterase oxygen therapy or those with upper airway inhibitor – Neostigmine(Prostigmine) is obstruction or who need *POSITIVE- administered PRESSURE mechanical ventilation  NURSING RESPONSIBILITIES FOR  Tracheostomy tube – indicated for chronic NEUROMUSCULAR BLOCKER: ventilator support  PRIOR TO ADMINSTRATION –  MECHANICAL VENTILATION – indicated when ASSESS placement of ET and alveolar ventilation is inadequate to maintain ensure that mechanical blood O2 and CO2 levels ventilator is functioning  Specific indications of Mechanical effectively – to prevent ventilation: hypoxemia  Apnea or acute ventilator failure  Administer slow IV or by  Hypoxemia – unresponsive to oxygen infusion therapy  Keep antagonist at the bedside  Increase work pf breathing leading to for rapid reversal of progressive fatigue neuromuscular effects  TYPES, MODES and SETTINGS of necessary Mechanical Ventilation:  Administer neuromuscular  Negative pressure ventilator blocker with Morphine SO4,  Example: Iron lung machine Diazepam or other antianxiety  Positive Pressure Ventilator agent or sedative  Positive-cycled ventilator  Administer only fresh solution –  Example: Bird mark 7 or DO NOT store in the syringe Bennett PR II  Instill artificial tears every 2-4H  Volume-Cycled Ventilator – – to lubricate the eyes since  Example: MA-1 or Bennett 7200 client is unable to blink  Suction oral cavity D. OTHER THERAPIES:  NEVER turn off ventilator alarm 1. Fluid and electrolyte status monitoring – –since the client is unable to MIO, daily weight breathe independently and  Swan-Ganz Catheterization unable to call help  CVP monitoring  Reassure client that ability to 2. Adequate nutrition move and communicate will be  Parenteral nutrition or Enteral restored when medication is feeding via NGT or PEG or J-tube discontinued 3. Lung Transplant  Teach family about the effects of the drug and reason for its use Abigail marie Prelims | Medical Surgical 3 14 NURSING INTERVENTION: LUNG TRANSPLANT:  Lung transplantation is a viable option for those 1. INABILITY TO SUSTAIN SPONTANEOUS with end-stage pulmonary disease without end- VENTILATION stage cardiac disease.  Assess & document vital signs every 15-30  COPD remains the predominant reason for lung min. transplantation  Assess for S/SX of respiratory distress  Considered: when the patients risk of mortality  Monitor ABG/pulse oximeter for evidence of is greater than 50% within the next 2 years improving or worsening respiratory status – report changes promptly TYPES:  Administer oxygen, monitor – monitor response, observe closely for signs of 1. SINGLE-LUNG TRANSPLANTATION respiratory depression  Some advantages of a single-lung transplant  Place in fowler’s position- promote lung include shorter extubation time, less need for expansion cardiopulmonary bypass, and a shorter  Minimize activities & energy expenditures by hospitalization. assisting client with care, spacing procedures  If both lungs has the same impaired function = and activities allowing uninterrupted rest the right lung is chosen for explantation and a periods – rest is vital new donor is inserted to avoid maneuvering  Avoid sedatives and respiratory depressant around the heart of the patient drugs  Most common complication  Prepare for intubation and mechanical  Lung hyperinflation – because of graft ventilation compression by the hyperinflated native lung 2. INEFFECTIVE AIRWAY CLEARANCE  Graft- is the donated lung or  Assess respiratory status including the rate, transplanted lung that would ventilator settings, chest movement and lung cause mediastinal shift and sounds frequently. respiratory failure  Assess coordination of respiratory effort and ventilator 2. DOUBLE-LUNG TRANSPLANTATION  Monitor and assess O2 sat and ABG  Double-lung transplantation is the preferred  Suction PRN to maintain patent airway surgical procedure for patients with CF (Cystic  Indicators of suctioning: fibrosis) or bronchiectasis  Crackles and rhonchi on  Can be done simultaneously – end block auscultation  The lung is