ECG Rhythms: Sinus Rhythm, Atrial Fibrillation, VTach

ECG Rhythms

• Key ECG rhythms to be recognized are sinus rhythm, atrial fibrillation, and ventricular tachycardia

Sinus Rhythm

• Ventricular and atrial rate in adults is 60 to 100 bpm
• Ventricular and atrial rhythm is regular
• QRS shape and duration is usually normal, but might regularly be abnormal
• P wave shape is normal and consistent
• P wave shape is always in front of the QRS
• PR interval is consistent, between 0.12 and 0.20 seconds
• P:QRS ratio is 1:1

Atrial Fibrillation

• Atrial rate is 300 to 600 bpm
• Ventricular rate is usually 120 to 200 bpm in untreated atrial fibrillation
• Ventricular and atrial rhythm is highly irregular
• QRS shape and duration is usually normal, but might be abnormal
• No discernible P waves seen
• Irregular undulating waves vary in amplitude and shape and are referred to as fibrillatory or f waves
• PR interval cannot be measured
• P:QRS ratio is many:1

Ventricular Tachycardia

• Ventricular rate is 100 to 200 bpm
• Atrial rate depends on the underlying rhythm (e.g., sinus rhythm)
• Ventricular and atrial rhythm is usually regular; atrial rhythm may also be regular
• QRS duration is 0.12 seconds or more and has a bizarre, abnormal shape
• P wave is difficult to detect, so the atrial rate and rhythm might be indeterminable
• PR interval is very irregular, if P waves are seen
• P:QRS ratio is difficult to determine, but if P waves are apparent, there are usually more QRS complexes than P waves

Medical Management for Ventricular Tachycardia

• Administer anti-arrhythmic medications like amiodarone, procainamide, or lidocaine
• Anti-tachycardia pacing, direct cardioversion, and defibrillation are medical interventions

Causes of Sinus Tachycardia

• Physiologic or psychological stress like acute blood loss, anemia, shock, hypervolemia, hypovolemia, heart failure, pain, hypermetabolic states, fever, exercise, and anxiety can cause sinus tachycardia
• Medications that stimulate the sympathetic response (e.g., catecholamines, aminophylline, atropine), stimulants (e.g., caffeine, nicotine), and illicit drugs (e.g., amphetamines, cocaine, ecstasy) can cause sinus tachycardia
• Enhanced automaticity of the SA node and/or excessive sympathetic tone with reduced parasympathetic tone that is out of proportion to physiologic demands, a condition called inappropriate sinus tachycardia
• Autonomic dysfunction results in postural orthostatic tachycardia syndrome (POTS)
• POTS is characterized by tachycardia without hypotension, and by presyncopal symptoms like palpitations, lightheadedness, weakness, and blurred vision, which occur with sudden posture changes

Causes of Sinus Bradycardia

• Lower metabolic needs (e.g., sleep, athletic training, hypothyroidism)
• Vagal stimulation (e.g. from vomiting, suctioning, severe pain)
• Medications (e.g. calcium channel blockers [e.g. nifedipine, amiodarone], beta-blockers [e.g. metoprolol])
• Idiopathic sinus node dysfunction
• Increased intracranial pressure
• Coronary artery disease, especially myocardial infarction of the inferior wall
• Unstable and symptomatic bradycardia is frequently due to hypoxemia
• Acute altered mental status (e.g. delirium)
• Acute decompensated heart failure

Risk Factors for Atrial Fibrillation

• Increasing age
• Hypertension
• Diabetes
• Obesity
• Valvular heart disease
• Heart failure
• Obstructive sleep apnea
• Alcohol abuse
• Hyperthyroidism
• Smoking
• Exercise
• Cardiothoracic surgery
• Increased pulse pressure
• European ancestry
• Family history

Clinical Manifestations of Atrial Fibrillation

• Some patients are asymptomatic
• Palpitations and clinical manifestations of heart failure (e.g. SOB, hypertension, dyspnea on exertion, fatigue) are clinical manifestations
• A high ventricular rate of response during atrial fibrillation (greater than 80 bpm) can eventually lead to mitral valve dysfunction, mitral regurgitation, intraventricular conduction delays, and dilated ventricular cardiomyopathy

Stroke Risk Assessment

• Stroke risk assessment for atrial fibrillation uses the CHA2DS2-VASC scoring system

Risk Factors for Stroke

• Congestive Heart Failure (left ventricular systolic dysfunction)
• Hypertension (BP >130/80 mm Hg)
• Age ≥75 years (score=2)
• Diabetes
• Prior Stroke/TIA/Thromboembolism (score=2)
• Vascular disease (i.e., prior MI, PAD, or aortic plaque)
• Age 65–74 years
• Sex category (female gender)

