COPD and ARDS: A Comprehensive Overview PDF

**COPD** **DEFINITION** - Chronic Obstructive Pulmonary Disease (COPD) is a condition of chronic dyspnea with expiratory airflow limitation that does not significantly fluctuate - It has been defines as a preventable and treatable disease with some significantly It has ben defined...

**COPD** **DEFINITION** - Chronic Obstructive Pulmonary Disease (COPD) is a condition of chronic dyspnea with expiratory airflow limitation that does not significantly fluctuate - It has been defines as a preventable and treatable disease with some significantly It has ben defined extrapulmonary effects that may significantly contribute to the severity in individual patients. (The Global Initiative for Chronic Obstructive Pulmonary Disease) **Classification:** - Chronic Bronchitis - Emphysema These two classifications of COPD can be confusing because there are patients who have overlapping signs and symptoms **CHRONIC BRONCHITIS** - is a disease of the airways that is characterized by cough and sputum production for at least 3 months - BLUE BLOATERS - large edematous, cyanotic and with minimal dyspnea. - Airway obstruction leads to hypoxia, subsequently causing vasoconstriction (pulmonary hypertension) further causing reduced circulatory blood volume and right sided heart failure which can lead to cor pulmonale. This leads to hypoxemia and polycythemia causing cyanosis. A wide range of viral, bacterial and mycoplasmal infections can produce acute episodes of bronchitis **EMPHYSEMA** - PINK PUFFER-is a thin, cathetic person with marked shortness of breath. The blood remains well oxygenated because both ventilation and perfusion are reduced - Loss of elastin fibers reduces structural support for alveoli and small airways, which makes them prone to collapse on expiration, leading to air trapping. - Pursed lip breathing allows maintenance of positive end expiratory procedure (PEEP) which keeps the airway open. The decreased lung compliance leads to increased work of breathing and dyspnea. - There is abnormal distention of airspaces beyond the bronchioles and destruction of the walls of the alveoli. There is impaired carbon dioxide and oxygen exchange due to the destruction of the walls of the overdistended alveoli - They can be **Panlobular -** there is destruction of the respiratory bronchioles, alveolar duct and the alveolus - **Centrilobular -** changes occur in the secondary lobules **PATHOPHYSIOLOGY** - In COPD, the airflow is both progressive and associated with an abnormal inflammatory response of the lungs to noxious gases or particles **What happens?** - An inflammatory response happens throughout the proximal and peripheral airways, Lung parenchyma and pulmonary blood vessels - Due to this chronic inflammation, changes and narrowing occurs in the airways - There is an increase in the number of goblet cells and enlarged submucosal glands causing the increased secretion of mucus - Causes scar formation in the long term and narrowing of airways - Wall destruction leads to loss of alveolar attachment and decrease in elastic recoil - This chronic inflammatory process affects the pulmonary vessels and subsequent thickening of the vessel lining and hypertrophy of smooth muscle. **CAUSES** 1. **Smoking** depresses the activity of scavenger cells and affects the respiratory tract\'s ciliary cleansing mechanism 2. **Occupational exposure**- prolonged and intense exposure to work related dusts and chemicals, indoor air pollution, and outdoor air pollution 3. **Genetic abnormalities**- deficiency in the alpha 1-antitrypsin, an enzyme inhibitor that protects the lung surface from injury **CLINICAL MANIFESTATION** - The natural history of COPD is variable but is a generally progressive disease 1. Chronic cough 2. Sputum production 3. Dyspnea on exertion 4. Dyspnea at rest 5. Weight loss 6. Barrel chest **PREVENTION** 1. **STOP SMOKING**- this is the single most cost effective intervention 2. As nurses we can help promote the stoppage of smoking by explaining the risks of smoking personally to the patient **COMPLICATIONS** - Two major life threatening complications - Respiratory failure - Respiratory insufficiency **ASSESSMENT AND DIAGNOSTIC FINDINGS** Carefully assess the history and findings 1. Health history 2. Pulmonary function studies - Spirometry - ABG - Chest x-ray - CT scan - Bronchogram - Lung scan - CBC - Blood chemistry - Sputum cultures - Cytology exams - ECGS - Stress test **MEDICAL MANAGEMENT** - PHARMACOLOGIC THERAPHY \- Bronchodilators \- Corticocosteroids \- Others - Alpha 1-antitrysin augmentation therapy - Antibiotics - Mucolytics - Antitussive - Vasodilators - Narcotics **MANAGEMENT OF EXACERBATIONS** Bronchodilators Hospitalization Oxygen therapy Antibiotics **SURGERY** Bullectomy Lung volume reduction surgery Lung transplantation **NURSING MANAGEMENT** - Management should be incorporated with teaching and improving the respiratory status of the patient **Nursing Assessment** - Respiratory system assessment should be done rapidly but accurately - Exposure to risk factors - Past and present medical history - Signs of COPD and how severe are they - Knowledge of disease by the patient - Vital signs - Breath sounds and pattern **Nursing Diagnosis: (depends on the assessment data gathered)** - Impaired gas exchange due to chronic inhalation of toxins - Ineffective airway clearance related to bronchoconstriction, increased mucus production, ineffective cough and other complications - Ineffective breathing patterns related to shortness of breath, mucus, bronchoconstriction, and airway irritants - Self care deficit related to fatigue - Activity intolerance related to hypoxemia and ineffective breathing patterns **Planning and Goals** - Improvement in gas exchange - Achievement in airway clearance - Improvement in breathing pattern - Independence in self care activities - Improvement in activity intolerance - Ventilation/oxygenation adequate to meet self care needs - Nutritional intake meeting caloric needs - Infection treated/prevented - Disease process/prognosis and therapeutic regimen understood - Plan in place to meet needs after discharge **Nursing Priorities** - Airway patency - Measures to facilitate gas exchange - Enhance nutritional intake - Prevent complications, slow progression - Provide information about disease process/prognosis and treatment regimen **Nursing interventions** Patient and family teachings for enhanced self management - **Airway clearance** - Bronchodilators - Diaphragmatic breathing - Pursed lip breathing - **Activity Tolerance** - Manage daily activities - Exercise training - Walking aids **Manage and monitor potential complications** - Monitor cognitive changes - Monitor pulse oximetry changes - Prevent infection **Evaluation** - Identifies the hazards of smoking - Identifies resources for stopping smoking - Minimizes or eliminates exposure - Verbalizes the needs for fluids - Is free of infection - Practices breathing exercises - Performs activities with less shortness of breath **DISCHARGE AND HOME CARE GUIDELINES** - Setting goals - Temperature - Activity moderation - Breathing retraining **ACUTE RESPIRATORY DISTRESS SYNDROME** - Is a life threatening lung condition where there is a failure in breathing that can occur in the very ill or severely injured people. - This is not a specific disease - It starts with the swelling of tissue in the lungs and build up of fluids in the tiny air sacs that transfer oxygen to the bloodstream subsequently leading to low blood oxygen levels. - This is similar to the infant respiratory distress syndrome. Though they differ in the causes and the treatment. ARDS can occur in anyone over the age of one. **Causes** **DIRECT INJURY TO THE LUNGS** - Chest trauma (heavy blow) - Breathing vomit - Breathing smoke, chemicals or saltwater - Burns **INDIRECT INJURY TO THE LUNGS** - Severe infection - Massive blood transfusion - Pneumonia - Severe inflammation of the pancreas (pancreatitis) - Alcohol or drug overdose - Lung and bone transplantation **SYMPTOMS** - Shortness of breath - Fast, labored breathing - Bluish skin or fingernails - Rapid pulse **Pathophysiology** - When lung tissues are injured, the alveoli becomes permeable to lung proteins - Entry of more proteins, debris and fluids into the lungs - Inflammation breaks down surfactant making the lungs less compliant **Three stages:** **-Exudative** **-Proliferative** **-Fibrotic** Initially mild symptoms like dyspnea, cough, tachypnea and restlessness are observed, but as the syndrome progresses the symptoms worsen as fluid accumulation increases. Respiratory muscle fatigue becomes evident and ABG results declines. **Nursing Assessment** 1. Review health history - assess the patient\'s general symptoms (dyspnea, cough, tachypnea, restlessness) - Determine the underlying cause - Sepsis-most common - Multi organ dysfunction - Pneumonia - Aspiration - Burns - Drug overdose - Pancreatitis - Fractures of long bones - Determine the patients\' risk factors - Old age - Female (in cases of trauma) - Tobacco use - Alcohol use - Chronic lung disease - High risk surgeries - Assess the patients environment, occupation or lifestyle habits **Physical Assessment** A. Closely monitor the respiratory status B. Monitor the vital signs C. Determine the presence of infection or sepsis D. Auscultate the lung sounds **Nursing Interventions** **Provide supportive care** - Manage the underlying conditions - Administer medications as prescribed - Adores the cause of sepsis - Prevent complications associated with mechanical ventilation and ICU stay - Provide Oxygenation **5 Ps of the ARDS Therapy** -Perfusion -Positioning -Protective lung ventilation -Protocol weaning -Preventing complications - Administer oxygen as ordered - Consider mechanical ventilation - Consider tracheostomy - Turn the patient to PRONE POSITION - Administer fluids with caution - Administer nutritional support - Promote bed rest - Minimize sedation - Refer for rehab **Nursing Care Plans** **Impaired gas exchange** Related to: - Damage to the alveolar capillary membrane - Change in lung compliance - Imbalance in ventilation perfusion - Ineffective breathing pattern As evidenced by: - Abnormal arterial pH - Cyanosis - Altered respiratory depth and rhythm - Hypoxemia - Hypoxia - Nasal flaring - Altered mental status **Impaired spontaneous ventilation** Related to: - Damage to the alveolar-capillary membrane - Respiratory muscle fatigue - Disease process - Pulmonary inflammatory process As evidenced by: - Decreased arterial 02 saturation - Decreased tidal volume - Increased accessory muscle use - Increased HR - Restlessness an decreased cooperation **Ineffective airway clearance** Related to: - Excessive mucus - Retained secretions - Airway spasm - Inflammatory process - Lung injury - Decreased surfactant As evidenced by: - Adventitious breath sounds - Altered respiratory rate and rhythm - Tachypnea - Tachycardia - Cyanosis - Excessive sputum - Nasal flaring - Shortness of breath **Ineffective Breathing Pattern** Related to: - Alveolar impairment - Poor lung expansion - Reduced surfactant - Lung fibrosis - Fluid in the lungs As evidenced by: - Tachypnea - Dyspnea - Accessory muscle use - Anxiety - Restlessness - Respiratory muscle fatigue **Risk for infection** Related to: - Sepsis - Invasive lines **Surgical incisions** - Wounds - Stress - Prolonged hospital stay - Prolonged immobility **PULMONARY EMBOLISM** - Refers to the obstruction of the pulmonary artery or one of its branches by a thrombus (or thrombi) that originates somewhere in the venous system or in the right side of the heart - The cause is usually a blood clot in the leg called a deep vein thrombosis that breaks, loose and travels through the bloodstream to the lungs. - It can damage part of the lungs due to restricted blood flow, decrease oxygen levels in the blood, and affect other organs as well. Large or multiple blood clots can be fatal. - The blockage can be life-threatening - Most commonly, pulmonary embolism is due to a blood clot or thrombus, but there are other types of emboli: fat, air, amniotic fluid, and septic. - **Fat emboli.