transplanted one after the other →  Frequent coughing or setting off bilateral sequential transplant/ bilateral the high-pressure alarm single lung transplant  Increase restlessness or anxiety  Obtain specimen for culture if sputum appears The general indications for lung transplantation are purulent or odorous as follows:  Perform CPT as ordered 1. Advanced lung disease (World Health  Use minimal occluding volume technique, Organization (WHO) functional class III or IV) minimal leak technique or measured 2. Lung disease which is progressive and refractory pressured of 20-25mmhg in the cuff of ET. to maximum medical intervention  For minimal leak – inflate the cuff as 3. Estimated survival chance of /= 94% dysfunction, and patients at high risk for clinical b) Without pneumonia but with risk deterioration factors for progression: elderly and/or CRITICAL CARE AND RESPIRATORY with comorbidities MANAGEMENT: 2. Severe COVID-19 - with pneumonia and signs of  For patients with mild COVID-19 disease, respiratory distress, oxygen saturation < 94%; RR supportive care is recommended. >30 breaths/minute, requiring oxygen  These include: antipyretics for fever, oral fluids supplementation for hydration, isolation at home or in temporary treatment and monitoring facilities. 3. Critical COVID-19 - with pneumonia and impending respiratory failure , in acute respiratory Abigail marie Prelims | Medical Surgical 3 18 1. Anti-Viral therapy: Remdesivir given to hospitalized adult patients with severe COVID-19 5. Ad26.COV2.S (Janssen/Johnson&Johnson)  Dosing regimen of Remdesivir is 200 mg IV (given as 0.5ml single dose intramuscular injection loading dose on  Day 1 followed by 100 mg IV once a day for 5-10 days. Initial assessment of patient with COVID-19.  Immunomodulatory drug such as Tocilizumab (antihuman IL-6 receptor antibody) ACDE approach of history: 2. Corticosteroids e.g. Dexamethasone or Methylprednisolone Airway (A) 3. Prophylactic anticoagulation  Ensure the patency of airway 4. Norepinephrine is the first-line vasopressor in  Assess for dyspnea, abnormal breathing, patients with hemodynamic instability sounds, cough and sputum expectoration. 5. Vasopressin might be used as first vasopressor 6. Inotropics e.g Dobutamine Breathing (B) 7. Loop diuretics (oral or intravenous) - for patients  Assess for tachypnea (>20/ min), dyspnea, without indication of RRT abnormal breathing, sounds, cough and sputum 8. Conservative fluid management expectoration. 9. Prone positioning and inhaled selective  Measure oxygen saturation (SpO2>96%) pulmonary vasodilators have been used for patients with refractory hypoxemia Circulation (C) 10. High-flow nasal cannula oxygenation rather than  Asses for cyanosis, capillary refill time (100 beats/min) and BP NIV) in patients with COVID-19 infection and acute  Assess for any signs of shock (hypotension, hypoxemic respiratory failure who do not respond to tachycardia etc.) conventional oxygen therapy. 11. Lung protective ventilation strategy (Tidal volume Disability (D) 4-8 mL/kg predicted body weight and plateau  Assess the level of consciousness using AVPU, pressure less than 30 cmH2O) in patients with pupillary reflex COVID-19 infection and ARDS.  Previous history of any co-morbidity, drug intake 12. Use of VV-ECMO/ VA ECMO - for COVID-19 history of fever, headache, coughing and patients with refractory ARDS malaise 13. Continuous renal replacement therapy (CRRT) or  Measure blood glucose level Sustained Low-Efficiency Dialysis (SLED) - for patients with AKI Exposure (E)  SLED - a form of RRT  Assessing for contact history as defined by 14. Hemoperfusion (HP) WHO: Exposures during 2 days before and the 14 days after the onset of symptoms: 1. Face-to-face contact with a probable or VACCINES confirmed case within 1 meter and for -use of the following vaccines to prevent symptomatic more than 15 minutes; SARS-CoV-2 infection in adults: 2. Direct physical contact with a probable or confirmed case; 1. BNT162b2 (Pfizer/BioNTech) (given as 0.3ml 3. Direct care