Cardiovascular Pathophysiology and Pharmacology PDF

Cardiovascular Pathophysiology and Pharmacology This presentation explores the anatomy, physiology, and pharmacology of the cardiovascular system, focusing on common diseases and their treatment.  Electrical Conduction System The heart's electr...

Cardiovascular Pathophysiology and Pharmacology This presentation explores the anatomy, physiology, and pharmacology of the cardiovascular system, focusing on common diseases and their treatment.  Electrical Conduction System The heart's electrical conduction system is a network of These impulses trigger muscle contractions, ensuring specialized cells responsible for generating and transmitting coordinated pumping of blood throughout the body. electrical impulses.  Action Potential of the Cardiac Myocyte Phase 0: Rapid Phase 1: Early Phase 2: Plateau Phase 1 2 3 Depolarization Repolarization Calcium influx, balancing Sodium influx into the cell. Sodium channels close, potassium efflux. potassium channels open. Phase 3: Rapid Repolarization Phase 4: Resting Membrane Potential 4 5 Potassium efflux dominates, returning to resting The cell is polarized, ready for the next action potential. potential.  Specialized Cardiac Conduction System Sinoatrial (SA) Node Atrioventricular (AV) Node Bundle of His Purkinje Fibers The pacemaker of the heart, generating electrical Slows conduction, allowing atria to contract Transmits the impulse from the AV node to the Rapidly conduct the impulse throughout the impulses at a rate of 60-100 beats per minute. before ventricles. ventricles. ventricular myocardium, ensuring synchronized contraction.  Sinus Node Pacemaker Rhythm Generates the electrical impulses Controls the heart rate, typically that initiate the heartbeat. 60-100 beats per minute. Conduction Transmits impulses to the atria and then to the ventricles.  Atrioventricular Node Conduction Gatekeeper Rhythm Delay Acts as a Regulation The AV node slows gatekeeper, Helps maintain a the electrical preventing too-fast regular heart rhythm impulse, allowing ventricular by controlling the the atria to contract contractions. rate at which before the impulses reach the ventricles. ventricles.  Bundle of His Pathway Septum Transmits the electrical Located within the impulse from the AV node to interventricular septum, the left and right bundle separating the left and right branches. ventricles. Conduction Rapidly conducts the impulse, allowing synchronized contraction of the ventricles.  Purkinje Fibers Branching Rapid Myocardial Network Conduction Stimulation Extends from the Efficiently conduct Stimulate the bundle branches, the electrical ventricular muscle forming a vast impulse, ensuring fibers, initiating the network that synchronized pumping action of spreads throughout contraction of the the heart. the ventricular ventricular muscle. myocardium.  Tachyarrhythmia Pharmacology Management Ventricular Tachycardia Supraventricular Tachycardia Ventricular (VTach) (SVT) Fibrillation/PEA/Asystole Amiodarone: 150mg IV bolus, then Adenosine: 6mg rapid IV push, Epinephrine: 1mg IV q3-5min infusion, 300mg IV then 12mg if needed Amiodarone: 300mg IV bolus for Lidocaine: 1-1.5 mg/kg IV bolus Verapamil: 5-10mg IV over 2 min VFib Procainamide: 20-50 mg/min until Diltiazem: 0.25mg/kg IV over 2 min Sodium bicarbonate: Consider for arrhythmia suppressed prolonged arrest Magnesium Sulfate: 2g IV for Beta blockers: Metoprolol 5mg IV Calcium chloride: For suspected Torsades de Pointes q5min x3 doses hyperkalemia Consider cardioversion if Vagal maneuvers as first-line Immediate defibrillation for VFib; hemodynamically unstable treatment high-quality CPR for all  Bradyarrhythmia Pharmacology Management First-Line Treatment: Second-Line Agents: Special Considerations Atropine Sympathomimetics Glucagon: 3-10mg IV bolus for 0.5-1mg IV bolus every 3-5 Dopamine: 2-20 mcg/kg/min beta-blocker induced minutes (max total 3mg) IV infusion bradycardia Blocks parasympathetic Epinephrine: 2-10 mcg/min IV Calcium: For calcium-channel influence on SA/AV nodes infusion blocker toxicity Used for symptomatic sinus Isoproterenol: 2-10 mcg/min Temporary pacing: Consider if bradycardia or AV block IV infusion medications ineffective Remember to monitor vital signs and ECG continuously during treatment. Be prepared for temporary pacing if pharmacological management fails. Treat underlying causes when possible. Heart Function Equation CO = SV × HR Cardiac Output (CO) Stroke Volume (SV) Heart Rate (HR) The volume of blood pumped by the heart per The volume of blood pumped out by the The number of heartbeats per minute, minute, measured in L/min ventricle in each contraction, measured in measured in beats/min mL/beat This fundamental equation demonstrates how cardiac output is determined by both the amount of blood ejected with each heartbeat (stroke volume) and the frequency of heartbeats (heart rate). Definition and Pathogenesis: Myocardial Infarction Definition Pathogenesis A heart attack occurs when a Atherosclerosis, a buildup of coronary artery is blocked, plaque in the arteries, can leading to a lack of oxygen rupture, triggering a blood clot and nutrients to the heart that blocks the artery. muscle. Myocardial Infarction 1 2 3 1 Myocardial Infarction Heart attack, occurs when a coronary artery is blocked. 