** Fat emboli are cholesterol or fatty substances that may clog the arteries when fatty foods are consumed more. - **Air emboli.** Air emboli usually come from intravenous devices. - **Amniotic fluid emboli.** Amniotic fluid emboli are caused by amniotic fluid that has leaked towards the arteries. - **Septic emboli.** Septic emboli originate from a bacterial invasion of the thrombus. - Blood clots can form for a variety of reasons. Pulmonary embolisms are most often caused by deep vein thrombosis, a condition in which blood clots form in veins deep in the body. The blood clots that most often cause pulmonary embolisms begin in the legs or pelvis. - Blood clots in the deep veins of the body can have several different causes, including: - **Injury or damage**: Injuries like bone fractures or muscle tears can cause damage to blood vessels, leading to clots. - **Inactivity:** During long periods of inactivity, gravity causes blood to stagnate in the lowest areas of your body, which may lead to a blood clot. This could occur if you\'re sitting for a lengthy trip or if you\'re lying in bed recovering from an illness. - **Medical conditions:** Some health conditions cause blood to clot too easily, which can lead to pulmonary embolism. Treatments for medical conditions, such as surgery or chemotherapy for cancer, can also cause blood clots. - Includes immobility, trauma to the legs, childbirth, congestive heart failure, dehydration, increased coagulability of the blood, and cancer - Thrombi tend to break off with sudden muscle action or massage, trauma, or changes in the blood flow - Post operative risk can be reduced by early ambulation or use of TEDS (thromboemobolic) stockings - Other types include fat emboli from the bone marrow resulting from fracture of a large bone, vegetations resulting from endocarditis in the right side of the heart, amniotic fluid emboli from placental tears occuring during labor delivery, tumor cell emboli that break away from a malignant mass, or air embolus injected into a vein. **Pathophysiology** - The effects of pulmonary embolus depend somewhat on the material but largely on the size and therefore on the location of the obstruction. - Because lung tissue is supplied with oxygen and nutrients by the bronchial circulation, infarction does not follow obstruction of the pulmonary circulation unless the general circulation is compromised or there is prior lung disease. - Infarction usually involves a segment of the lung and the pleural membrane in the area. **Small pulmonary emboli** are frequently \"silent\" or asymptomatic. However, multiple small emboli (\"a shower\") often have an effect equal to that of a larger embolus Emboli that block moderate-sized arteries usually causes respiratory impairment because fluid and blood fill the alveoli of the involved area. Reflex vasoconstriction often occurs in the area, further increasing the pressure in the blood vessels.  **Large emboli** (usually those involving more than 60% of the lung tissue) affect the cardiovascular system, causing right-sided heart failure and decreased cardiac output (shock). Sudden death often results in these cases, which involve greatly increased resistance in the pulmonary arteries because of the embolus plus reflex vasoconstriction due to released chemical mediators such as serotonin and histamine. This resistance to the output from the right ventricle causes acute cor pulmonale. Also, there is much less blood returning from the lungs to the left ventricle and then to the systemic circulation (decreased cardiac output). This can be appreciated by visualizing a large embolus lying across the bifurcation of the pulmonary artery (a \"saddle embolus\") and totally blocking the flow of the blood from the right ventricle into the lungs. **Pathophysiology** A series of happenings occur inside a patient\'s body when he or she has emboli. - **Obstruction.** When a thrombus completely or partially obstructs the pulmonary artery or its branches, the alveolar dead space is increased. - **Impairment.** The area receives little to no blood flow and gas exchange is impaired. - **Constriction.** Various substances are released from the clot and surrounding area that cause constriction of the blood vessels and results in pulmonary resistance. - **Consequences.** Increased pulmonary vascular resistance due to regional vasoconstriction leading to increase in pulmonary arterial pressure and increased right ventricle workload are the consequences that follow. - **Failure.** When the workload of the right ventricle exceeds the limit, failure may occur **Signs and Symptoms** a. **Small emboli** - a transient chest pain, cough, or dyspnea may occur. Often unnoticed but can be significant because it may be a warning of more emboli developing b. **Larger emboli** - chest pain that increases with coughing or deep breathing, tachypnea, and dyspnea develop suddenly. Later, hemoptysis and fever are present. c. **Hypoxia** stimulates a sympathetic response, with anxiety and restlessness, pallor and tachycardia d. **Massive emboli** - cause severe crushing chest pain, low blood pressure, rapid weak pulse, and loss of consciousness. e. **Fat emboli** - development of acute respiratory distress, a petechial rash on the trunk, and neurologic signs such as confusion and disorientation **Diagnostic Test** 1. **Chest X-ray** - usually normal but may show infiltrates, atelectasis, elevation of the diaphragm on the affected side, or a pleural effusion. 2. **ECG** - usually shows sinus tachycardia, PR-interval depression, and nonspecific T-wave changes. 3. **ABG analysis** - ABG analysis may show hypoxemia and hypocapnia; however, ABG measurements may be normal even in the presence of PE. 4. **Pulmonary angiography** - allows for direct visualization under fluoroscopy of the arterial obstruction and accurate assessment of the perfusion deficit. 5. **duplex venous ultrasound** - This test uses radio waves to visualize the flow of blood and to check for blood clots in your legs. 6. **Venography** - This is a specialized X-ray of the veins of your legs. 7. **D-dimer test** - A type of blood test that is used to help rule out the presence of an inappropriate blood clot. 8. **V/Q scan (ventilation/perfusion lung scan)** - evaluates the different regions of the lung and allows comparisons of the percentage of ventilation and perfusion in each area. The normal range for D-dimer is **500ng/mL** fibrinogen equivalent units (FEU) - A **negative D-dimer** result means that it is most likely that the person tested does not have an acute condition or disease causing abnormal clot formation or breakdown. - A **positive D-dimer** result may indicate the presence of an abnormally high level of fibrin degradation products Because PE is often a medical emergency, emergency management is of primary concern. - **Anticoagulation therapy.** Heparin, and warfarin sodium has been traditionally been the primary method for managing acute DVT and PE. - **Thrombolytic therapy.** Urokinase, streptokinase, alteplase are used in treating PE, particularly in patients who are severely compromised. **Surgical Management** Removal of the emboli may sometimes need surgical management. - **Surgical embolectomy.** This is the removal of the actual clot and must be performed by a cardiovascular surgical team with the patient on cardiopulmonary bypass. - **Transvenous catheter embolectomy.** This is a technique in which a vacuum-cupped catheter is introduced transvenously into the affected pulmonary artery. - **Interrupting the vena cava.** This approach prevents dislodged thrombi from being swept into the lungs while allowing adequate blood flow. **Nursing Management** 1. **Prevent venous stasis**. Encourage ambulation and active and passive leg exercises to prevent venous stasis. 2. **Manage pain.** Turn patient frequently and reposition to improve ventilation-perfusion ratio. 3. **Manage oxygen therapy.** Assess for signs of hypoxemia and monitor the pulse oximetry values. 4. **Relieve anxiety.** Encourage the patient to talk about any fears or concerns related to this frightening episode. 5. **Monitor thrombolytic therapy.** Monitoring thrombolytic and anticoagulant therapy through INR or PTT. - **INR (International Normalized Ratio)** and PTT (partial thromboplastin time) are used to monitor effectiveness of the anticoagulant warfarin. - **Extended PTT** times can be a result of anticoagulation therapy, liver problems, lupus, and other diseases that result in poor clotting. Normal range of INR is **1 to 2**, while for PTT is **30 to 45** seconds. **Discharge and Home Care Guidelines** 1. **Prevent recurrence.** The nurse should instruct the patient about preventing recurrence and reporting signs and symptoms. 2. **Adherence.** The nurse should monitor the patient\'s adherence to the prescribed management plan and enforces previous instructions. 3. **Residual effects.** The nurse should also monitor for residual effects of the PE and recovery. 4. **Follow-up checkups.** Remind the patient about keeping up with follow-up appointments for coagulation tests and appointments with the primary care provider. **RESPIRATORY FAILURE** Respiratory failure is a condition where there Is not enough oxygen or too much carbon dioxide in your body. There is a sudden and lite threatening deterioration of the gas exchange function of the lungs. There is a failure to provide adequate oxygenation or ventilation for the blood. This is a condition where there is: - Not enough oxygen in the tissues in your body (hypoxia) - Too much carbon dioxide in your blood (hypercapnia) This is a medical emergency - Can come on suddenly (acute) or over time (chronic) **Types of Respiratory Failure** **Hypoxemic Respiratory Failure (Type 1)** - Happens when you don't have enough oxygen in the blood (hypoxemia) - Also known as hypoxic respiratory failure - Causes: heart and lung conditions **Hypercapnic Respiratory Failure (Type II)** - Too much carbon dioxide in the blood - If your body can't get rid of carbon dioxide there wont be enough room for blood cells to carry oxygen - Causes: heart, lung, muscle and neurological conditions (Guillain-Barre Syndrome, Myasthenia Gravis, Polymyositis or Multiple Sclerosis) - COPD **Perioperative respiratory failure** - Surgery - Anesthesia can affect breathing that could lead air sacs to collapse (atelectasis) and further leading oxygen out from the blood **Respiratory Failure due to Shock** - Causes low blood pressure, pulmonary edema and other conditions like sepsis or heart attacks or blood loss. **Pathophysiology** **Impaired ventilation or perfusion mechanisms** - Impaired function of the CNS (e.g. drug overdose, head trauma, infection, sleep apnea, hemorrhage) - Neuromuscular dysfunction (eg. Guillain-Barre Syndrome, Myasthenia Gravis, ALS or spinal cord trauma) - Musculoskeletal dysfunction (e.g. chest trauma, kyphoscoliosis, malnutrition - Pulmonary dysfunction (e.g. COPD, asthma, cystic fibrosis) **Oxygenation failure mechanisms** - Pneumonia - ARDS - CHF - COPD - PE - Restrictive lung diseases interstitial lung disease, pulmonary fibrosis, sarcoidosis) **Post-operative Period** - Major thoracic or abdominal surgery may cause inadequate ventilation and respiratory failure - Caused by: anesthesia, analgesics or sedatives **Clinical Manifestations** Early signs: - Impaired oxygenation - Restlessness, fatigue, headache, dyspnea, air hunger, tachypnea and increased BP - As hypoxemia progresses - Confusion - Lethargy - Tachycardia, tachypnea - Central cyanosis - Diaphoresis - Respiratory arrest - Physical findings - ARDS (increase use of accessory muscles) - Decrease breath sounds (if patient cannot adequately ventilate) - Related to underlying disease - Hypotension with signs of poor perfusion suggests severe sepsis or severe pulmonary embolism - Hypertension with signs of poor perfusion suggests cardiogenic pulmonary edema - **Symptoms depend on the cause:** - Dyspnea - Tachypnea - Fatigue - Heart palpitations - Hemoptysis - Diaphoresis - Restlessness - Pallor - Cyanosis - Blurred vision - Agitation, confusion - Behavioral changes **Diagnosis: History** - Sepsis - Pneumonia - Pulmonary embolus suggested by sudden onset of shortness of breath of chest pain - COPD exacerbation suggested by history of heavy smoking, cough, sputum production - Cardiogenic pulmonary edema suggested by chest pain, paroxysmal nocturnal dyspnea, and orthopnea **Diagnosis: Physical Findings** - Hypotension usually with signs of poor perfusion suggests severe sepsis or massive pulmonary embolus. - Hypertension usually with signs of poor perfusion suggests cardiogenic pulmonary edema. - Wheezing suggests airway obstruction: - Bronchospasm - Secretions - Pulmonary edema - Stridor suggests upper airway obstruction - Elevated jugular venous pressure suggests right ventricular dysfunction due to accompanying - Pulmonary hypertension - Tachycardia and arrhythmias may be the cause of cardiogenic pulmonary edema **Laboratories** - ABG - Complete blood count - Cardiac serologic markers - Microbiology - Pulmonary function tests/bedside spirometry - Bronchoscopy - Chest radiography - Electrocardiogram - Echocardiography **Management** **ABC's** - Ensure airway is adequate - Ensure adequate supplemental oxygen and assisted ventilation, if indicated. Support circulation as needed **Treatment of a specific cause when possible** - Infection **Antimicrobials, source control** - Airway obstruction Bronchodilators, glucocorticoids. - Improve cardiac function - Positive airway pressure, diuretics, vasodilators morphine, inotropes **Mechanical ventilation** - Non-invasive - Mask: usually orofacial to start - Invasive - Endotracheal tube (ETT) - Tracheostomy - if upper airway is obstructed **Indications for Mechanical Ventilation** - Cardiac or respiratory arrest. - Tachypnea or bradypnea with respiratory fatigue. - Acute respiratory acidosis. - Inability to protect the airway associated with depressed level of consciousness of consciousness - Shock associated with excessive respiratory work - Inability to clear secretions with impaired gas exchange - Short term adjunct in management of acutely increased intracranial pressure (ICP) - Consider Non Invasive ventilation particularly in the following settings: - COPD exacerbation - Cardiogenic pulmonary edema - Obesity hypoventilation syndrome **Nursing Management** - Assess the patient's tissue oxygenation status regularly. - Evaluate ABG results. - To enhance V/Q matching, tum the patient on a regular and timely basis-lo rotate and maximize lung zones. - Regular, effective use of incentive spirometry - Regular patient turning and repositioning enhances diffusion by promoting a healthy, well-perfused alveolar surface. - These actions, as well as suctioning, help mobilize sputum or secretions. - Regular, effective use of incentive spirometry - Regular patient turning and repositioning enhances diffusion by promoting a healthy, well-perfused alveolar surface. - These actions, as well as suctioning, help mobilize sputum or secretions. **PNEUMOTHORAX AND HEMOTHORAX** - PNEUMOTHORAX is a collection of air outside the lung but within the pleural cavity. - It occurs when air accumulates between the parietal and visceral pleura inside the chest - In a normal lung, negative pressure exists b/n the visceral and parietal pleural (pleural space) - This pleural space contains minimal fluid that serves as lubricant when the tissues move. - When air enters this space, pressure changes will cause the lungs to collapse (partial or complete) **Types** - Spontaneous pneumothorax- rupture of air-filled sacs on the lung surface - Primary's spontaneous pneumothorax- occurs without an evident cause - Secondary spontaneous pneumothorax- occurs due to an underlying Illness (COPD, asthma, tuberculosis, cystic fibrosis and other lung disease) - latrogenic pneumothorax- occurs due to puncture or laceration of the lungs during a medical procedure (lung biopsy, tracheostomy or catheter insertion) - Tension pneumothorax-occurs when the air enters the pleural space and cannot escape due to trauma (stab wound, gunshot wound, fractured rib) **Nursing Process** - Check patient's ABCs and hemodynamic stability - If the patient is stable and has minimal air or fluid accumulation in the pleural space, no treatment may be necessary as it may resolve spontaneously. - But it severe immediate medical care is needed **Nursing Assessment** Review heath History 1. Determine cause - Chest trauma/injury - Ruptured blebs or bullae (collection of air or fluid) - Underlying lung disease - Recent surgery or invasive procedures 2. Obtain past medical history. Note existing lung disease - COPD - Cystic fibrosis - Lung cancer - Sarcoidosis - Tuberculosis - HIV AIDS with pneumonia 3. Risk Factors - Gender- Male - Age- 20 to 30 year old - Tall, thin - Smoking - Pregnancy - Marfan syndrome - Family history of pneumothorax 4. Genetics - Patients with Marfan syndrome, homocystinuria and Brd-Hogg-Dube syndrome are linked with spontaneous pneumothorax 5. Previous History of Pneumothorax - Smoker - Younger - Taller and thinner - History of COPD, AIDs and pulmonary fibrosis - May recur within the first 6 months to 3 years 6. Review past medical procedures - Transthoracic needle aspiration (main factor in iatrogenic pneumothorax) - CVP insertion - Tracheostomy - CPR - ARDS - NGT placement 7. Patient lifestyle and occupation - Drug use (inhaled) marijuana or cocaine - Flying, scuba or deep sea diving (can cause drastic air pressure changes) **Physical Assessment** 1. Symptoms - Sudden chest pain- sharp, severe and becomes worse with inspiration that radiates to the ipsilateral shoulder - Dyspnea becomes more severe with secondary pneumothorax 2. Monitor VS - ↑ RR and PR - ↓ BP & O2 saturation - Closely monitor changes for hemodynamic instability 3. Assess respiratory status - IPPA - Inspection: respiratory discomfort, airway patency, tracheal - Deviation - Palpitation: ↓ Tactile fremitus, asymmetrical expansion - Percussion: hyperresonance - Auscultation: ↓or absent breath sounds 4. Assess the cardiovascular status - ↑ HR - ↓BP - Jugular vein distention - Cyanosis - Cardiac arrest **Diagnostic Procedures** 1. Chest x-ray 2. Imaging scans 3. ABGs **Nursing Interventions** - Administer medications - Prophylactic antibiotics prior to chest tube insertion - Analgesics or nerve block - Prepare for decompression - Inserting a large bore catheter into the chest wall to draw out excess air - Assist in thoracostomy tube insertion - Placing a chest tube following needle decompression - Heimlich valves are one-way valves that allow air to escape without using suction - SSP typically requires suction - Watchful approach to small pneumothraces - For small asymptomatic, observation is advised with 02 therapy because it will likely resolve on its own - 02 therapy - 3 Ipm via cannula or higher to treat hypoxemia - Surgical intervention - Thoracoscopy - Electrocautery - Laser treatment - Resection of blebs or pleura - Open thoracotomy - VATS - Decrease pneumothorax recurrence - Pleurodesis (sclerotherapy)-creates scar tissue b/n layers of the pleura causing the sticking them together to prevent reaccumalation of fluid or air in the pleural space **Prevention** ► Stop smoking ► Avoid activities with drastic changes in air pressure ► Limit air travel ► Treat lung infection **Nursing Care Plans** **ACUTE PAIN** Related to: - Chest injury - Pneumothorax As evidenced by: - Distraction behavior - Expressive pain behavior - Guarding - Positioning to ease pain - Hesitancy to take deep breathing/shallow breathing Expected outcomes; - Patient report a reduction of pain when breathing - Patient will demonstrate an even RR without expressing pain Assessment: - A Comprehensive pain assessment - Monitor effectiveness of analgesics Interventions: - Use of chest splint when breathing or coughing - Assist the patient in position of comfort - Analgesics as prescribed - Provide diversional activities **IMPAIRED SPONTANEOUS VENTILATION** Related to: - Respiratory muscle fatigue - Limited lung expansion - Comorbid conditions - Hemodynamic instability As evidenced by: - Dyspnea - Decreasing SpO2 - Increased accessory muscle use - Restlessness - Fatigue Expected outcomes: - Patient will exhibit clear lung sounds and SpO2 within normal limits - Patient will demonstrate an absence of complications from pneumothorax Assessment: - Monitor ABG5 - Assess CT Scan results **INEFFECTIVE AIRWAY CLEARANCE** Related to: - Underlying lung disease (COPD, asthma, pneumonia) - Tracheal deviation - Ineffective cough As evidenced by: - Altered respiratory rate & rhythm - Abnormal breath sounds - Dyspnea - Orthopnea - Restlessness - Cyanosis Expected outcomes; - Patient will maintain clear, open airways as evidenced by normal breath sounds and RR and depth within normal minutes - Patient will demonstrate ABG results within acceptable limits Assessment: - Monitor and measure the rate and depth respirations, chest movement and the use of accessory muscles - Assess lung sounds Interventions: - Encourage coughing and breathing - Upright position - Administer analgesics - Monitor ABGs and SpO2 **INEFFECTIVE BREATHING PATTERN** Related to: - Pain - Asymmetrical lung expansion - Body position that inhibits the lung expansion As evidenced by: - Abdominal paradoxical respiratory pattern - Altered chest excursion - Altered tidal volume - Bradypnea - Decreased expiratory and inspiratory pressure - Accessory muscle use Expected outcomes; - Patient will maintain an 02 saturation of 94% or greater - Patient will demonstrate an effective - Breathing pattern as evidenced by an RR and depth within expected limits Assessment: - Assess the Ct drainage system - Assess the patient's respiratory function - Review imaging tests Interventions: - Assist with thoracentesis - Encourage ambulation - Consult with respiratory therapy - Maintain the closed-drainage system **PNEUMONIA** - One of the most common respiratory problems that can affect all stages of life - An inflammation of the lung parenchyma that is caused by many microorganisms (bacteria, mycobacteria, fungi or viruses) - PNEUMONITIS-describes the inflammatory process in the lung tissue that con predispose and place a patient at risk for microbial Invasion. **Classification** 1. **Community-Acquired Pneumonia (CAP)** - Occurs in the community setting or within the 48 hours after hospitalization/admission - Usual needing admission