Pharmacologic Therapy for Atrial Fibrillation

• Antithrombotic Medications: anticoagulants and antiplatelet drugs depending on stroke risk: aspirin daily, warfarin (Coumadin), dabigatran (Pradaxa), rivaroxaban (Xarelto)
• Medications that Control Heart Rate: beta blockers or calcium channel blockers

Beta Blockers

• Actions: Decreases automaticity and conduction
• Treats atrial and ventricular arrhythmias
• Drug names: acebutolol, atenolol, bisoprolol/HCTZ, esmolol, labetalol, metoprolol, nadolol, propranolol, sotalol (also has class III actions), timolol
• Side effects: Bradycardia, AV block, decreased contractility, bronchospasm, nausea, asymptomatic and symptomatic hypotension, masks hypoglycemia and thyrotoxicosis, CNS disturbances (e.g., confusion, dizziness, fatigue, depression)
• Nursing interventions: Monitor heart rate, PR interval, signs and symptoms of HF, especially in those also taking calcium channel blockers. Monitor blood glucose level in patients with type 2 diabetes. Caution the patient about abrupt withdrawal to avoid tachycardia, hypertension, and myocardial ischemia

Calcium Channel Blockers

• Actions: Blocks Calcium channel. Treats and prevents paroxysmal atrial arrhythmias
• Drug names: verapamil, diltiazem
• Side effects: bradycardia, AV blocks, hypotension with IV administration, HF, peripheral edema, constipation, dizziness, headache, and nausea
• Nursing interventions: Monitor heart rate and PR interval. Closely monitor blood pressure with IV administration. Monitor for signs and symptoms of HF. Do not crush sustained-release medications
• Medications for Pharmacologic Cardioversion: dofetilide (Tikosyn), amiodarone

Nursing Management of Arrhythmia

• Monitor rhythm and vitals
• Assess for decreased cardiac output: dizziness, hypotension, chest pain, SOB
• Administer medications per protocol
• Educate patient:
  • Avoid stimulants
  • Medication adherence
  • Monitoring for side effects
• Prepare for procedures:
  • Synchronized cardioversion
  • Anticoagulation teaching if on warfarin (diet, INR monitoring)

Risk Factors for Coronary Artery Disease (CAD)

Nonmodifiable Risk Factors

• Family history of CAD (first-degree relative with cardiovascular disease at 55 years of age or younger for men and at 65 years of age or younger for women)
• Increasing age (more than 45 years for men; more than 55 years for women)
• Gender (men develop CAD at an earlier age than women)
• Race (higher incidence of heart disease in African Americans than in Caucasians)
• History of premature menopause (before age 40) and history of pregnancy-associated disorders such as preeclampsia
• Primary hypercholesterolemia (a genetic condition resulting in elevated LDL)

Modifiable Risk Factors

• Hyperlipidemia
• Tobacco use
• Hypertension
• Diabetes
• Metabolic syndrome
• Obesity
• Physical inactivity
• Chronic inflammatory conditions (e.g., rheumatoid arthritis, lupus, HIV/AIDS)
• Chronic kidney disease

Clinical Manifestations of Angina Pectoris

• Frequently retrosternal and may radiate to neck, jaw, shoulders, back or arms (usually left)
• Tightness, choking, or a heavy sensation in upper chest
• Anxiety frequently accompanies the pain
• Other symptoms may occur: dyspnea or shortness of breath, dizziness, nausea, and vomiting
• Pain of typical angina subsides with rest or NTG
• Pain that is characterized by increased frequency and severity and is not relieved by rest and NTG requires medical intervention

Pharmacologic Therapy for Angina Pectoris

• Nitrates: Nitroglycerin - short- and long- term reduction of myocardial oxygen consumption through selective vasodilation
• Beta-Blockers: Metoprolol, Atenolol - reduction of myocardial oxygen consumption by blocking beta-adrenergic stimulation of the heart
• Calcium Channel Blockers: Amlodipine, Diltiazem- negative inotropic effects; indicated in patients not responsive to beta-blockers; used as primary treatment for vasospasm
• Antiplatelet Meds: Aspirin, Clopidogrel, Prasugrel, Ticagrelor - prevention of platelet aggregation
• Anticoagulants: Heparin (unfractionated), Low-molecular-weight heparins (Enoxaparin, Dalteparin) - prevention of thrombus formation