for a patient with probable or (30ug) intramuscular injections, in 2 doses, 21 confirmed COVID-19 disease without days apart) using proper personal protective equipment1; OR 2. mRNA-1273 (Moderna) (given as 0.5ml (100ug) 4. Other situations as indicated by local intramuscular injections, in 2 doses, 28 days risk assessments. apart) Care of patient with mid-moderate symptom 3. ChAdOx1 (AstraZeneca) (given as 0.5 ml (5 x 106 vp) intramuscular injections, in 2 doses, at  Provide complete bed rest, promote sound sleep least 12 weeks apart) and regularly monitor vital signs  Provide antipyretic drugs (e.g. acetaminophen) 4. Gam-COVID-Vac (Gamaleya) (given as rAd-26 for management of fever and myalgia 0.5ml intramuscular injection, then rAd-5S 0.5 ml  NSAIDs should be avoided. intramuscular injection 21 days after)  Non-pharmacological interventions Abigail marie Prelims | Medical Surgical 3 19  Encourage patients to take a bath regularly with A5. PULMONARY EMBOLISM soap and water and maintain good personal  PE refers to the obstruction of the pulmonary hygiene. artery or one of its branches by a thrombus that  Provide plenty of fluids be, a nutritious high originates somewhere in the venous system or protein diet with vitamins. in the right side of the heart.  Patients with respiratory difficulties may require  PE can be associated with trauma, surgery Fowler's positon, pulse oximeter to monitor (orthopedic, major abdominal, pelvic, oxygen saturation and oxygen administration gynecologic), pregnancy, heart failure, age older using nasal prongs or cannula to maintain SpO2 than 50 years, hypercoagulable states, and > 90%. prolonged immobility.  Collect blood samples and send them to the  Death from acute PE commonly occurs within 1 laboratory hour after the onset of symptoms CRITICAL CARE OF PATIENTS WITH COVID 19: PATHOPHYSIOLOGY  Close monitoring of patency of airway, SpO2 >  Most common cause: blood clot or thrombus. 90%, vital signs, level of consciousness, acid-  Other types of emboli: air, fat, amniotic fluid, and base balance, ECG, infection indicators, septic (from bacterial invasion of the thrombus). coagulation profile, renal and liver functions, signs of DVT and risk of pressure sores.  Complete or partial obstruction of a pulmonary  Position patient in semi-fowler's position and artery or its branches by a thrombus → increase change every two hourly alveolar dead space → little / no blood flow →  Administer oxygen therapy to maintain SpO2 > impaired / absent gas exchange in the area. 90%; initially through nasal prongs or cannula or  various substances are released from the clot mask. If this fails to maintain the desired SpO2, and surrounding area → constriction of regional then high flow nasal oxygen (HFNO), non- blood vessels and bronchioles → results invasive ventilation (NIV) or invasive mechanical increase in pulmonary vascular resistance → ventilation should be implemented. compounding the V./Q. imbalance.  Early initiation of nasogastric tube feeding  increased pulmonary vascular resistance (within 48- hours) or parenteral nutrition with diet results → in an increase in pulmonary arterial rich in protein and vitamins. pressure → an increase in right ventricular work  Assist in insertion of oropharyngeal airways and → when exceeds → right ventricular failure → endotracheal intubation with aerosol and contact lead to decrease cardiac output → decrease in precautions. systemic blood pressure and shock.  