if infectious agents are any of Streptococcus pneumoniae (most common). H. influenza, Legionella and Pseudomonas Aeruginosa - 50% of specific causative agent are identified - In infants or children viruses are the causative agent 2. **Hospital- Acquired Pneumonia (Nosocomial Pneumonia)** - Is defined as the onset of symptoms more than 48 hours after admission in patients with no evidence of infection at the time of admission - Most lethal and leading cause of mortality is patients with pneumonia - Most common causative agent: Enterobacter species, Escherichia coli, influenza, klebsiella, proteus, serratia marcescens, S. aureus, and S. pneumonia - Usual presentation: pulmonary infiltrates on xray and more evidence of infection 3. **Pneumonia in the Immunocompromised Host** - Includes: pneumocystis pneumonia, fungal pneumonias and mycobacterium tuberculosis - Immunocompromised patients develop pneumonia from organisms of low virulence 4. **Aspiration Pneumonia** - Caused by the entry of endogenous or exogenous substances into the lower airway - Most common form: Bacteria Infection from aspiration of bacteria in the upper airways - Most common cause: - S. pneumonia, H. influenza and S. aureus **Pathophysiology** Arises from normal flora from an patient with altered resistance or from the aspiration of flora present in the oropharynx ↓ Inflammatory reaction in the alveoli ↓ Production of exudates that may interfere with O2 and CO2 diffusion ↓ WBCs enter the alveoli and fill up air filed spaces ↓ Decreased ventilation and causing obstruction of the alveoli or bronchi ↓ Mixing of oxygenated blood and poorly oxygenated blood ↓ Hypoxemia **Causes** - **CAP** - Streptococcus pneumoniae- leading cause - H. influenza- elderly - Mycoplasma pneumoniae - **HAP** - Staphylococcus aureus-Inhaled - Impaired host defenses - Comorbid conditions - Prolonged supine position - Prolonged hospitalization **Clinical Manifestations** - S/S varies depending on its type - Fever-rapidly rising - Pleuritic chest pain - Rapid and bounding pulse - Tachypnea - Sputum-purulent **Prevention** - Vaccination-pneumococcal vaccine (65-85% effective in healthy patients) - Surveillance-infection and microbiologic **Complications** - Shock and respiratory failure - Pleural effusion **Assessment and Diagnostic Findings** - History Taking-recent respiratory tract infection - Physical Examination-breath sounds - Chest x-ray-structural distribution - Abscesses/infiltrates, empyema (staphylococcus), - Scattered or localized infiltration (bacteria) - Diffuse /extensive nodular infiltrates (viral - Clear (mycoplasma) - ABGs/pulse oximetry - Gram stain/cultures - Helps identity causative organism - CBC-leukocytosis, ↑ ESR - Serologic studies- viral or legionella liters - Electrolytes - Bilirubin - Percutaneous aspiration/open biopsy of lung tissue **Medical Management** - Blood culture-identify - Macrolides-for drug resistant - Hydration - Antipyretics - Bed rest - 02 administration - Pulse oximetry - Aggressive respiratory measures-high concentration oxygen, ET intubation, mechanical ventilation **Nursing Management** - Nursing Assessment - Assess respiratory symptoms - Assess clinical manifestations - Physical assessment - Assessment in elderly patients **Diagnosis** 1. **[Ineffective airway clearance]** related to copious tracheobronchial secretions 2. **[Activity intolerance]** related to impaired respiratory function 3. **[Risk for deficient fluid volume]** related to fever and a rapid respiratory rate **Nursing Care Planning and Goals** - Improve airway patency - Rest to conserve energy - Maintenance of adequate nutrition - Understanding of treatment process and how to prevent - Absence of complications **Nursing Priorities** - Maintain/improve respiratory function - Prevent complications - Support recuperative process - Provide information about disease process, prognosis and treatment **Nursing Interventions** [Improve Airway Patency] - Remove secretions - Hydration - Humidification - Coughing exercises - Chest physiotherapy [To promote rest and conserve energy] - Avoid overexertion - Semi fowlers position [To promote fluid intake] - Fluid intake [To maintain nutrition] - Fluids with electrolytes - Nutrition enriched beverages [To promote patient's knowledge] - Educate patient and family about disease PULMONARY HYPERTENSION - a severe, rare lung disease characterized by high blood pressure in the pulmonary arteries, which deliver blood from the heart to the Lungs - The increased pressure in the blood vessels of the lungs means that your heart has to work harder to pump blood into the lungs. - A serious health condition that results when the arteries carrying blood from the right side of the heart to the lungs are constricted, disrupting blood flow. - Blood must travel through the lungs for air exchange in order to pick up oxygen that it delivers to all the organs, muscles, and tissue in the body. - When the arteries between the heart and lungs become narrowed and flow is constricted, the heart has to work extra hard to pump Blood to the lungs. - Over time, the heart con grow weak and proper circulation can diminish throughout the body **Classification** - **Class I:** Although you've been diagnosed with pulmonary hypertension, you have no symptoms with normal activity. - **Class II.** You don't have symptoms at rest, but you experience symptoms such as fatigue, shortness of breath or chest pain with normal activity. - **Class III.** You're comfortable al rest, but have symptoms when you're physically active. - **Class IV.** You have symptoms with physical activity and while at rest. **TYPES** - Group 1 PAH (Pulmonary arterial hypertension) - Group 2 PAH (Left heart disease) - Group 3 PAH lung disease) - Group 4 PAH (thromboembolic disease) - Group 5 PAH (multifactorial) **GROUP I** - Pulmonary hypertension is associated with the narrowing of the small blood vessels in the lungs. - It also called Pulmonary Arterial Hypertension (PAH) and includes cases where the underlying cause of the narrowing is not known - idiopathic pulmonary hypertension). - There are multiple other subgroups in group 1, including: - Familial, or heritable pulmonary hypertension (FPAH) or (HPH) - PAH caused by certain drugs or toxins including some recreational drugs and diet medications - PAH associated with other conditions such as connective tissue diseases like: - Scleroderma or lupus (connective tissue diseases certain autoimmune diseases) - Congenital heart problems - High blood pressure in the fiber - HIV - Certain infections like schistosomiasis (a type of parasitic infection) - Sickle cell anemia - Liver disease **Group 2: pulmonary hypertension due to left heart disease** - Group 2 refers to pulmonary hypertension caused by left heart disease. - Long-term problems with the left side of the heart can lead to changes in the pulmonary arteries and cause pulmonary hypertension. This may include: - Left ventricular systolic dysfunction, when the heart cannot pump blood effectively - Left ventricular diastolic dysfunction, when the heart cannot properly relax to allow enough blood to flow in - Valvular disease, when the valves of the left side of the heart are allowing blood to leak - Congenital heart defects (heart defects from birth), which can lead to problems with blood flowing in or out of the heart **Group 3: pulmonary hypertension due to lung disease and/or chronic hypoxia** - Group 3 Includes: pulmonary hypertension resulting from lung diseases or shortage of oxygen in in the body (hypoxia). - The common diseases associated with group 3 pulmonary hypertension are: - Chronic obstructive pulmonary disease (COPD) - Interstitial lung disease (such as pulmonary fibrosis), which can cause scarring on lung tissue - Sleep-disordered breathing, a group of diseases that affect breathing during sleep Like obstructive sleep apnea (OSA) - Chronic high-altitude exposure - Lung developmental abnormalities - Alveolar hypoventilation disorders **Group 4: pulmonary hypertension due to blood clots in the lungs** - Refers to pulmonary hypertension caused by blood clots obstructing the pulmonary arteries. - This also can be referred to as chronic thromboembolic pulmonary hypertension (CTEPH). - Clots are the body's response to bleeding and injuries, but can harm the heart and lungs when they occur without an apparent cause. Pulmonary emboli are blood clots that travel to the lungs, and pulmonary thrombosis are clots that are formed in the lungs, which can block the pulmonary arteries. **Group 5: pulmonary hypertension due to blood and other disorders** - the last category and includes other less-common causes that do not fit into any of the other four groups. These are widely split into four categories: - Blood disorders, such as some types of anemia (polycythemia vera and thrombocythemia) - Systemic disorders, such as sarcoidosis (a condition that results in inflammation of different organs like the lungs and lymph nodes) and histiocytosis (a rare disorder that causes scarring) - Metabolic disorders, such as glycogen storage diseases and thyroid disorders - Other disorders, such as chronic kidney failure or tumors obstructing pulmonary arteries  **PREDISPOSING FACTORS** - **Family history & Genetics** - Certain genetic disorders, such as Down syndrome, congenital heart disease, and Gaucher disease, can Increase your risk of developing pulmonary hypertension - A family history of blood clots or pulmonary embolism also increases your risk of developing Pulmonary hypertension. - Age - Risk goes up as you get older, although it may occur at any age. The condition is typically diagnosed between ages 30 and 60 - Sex - More common in women that men. PH with certain types of heart failure is also more common in women - Lifestyle habits - Unhealthy lifestyle habits can increase the risk of PH - Illegal drugs - Such as cocaine and amphetamines - Smoking - Overweight - Appetite-suppressant medications **CLINICAL MANIFESTATIONS** Early symptoms include: - SOB during routine activity and eventually while at rest - Fatigue - Chest pain - Rapid heartbeat - Pain in upper right side if abdomen - Decreased appetite Later symptoms include: - Feeling ligh0headed, especially during physical activity - Dizziness or fainting (syncope) - Swelling in the ankles or legs - Bluish color to lips or skin (cyanosis) **LABORATORY AND DIAGNOSTIC TESTS** - Echocardiogram - Chest X-ray - Electrocardiogram - Right heart catheterization - Blood tests - Cardiac MRI **COMPLICATIONS:** - Right-sided heart enlargement and heart failure (cor pulmonale). In cor pulmonale, your heart's Right ventricle becomes enlarged and has to pump harder than usual to move blood through narrowed or blocked pulmonary arteries. - At first, the heart tries to compensate by thickening its walls and expanding the chamber of the right ventricle to increase the amount of blood it can hold. But this thickening and 1 enlarging works only temporarily, and eventually the right ventricle fails from the extra strain - Blood clots. Clots help stop bleeding after you've been injured. But sometimes clots form where They're not needed. A number of small clots or just a few large ones dislodge from these veins and travel to the lungs, leading to a form of pulmonary hypertension that can generally be reversible with time and treatment. - Having pulmonary hypertension makes it more likely you'll develop clots in the small arteries in your lungs, which is dangerous if you already have narrowed or blocked blood vessels. - Arrhythmia. Irregular