Self-Administration of Nitroglycerine

• Instruct the patient to make sure that the mouth is moist, the tongue is still, and saliva is not swallowed until the nitroglycerin tablet dissolves
• If the pain is severe, the patient can crush the tablet between the teeth to hasten sublingual absorption
• Advise the patient to carry the medication at all times as a precaution
• Nitroglycerin is very unstable, it should be carried securely in its original container (e.g., capped dark glass bottle); tablets should never be removed and stored in metal or plastic pillboxes
• Nitroglycerin is volatile and is inactivated by heat, moisture, air, light, and time. Instruct the patient to renew the nitroglycerin supply every 6 months
• Inform the patient that the medication should be taken in anticipation of any activity that may produce pain
• Nitroglycerin increases tolerance for exercise and stress when taken prophylactically (i.e., before angina-producing activity, like exercise etc), it is best taken before pain develops
• Recommend that the patient note how long it takes for the nitroglycerin to relieve the discomfort
• Advise the patient that if pain persists after taking three sublingual tablets at 5-minute intervals, emergency medical services should be called
• Discuss possible side effects of nitroglycerin, including flushing, throbbing headache, hypotension, and tachycardia
• Advise the patient to sit down for a few minutes when taking nitroglycerin to avoid hypotension and syncope

Clinical Manifestations of ACS

• Chest pain that occurs suddenly and continues despite rest and medication is the presenting symptom in most patients w/ ACS
• Other manifestations are chest pain, shortness of breath, indigestion, nausea, and anxiety
• Cool, pale, and moist skin is also a manifestation
• Pt heart rate and respiratory rate may be faster than normal

Treatment Guidelines for Acute Myocardial Infarction

• Use rapid transit to the hospital
• Obtain a 12-lead electrocardiogram to be read within 10 minutes
• Obtain laboratory blood specimens of cardiac biomarkers, including troponin
• Obtain other diagnostics to clarify the diagnosis
• Begin routine medical interventions: Supplemental oxygen, Nitroglycerin, Morphine, Aspirin, Beta-blocker, Angiotensin-converting enzyme inhibitor within 24 hours, Anticoagulation with heparin and platelet inhibitors, and Statin
• Evaluate for indications for reperfusion therapy (Percutaneous coronary intervention and Thrombolytic therapy.)
• Continue therapy as indicated with IV heparin, low-molecular-weight heparin, bivalirudin, or fondaparinux, Clopidogrel, Glycoprotein IIb/IIIa inhibitor
• Bed rest for a minimum of 12–24 hours
• Statin prescribed at discharge

Nursing Management of ACS/MI

• Goals for a patient with MI: Relieve pain, preserve myocardium by facilitating early reperfusion, prevent complications (like arrhythmias, heart failure), provide emotional support, and educate about rehabilitation and lifestyle changes
• Pain and anxiety management: ensure adequate pain relief (usually IV morphine) and bed rest to minimize stress on the heart
• Unnecessary reduce stimulation
• Keep the patient informed of what is happening
• Continuous monitoring: Place the patient on continuous ECG monitoring (telemetry or in ICU)
• Watch for dysrhythmias; ventricular fibrillation is the leading cause of death in the first hour of MI
• Have a defibrillator nearby
• Also monitor oxygen saturation and vital signs frequently (every 15-30 min in acute phase)
• If arterial line is present, monitor real-time BP
• Assess lung sounds and urine output to detect heart failure (pulmonary congestion or cardiogenic shock signs)
• Enhance oxygenation: If the patient is hypoxic or pulmonary edema is present, titrate oxygen appropriately
• High Fowler's position can improve breathing if pulmonary edema occurs (along with IV diuretics like furosemide as ordered)
• Maintain a patent IV access: Preferably two IV lines one for medications (e.g., IV nitroglycerin, morphine, heparin, etc.) and one for fluids if needed
• Avoid fluid overload, but ensure adequate IV access for emergency drugs
• Rest and gradual activity: Initially strict bed rest with bedside commode to avoid Valsalva (which can strain the heart)
• Prevent straining: give stool softeners to avoid constipation and vagal strain. After 24 hours (and if stable), patients with uncomplicated MI are often encouraged to progressively increase activity
• Observe for any chest pain or dyspnea with activity
• Cardiac rehabilitation usually begins in hospital with mild exercises and continues after discharge in a structured program
• Relieve fear: Provide clear information about what happened and the plan and involve them in care decisions when appropriate
• Prevent complications
  • Arrhythmias: as noted, monitor ECG
  • If on amiodarone or lidocaine for arrhythmias, monitor for side effects
  • Keep potassium and magnesium within normal range to reduce ectopy (correct any electrolyte imbalances)
  • Heart failure/cardiogenic shock: Monitor fluid status (I&O, daily weights, lung sounds). An S3 gallop or new crackles in lungs could mean onset of left ventricular failure report promptly
  • Administer ACE-inhibitors, diuretics, or inotropes as ordered if heart failure signs appear
  • Pericarditis: After an MI (especially large transmural MI), Dressler's syndrome (post-MI pericarditis) can occur days to weeks later
  • Watch for pericardial friction rub and chest pain that changes with position, and treat with anti-inflammatory agents
  • Recurrent ischemia: Continue anti-ischemic therapies (beta-blockers, nitrates). If chest pain returns, treat as described, and notify the physician the patient might need repeat cath evaluation