Endotracheal intubation is done after five minutes pre-oxygenation via the Atrial fibrillation can also cause PE. continuous positive airway pressure (CPAP) method. Massive PE: an occlusion of the outflow tract of the  Use closed endotracheal suctioning system with main pulmonary artery or of the bifurcation of the low suction pressure. pulmonary arteries  Patient on mechanical ventilation requires use of separate ventilator circuit, implement Ventilator Associated Pneumonia (VAP) prevention CLINICAL MANIFESTATIONS bundle, catheter-related urinary tract infections 1. Dyspnea is the most frequent symptom (CAUTI) prevention bundle, catheter-related 2. Sudden chest pain is common - pleuritic in sepsis (CLEBSI), bundle, deep vein thrombosis origin. (DVT) prevention interventions and regular  It may be substernal and may mimic check the readiness for weaning. angina pectoris or a myocardial  Regularly provide oral care (every 6-hourly), infarction. central line care (change dressing every 72- 3. Tachypnea - most frequent sign hours with transparent dressing), daily eye care, 4. Other symptoms include anxiety, fever, eye patching, urinary catheter care, back care, tachycardia, apprehension, cough, diaphoresis, bed bath (with disposal wet sponges). hemoptysis, and syncope.  Provide intermittent pneumatic compression and prophylactic anticoagulant for prevention of deep DIAGNOSTIC TEST: vein thrombosis and its complications. 1. S. electrolytes, CBC, and coagulation studies  Intake and output monitoring. 2. Chest x-ray: usually normal but may show infiltrates, atelectasis, elevation of the diaphragm on the affected side, or a pleural effusion. Abigail marie Prelims | Medical Surgical 3 20 3. ECG: sinus tachycardia, and non- specific ST-T a reoccurrence or extension of the wave abnormalities thrombus and may continue up to 10 4. Pulse oximetry days 5. ABG: hypoxemia and hypocapnia (from  Long-term anticoagulation is indicated tachypnea) from 10 days to 3 months following the 6. V./Q. scan - evaluate different regions of the PE and is critical in the prevention of lungs and allow comparisons of the percentage recurrence of VTE. of V/Q in each area  Low molecular weight heparin 7. Multidetector-row computed tomography (e.g., Enoxaparin), unfractionated angiography (MDCTA) - is the criterion heparin, or one of the new oral standard for diagnosing PE anticoagulants (NOACs) e.g. 8. Pulmonary angiography - alternative Direct Thrombin Inhibitor (e.g., diagnostic allows for direct visualization under Dabigatran), or a Factor Xa fluoroscopy of the arterial obstruction and Inhibitor (e.g., Fondaparinux, accurate assessment of the perfusion deficit. Rivaroxaban, Apixaban, or PREVENTION Edoxaban) 1. Active leg exercises to avoid venous stasis  Unfractionated heparin is 2. Early ambulation preferred in patients who are 3. Use of anti-embolism stockings hemodynamically unstable in MEDICAL MANAGEMENT anticipation of a potential need for thrombolysis or embolectomy.  PE is often a medical emergency  Long-term treatment: Warfarin and the  EMERGENCY MANAGEMENT CONSISTS OF NOACs. THE FOLLOWING ACTIONS: A. Nasal oxygen is given immediately to relieve B. Thrombolytic Therapy hypoxemia, respiratory distress, and central  Thrombolytic therapy is used in patients cyanosis with an acute PE who have hypotension B. Emergent endotracheal intubation and and do not have a contraindication or mechanical ventilatory - severe hypoxemia potential bleeding risk C. Insertion of IV infusion lines to establish  Recombinant Tissue Activator routes for medications or fluids. (Activase) or other thrombolytic D. For hypotension that does not resolve with IV agents like kabikinase (Streptase) fluids - prompt administration of vasopressor are used in treating massive PE, therapy. particularly in patients who are E. Hemodynamic measurements and evaluation severely compromised for hypoxemia F. ECG is monitored continuously for  Thrombolytic therapy resolves the dysrhythmias and right ventricular failure thrombi or emboli quickly and restores G. Insertion of indwelling urinary catheter - for more normal hemodynamic functioning hypotensive patient and suffered massive of the pulmonary circulation - reducing embolism. pulmonary hypertension and improving H. Small doses of IV morphine or sedatives: to perfusion, oxygenation, and cardiac relieve patient anxiety, alleviate chest output discomfort, improve tolerance of the  Risk of bleeding is significant. endotracheal tube and ease adaptation to the  Contraindications to thrombolytic mechanical ventilator therapy: includes: CVA within the past 2 months, other active intracranial processes, active bleeding, surgery within 10 days of the thrombotic event, GENERAL MANAGEMENT recent labor and delivery, trauma, or severe hypertension. 