heartbeats (arrhythmias) from the upper or lower chambers of the heart are complications of pulmonary hypertension. These can lead to palpitations; dizziness or fainting and can be fatal. - Bleeding. Pulmonary hypertension can lead to bleeding into the lungs and coughing up blood (hemoptysis, this is another potentially fatal complication. **NURSING MANAGEMENT** - Although medical treatment can't cure pulmonary hypertension, it can lessen symptoms. Lifestyle changes also can help improve your condition. Consider these tips: - Get plenty of rest. Resting can reduce the fatigue that might come from having pulmonary hypertension. - Stay as active as possible. Even the mildest forms of activity might be too exhausting for some people who have pulmonary hypertension. For others, moderate exercise such as walking might be beneficial -- especially when done with oxygen. Discuss the level of activity with your doctor about specific exercise restrictions. Avoid straining or lifting heavy weights. Rest when you need to. - Don't smoke. If you smoke, the most important thing you can do for your heart and lungs is to stop. If you can't stop smoking by yourself, ask your, doctor to prescribe a treatment plan to help you quit. Also, avoid secondhand smoke if possible. - Avoid pregnancy and birth control pills. If you're a woman of childbearing age, avoid pregnancy. Pregnancy can be life-threatening for both you and your baby. Also avoid using birth control pills, which san increase your risk of blood clots. Talk to your doctor about alternative forms-of birth control. If you do become pregnant, it's important to consult with your doctor as pulmonary hypertension can cause serious complications to both you and the fetus. - Avoid traveling to or living at high altitudes. High altitudes can worsen the symptoms of pulmonary hypertension. If you live at an altitude of 8,000 feet (2,438 meters) or higher, your doctor might recommend that you move to a lower altitude. Be cautious about air travel or high-altitude locales. You may need to travel with extra oxygen. - Get vaccines. Your doctor may recommend getting an influenza and pneumonia vaccine, as these conditions can cause serious issues for people with pulmonary hypertension. - Get support. If you're feeling stressed or worried due to your condition, get support from family or friends. Or, consider joining a support group with others who have pulmonary hypertension - Heart-healthy eating, which includes eating less salt, to lower blood pressure or cholesterol if high levels of these contributed to the cause of your pulmonary hypertension. Eating less salt will help control your body fluids and may improve heart function. Aim to eat a healthy diet of whole grains, a variety of fruits and vegetables, lean, meats and low-fat dairy products. - Avoid saturated fat, trans fat and cholesterol. Aim to maintain a heathy weight. - Physical rehabilitation to improve your ability to exercise and also boost your quality of life - Ask your doctor about medications. Take all your medications as prescribed. Ask your doctor about any other medications before taking them, as some can interfere with your medication or worsen your condition. - Watch your weight. A daily record of your weight can help you be aware of rapid weight gain, which may be a sign that your pulmonary hypertension is worsening. - Anticoagulation or blood thinners to prevent blood clots in people whose pulmonary hypertension is caused by chronic blood clots in the lungs. These thinners also can help some people who have pulmonary arterial hypertension, heart failure, or other risk factors for blood clots. - Digitalis, or digoxin to control the rate blood is pumped throughout the body. **SURGICAL MANAGEMENT** - Atrial septostomy. If medications don't control your pulmonary hypertension, this open-heart surgery might be an option. In an atrial septostomy, a surgeon will create an opening between the upper left and right chambers of your heart (aria) to relieve the pressure on the right side of your heart. - Atrial septostomy can have serious complications, including heart rhythm abnormalities (arrhythmias). - Transplantation. In some cases, a lung or heart-lung transplant might be an option, especially for younger people who have idiopathic pulmonary arterial hypertension. - Major risks of any type of transplantation include rejection of the transplanted organ and serious infection, and you must take immunosuppressant drugs for life to help reduce the chance of rejection - Oxygen therapy if oxygen levels in the blood are too low. - Balloon atrial septostomy to decrease pressure in the right heart chambers and improve the output of the left heart and oxygenation of the blood. In this procedure, a small hole is made in the wall between the right and left atria to allow blood to flow from the right to the left atrium. - Balloon pulmonary angioplasty to lower the blood pressure in your pulmonary artery and improve heart function in people who cannot have a pulmonary endarterectomy. - Pulmonary endarterectomy surgery to remove blood clots from the inside of the blood vessels of the lungs. - Blood pressure medicines such as angiotensin- converting enzymes inhibitors, beta blockers, or calcium channel blockers when left heart disease is the cause - Blood transfusions or hydroxyurea to treat sickle cell disease - Heart valve repair **MS -- MIDTERM** **CORONARY ARTERY DISEASE** **DEFINITION** Is the narrowing or blockage of the coronary arteries, usually caused by artherosclerosis: **Artherosclerosis** (the hardening or clogging of the arteries) is the build-up of cholesterol and fatty deposits plaques) on the inner walls of the arteries. These plaques can restrict the blood flow to the heart muscle by physically clogging the artery or by causing abnormal artery tone function. This can also lead to chest pain or angina, or a heart attack. Over time, CAD can also weaken the heart muscle and contribute. To heart failure and arrhythmias. Heart failure means the heart can't pump blood well to the rest of the body, Arrhythmias are changes in the normal rhythm of the heart. CVDs are the number 1 cause of death globally: more people die annually from CVDs than from any other cause. An estimated 17.9 million people died from CVDs in 2016, representing 31% of all global deaths. Of these deaths 85% are due to heart attack and stroke. Over three quarters of CVD deaths take place in low- and middle-income countries. Out of 17 million premature deaths (under 70 years old) due to non-communicable diseases in 2015, 82% are in low- and middle-income countries, and 37% are caused by CVDs. **In the PHILIPPINES:** Reacted Coronary Heart Disease (CHD) deaths reached 122,950 or 19.86% of total deaths. The age adjusted rate is 11.82 per 100,000 of population ranks Philippines 116^th^ in the world. **RISK FACTORS** - **Non-modifiable** - Gender - Age - Family History - Race - **Modifiable** - Cigarette smoking - High blood cholesterol - High triglycerides - Hypertension - Uncontrolled Diabetes - Sedentary Lifestyle Obesity - Uncontrolled Stress and anger - Unhealthy Diet **SYMPTOMS** - Chest part (Angina Pectoris) it may also be felt in the left shoulder, dims, neck, back or jaw. - Chest discomfort, heaviness, tightness, pressure, aching burning, numbness, fullness, or squeezing - Shortness of breath - Irregular heart beats or rapid heart beats - Dizziness - Sweating - Fatigue - Nausea - Palpitations **DIAGNOSTIC TESTS** 1. **ECG or EKG** Measures the electrical activity, rate and regularity of your heartbeat 2. **Echocardiogram** Uses Ultrasound to assess cardiac structure and mobility 3. **Exercise stress test** Measures, heart rate while walking on a treadmill, Helps to determine how well the heat Junction while it has to pump more blood 4. **Heart CT Scan** To the calcium deposits in arteries that con narrow arteries. 5. **Cardiac Catheterization** To assess 02 level blood flow, CO. heart structures and coronary artery visualization 6. **Angiogram** Involves introduction of contrast medium into the vascular system to outline the heart and blood vessel **ECG** **EXERCISE STRESS TEST** **HEART CT SCAN** **CARDIAC CATHETERIZATION AND ANGIOGRAM** **LABORATORY TESTS** - **Hemoglobin -** decreased hgb increases the risk of oxygen deficit in the tissues when cardiovascular disease is present. - **Total cholesterol -** high level can increased risk of heart disease. - **LDL**- too much (DL in the blood causes accumulation of fatty deposits in arteries: which reduces Hood low. - **HDL**- the good cholesterol. - **Triglycerides -** high levels of these con increase the risk of heart disease. - **Lipoprotein -** is a DL. High level of this increase the risk of heart attack, stroke, blood clots, fatty build-up. - **Creatinine-Kinase CK-MB-** is, o cardiac muscle cells that therefore increase then there is damage these cells **WHAT ARE THE DIFFERENT CORONARY ARTERIES?** The 2 main coronary arteries are the left main and right coronary arteries. - **Left main coronary artery (LMCA).** The left main coronary artery supplies. Blood to the left side of the heart muscle (the left ventricle and left atrium). The left main coronary divides into branches: - The left anterior descending artery branches off the left coronary A artery and supplies blood to the front of the left side of the heart. - The circumflex artery branches off the left coronary artery and encircles the heart muscle, This artery supplies blood, to the outer side and back of the heart. - **Right coronary artery (RCA).** - The right coronary artery supplies blood to the right ventricle, the right atrium, and the SA (sinoatrial) and AV (atrioventricular) nodes, which regulate the heart rhythm. - The right coronary artery. Divides into smaller branches, including right posterior descending artery and the acute marginal-artery. The - Together with the left anterior descending artery, the right coronary artery helps supply blood to the middle or septum of the heart. **PATHOPHYSIOLOGY** **MEDICAL MANAGEMENT** - **Pharmacologic Therapy** - **Cholesterol-modifying medications** - by decreasing the amount of cholesterol in the blood, especially, IDL, these drugs decrease the primary material that deposits on the coronary arteries. - **Platelet Aggregation Inhibitors** - Class of drug that decreases platelet aggregation and inhibit thrombus formation - **Beta-adrenergic Blockers -** it decreases blood pressure and heart rate. If reduces the risk for future heart attacks. - **Calcium-channel Blockers -** it inhibits the transport of calcium into myocardial and vascular smooth muscle cells, resulting in inhibition of excitation-contraction coupling and subsequent contraction,, It has systemic vasodilation effect resulting in decreased BR, Coronary vasodilation resulting in decreased frequency and severity of attacks of angina. - **Nitroglycerin** - Increases blood flaw by dilating coronary arteries and improving collateral flow to ischemic regions. Decreases blood pressure) - **ACE inhibitors and ARBs-** these similar drugs- decrease blood pressure and help in preventing the progression of coronary artery disease - **Analgesic -** [Morphine sulfate], may be used in acute onset because of its several beneficial effects, example: causes peripheral vasodilation and reduces myocardial workload has sedative effect to produce relaxation - **Angioplasty and stent replacement (Percutaneous coronary revascularization)-** mechanical dilation of the coronary vessel wall by compressing the atheromatous plaque. - A specially designed balloon-tipped catheter is inserted under fluoroscopic guidance and advanced to the site of the coronary obstruction. - Stent helps prevent the artery from closing up again, A drug- eluting stent has a medicine embedded in it that helps prevent The artery from closing in the long term.   **NURSING INTERVENTIONS IN DRUG THERAPY** 1. **Nitroglycerin therapy** - Assume sitting or reclining position when taking the drug - Caution patient to change position slowly. - If to be taken sublingually, offer sips of water before administration because dryness of mouth may Inhibit drug absorption. - Instruct client to avoid drinking alcohol, to avoid hypotension, weakness and faintness - Inform patient that headache, flushed face, dizziness, faintness, tachycardia are common side effects during fist few doses. - Transderm - nitropatch applied OD In the morning. - Evaluate effectiveness: relief of chest pain 2. **Beta-adrenergic Blockers** - Assess pulse rate before administration of the drug, withhold if bradycardia is present - Administer after meals to prevent Gl upset. - Do not administer propranolol to asthma patients because it causes bronchoconstriction. - Do not give propranolol to patients with DM because it causes hypoglycemia. - Give with extreme caution to patients with heart failure. - Observe for side effects: nausea, vomiting, mental depression, mild diarrhea, fatigue and impotence. - Antidote for **beta blocker** poisoning is **Glucagon** **Calcium- channel Blockers** - Assess HR and BP - Monitor hepatic and renal function - Administer 1 hour before or 2 hours after meals. Food delays absorption and decreases plasma levels of the drug. - The antidote for **calcium-channel blocker** poisoning is **Glucagon**. **NURSING INTERVENTIONS** - Instruct patient and watchers to notify nurse immediately when chest pain occurs. - Identify precipitating event, if any: frequency, duration, intensity, and location of pain - Assess and document patient's response to medication. - Observe for associated symptoms: dyspnea, nausea and vomiting, dizziness; palpitations, desire to urinate. - Evaluate reports of pain in jaw, neck, shoulder, arm or hand usually in left side. - Obtain results of cardiac markers- creatinine, CK-MB, total Cholesterol, LDL, HDL, Lipoprotein, hemoglobin and triglycerides as ordered. - Place patient of complete rest during anginal episodes. - Position patient to moderate high back rest to improve chest expansion and oxygenation - Monitor patient's vital signs with pain and 02 saturation. Note the heart's rhythm - Monitor and obtain ECG results to note abnormal tracings - Provide oxygen as needed or as ordered. - Administer vasodilators, beta-blockers, calcium-channel blockers and platelet aggregation inhibitors as ordered - Monitor patient's vital signs every 15 minutes during initial-anginal attack. - Maintain quiet, comfortable environment. Restrict visitors as necessary. - Advise patient to minimize emotional outbursts, worry and tension because anginal points often precipitated by emotional stress. - Provide assistance with the activities of patient to avoid over exertion. - Stay with patient who is experiencing pain or appears anxious. - Provide light meals or small frequent feedings. Have patient rest for 1hr after meals**.** - Daily management of hypertension. Take medicines at regular basis. - Stop smoking. Smoking reduces available oxygen to the heart and can precipitate angina, it also increases heart rate and blood pressure. - Follow a heart healthy diet- Low sodium, low fat, low cholesterol and high fiber. Diet. Avoid saturated fats. - If obese or overweight, lose weight. - Reduce stress Because stress stimulates increase of norepinephrine that causes vasoconstriction and tachycardia. Stress also causes anginal pain - Allow adequate time for rest and relaxation. **HYPERTENSIVE CRISIS** **DEFINITION** - An elevated blood pressure associated with evidence of acute end- organ damage. - With acute damage to vital organs, such as the kidney, heart, and brain, there is a significant risk of morbidity in hours without therapeutic intervention. - The absolute level of blood pressure and the time course of blood pressure elevation determine the development of hypertensive crisis. In general, with hypertensive crisis, the diastolic blood pressure is greater than 130 mmHg - In the Philippines 37% of Filipinos are - Severe hypertension (diastolic BP \> 120 mmHg) can cause irreversible damage to the brain, heart and kidneys that can lead to possible death - A hypertensive crisis can occur in patients with either - **ESSENTIAL HYPERTENSION or PRIMARY HYPERTENSION** - **SECONDARY HYPERTENSION** (due to renal or endocrine disease) **ETIOLOGY** - Noncompliance with medications - Exacerbation of chronic hypertension - Renovascular hypertension - Drugs(cocaine, amphetamines) - Rebound hypertension (from abrupt withdrawal of some hypertensive drugs such as clonidine or beta adrenergic blockers - Necrotizing vasculitis (inflammation of blood vessels) - Head injury - Post op state - Preeclampsia and eclampsia **CLASSIFICATION** - HYPERTENSIVE CRISIS is classified by the degree of organ damage and the rapidity with which the **BP must be lowered** - ***Hypertensive emergency***, which [develops over hours to days], situation in which a patient's BP is severely elevated (\> 180/120mm Hg) with [evidence of acute target organ damage, especially damage] to the CNS - ***Hypertensive urgency***, which develops [over days to weeks,] is a situation in which a patient's [BP is severely elevated] but there is [no clinical evidence of target organ damage.] **PATHOPHYSIOLOGY** - **UNKNOWN** - Sudden increase - Transition from simple hypertension or normotension to hypertensive crisis. - The product of cardiac output and peripheral vascular resistance determines blood pressure. - The initial blood pressure increase is likely secondary to an increase in vascular resistance. - The end result of these changes is a significant increase in peripheral vascular resistance with ischemia of heart, brain, and kidneys **CLINICAL FEATURES** - Headache, usually worse in morning. Location is occipital or anterior with steady quality. - Visual disturbances(diplopia, hemianopia, blindness) - Altered level of consciousness - Ischemic chest pain - Renal symptoms (nocturia, polyuria, hematuria), decreased urine output - Back pain - Gastrointestinal disturbances (nausea, vomiting) **MEDICAL MANAGEMENT** **TARGET:** rapid lowering of BP, reduce the 58P by no more than 25% within the first hour of treatment and if stable then 160/100 mm Hg within 2-6 hours and back to normal in 24-48 hours - Vasoactive intravenous drips (labetalol, esmolol, nicardipine, nitroglycerine) - rapidly acting and titratable - Don't give clonidine or catapres **REPORT:** altered LOC, unresponsiveness and increased BP despite treatment **NURSING MANAGEMENT** a. Monitor blood pressure, vital signs b. Antihypertensives as ordered c. Large bore IV needle d. 02 saturation levels e. Monitor urine output f. Limit fluid intake if with CHF g. Monitor ECGs, chest x-ray h. Auscultate heart and lung sounds i. Monitor renal and electrolyte levels j. Encourage rest periods k. Educate patient of disease and how to manage stress l. Diet low salt, exercise and healthy foods m. COMPLIANCE to medications **CARDIOMEGALY** **DEFINITION** - Cardiomegaly, also known as an enlarged heart, is a medical condition in which the heart becomes larger than its normal size. It is often referred to simply as "having an enlarged heart." - The cardiac enlargement process can be generalized to all chambers or involve only the left or right heart chambers, or even a single chamber, depending on the location and type of underlying lesion(s). **ETIOLOGY** - Congenital - Acquired **ACQUIRED ETIOLOGY** The most common causes of cardiomegaly are: - **Ischemic cardiac disease** - The ischemic cardiac disease occurs when narrowed arteries, caused by fatty deposits that build up in arteries, prevent blood from getting to heart - **High blood pressure** - **Cardiomyopathy** - Cardiomyopathy may be a progressive cardiac disease with several types. Diseases that damage thin cardiac muscle can cause it to enlarge The more damage that happens, the weaker and less able to pump the heat becomes.  - **Heart valve disease** - Infections, connective tissue diseases, and a few medications can damage the valves that keep blood flowing within the right direction through heart. When blood flows backwards, the heart needs to work harder to push it out. - **Heart attack** - During heart failure, blood flow to a part of the heart is blocked completely. The shortage of oxygen-rich blood damages the heart muscle. - **Thyroid disease** - The thyroid gland produces hormones that regulate the body's metabolism. Both overproduction (hyperthyroidism) and underproduction (hypothyroidism) of those hormones can affect the pulse rate, blood pressure, and size of the heart. - **Irregular cardiac rhythm (arrhythmia)** - If you have an irregular heartbeat, rather than beating in its familiar lub-dub pattern, the heart flutters or beats too slowly or quickly. An irregular cardiac rhythm can cause blood to back up within the heart and eventually damage the muscle **CONGENITAL ETIOLOGY** Congenital conditions - Congenital cardiomegaly may be a heart disorder born with. Congenital heart defects that cause this symptom to include - **Atrial septal defect (ASD)** - a hole within the wall separating the two upper chambers of the heart - **Ventricular septal defect (VSD)** - a hole within the wall separating the two lower chambers of the heart  - **Coarctation of the aorta** - a narrowing of the aorta, the main artery that carries blood from the heart to the whole of the body - **Patent ductus botalli** - a hole within the aorta  - **Ebstein's anomaly** - the issue with the valve that separates the two right chambers of the heart (atrium and ventricle) - **Tetralogy of Fallot (TOF)** - a mixture of birth defects that disrupt the regular flow of blood through the heart  **OTHER POSSIBLE CAUSES OF CARDIOMEGALY INCLUDE:** - Lung disease -- including Chronic Obstructive Pulmonary Disease (COPD) - Myocarditis - Pulmonary hypertension - Anemia - Connective tissue disease, like Scleroderma - Drug & alcohol use - Pulmonary hypertension - Myocarditis **PATHOPHYSIOLOGY** Development of cardiac remodeling and hypertrophy with genetic and non-genetic components. ↓ pathophysiological changes resulting in cardiomegaly include dilated hypertrophy, fibrosis, and contractile malfunction ↓ Can cause cardiomyopathy or dilated cardiomyopathy. ↓ Mechanical stretching, circulating neurohormones and oxidative stress are significant changes in structural proteins and proteins that regulate excitation-contraction ↓ cardiomyopathy mutations result in a molecular phenotype of hyperdynamic contractility, poor relaxation, and increased energy consumption. **RISK FACTORS** a. **High blood pressure:** Having a blood pressure measurement above 140/90 millimeters of mercury. b. **A family history of enlarged hearts or cardiomyopathy:** If an instantaneous loved one, like a parent or sibling, has had cardiomegaly, you'll be more susceptible c. **Congenital cardiac disease:** If you're born with a condition that affects the structure of your heart, you'll be at increased risk. d. **Heart valve disease:** the heart has four valves aortic, mitral, pulmonary and tricuspid that open and shut to direct blood flow through your heart. Conditions that