Deep Vein Thrombosis (DVT) Implications after an MI

• Immobility and infarction can increase risk, so preventive measures like compression stockings or heparin prophylaxis should be used if patient is not fully ambulatory

Caring for the Patient After Cardiac Surgery

• ICU care: Monitor hemodynamics (arterial line, central venous or PA pressures), maintain ventilator and chest tube management
• Assess for bleeding – chest tube drainage >150mL/hr could indicate hemorrhage and needs reporting
• Maintain patency of chest tubes (no kinks, and do not strip tubes aggressively as it can cause high pressure)

Temperature Regulation After Cardiac Surgery

• Patients often come out of OR cold; warm them gradually to prevent shivering (shivering increases oxygen demand)

Fluid and Electrolytes Management After Cardiac Surgery

• Strict I&O; watch for edema or signs of cardiac tamponade (which can occur if fluid accumulates around heart signs include rising CVP, JVD, muffled heart sounds)
• Electrolyte imbalances (especially K and Mg) are common post-bypass and need correction to prevent arrhythmias

Pain Control After Cardiac Surgery

• Differentiate incisional pain (sternotomy pain, musculoskeletal) from anginal pain
• Adequate analgesia (IV opioids) and splinting the incision with a pillow during coughing can improve breathing and prevent pulmonary complications

Pulmonary Hygiene After Cardiac Surgery

• Suction as needed while intubated; after extubation (usually within 6-24 hours), encourage incentive spirometry, deep breathing, and coughing to prevent atelectasis
• Monitor for atelectasis or pneumonia

Mobilization After Cardiac Surgery

• Within 24-48 hours post-op, the patient is usually helped out of bed to a chair and then ambulating short distances by day 2 or 3 to reduce risk of DVT and helps recovery

Wound Care After Cardiac Surgery

• Maintain aseptic technique with chest and graft site incisions (e.g. leg incisions if saphenous vein graft)
• Monitor for signs of infection (redness, drainage, fever)

Emotional Support Post-Cardiac

• Patients and families may experience anxiety or emotional swings post-surgery (ICU delirium can happen)
• Provide reassurance that mood changes can be temporary

Patient Education Before Discharge After Cardiac Surgery

• Teach sternal precautions (like avoiding heavy lifting >5-10 lbs for ~6-8 weeks, not driving for several weeks), incisional care, recognizing signs of infection, and follow-ups
• Patients will go to cardiac rehab for supervised exercise and education on lifestyle

Rehabilitation After Cardiac Surgery

• Start plans for cardiac rehab early
• Provide dietary consultation (likely a low-fat, low-salt, low-cholesterol diet)
• Make sure the patient can recognize symptoms (like differentiating angina vs. other discomfort) and knows how to respond
• Sexual activity can usually resume when the patient can climb 2 flights of stairs without chest pain or significant breathlessness (often ~4-6 weeks post-MI; clarify this with the provider)
• Discuss any needed home support and follow-up appointments

Age-Related Changes in Immunologic Function

Immune

• Impaired function of B and T lymphocytes
• Failure of lymphocytes to recognize mutant or abnormal cells
• Decreased antibody production
• Failure of the immune system to differentiate "self" from “non-self"
• Suppressed phagocytic immune response

Consequences of Immunity Changes

• Suppressed responses to pathogenic organisms with increased risk for infection
• Increased incidence of cancers
• Anergy (lack of response to antigens applied to the skin [allergens])
• Increased incidence of autoimmune diseases
• Absence of typical signs and symptoms of infection and inflammation
• Dissemination of organisms usually destroyed or suppressed by phagocytes (e.g., reactivation or spread of tuberculosis)

Gastrointestinal Alterations

• Decreased gastric secretions and motility
• Decreased phagocytosis by the liver's Kupffer cells
• Altered nutritional intake w/ inadequate protein intake

Gastrointestinal Consequences

Proliferation of intestinal organisms resulting in gastroenteritis and diarrhea Increased incidence and severity of hepatitis B Increased incidence of liver abscesses Suppressed immune response