1. Oxygen therapy is given to correct the hypoxemia,  Obtain: INR, partial thromboplastin time relieve the pulmonary vascular vasoconstriction, and (PTT), hematocrit, and platelet counts reduce the PH. before starting thrombolytic therapy 2. Anti-embolic stockings or intermittent pneumatic leg  DC anticoagulant prior to administration compression devices reduces venous stasis. of a thrombolytic agent. 3. Elevating the leg (above the level of the heart) -  During therapy, all but essential invasive increases venous flow. procedures are avoided. 4. Pharmacologic Therapy A. Anticoagulation Therapy C. Surgical Management  Immediate anticoagulation: to prevent  EMBOLECTOMY is rarely performed Abigail marie Prelims | Medical Surgical 3 21 but may be indicated if the patient has a questions concisely and accurately, explains the massive PE or hemodynamic instability therapy, and describes how to recognize or if there are contraindications to untoward effects early. thrombolytic (fibrinolytic) therapy. 7. Monitoring for Complications NURSING MANAGEMENT A. The nurse must be alert for the potential complication of cardiogenic shock or right 1. Preventing Thrombus Formation: is a major ventricular failure subsequent to the effect of PE nursing responsibility. on the cardiovascular system A. Encourages ambulation and active and passive leg exercises 8. Providing Postoperative Nursing Care B. Instructs the patient to move the legs in a A. Post embolectomy, measures pulmonary arterial “pumping” exercise pressure and urinary output. C. Advise patient not to sit or lie in bed for B. Assesses the insertion site of the arterial prolonged periods, not to cross the legs, and catheter for hematoma formation and infection. not to wear constrictive clothing. C. Maintain BP at a level that supports perfusion of D. Apply Intermittent pneumatic compression vital organs. (IPC) devices as advised D. Elevate the foot of the bed and encourages  The nurse must pay attention to isometric exercises optimal fitting of the compression sleeves and adherence to keeping the sleeves on when the patient is in a seated or supine position. PNEUMONIA (COMMUNITY ACQUIRED; E. Legs should not be dangled or place feet in a dependent position while the patient sits on VENTILATOR AQCUIRED) the edge of the bed; but instead the feet should rest on the floor or on a chair. PNEUMONIA F. IV catheters should not be left in place for  is an inflammation of the lung parenchyma prolonged periods. caused by various microorganisms, including bacteria, mycobacteria, fungi, and viruses 2. Assessing Potential for Pulmonary Embolism (Cytomegalovirus, RSV)  Careful assessment of the patient’s health  Pneumonitis describes an inflammatory history, family history, and medication record. process in the lung tissue that may predispose  Asked patient about pain or discomfort in the or place the patient at risk for microbial invasion extremities.  Evaluate extremities for warmth, redness, and CLASSIFICATION inflammation.  Pneumonia can be classified into four types: Community-Acquired Pneumonia (CAP), Health 3. Monitoring Thrombolytic Therapy Care–Associated Pneumonia (HCAP), Hospital-  During thrombolytic infusion assess VS every 2 Acquired Pneumonia (HAP) and VAP hours and invasive procedures are avoided.  