damage the valves may cause the heart enlargement. **DIAGNOSIS** - A **chest X-ray** could also be the primary test your doctor does because it can show whether your heart is enlarged. - **Echocardiogram (ECG or EKG)** uses sound waves to look for problems along with your heart's chambers. - **Electrocardiogram** monitors the electrical activity in your heart. It can diagnose irregular cardiac rhythm and ischemia. - **Blood tests** check for substances in your blood produced by conditions that cause cardiomegaly like thyroid disease. - A **cardiovascular test involves walking on a treadmill or pedalling** a stationary bike while your cardiac rhythm and breathing are monitored. It can show how hard your heart is functioning during exercise. - **Computerized tomography (CT) scans** use X-rays to provide detailed images of your heart and other structures in your chest. It can help diagnose valve disease or inflammation. - **Magnetic resonance imaging (MRI)** uses strong magnets and radio waves to provide pictures of your heart. - **Chest radiography** **In pregnancy** - During pregnancy, doctors can use a test called a **fetal echocardiogram** to diagnose heart defects within the unborn baby. This test uses sound waves to form pictures of the baby's heart. - Your doctor might recommend a fetal echocardiogram if you've got a family history of heart enlargement or heart defects, or if your baby has a genetic disease like Down syndrome. **TREATMENT/MANAGEMENT** - Treatment of mild cardiomegaly centers upon the treatment of the underlying condition. In moderate to severe cardiomegaly related to congestive heart failure.. standard HF treatment guidelines also apply - Patients at risk of cardiomyopathy have the benefit of risk factor modification like smoking cessation, limiting alcohol intake, weight loss, exercise, and consuming a healthy diet. Recommendations include treating any underlying risk factors like hypertension, dyslipidemia, and diabetes. - Other underlying conditions, including obstructive sleep disorder, arrhythmias, anemia, and thyroid disorders also require treatment. - Patients with early-onset hypertrophic cardiomyopathy who are asymptomatic are managed with risk factor modification and also the addition of ACE inhibitor or ARB (if intolerant to ACE) and ẞ-blocker if there's a history of Ml or reduced ejection fraction (EF) - Diuretics and salt restriction - Ace inhibitor or arb (if intolerant to ace) and beta-adrenergic blocker if they have reduced EF - A hydralazine/nitrate combination when added to ace inhibitor, beta-adrenergic blocker, and diuretics improve outcomes - An ICD (implantable cardioverter-defibrillator) is placed in patients with EF 35% - CRT (cardiac resynchronization) is performed with or without ICD in patients with EF 35% or less and moderate to severe symptoms with evidence of left bundle branch block - Patients with refractory congestive heart failure should receive optimal medical management. Also, eligible patients are often considered for cardiac transplantation and bridge therapy like ventricle assist device **PREVENTION** - Eating a heart healthy diet high in fruits and vegetables, lean poultry, fish, low-fat dairy, and whole grains - Limiting salt, alongside saturated and trans fats - Avoiding tobacco and alcohol - Doing aerobic and strength-training exercises on most days of the week - Checking your blood pressure and cholesterol level regularly, and working along with your doctor to lower them if they're high **COMPLICATIONS** A. **Heart failure** - An enlarged heart ventricle, one among the most serious kinds of cardiomegaly, increases the chance of heart failure. In heart failure, your cardiac muscle weakens, and also the ventricles stretch (dilate) to the point that the heart can't pump blood efficiently throughout your body. B. **Blood clots** - Having cardiomegaly may cause you to more at risk of forming blood clots within the lining of your heart. If clots enter your bloodstream, they will block blood flow to vital organs, even causing an attack or stroke. Clots that develop on the right side of your heart may travel to your lungs, a dangerous condition called a pulmonary embolism (PE) C. **Heart Murmur** - For people who's heart is enlarged, 2 of the heart's 4 valves (mitral-tricuspid valves) might not close properly because they become dilated, resulting in back flow of blood. This flow creates sound called HEART MURMURS. Although not necessarily harmful, but this could be monitored by your doctor. D. **Cardiac arrest and sudden death** - Sometimes cardiomegaly can result in disruptions in your heart's beating rhythm. Heart rhythms that are too slow to move blood or too fast to permit the heart to beat properly may result in fainting or, in some cases, cardiopulmonary arrest or sudden death **HEART FAILURE** - **Heart failure is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood to meet the metabolic demands of the body** - **This means less oxygen is reaching the organs and muscles, which can make feel tired and short of breath.** - **CONGESTIVE HEART FAILURE -- refers to the state in which abnormal circulatory congestion exists a result of heart failure. It is the inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients. The heart fails because of changes in the systolic and diastolic function of the left ventricle.** - **The heart fails when because of intrinsic disease or structural, it cannot handle a normal blood volume or, in the absence of disease, cannot tolerate a sudden expansion in blood volume. This is caused by various cardiovascular conditions like chronic conditions, coronary artery disease and valvular disease.** - **There is heart disease where there are problems, which may or may not cause pulmonary or systemic congestion.** - **Contraction of the heart (systolic dysfunction)** - **Filling of the heart (diastolic dysfunction)** - **This progressive, life-long condition can be managed with lifestyle changes and medications to prevent decompensated heart failure.** **ETIOLOGY** - Systemic hypertension in 75% of cases. - Structural heart changes, such as valvular dysfunction, cardiomyopathy, inflammatory heart diseases - Arrhythmias - Coronary Artery disease - Increase in Pulmonary pressure results fluid in alveoli - **(PULMONARY EDEMA) -** This is not disease in itself but is a syndrome characterized by volume overload, inadequate tissue perfusion and poor exercise tolerance **PRECIPITATING FACTORS** - **Congenital heart defects** - **Severe lung disease** - **Diabetes** - **Severe anemia** - **Overactive thyroid gland (hyperthyroidism)- cause of overactive hormones , can cause tachycardia, restlessness body** - **Hypervolemia** **CLASSIFICATION OF THE HEART FAILURE** **ACCORDING TO THE COURSE OF DISEASE:** - **Acute HF** - **Chronic HF** **ACCORDING TO THE SEVERITY:** - **Mild HF or complete compensation** - **Moderate HF or incomplete compensation** - **Severe HF or decompensation** **ACCORDING TO THE LOCATION OF HEART FAILURE** - **Left- side heat failure** - **Right- side heart failure** - **Biventricular failure (whole heart failure)** **ACCORDING TO THE FUNCTION IMPAIRED** - **Systolic failure** - **Diastolic failure** **ACCORDING TO THE CARDIAC OUTPUT (CO)** - **Low-output HF** - **High-output HF** **ACCORDING TO THE AMERICAN HEART ASSOCIATION** **CLASSIFICATION:** - **Stage A** - **Patients at high risk for developing left ventricular dysfunction but without structural heart disease or symptoms of heart failure** - **Stage B** - **Patients with left ventricular dysfunction or structural heart disease that has not developed symptoms of heart failure** - **Stage C** - **Patients with left ventricular dysfunction or structural heart disease with current or prior symptoms of heart failure** - **Stage D** - **Patients with refractory end stage heart failure requiring specialized intervention** **PATHOPHYSIOLOGY** In order to maintain normal cardiac output, several compensatory mechanisms play a role to maintain normal tissue perfusion including Compensatory enlargement in the form of cardiac hypertrophy, cardiac dilatation, or both. **Compensatory Mechanisms:** 1. **Sympathetic nervous system stimulation** - Baroreceptors - Nerve cells in carotid artery & aortic arch - Maintain BP during normal activities - React to increases & decreases in BP - Decreased BP -- activates SNS; Release of catecholamine's, vasoconstriction of arterioles; increases HR & heart contractility 2. **Renin-angiotensin system activation** 3. **Ventricular hypertrophy** - Hypertrophy is an increase in muscle mass and cardiac wall thickness in response to overwork and strain - This will increase cardiac output initially 4. **Ventricular dilation** - Dilation is an enlargement of the chambers of the heart - It occurs when pressure in the heart chambers is elevated - More stretching resulting increased cardiac output initially **COUNTER REGULATORY MECHANISMS** - Body will try to maintain a balance in compensatory mechanism - Heart muscles produce Natriuretic peptides - **Atrial Natriuretic peptide(ANP)** - **B-type natriuretic peptide(BNP)** - These are **endothelin and aldosterone antagonists,** which will cause **diuresis** and **vasodilation**, **prevent hypertrophy** - Nitric oxide release vascular endothelium causes vasodilation **CLINICAL MANIFESTATIONS** It can affect the heart's one side or both sides. Though it usually affects the left side first, the signs and symptoms are based on which ventricle is affected. - Dyspnea - Exertional dyspnea - Orthopnea - Paroxysmal nocturnal dyspnea - Fatigue - Tachycardia - Edema - Behavioral changes - Skin changes (poor skin turgor) I. **LEFT-SIDED HEART FAILURE** **(DOCHAP)** - **Dyspnea** (may be precipitated by minimal to moderate activity) - **Orthopnea** (dyspnea that develops in the recumbent position that is relieved by placing a pillow under the head) - **Cough** (initially dry and non-productive. In severe pulmonary congestion, the sputum may be pinkish and frothy) - **Hemoptysis** (pink or blood tinged) - **Adventitious Breath Sounds** (Pulmonary crackles which initially bibasilar but may be heard across all lung fields if worsening) - **Pulmonary congestion** (sustained pressure in the pulmonary veins forces some fluids from the blood to the alveoli, which transfer O2 to the blood stream - **Pulmonary edemam(crackles)** - **Pleural effusion** - **S3 & S4** II. **RIGHT SIDED HEART FAILURE (AWHEAD)** - **Anorexia and Nausea** (from venous engorgement and venous stasis within the abdominal organ) - **Weight gain** (edema/fluid accumulation) - **Hepatomegaly** (from venous engorgement of the liver causing liver dysfunction) - **Edema** (bipedal) pink or blood tinged sputum - **Ascites** (peritoneal cavity) - **Distended neck vein** (due to increased venous pressure) - **Jugular venous distention** - **Anasarca** - **Edema (pitting edema)** - **Tachycardia** - **Murmurs** **COMPLICATIONS** Related to diuretic use: a. **Hyperkalemia**- may occur with the occur with the use of ACE inhibitors, ARBs or spironolactone b. **Hypokalemia**- excessive and repeated diuresis c. **Hyponatremia**- due to prolonged diuretic therapy that can result to disorientation, fatigue, apprehension, weakness and muscle cramps d. **Dehydration, hypotension**- from excessive fluid loss **DIAGNOSIS** - **History:** Risk factors for ischemic heart disease, family history - **Physical exam:** S3, JVD more specific signs of HF than rales, peripheral edema - **Chest X-ray:** cardiomegaly and pulmonary edema; Kerley's B