Urinary Dysfunction

• Decreased kidney function and changes in lower urinary tract function (enlargement of prostate gland, neurogenic bladder)
• Altered genitourinary tract flora

Urinary Consequences

• Urinary stasis and increased incidence of urinary tract infections

Pulmonary Alterations in immunity

• Impaired ciliary action due to exposure to smoke and environmental toxins

Pulmonary Consequences in relation to immunity

• Impaired clearance of pulmonary secretions; increased incidence of respiratory infections

Integumentary Alterations in immunity

• Thinning of skin w/ less elasticity; loss of adipose tissue
• Impaired microcirculation
• Decreased sensation and slowing of reflexes

Integumentary Consequences in relation to immunity

• Increased risk of skin injury, breakdown, and infection
• Stasis and pressure injuries
• Increased risk of injury, skin ulcers, abrasions, and burns

Assessment for Immune Dysfunction

• Symptoms for respiratory system infections include a changed respiratory rate, cough, abnormal lung sounds, rhinitis, hyperventilation, bronchospasm
• Symptoms for cardiovascular system infections include hypotension, tachycardia, arrhythmia, vasculitis, anemia
• Symptoms of gastrointestinal infections include hepatosplenomegaly, colitis, vomiting, diarrhea
• Symptoms for genitourinary system infections include increased frequency and burning on urination, hematuria, discharge
• Symptoms in the musculoskeletal system for infections include edema or pain
• Skin manifestations includes rashes, lesions, or dermatitis
• Neurosensory manifestations includes cognitive dysfunction, hearing loss, visual changes, headaches and migraines, ataxia, and tetany

Clinical Manifestations of a Primary Immune Deficiency Disorder

• Multiple infections
• Infections despite aggressive treatment
• Infections with unusual or opportunistic organisms
• Failure to thrive or poor growth
• Significant family history

HIV Risks and Prevention

• Sharing infected injection drug use equipment
• Having sexual relations with infected persons (both genders)
• Infants born to mothers with HIV infection or who are beast-fed by HIV-infected mothers
• People who received organ transplants, HIV-infected blood, or blood products (especially between 1978 and 1985) is a risk

HIV Prevention

• Abstaining from exchanging sexual fluids (semen and vaginal fluid)
• Reduces the number of sexual partners to one
• Always use latex condoms
• If the patient is allergic to latex, nonlatex condoms should be used; however, they will not protect against HIV infection
• Not reuse condoms
• Avoid using cervical caps or diaphragms without using a condom as well
• Always use dental dams for oral-genital or anal stimulation
• Avoid anal intercourse, because this practice may injure tissues; if not possible, use lubricant- there are water and silicone-based products designed for anal sex and avoid manual-anal intercourse (“fisting”)
• Avoid sharing needles, razors, toothbrushes, sex toys, or blood-contaminated articles and consider PrEP if regularly engage in high-risk behaviors and use needle-exchange programs (as appropriate) and do not share drug-using equipment for drug equipment

Advice for HIV Seropositive Patients

• Take ART regularly to achieve viral suppression
• Inform previous, present, and prospective sexual and drug-using partners of their HIV-positive status. If the patient is concerned for their safety, advise the patient that many states have established mechanisms through the public health department in which professionals are available to notify exposed contacts
• Avoid having unprotected sex with another HIV-seropositive person
• Do not donate blood, plasma, body organs, or sperm

Clinical Manifestations of HIV

• Several stages of IV infection: acute infection, asymptomatic (latent) period, early symptomatic, and AIDS (advanced disease with opportunistic infections). Manifestations are widespread and can involve virtually any organ system because HIV affects the immune system globally (particularly CD4 T-lymphocytes), allowing opportunistic infections (OIs) and certain cancers to develop

Stages of HIV

• Acute HIV infection (seroconversion): Occurs 2-4 weeks after infection; often a mononucleosis-like syndrome with fever, swollen lymph nodes, sore throat, rash, muscle/joint aches, diarrhea
• Chronic Asymptomatic (Latency):After seroconversion, patients may have no symptoms for years while the virus replicates at low levels; lymphadenopathy might be present as well with this phase lasting ~8-10 years without ART, shorter if the virus is aggressive
• Early symptomatic HIV (CD4 count dropping): Patients start to get generalized lymphadenopathy, persistent fever, night sweats, chronic diarrhea, weight loss (>10% body weight, “HIV wasting”), fatigue, and more frequent candida infections