Monitor INR or PTT result, refer. A. COMMUNITY-ACQUIRED PNEUMONIA 4. Managing Pain  CAP: a common infectious disease, occurs A. Place in semi-Fowler’s position either in the community setting or within the first B. Turn patients frequently and reposition 48 hours after hospitalization or C. administers opioid analgesic agents as institutionalization (placed in a facility) prescribed ETIOLOGY: 5. Managing Oxygen Therapy  Severe Community-Acquired Pneumonia A. Assesses the frequently for signs of hypoxemia  Pathogens that can cause severe CAP and monitor the pulse oximetry values include Streptococcus pneumoniae, B. Deep breathing and incentive spirometry as Legionella species, Haemophilus indicated influenzae, Moraxella catarrhalis, C. Nebulizer therapy or percussion and postural Staphylococcus aureus, Mycoplasma drainage as ordered pneumoniae, respiratory viruses, Chlamydia pneumoniae, and 6. Relieving Anxiety Pseudomonas aeruginosa. A. Encourages patient to talk about any fears or concerns, answers the patient’s and family’s Abigail marie Prelims | Medical Surgical 3 22 S. Pneumoniae (pneumococcus)  is the most common cause of CAP in people younger than 60 years without comorbidity and in those 60 years and older with comorbidity H. influenzae  causes a type of CAP that frequently affects older adults and those with comorbid illnesses (e.g. COPD, alcoholism, and diabetes). M. Pneumoniae  causes: Mycoplasma pneumonia is spread by infected respiratory droplets through person-to- person contact. Viruses  are the most common cause of pneumonia in infants and children but are relatively uncommon causes of CAP in adults. RISK FACTORS  Cytomegalovirus 1. Conditions that produce mucus or bronchial  is the most common viral pathogen in obstruction and interfere with normal lung immunocompromised adults, followed by drainage e.g cigarette smoking, cancer, COPD Herpes Simplex Virus, Adenovirus, and RSV. 2. Immunosuppressed patients and those with neutropenia 3. Smoking B. VENTILATOR-ASSOCIATED PNEUMONIA 4. Prolonged immobility and shallow breathing pattern Ventilator Acquired Pneumonia VAP: 5. Depressed cough reflex due to medications,  A subtype of HAP that develops ≥48 hours after debilitated state, weak respiratory muscles, endotracheal tube intubation and has received aspiration of foreign material into the lungs mechanical ventilatory support during a period of unconsciousness or abnormal  VAP occurring within 96 hours of the onset of swallowing mechanism mechanical ventilation is usually due to 6. NPO status, placement of NGT, orogastric or antibiotic-sensitive bacteria that colonize the endotracheal tubes patient prior to hospital admission, whereas 7. Supine position in patients who are unable to  VAP developing after 96 hours of ventilatory protect their airway support is more often associated with MDR 8. Antibiotic therapy bacteria 9. Alcohol intoxication  Pathogens that causes VAP: S. aureus and P. 10. General anesthetics, sedatives, or opioid aeruginosa. preparation 11. Advanced age 12. Respiratory therapy with improperly cleaned PATHOPHYSIOLOGY equipment  Lobar pneumonia: one or more lobes is 13. Transmission of organism from health care providers. involved  Bronchopneumonia: is used to describe CLINICAL MANIFESTATIONS pneumonia that is distributed in a patchy fashion, originated in one or more localized  Acute rapid onset of chills, fever and cough areas within the bronchi and extending to the productive of rust-coloured or purulent sputum adjacent surrounding lung parenchyma  Chest pain or pleuritic pain (sharp localized  Portal of entry: pain) 1. Aspiration of oropharyngeal secretions -  Limited or decreased breath sounds and fine Most common crackles 2. Droplet transmission as infected person  Pleural friction rub coughs, sneezes or talks  Dyspnoea and cyanosis may be noted 3. Bloodstream infection  Bronchopneumonia - more insidious onset with low-grade fever, cough and scattered crackles  Older adult or debilitated person may have atypical manifestations of pneumonia: with little Abigail marie Prelims | Medical Surgical 3 23 cough,scant sputum and minimal evidence of with flow rates of 2 to 6 L/min. respiratory distress. Fever, tachypnoea and  Simple face mask delivers 40– altered mentation or agitation may be the 60% oxygen concentrations primary presenting symptoms. with flow rates of 5 to 8 L/min.  Non-rebreather mask can be DIAGNOSTIC TEST: deliver the highest 1. Chest x-ray : Fluid, infiltrates, consolidated concentration possible up to lung tissue and atelectasis 100% oxygen without 2. CT scan provides a more detailed image of mechanical ventilation. pulmonary tissue and used when CXR is not  High-flow system: Venturi mask diagnostic.  