Lines - **Electrocardiogram:** Anterior Q waves, LBBB, LVH - **Echocardiogram:** enlarged chambers, decreased ejection fraction - **Lab values:** elevated ANP,BNP Levels - **Hemodynamic:** Reduced EF, Increased Pulmonary Cap Wedge Pressure - **Heart scan (MUGA):** Multigated Acquisition Scan-measures the cardiac volume, ejection fraction and wall motion - **PET Scan:** sensitive test for evaluating myocardial ischemia and viability - **Cardiac catheterization:** assesses pressures - **Liver enzymes:** elevated - **Myocardial biopsy** **DECREASING INTRAVASCULAR VOLUME** - Administration of diuretics - Loop diuretics -- LASIX (furosemide)- given slowly - Ultrafiltration - Achieved by hemodialysis **DECREASING VENOUS RETURN** - It decreases the amount of volume returned to the left ventricle during diastole - Provide high fowlers position - Administration of nitroglycerin **DECREASING AFTERLOAD** - Decreasing the systemic vascular resistance - IV sodium nitropusside - Morphine sulfate - Nesritide - Recombinant form of BNP. It causes both arterial and venous dilation **IMPROVING GAS EXCHANGE** - Administration of oxygen by oxygen mask or mechanical ventilation - Administration of IV morphine sulfate **IMPROVING CARDIAC FUNCTION** - Digitalis - it is a positive inotrope that increases force of left ventricular contraction - Dopamine -- beta adrenergic agonist. It will increases contractility and heart rate - Dobutamine -- synthetic beta adrenergic agonist, it does not increase SVR - Milrinone and Inamrinone -- these are phosphodiesterase inhibitors. They will enhances calcium entry into cell and increases contractility **REDUCING ANXIETY** - Morphine sulfate - benzodiazepines **CHF -- DRUG THERAPY** - diuretics **MEDICAL MANAGEMENT (DABONDCLASH)** - **Digitalis** - increases the force of myocardial contraction and slow conduction through the AV node; improves contractility left ventricular output and enhances diuresis. - **ACE inhibitors** - promotes vasodilation and diuresis by decreasing afterload and preload, ultimately decreasing the workload of the heart - **Dobutamine** - IV medication administered to patients with left ventricular dysfunction and hypoperfusion - **Beta-blockers** - reduces mortality and morbidity by heart failure by reducing the adverse effects from the constant stimulation of the SNS - **Oxygen** - need is based on the degree of pulmonary congestion and resulting hypoxia - **Nitrates** - causes venous dilation, which reduces the amount of blood return to the heart and lowers preload - **Digitalis** - to remove excess extracellular fluid by increasing the rate of urine produced in patients with fluid overload. - **Calcium channel blockers** - causes vasodilation, reducing systemic vascular resistance - **Lifestyle changes** - restriction of dietary sodium, avoidance of excess fluid intake, weight reduction, and regular exercise - **Angiotensin II Receptor Blockers** - they block the effects of angiotensin II at its receptors: have similar hemodynamic effects as of ACE Inhibitors. Serves as alternative for patients who cannot tolerate ACE Inhibitors - **Sodium restrictions** - a low Na diet and fluid restrictions. - **Hydralazine** - lowers systemic vascular resistance and left ventricular afterload **PHARMACOLOGIC THERAPY** 1. **ACE inhibitors** - ACE inhibitors slow the progression of heart failure, improve exercise tolerance, decrease the number of hospitalizations and promote vasodilation and diuresis. 2. **Angiotensin II Receptor Blockers** - They block the conversion of angiotensin I at the angiotensin 2 receptor and cause decreased BP, vascular resistance and improved cardiac output. 3. **Beta Blockers** - reduce the adverse effects from the constant stimulation of the SNS. 4. **Diuretics** - Removes excess extracellular fluid by increasing the rate of urine produced in the patients with signs and symptoms of fluid overload. 5. **Calcium channel blockers** - Cause vasodilation by reducing systemic vascular resistance but contraindicated in patients with systolic heart failure. **NURSING PROBLEM PRIORITIES** 1. Improve myocardial contractility and perfusion. 2. Manage fluid volume 3. Prevent complications 4. Promote activity tolerance 5. Reduce anxiety 6. Minimize powerlessness 7. Provide disease information and prevention education **NURSING DIAGNOSIS** - Decreased cardiac output related to impaired myocardial function as evidenced by signs of fatigue, dyspnea, and abnormal heart rate or blood pressure. - Risk for ineffective health related to lack of knowledge regarding diagnostic and laboratory procedures necessary for monitoring heart status - Impaired gas exchange related to fluid overload and pulmonary congestion as evidenced by orthopnea - Excess fluid volume related to compromised heart function and renal perfusion as evidenced by peripheral edema - Acute pain related to decreased myocardial oxygenation as evidenced by discomfort worsened by stress - Ineffective tissue perfusion related to decreased cardiac output as evidenced by decreased urine output - Imbalanced nutrition; less than body requirements related to dietary restrictions and fluid management in heart failure as evidenced by confusion about diet and fluid restrictions **ARRHYTHMIAS**  **CAUSES OF CARDIAC ARRHYTHMIAS** - Abnormal rhythmicity of the pacemaker - Shift of the pacemaker from the sinus node to another place of the heart - Blocks of different points in the spread of the impulse through the heart - Abnormal pathways of impulse transmission through the heart - Spontaneous generation of spurious impulses in almost any part of the heart. **HEART BLOCK:** E. **[Block at the level of AV node:]** a. ***[First degree heart block:]*** every atrial depolarization is followed by conduction to ventricle but delay. ECG changes prolongation of PR interval to more than 0.22 second b. ***[Second degree heart block:]* some P waves conducted but other not. ECG changes every second or third P wave conducted to the ventricles** c. ***[Third degree heart block (complete heart block):]*** - **Atrial: 60--100 bpm** - **ventricular: 40--60 bpm** - **Rhythm: Usually regular, but atria and ventricles act independently. It occurs when all atrial activity fails to conduct to the ventricle so the Bundle of His will be responsible form generation of impulses** **Caused by:** - **Acute myocardial infarction, calcify aortic stenosis, cardiomyopathy, drugs (digoxin).** - **Block below AV node: A. block at Bundle of His, B. Block at the branches (Right or Left branch).** **SINUS RHYTHM:** **It is caused by the changes of number of impulses emitted form SA node. Heart rates more than 100/min is called (tachycardia), while less than 60/min is called (bradycardia). It is usually of two types:** a. ***[Sinus bradycardia:]*** **Causes:** - **Extrinsic causes: hypothermia, hypothyroidism, and raised intra cranial pressure, drugs (beta-blockers, digitalis, and anti-arrhythmic drugs).** - **Intrinsic causes: acute ischemia, infarction of SA node. ECG changes: Prolonged R- R interval.** b. ***[Sinus tachycardia: ]*** **Causes:** - **acute causes: exercise, emotion, pain, fever, acute heart failure,** - **chronic causes: pregnancy, anemia, hyperthyroidism, excess catecholamine. ECG: short R-R interval.** **Ectopic beat (extra-systoles, premature beat):** **A premature contraction is contraction of heart before the time that normal contraction would have been expected. Most premature contraction result from ectopic foci in the heart, which emits abnormal impulses at odd time during cardiac rhythm. Possible causes of ectopic foci are:** - **Local area of ischemia** - **Small calcified plaques at different points in the heart, which press against the adjacent cardiac muscle so some fibers are irritated** - **Toxic irritation of the AV node, Purkinje system, or myocardium caused by drugs, nicotine, or caffeine. If an irritable ectopic focus discharges once, the result is ectopic beat. If the ectopic foci discharge repetitively at rate higher than that of SA node, it produces rapid, irregular tachycardia.** **It could be:** a. ***[Atrial ectopic]*** **The ECG changes are:** - **The P wave of this beat occurs too soon in the heart cycle** - **The P-R interval is shortened, indicating that the ectopic origin of the beat is near the A-V node** - **The interval between the premature and the next succeeding contraction is slightly prolonged, which is called (compensatory pause).**  b. ***[Ventricular ectopic: ]*** **ECG changes:** - **Premature beats that originate in an ectopic ventricular focus usually have bizarrely shaped prolonged and high voltage QRS complex** - **The P wave is usually buried in the QRS of the extra-systole** - **The T wave has an electrical potential polarity opposite to the QRS** **TACHYARRHYTHMIA** **Cardiac arrhythmia is a disturbance in electrical rhythm of the heart; this may be paroxysmal or continuous, and may cause sudden death, syncope, heart failure, palpitation, or no symptoms.** **There are two mechanisms for tachycardia:** F. ***[Increase automaticity (increase slop angle):]* when the tachycardia is sustained by repeated spontaneous depolarization of an ectopic focus or single cell.** G. ***[Re-entry:]* when the tachycardia is initiated by an ectopic beat but sustained by a closed loor re-entry circuit. Most tachyarrhythmia are due to re-entry.**  **CAUSES OF RE --ENTRY (CIRCUS MOVEMENT)** **TYPES OF TACHYARHYTHMIAS** **Causes:** - **ischemic heart disease** - **Mitral valve disease** - **rheumatic heart disease** - **hypertension** - **cardiomyopathy** - **thyrotoxicosis** - **atrial septal defect** - **acute and chronic alcohol abuse pulmonary embolus.** a. ***[Atrial fibrillation:]*** **ECG: normal but irregular QRS, there are no P waves but base line may show irregular fibrillation waves** b. **Atrial flutter:** **ECG: regular saw-tooth-like atrial flutters waves (F waves) between QRST complexes; with rate about 300 beats/min. the QRS conducted 150 if every other one is conducted**  c. ***[Atrial tachycardia:]*** **An ectopic atrial tachycardia due to increase automaticity is rare but is sometimes is manifestation of digitalis toxicity.** **Rate: 150--250 bpm** **Rhythm: Regular** **P Waves: Normal (upright and uniform) but differ in shape from sinus P waves** **TYPES OF VENTRICULAR TACHYARRHYTHMIA:** a. ***[Ventricular tachycardia: ]*** **it is usually a serious condition because:** - **This type of tachycardia does not occur unless considerable ischemic damage is present in the ventricles** - **Ventricular tachycardia frequently initiates the lethal condition of ventricular fibrillation** - **Cardiac output is decreased. The ECG changes including: a series of ventricular premature beats occurring one after another without any normal beat interspersed so QRS morphology is regular, the rate is between (140-220/min).** b. ***[Ventricular fibrillation: ]*** - **The fibrillating ventricles, like the fibrillating atria, look like a quivering "bag of worms".** - **The fibrillating ventricles cannot pump blood effectively and circulation of the blood stops.** - **Therefore, in the absence of emergency treatment, ventricular fibrillation that last more than a few minutes is fatal.** - **The most common cause of sudden death in patients with myocardial infarction is ventricular fibrillation. The ventricular fibrillation can often be stopped and converted to normal sinus rhythm by mean of electrical shock.** - **The ECG changes: it shows undulating waves of varying frequency and amplitude.**  **ANTIARRHYTHM