AIDS

• AIDS (Acquired Immune Deficiency Syndrome): Defined by CD4+ T-cell count < 200 cells/µL and/or AIDS-defining illnesses
• At this stage, the immune system is severely compromised
• Opportunistic infections and cancers occur, which can involve any organ
  • Respiratory: Pneumocystis pneumonia (PCP) – causing fever, cough, and hypoxia; Tuberculosis (can be pulmonary or disseminated); fungal infections like Histoplasmosis
  • GI: Chronic Cryptosporidium diarrhea; Candida esophagitis (painful swallowing); wasting syndrome from malabsorption
  • Neurologic: Toxoplasmosis of the brain (causing headaches, confusion, seizures); Cryptococcal meningitis; HIV-related dementia (HIV-associated neurocognitive disorder); Progressive multifocal leukoencephalopathy (PML) due to JC virus
  • Skin/Mucous membranes: Oral thrush, recurrent herpes simplex ulcers, Kaposi's sarcoma lesions (violaceous skin lesions and can involve GI/lungs), molluscum contagiosum, severe psoriasis
  • Hematologic/Oncologic: Opportunistic cancers like Kaposi's sarcoma (cancer of blood vessel lining), Non-Hodgkin's lymphoma, Primary CNS lymphoma, and invasive cervical cancer in women General: Profound fatigue, cachexia (muscle wasting), persistent high fevers, night sweats, chronic skin rashes
• Pediatric differences: Infants might fail to thrive, have developmental delays, or get recurrent infections like severe thrush, chronic diarrhea, etc

Nursing for HIV Sufferers

• Because HIV can affect any organ via opportunistic diseases, it's important to maintain a broad index of suspicion in advanced HIV for unusual presentations as signs and symptoms are widespread and may involve virtually any organ system
• Patients with HIV should be monitored for even subtle changes (new cough, headaches, vision changes, weight loss, etc.) as these could indicate an OI
• Prophylactic medications are given at certain CD4 levels (e.g., TMP-SMX for PCP when CD4 <200, azithromycin for MAC when CD4 <50, etc.)

Goals of ART

• HIV treatment is lifelong and uses combinations of antiretroviral drugs to suppress the virus
• Goals are to maximally and durably suppress HIV viral load
  • This means reducing the amount of HIV in the blood to undetectable levels and keeping it there. Achieving an undetectable viral load (<50 copies/mL) stops disease progression and greatly reduces risk of transmission
• Restore and preserve immunologic function by suppressing the virus
• CD4+ T-cell counts can rebound or be maintained, improving the patient's immune response. The goal is to allow the immune system to recover so it can fight off infections and prevent opportunistic diseases
• Reduce HIV-related morbidity and prolong survival
• Effective ART should improve quality of life and help people with HIV live long, healthy lives comparable to HIV-negative individuals. It prevents progression to AIDS and reduces complications
• Prevent HIV transmission (Treatment as prevention)
• When patients adhere to ART and maintain an undetectable viral load, the risk of transmitting HIV sexually is effectively zero
• Improve quality of life Free from frequent illness, the person can work, have relationships, and plan for the future

Treatment for HIV Sufferers

Combination ART (usually 3 or more drugs from at least two different classes) which attacks the virus at multiple points in its life cycle, minimizing chance of resistance

Promoting Adherence to ART

Use a multidisciplinary team approach: - Nonjudgmental providers, nurses, social workers, pharmacists, and medication managers Strengthen early linkage to care and retention in care: - Encourage health care team participation in linkage to and retention in care Assess patient readiness to start ART Evaluate patient's knowledge about HIV disease, prevention and treatment and, on the basis of the assessment, provide HIV-related information Identify facilitators, potential barriers to adherence, and necessary medication management skills before starting ART medication Provide needed resources Involve the patient in ARV regimen selection Assess adherence at every clinic visit Use positive reinforcement to foster adherence success

Severe Anaphylaxis and its Manifestations

Mild Manifestations

• Peripheral tingling and a sensation of warmth
• Possibly accompanied by a sensation of fullness in the mouth and throat
• Nasal congestion
• Periorbital swelling

Moderate Manifestations

• Warmth
• Anxiety
• Itching in addition to any of the milder symptoms

Severe Manifestations

• Symptoms are an Abrupt onset w/ same signs and symptoms as above
• Symptoms progress rapidly to bronchospasm, laryngeal edema, severe dyspnea, cyanosis, hypotension, dysphagia, abdominal cramping, vomiting, diarrhea, seizures, and cardiac arrest/coma

