'6 rcp 120' with you.pdf

Oxygen Therapy Goals and Effects  OXYGEN THERAPY Objectives… ◼ Indications ◼ Risks or Hazards ◼ Clinical Signs of Hypoxemia  OXYGEN THERAPY ◼ You, the RCP, must be well-versed in both the goals and objectives of this therapy, and its use in clinical practice. ◼...

Oxygen Therapy Goals and Effects  OXYGEN THERAPY Objectives… ◼ Indications ◼ Risks or Hazards ◼ Clinical Signs of Hypoxemia  OXYGEN THERAPY ◼ You, the RCP, must be well-versed in both the goals and objectives of this therapy, and its use in clinical practice. ◼ You will be the “Go-To” caregiver for oxygen administration.  General Goals and Clinical Objectives ◼ The overall goal of oxygen therapy is to maintain adequate tissue oxygenation while minimizing cardiopulmonary work.  Objectives for O2 Therapy ◼ Correct documented or suspected acute hypoxemia. ◼ Decrease the symptoms associated with chronic hypoxemia. ◼ Decrease the workload hypoxemia imposes on the cardiopulmonary system. 1st Things st 1 : How Do We Breathe? Intentionally Left Blank Intentionally Left Blank  Signs of Hypoxia ◼ Respiratory ◼ Tachypnea, dyspnea, cyanosis, accessory muscle use ◼ Cardiac ◼ Tachycardia, hypertension ◼ Neurological ◼ Somnolence, confusion, blurred vision, loss of coordination, impaired judgment, change in mental status!  Hypoxia vs. Hypoxemia ◼ Hypoxia – Low, or failed, supply of oxygen to tissues. ◼ Hypoxemia – Condition where the oxygen content in the arterial blood is below normal. ◼ Terms are often used interchangeably, but they are NOT the same. ◼ Hypoxemia may cause hypoxia, but there are other causes of hypoxia as well.  Indications for Oxygen ◼ Documented hypoxia ◼ Suspected hypoxia ◼ Myocardial infarction ◼ Severe trauma ◼ Post anesthesia ◼ Low PaO2 from an ABG Clinical Signs of Hypoxia Findings Mild to Moderate Severe Respiratory Tachypnea Tachypnea Dyspnea Dyspnea Paleness Cyanosis Cardiovascular Tachycardia Tachycardia, eventual Mild hypertension; bradycardia peripheral arrhythmias vasoconstriction Neurologic Restlessness Confusion Disorientation Blurred vision Headaches Tunnel vision Lassitude Loss of coordination Impaired judgement Slow Reaction time Manic-depressive activity Coma Other Clubbing*  Digital Clubbing Which example to the right is clubbing and which one is normal?  Correcting Hypoxemia ◼ Oxygen therapy corrects hypoxemia by raising alveolar and blood levels of oxygen. ◼ This is the most tangible objective for 02 therapy, and the easiest to measure and document.  RA Pb of 760 Thickening of A-C Membrane PAO2 149 torr More partial Pressure of O2 required to pass A-C =PaO2 55 torr Membrane  4l/m NC FiO2 37% of Pb760 Thickening of A-C Membrane PAO2 263 torr More partial Pressure of O2 required to pass A-C =PaO2 95 torr Membrane  Minimizing Cardiopulmonary Workload ◼ The cardiopulmonary system compensates for hypoxemia by increasing ventilation and cardiac output: INCREASED HR &/or INCREASED RR What is normal? ◼ Supplemental oxygen can decrease demands on both the heart and the lungs. ◼ 02 therapy can reduce both the high ventilatory demand and the work of breathing.  Assessing the Need for Oxygen Therapy ◼ There are three basic ways to determine if a patient needs oxygen therapy. ◼ First, you can use laboratory measurements (e.g. ABG) to document hypoxemia. ◼ Second, you can base a patient’s need for 02 therapy on his or her specific clinical problem or condition. ◼ Last, you can use astute bedside assessment techniques to determine the need for supplemental oxygen.  Assessing the Need for Oxygen ◼ Laboratory measures used to document hypoxemia include either Hb saturation or PaO2, as determined by either invasive or noninvasive means. Normal PaO2 80 torr - 100 torr Mild Hypoxemia 79 torr - 60 torr Moderate Hypoxemia 59 torr - 40 torr Severe Hypoxemia < 40 torr  What is Hemoglobin? ◼ The protein molecule in red blood cells that carry oxygen from the lungs to the body’s tissues, and then returns to the lungs carrying carbon dioxide from the tissues.  