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MED SURG II EXAM 2
Review of Respiratory
| Question | Answer |
|---|---|
| Respiration | Gas exchange between the lungs and blood, and between the blood and tissues |
| Diffusion | Exchange of oxygen and carbon dioxide from the alveoli into the blood |
| Metabolic Alkalosis | Loss of acid from prolonged vomiting or NG suction. |
| Metabolic Acidosis | Acid increases due to metabolic or endocrine causes. Or the body is unable to excrete acid |
| Respiratory Acidosis | Increased CO2 retention due to hypoventilation |
| Respiratory Alkalosis | Increased CO2 excretion due to hyperventilation |
| Metabolic Alkalosis Compensation | Lungs retain CO2 to compensate |
| Metabolic Acidosis Compensation | The lungs compensate by increasing CO2 excretion |
| Respiratory Alkalosis Compensation | Kidneys excrete HCO3 to compensate |
| Respiratory Acidosis Compensation | Kideys retain HCO3 to compensate |
| Metabolic Alkalosis Symptoms | Irritability, dysrhythmias from hypokalemia, lethargy, nausea, vomitng, seizures, hypertonic muscles |
| Respiratory Alkalosis Symptoms | Tachycardia, Tachypnea, Dizziness, Syncope, Confusion, Cramps, Paresthesia, Hyperreflexia |
| Respiratory Acidosis Symptoms | Warm, Flushed, Skin, Respiratory Distress, Altered Mental Status, Sleepiness or Fatigue, Headache, Seizures, Hypotension |
| Metabolic Acidosis Symptoms | Nausea, Vomiting, Diarrhea, Headache, Muscle weakness, coma, Deep, Rapid, Respirations, termed Kussmaul Respirations |
| Metabolic Alkalosis Causes | Vomiting, excess bicarbonate intake, nasogastric suctioning, diuretic therapy, hypokalemia, mineralocorticoid use. |
| Respiratory Acidosis Causes | Asthma, COPD, Pulmonary Edema, Respiratory Failure, Atelectasis, Obstructed Airway, Overdose |
| Respiratory Alkalosis Causes | Hyperventilation, liver failure, mechanical ventilation, stimulated respiratory center in septicemia, stroke, meningitis |
| Metabolic Acidosis Causes | Diabetic Ketoacidosis, lactic acidosis, shock, starvation, renal failure |
| Pulmonary Embolism | Obstruction of the pulmonary artery, or one of its branches by a thrombus. Often originates in the lower extremities. Clot can dislodge and travel to the lungs. Results in a decreased or absent gas exchange. Can be associated with trauma, surgery, pregnancy, HF, over 50 years of age, hypercoagulable states, prolonged immobility |
| Pulmonary Embolism Symptoms | Tachypnea (most common), SOB that appears suddenly, chest pain, cough (blood or blood-tinged), anxiety, feeling of suffocation, irregular heartbeat, syncope, lightheadedness, dizziness, excessive sweating, clammy or cyanosis of the skin, leg pain and swelling |
| Pulmonary Embolism Diagnostics | Chest X ray which is usually normally but may show infiltrates, atelectasis, elevation of the diaphragm on effected side, and possible pleural effusion. ECHO allows monitoring for enlarged right-sided or tricuspid regurgitation. ECG to rule out MI. Pulse OX to monitor for hypoxia, ABGs to monitor for hypoxemia and hypocapnia |
| VQ Scan | Compares the amount of perfusion in a lung segment with the degree of ventilation in the segment |
| Pulmonary Angiogram | Allows for direct visualization under fluroscopy of the arterial obstruction and accurate assessment of the perfusion deficit |
| Multidetector Computed Tomographic Angiography | Standard for diagnosis of PE, can be performed quickly, and provides the advantage of high-quality visualization of the lung parenchyma. |
| Pulmonary Embolism Treatment | Initial treatment is to dissolve the clot with thrombolytics. Second is long-term anticoagulants to prevent future clots. For recurrent embolis despite anticoagulant therapy an IVC filter may be used. Rarely an embolectomy is used. |
| Prevention of Venous Stasis | Do not dangle legs, use compression stockings, encourage ambulation and active or passive exercises, avoid sitting or staying in bed too long, encourage leg pumps |
| Acute Respiratory Distress Syndrome | Severe, life-threatening medical condition. Characterized by widespread inflammation in the lungs. The endothelial damage and leakage of protein-rich fluid into the alveoli. Results in noncardiogenic pulmonary edema and diffuse alveolar damage. Results in nonfunctioning alveoli and refractory hypoxemia |
| Acute Respiratory Distress Syndrome Assessment | Severe VQ mismatching occurs. Alveoli collapse due to the inflammatory infiltrate, and blood, fluid, and surfactant dysfunction. Small airways are narrowed because of interstitital fluid and bronchial obstruction. Lung Compliance is markedly decreased resulting in decreased functional residual capacity. Initially resembles pulmonary edema, rapid onset of dyspnea, arterial hypoxemia, that DOES NOT RESPOND TO OXYGEN |