Intubation and mechanical Ventilation - 3. Sputum Gram stain severe hypoxia 4. Sputum culture and sensitivity 6. Chest physiotherapy to reduce lung 5. Full blood count (FBC) with white blood cell consolidation and prevent atelectasis. (WBC) differential shows an elevated WBC  Percussion is performed by (>10 × 109 /L) with increased circulating rhythmically striking the chest wall with immature leucocytes cupped hands using rapid wrist flexion  Immunocompromised patient- WBC and extension. is decreased  The breasts, sternum, spinal  Sepsis- WBC is decreased column and kidney regions are 6. Serology testing avoided during percussion. 7. Pulse oximetry  Vibration facilitates secretion  The saturation of peripheral oxygen movement into larger airways. (SpO2 ) is normally 95% or higher.  It usually is combined with  An SpO2 of less than 95% may percussion but may be used indicate impaired alveolar gas when percussion is exchange. contraindicated or poorly  An arterial oxygen tension (PaO2 ) of tolerated. less than 75 to 80 mmHg indicates  Postural drainage done in conjunction impaired gas exchange or alveolar with percussion and vibration ventilation  uses gravity to facilitate 8. Arterial blood gases (ABGs) removal of secretions from a 9. Fibre-optic bronchoscopy particular lung segment. MEDICAL MANAGEMENT  The person is positioned with the segment to be drained A. Pharmacologic Therapy superior to or above the 1. Broad-spectrum antibiotic therapy trachea or mainstem bronchus. 2. Bronchodilators may be ordered to improve ventilation and reduce hypoxia. NURSING MANAGEMENT: 2.a. Sympathomimetic drugs e.g. Salbutamol (Ventolin) NURSING DIAGNOSES 2.b. Anticholinergic drugs, e.g. Ipratropium 1. Ineffective airway clearance related to copious bromide (Atrovent) tracheobronchial secretions 3. Mucolytic agent helps to liquefy mucus e.g. A. Assess respiratory status, including vital Acetylcysteine (Fluimucil) signs, breath sounds, SpO2 and skin colour, at least every 4 hours. B. Treatments B. Assess cough and sputum (amount, 1. Increase fluid intake to 2500 to 3000 mL per colour, consistency and possible odour). day C. Monitor ABG results; report increasing 2. Intravenous fluids and nutrition hypoxaemia and other abnormal results to 3. Incentive spirometry the doctor. 4. Endotracheal suctioning for ineffective D. Place in Fowler’s or high-Fowler’s cough. position. Encourage frequent position 5. Oxygen therapy may be administered by changes and ambulation as allowed. either a low-flow or a high-flow system. E. Assist to cough, deep breathe and use  Low-flow systems: nasal prongs, assistive devices. simple face mask, partial rebreathing F. Provide endotracheal suctioning using mask and non-rebreathing mask aseptic technique as required if is  Nasal prongs can deliver 24– intubated. 45% oxygen concentrations G. Provide a fluid intake of at least 2500 to Abigail marie Prelims | Medical Surgical 3 24 3000 mL per day. further irritation of the lungs H. Administer prescribed medications as 6. Manifestations to report to the doctor, such as ordered and monitor their effects. increasing shortness of breath, difficulty I. Promptly report signs of respiratory breathing, increased fever, fatigue, headache, distress, including tachypnea, tachycardia, sleepiness or confusion. nasal flaring, J. use of accessory muscles, intercostal retractions, cyanosis, increasing PULMONARY HYPERTENSION restlessness, anxiety or decreased level of consciousness (LOC) - early PULMONARY HYPERTENSION manifestations of respiratory failure and  The normal mean arterial pressure in the inability to maintain ventilatory effort. pulmonary system is 12 to 15 mmHg (25 to 28 systolic/8 diastolic). 2. Ineffective breathing pattern  Pulmonary hypertension (PH) is characterized A. Provide for rest periods. by elevated pulmonary arterial pressure and B. Assess for pleuritic discomfort. Provide secondary right heart ventricular failure. analgesics as ordered.  