Assessing the Need for Oxygen Therapy M.I. Good examples are: Postoperative patients Carbon monoxide poisoning Cyanide poisoning Shock Trauma Acute myocardial infarction  Hazards and Precautions of Supplemental Oxygen 1. Oxygen toxicity 2. Depression of ventilation 3. Retinopathy of Prematurity 4. Absorption atelectasis 5. Equipment contamination with humidifiers  Oxygen Toxicity ◼ Oxygen toxicity primarily affects the lungs and central nervous system (CNS). ◼ Two primary factors determine oxygen’s harmful effects: ◼ the exposure time ◼ the PO2  RULE OF THUMB ◼ Avoiding Oxygen Toxicity - Limit patient exposure to 100% O2 to less than 24 hours whenever possible. ◼ High FiO2s are acceptable if the concentration can be lowered to 70% within 2 days and 50% or less in 5 days.  Oxygen Toxicity ◼ Patients exposed to high oxygen levels for a prolonged period of time have lung damage. ◼ First damage is capillary epithelium, leading to edema, thickened membranes and finally to pulmonary fibrosis and hypertension.  Depression of Ventilation ◼ When breathing moderate to high oxygen concentrations, COPD patients with chronic hypercapnia tend to ventilate less. ◼ The primary reason why some COPD patients hypoventilate when given oxygen is most likely suppression of the hypoxic drive. ◼ In these patients, the normal response to high PaCO2 is depressed, with the primary stimulus to breathe being oxygen.  Retinopathy of Prematurity ◼ Hemorrhage of these new vessels causes scarring behind the eye’s retina. ◼ Scarring leads to retinal detachment and blindness. ◼ ROP mostly affects neonates up to about 1 month of age, by which time the retinal arteries have sufficiently matured.  Atelectasis ◼ A collapsed or airless state of the lung, which may be acute or chronic, and may involve all or part of the lung. ◼ The primary cause is obstruction of the bronchus serving the affected area. ◼ But other causes...  Absorption Atelectasis ◼ FiO2 above 0.50 present a significant risk of absorption atelectasis. ◼ Nitrogen is the most plentiful gas in both the air & the alveoli. Breathing high levels of oxygen quickly depletes body nitrogen levels.  Absorption Atelectasis ◼ Absorption atelectasis is the result of nitrogen being 'washed out' of alveoli. Nitrogen does not diffuse into the blood well, so it stays in the alveoli. This helps to keep them open. When this gas is replaced by another gas, the alveoli can collapse. Administering high levels of oxygen over longer periods of time can cause this. The oxygen flushes out the nitrogen, and the alveoli collapse.  Infection Control ◼ Therapist must use an aseptic technique when handling supplemental oxygen and humidity equipment ◼ Never drain water from the tubing back into the heated humidifier (Large Volume Nebulizer) ◼ Always date the opened container (replace?) ◼ Only use sterile liquids in reservoirs  Oxygen: a fire hazard ◼ Supports Combustion ◼ NEVER smoke while using supplemental oxygen ◼ Severe facial burns can and do happen  Clinical Guidelines for Oxygen ◼ Try to keep oxygen below 50% if possible. ◼ Use it for the shortest possible time. ◼ Check equipment regularly for contaminants. PULSE OXIMETRY Hess – Ch. 2, pages 24- 29  Respiratory Care Process ◼ O – G – P – A – E – R & WASH ◼ O = Orders ◼ G = Gather the required equipment ◼ P = Prepare Equipment and Pt ◼ A = Assess the pt ◼ E = Evaluate the Therapy / Tx ◼ R = Record and Report ◼ Wash Hands before and after all pt contact.  