| Causes of Acute Respiratory Distress Syndrome | Often presents in those with preexisting conditions and can caused by sepsis, inhalation of harmful substances, severe pneumonia, burns, COVID |
| Symptoms of Acute Respiratory Distress Syndrome | SOB, Fasting breathing, lots of rapid, shallow breaths, coughing up phlegm, cyanosis on fingernails, skin, or lips. Extremem tiredness, chest pain when deep breathing, intercostal retractions and crackles in severe ARDS |
| ARDS Diagnostics | BNP levels to rule out pulmonary edema. Chest X-Ray shows like cardiogenic pulmonary edema, there are visible bilateraly infiltrates that quickly worsen. Mild ARDs progresses to fibrosing of the alveolitis with persistent, severe hypoxemia. Patient will also show increased alveolar dead space. Typically has decreased pulmonary compliance (stiff lungs). ECHO, TEE to monitor structures, valvular disease, or decreased blood flow. EKG to monitor for arrythmias or ischemia. Bronchoscopy identifies the cause. |
| ARDS Medical Management | Almost always includes ET intubation or tracheostomy, mechanical ventilation, circulatory support, adequate fluid volume and nutrition, supplemental oxygen, PEEP, treatment for hypovolemia, nebulizer treatments, chest physiotherapy, suctioning, bronchoscopy, frequent turning, reducing anxiety, and prone positioning may be neccessary + |
| PEEP | A positive pressure maintained by the ventilator at the end of exhalation. Used to increase functional residual capacity. Opens collapsed alveoli. Improves oxygenation with a lower fraction of inspired oxygen. Unnatural pattern of breathing that feels strange to the patient. May require sedatives as lorazepam. |
| Mechanical Ventilator | Positive or negative pressure breathing device. Maintains ventilation and oxygen delivery for a prolonged period of time. May fight the vent. Assess for pneumothorax, possible malfucntioning. Sedatives or paralytics may be used |
| Ventilator Acquired Pneumonia | Prevention includes elevation of the head of bed 30-45 degrees, daily sedation vacations and readiness to extubate, peptic ulcer disease prophylaxis, DVT prophylaxis, daily oral care with chlorhexidine. |
| Weaning off the Ventilator | Patient must by physiologically and hemodynamically stables, demonstrates spontaneous breathing capability, recovering from the acute stage of medical and surgical problems, cause of respiratory failure is sufficiently reveresed. |
| Pulmonary Edema | Abnormal accumulation of fliuid in the interstitial spaces and the alveoli of the lungs. An acute event that results from left ventricular failure. Can occur following an acute MI, or as an exacerbation of chronic HF. When the left ventricle begins to fail, the blood backs up into the pulmonary circulation and causes pulmonary interstitial edema |
| Pulmonary Edema Symptoms | Dyspnea, extreme SOB that worsens with activity or lying down A feeling of suffocating or drowning when lying flat. A cough with frothy sputum tinged with blood. Wheezing, gasping for breath, cold, clammy skin, anxiety, restlessness, or sense of apprehension, cyanosis, tachycardia, irregular heartbeats, palpitations, JVD, confusion and stupor |
| Pulmonay Hypertension | High BP in the arteries of the lungs. Narrow, hard to pump heart, and the heart has to work harder. Symptoms include SOB with activity, fatigue, weakness, substernal chest pain, racing heart, pain on upper right side of abdomen, and decreased appetite. As the disease worsens it is hard to do any physical activity. There is no cure, we treat symptoms. Diagnostics include ABG, electrolytes, BUN, creatinine, BNP, chest x ray, CT scan, EKG, ECHO, VQ scan. Give oxygen, anticoagulation meds, digoxin, diuretics |
| Respiratory Failure | Sudden and life-threatening deterioration of the gas exchange function of the lungs and indicates their failure to provide adequate oxygenation or ventilation. The ventilation or perfusion mechanisms in the lung are impaired. Results in the blood not receiving enough oxygen or has too much carbon dioxide OR BOTH |
| Acute Respiratory Failure | Defined as hypoxemia with decreased arterial PaO2 to less than 60, hypercapnia with increased arterial carbon dioxide tension PaCO2 to greater than 50, and acidosis with pH less than 7.35 |
| Respiratory Failure Management | Nurses will assist with intubation and maintaining mechanical interventions, monitor respiratory status, level of responsiveness, vital signs, pulse ox, and provide care to prevent complication such as turning, mouth care, skin care, and ROM. The objective of treatment is to correct any underlying cause and restore adequate gas exchnage in the lungs |
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