Dyspnea with exertion without other clinical C. Provide reassurance during periods of manifestations - may indicate pulmonary respiratory distress. hypertension D. Administer oxygen as ordered.  Clinical recognition becomes the only indicator E. Teach slow abdominal breathing. of PH. 3. Activity intolerance  Defined as a disorder of pulmonary vasculature A. Assess activity tolerance, noting any with pulmonary arterial systolic pressure increase in pulse, respirations, dyspnoea, >25mmHg diaphoresis or cyanosis. B. Schedule activities, planning for rest Risk Factors periods. C. Provide assistive devices. 1. Collagen vascular disease D. Enlist the family’s help to minimise stress 2. Congenital heart disease and anxiety levels. 3. Portal hypertension E. Perform active or passive range-of-motion 4. HIV infection (ROM) exercises. 5. Drugs and toxins – anorexigens- appetite F. Provide emotional support and depressant – may cause PH, chronic use of reassurance that strength and energy will stimulants return to normal when the infectious 6. Pregnancy process has resolved and the balance of oxygen supply and demand is restored. PATHOPHYSIOLOGY  Pulmonary hypertension can develop as a primary disorder, but usually occurs secondarily to another condition. Nursing Alert: Activity intolerance may be an early sign  The three major components in the of cardiorespiratory compromise, particularly in the older pathogenesis of chronic PH are: adult or person with preexisting heart disease. New or 1. Endothelial dysfunction and worsening manifestations of activity intolerance should vasoconstriction be reported to the doctor 2. Vascular remodeling 3. Thrombosis. – endothelial dysfunction HEALTH EDUCATION:  Development of plexiform lesions that Discuss the following topics when preparing the person irreversibly obliterate (obstruction) the and family for home care: pulmonary arterioles. 1. The importance of completing the prescribed  Triggered by: inflammation –increase medication regimen as ordered monocyte, macrophages, T and B lymphocyte, 2. Recommendations for limiting activities and increase cytokines and chemokine level, increasing rest activation of fibroblasts (activation and retention 3. Maintaining adequate fluid intake to keep mucus of macrophage and monocytes in the pulmonary thin for easier expectoration artery that is affected = development of 4. Ways to maintain adequate nutritional intake, plexiform lesions such as small, frequent, well-balanced meals  Impaired endothelial cell function (Smooth 5. The importance of avoiding smoking or muscle cells and fibroblasts proliferate) → exposure to second hand smoke to prevent vasoconstriction (due to decreased endothelial Abigail marie Prelims | Medical Surgical 3 25 cell-derived nitric oxide (NO), and decreased FUNCTIONAL CLASSIFICATION OF PULMONARY prostacyclin, and increased endothelin) → HYPERTENSION: WHO CLASSIFICATION thrombi within the pulmonary arterioles  Overproduction of substances that cause CLASS / SYMPTOMS vasoconstriction → further increase vasoconstriction and fibrosis of pulmonary vessels → increase pressures in the pulmonary Class I system increase workload of the right ventricle  No limitation of physical activity; ordinary physical → lead to right ventricular failure activity does not cause undue dyspnea or fatigue, chest pain or near syncope Class II  Slight limitation of physical activity; they are comfortable at rest; ordinary physical activity causes undue dyspnea or fatigue, chest pain or near syncope Class III  Marked limitation of physical activity; they are comfortable at rest; less than ordinary activity causes undue dyspnea or fatigue, chest pain or near syncope Class IV Primary pulmonary hypertension  Inability to carry out any physical activity without symptoms; these patients manifest signs of right uncommon disorder; idiopathic cause. heart failure. Dyspnea and/or fatigue may even

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