PULSE OXIMETRY ◼ Allows you to monitor the oxygen saturation in the arterial blood, without drawing blood. ◼ The pulse oximeter uses photospectrometry to measure the oxygen saturation of a capillary bed. PULSE OXIMETRY  Pulse Oximetry ◼ The various hemoglobin molecules absorb wavelengths between 500 and 1000 nm in the infrared and visible light regions. ◼ The Beer-lambert law defines the relationship between the concentration of a substance and the amount of light absorbed Pulse Oximetry – Video ◼ Please refer to your videos in BB. ◼ Entitled “Pulse Oximetry” ◼ Link is https://youtu.be/-wsLjj78DXY  PULSE OXIMETRY ◼ The light passes through the capillary bed, and depending upon the amount of saturated hemoglobin, the color of the vascular bed varies (desaturated hemoglobin being darker). ◼ Oxygenated blood is more permeable to red light, the oximeter is able to relate this color change to oxygen saturation.  Digital Clubbing ◼ Clubbing Oxyhemoglobin Dissociation Curve Hess – Pages 1218 - 1220 SaO2 Axis PaO2 Axis Standard Oxyhemoglobin Dissociation Curve showing the P50, and the SaO2 at PaO2 = 80 mmHg.  A Couple of Definitions ◼ PaO2 - A measurement of oxygen in arterial blood. It shows how well oxygen is able to move from the lungs to the blood. ◼ Partial pressure is the dynamic that explains why oxygen moves from the alveoli into the blood and why carbon dioxide moves from the blood into the alveoli.  A Couple of Definitions ◼ SaO2 - A measurement of the percentage of how much hemoglobin is saturated with oxygen. ◼ Oxygen is transported in the blood in two ways: oxygen dissolved in blood plasma (PaO2) and oxygen bound to hemoglobin (SaO2).  Oxyhemoglobin Dissociation Curve ◼ The standard curve is shifted to the right by an increase in temperature, 2,3-DPG, or PCO2, or a decrease in pH. The curve is shifted to the left by the opposite of these conditions.  2,3-DPG 2,3 diphosphoglycerate is a substance made in the red blood cells. It controls the movement of oxygen from red blood cells to body tissues. 2,3DPG testing is done to help investigate both a deficiency in red blood cells (anemia) and an unexplained increase of red blood cells, called erythrocytosis. Hemoglobin, the protein in the blood that carries oxygen, uses 2,3- DPG to control how much oxygen is released once the blood gets out into the tissues. The more 2,3 DPG in the cell, the more oxygen is delivered to body tissues. Conversely, the less 2,3DPG in the cell, the less oxygen is delivered. (PaO2) Standard Oxyhemoglobin Dissociation Curve showing the P50, and the SaO2 of 50% and a Pressure of ~27mmHg  Oxyhemoglobin Dissociation Curve ◼ A rightward shift causes a decrease in the affinity of hemoglobin for oxygen. This makes it harder for the hemoglobin to bind to oxygen, but it makes it easier for the hemoglobin to release bound oxygen. ◼ A leftward shift increases the affinity, making the oxygen easier for the hemoglobin to pick up but harder to release. Intentionally Left Blank  SpO2 Relationship to PaO2 ◼ SpO2 (saturation pulse O2) measured by Pulse Oximetry ◼ SaO2 is measured by a Blood Gas analysis ◼ + or - The Rule of 30 Example: if the Spo2 is 90 the PaO2 is 60 + or - If the PaO2 is 60 then the SpO2 is 90 + or – (JUST AN ESTIMATE)  92% 87% 57 torr 62% Standard Oxyhemoglobin Dissociation Curve showing the estimated relationship between SpO2 and O2 tension.  KEY POINTS ◼ Oxygen saturation value reflects the saturation of the hemoglobin. It does not tell or show you how much hemoglobin the Pt. has. ◼ Pulse oximetry measures saturation in the peripheral tissues. ◼ Other substances can bind to hemoglobin and give false reading with pulse ox.  Degree of Hypoxemia ◼ When Measured: Normal PaO2 = 80 torr to 100 mmHg Mild Hypoxemia = 60 torr to 79 mmHg Moderate Hypoxemia = 40 torr to 59 torr Severe Hypoxemia