Medical Management of Anaphylaxis

• Critical management involves rapid assessment and intervention, supporting airway, breathing, and circulation (ABCs), and to stop the effects of the allergen Follow Key Steps:
• Call for help / Activate emergency response
• Ensure airway patency, giving oxygen and sitting the patient up helps if they are breathing, but if blood pressure is low the patient should be lying flat to help perfusion. Protect airway first
• Administer 100% oxygen
• Administer CPR if in cardiac arrest and remove the antigen source where possible
• Lay the patient flat with legs elevated to improve venous return (if hypotensive) unless that impairs breathing
• Monitor cardiac rhythm, blood pressure, pulse oximetry, and level of consciousness
• Observe even after initial treatment in case there is a bi-phasic reaction, sometimes requiring admission for observation

Pharmacologic Therapy for Anaphylaxis

• Epinephrine, IM (thigh) promptly; IV if needed. Reverses airway obstruction and shock
• Oxygen, high-flow O2 for any respiratory difficulty or shock
• IV Fluids, large bore IV access and aggressive fluids for hypotension
• Antihistamines, IV H1 blocker and consider H2 blocker
• Bronchodilators, Nebulized albuterol for bronchospasm; consider Ipratropium
• Corticosteroids. IV Solu-Medrol or equivalent to prevent recurrence
• Vasopressors, IV infusion (e.g., norepinephrine) if persistent hypotension

Nursing Management of Anaphylaxis

• Rapid recognition and activation of emergency protocols and ensure patients airway, breathing, circulation are supported.
• Position and reassure anxious patients
• Administer drugs and monitor the patient while continuing constant observation

Patient Teaching for Allergy Management

State the Environmental Factors

• Dust
• Molds
• Perfumes Foods

State Changes

• Removing drapes, curtains, and venetian blinds and replacing them with pull shades, covering the mattress with a hypoallergenic cover that can be zipped, removing rugs and replacing them with wood flooring or linoleum
• Reducing dust in the house as a whole by using steam or hot water for heating and using high-efficiency particulate air (HEPA) purifiers or air-conditioning
• Washing the floor and dusting and vacuuming daily, using clean filters, wearing a mask whenever cleaning is being done
• Replacing stuffed furniture with wood pieces that can easily be dusted
• Avoiding the use of tufted bedspreads, stuffed toys, and feather pillows and replacing them with washable cotton material
• Avoiding the use of any clothing that causes itching
• Verbalize ways to reduce exposure to pollens or molds by identifying seasons of the year when pollen counts are high, wearing a mask at times of increased exposure (windy days and when grass is being cut), and avoiding contact with weeds, dry leaves, and freshly cut grass
• Rationale for seeking air-conditioned areas at the height of the allergy season
• Rationale for avoiding sprays and perfumes, using hypoallergenic cosmetics, and taking prescribed medications as prescribed
• Identify specific foods that may cause allergic symptoms and develop a list of foods to avoid, verbalizing ways to cope with stress successfully, plans for regular exercise, and rationale for obtaining adequate rest
• How to reach the primary provider with questions or complications
• State time and date of follow-up appointments, testing and and identify the need for health promotion, disease prevention, and screening activities

Nursing Management of a Patient with Latex Allergy

• Identify high-risk individuals: Ask every patient about latex allergy or sensitivity (and document it clearly). High-risk groups include healthcare workers (due to frequent exposure), patients with spina bifida, those who have had multiple surgeries or chronic catheterizations from a young age, and people with certain food allergies (banana, avocado, kiwi, chestnut can cross-react with latex), any unexplained intraoperative anaphylaxis. Patients with atopic allergies or asthma may be more prone to latex allergy
• Prevent exposure in the healthcare setting For known latex-allergic patients, the hospital room and chart must be labeled “Latex Allergy.” Use a latex-free cart or kit

Latex-Free List

Gloves, IV tubing, syringes, latex-free blood pressure cuffs/tourniquets, and catheters

Procedures for Latex Free Patients

Schedule latex-allergic patients as the first case of the day to minimize latex contamination. Use latex-free equipment (including vial stoppers or medication ampoules if they contain latex pharmacy may need to supply alternatives). All staff in contact should wear non-latex gloves Emergency preparedness: A latex-allergic patient should be managed similarly to other severe allergies and be educated to all healthcare workers

Nursing Education for Latex Allergy

Inform all healthcare providers (dentist, lab tech, etc.) about the latex allergy before any exam or procedure Everyday items contain latex, so be aware latex is in cleaning gloves, balloons, rubber bands, condoms, diaphragms, some bandages, shoe soles, sports equipment If applicable, involve occupational health to create a latex-safe work environment or reassign duties if necessary (healthcare workers with latex allergy may need non-patient-contact roles or strict latex-free protocols) Advise patients to notify local EMS and their pharmacy of their latex allergy Facilitate psychosocial support, as patients experience anxiety Advocate within their institutions for latex-safe policies, such as having latex-free carts and signage, and educating staff about latex allergy seriousness

Autoregulation of Blood Pressure and Kidney Function

The vasa recta constantly monitors BP as blood passes through the kidneys, when the vasa recta detects a decrease in BP, renin is then secreted which then converts angiotensinogen to angiotensin I. Angiotensin I is converted to angiotensin II, the most powerful vasoconstrictor, which then increases the BP The adrenal gland then releases aldosterone Failure of this feedback mechanism is one of the primary causes of hypertension Antidiuretic hormone (ADH), also called vasopressin, is secreted by the posterior pituitary gland in response to high blood osmolality or low blood volume/BP ADH acts on the kidneys (distal tubules and collecting ducts) to make them more permeable to water In the absence of ADH, the distal nephron is impermeable to water resulting in excretion of a large volume of very dilute urine When ADH is present, it causes the insertion of water channels (aquaporins) in the collecting duct, leading to increased water reabsorption back into the bloodstream. This produces a smaller volume of concentrated urine Thus, ADH helps the body conserve water and concentrate urine during dehydration or volume loss ADH also causes mild vasoconstriction (hence the name vasopressin), but its primary effect is water balance.

Clinical Correlation For ADH

If ADH is not produced or the kidneys don't respond, the patient will excrete large volumes of dilute urine (polyuria) and become dehydrated easily If too much ADH is produced, the patient retains excess water, causing very concentrated urine and dilutional hyponatremia

Assessment for ADH

• Low urine output with high specific gravity suggests high ADH effect, could be appropriate like in dehydration, or inappropriate like SIADH
• Conversely, high output with low specific gravity suggests lack of ADH effect

Sodium and Potassium Deficiencies

Sodium

Hyponatremia: Nausea, malaise, lethargy, headache, abdominal cramps, apprehension, seizures managed with diet, normal saline or hypertonic saline solutions Hypernatremia: Dry, sticky mucous membranes, thirst, rough dry tongue, fever, restlessness, weakness, disorientation managed with fluids, diuretic agents, and dietary restriction

Potassium

Hypokalemia: Anorexia, abdominal distention, paralytic ileus, muscle weakness, ECG changes, arrhythmias managed with diet, oral or parenteral potassium replacement therapy Hyperkalemia: Diarrhea, colic, nausea, irritability, muscle weakness, ECG changes managed with dietary restriction, diuretics, IV glucose, insulin and sodium bicarbonate, cation-exchange resin, calcium gluconate, dialysis

Causes of Acute Kidney Injury (AKI)

• AKI is a sudden decline in kidney function (hours to days) resulting in inability to excrete wastes and maintain electrolyte balance. It is often categorized by cause:
• Prerenal AKI due to insufficient blood flow to kidneys (perfusion problem) Causes Volume depletion: hemorrhage, severe dehydration, or burns Low cardiac output: heart failure and cardiogenic shock Systemic vasodilation: sepsis and anaphylaxis

Management of Pre-Renal AKI

• Restore perfusion quickly
• IV fluids for dehydration
• Blood transfusions if hemorrhage occurred
• treat heart failure (inotropes, relieve tamponade,etc), manage sepsis (IV fluids, vasopressors)
• Prerenal AKI often reverses with prompt correction of circulation before structural damage occurs
• Monitor urine output – it should improve with correction.

Causes of Intrarenal (Intrinsic) AKI

Due to direct damage to kidney tissue (parenchymal injury) Ischemia: untreated prerenal can progress to acute tubular necrosis (ATN) Nephrotoxic substances Certain antibiotics: aminoglycosides Contrast dye from CT scans: NSAIDs, chemotherapeutic agents, heavy metals, or hemoglobin/myoglobin from massive hemolysis or rhabdomyolysis Inflammatory conditions: acute glomerulonephritis, interstitial nephritis (e.g., allergic reaction in kidney) Intrinsic vascular issues: vasculitis, malignant hypertension causing vessel damage

Management on Kidney Injury

• Remove or treat the cause
• Stop nephrotoxic drugs (or flush out contrast post-procedure with IV fluids), treat glomerulonephritis (possibly steroids or immunosuppressants if indicated)
• Manage rhabdomyolysis: vigorous IV fluids, bicarbonate to alkalize urine and flush myoglobin, maybe dialysis
• Provide supportive care, maintain fluid balance (but avoid overload), correct electrolyte imbalances, and consider dialysis
• Adequate hydration is key to prevent further injury

Postrenal AKI

• Due to obstruction of urine outflow anywhere from renal pelvis to urethra and is characterized by kidney