2 Ischemia Reduced blood flow to the myocardium. 3 Cell Death Prolonged ischemia leads to cell death, damaging the heart muscle.  Acute Myocardial Infarction ST-Segment Elevation MI (STEMI) Non-ST-Segment Elevation MI (NSTEMI) Complete blockage, causing significant damage to the heart muscle, Partial blockage, causing less severe damage, resulting in ST-segment resulting in ST-segment elevation on an EKG. depression or T-wave inversion on an EKG.  Pharmacological Management of Mycardial Infarctions Aspirin Nitroglycerin Beta-blockers ACE Inhibitors Antiplatelet agent Vasodilator reducing heart Slow heart rate and reduce Reduce BP and improve preventing blood clots. Oral: workload. Sublingual: 0.4mg BP. Oral: Metoprolol heart function. Oral: 162-325mg initial dose, then every 5 min up to 3 doses. 25-50mg twice daily. IV: Lisinopril 2.5-10mg daily. IV: 81mg daily. IV: Cangrelor 30 IV: Start 5-10 mcg/min, Metoprolol 5mg every 5 min Enalaprilat 1.25mg every 6 μg/kg bolus, then 4 titrate to response. up to 3 doses. hours. Side Effects: Headache, Side Effects: Bradycardia, Side Effects: Dry cough, μg/kg/min infusion. Side Effects: Bleeding risk, hypotension, dizziness, fatigue, bronchospasm, hyperkalemia, angioedema, gastrointestinal irritation, flushing, tachycardia, hypotension, depression, hypotension, acute kidney tinnitus, allergic reactions, syncope. sexual dysfunction. injury. bronchospasm in asthmatics.  Reperfusion: Fibrinolytics Fibrinolytic therapy is a critical intervention in acute myocardial infarction that works by breaking down blood clots to restore blood flow to the heart muscle. Mechanism of Action Common Fibrinolytics Activates plasminogen to form plasmin, which breaks - Alteplase (tPA): 90-minute infusion protocol - Reteplase: down fibrin clots and restores coronary blood flow Double-bolus administration - Streptokinase: Less used due to antigenic properties Key Indications Contraindications - STEMI within 12 hours of symptom onset - When PCI is - Active bleeding or bleeding disorders - Recent surgery or not available within 120 minutes - Significant ST-segment trauma - Intracranial hemorrhage history - Severe elevation or new LBBB uncontrolled hypertension Time is critical - earlier administration leads to better outcomes, with greatest benefit when given within 3 hours of symptom onset.  Definition and Pathogenesis: Congestive Heart Failure Exacerbation Definition Pathogenesis A sudden worsening of heart failure symptoms, typically Caused by factors that further reduce the heart's ability characterized by fluid retention, shortness of breath, and to pump blood effectively, often triggered by underlying fatigue. conditions or lifestyle changes.  Congestive Heart Failure Exacerbation The progression of congestive heart failure involves a cascade of maladaptive mechanisms that perpetuate cardiac dysfunction: Initial Compensatory Response RAAS Activation Neuroendocrine Changes 1 2 3 Activation of sympathetic nervous system leads to reduced Decreased cardiac output triggers RAAS, causing salt/water Release of epinephrine, norepinephrine, ET-1, and vasopressin beta-receptor responsiveness and altered myocardial retention and vasoconstriction, while angiotensin II promotes increases vasoconstriction and afterload function myocardial remodeling Myocardial Stress 4 Increased cAMP and cytosolic calcium lead to impaired relaxation and higher oxygen demand This cascade creates a perpetual cycle where decreased cardiac output leads to compensatory mechanisms, which ultimately worsen the condition through increased neurohumoral stimulation and maladaptive responses.  Renin-Angiotensin-Aldosterone System (RAAS) The RAAS system plays a crucial role in regulating blood pressure, fluid volume, and electrolyte balance. 1. Low Blood Pressure Detection 2. Angiotensin I Formation 3. Angiotensin II Formation 4. Multiple Effects Kidneys detect decreased blood pressure or Renin converts angiotensinogen (from liver) ACE (mainly in lungs) converts angiotensin I Angiotensin II causes vasoconstriction, blood volume, triggering juxtaglomerular into angiotensin I to angiotensin II increases blood pressure, and stimulates cells to release renin aldosterone release 5. Aldosterone Action Aldosterone increases sodium and water reabsorption in kidneys, further increasing blood volume and pressure  Pharmacological Management Diuretics ACE Inhibitors and ARBs Beta-blockers Inotropic Agents Used for: Reducing fluid overload Used for: Reducing afterload and Used for: Reducing heart rate and Used for: Increasing cardiac and congestion by increasing preventing cardiac remodeling by workload, improving survival in contractility and output in acute urine output blocking the RAAS system heart failure decompensated heart failure Medications: Medications: Medications: Medications: Furosemide (Lasix) Lisinopril (ACE) Losartan (ARB) Metoprolol Carvedilol Dobutamine Milrinone Digoxin Bumetanide (Bumex) Dosing: Dosing: Dosing: Dosing: Dobutamine: 2.5-20 Oral: Metoprolol 25-200mg daily mcg/kg/min IV Milrinone: Oral: Furosemide 20-80mg daily Lisinopril: 2.5-40mg daily IV: Metoprolol 5mg q5min (max 0.375-0.75 mcg/kg/min IV IV: Furosemide 20-40mg bolus Losartan: 25-100mg daily 15mg) Digoxin: 0.125-0.25mg daily Side Effects: Electrolyte Side Effects: Dry cough (ACE) Side Effects: Bradycardia Side Effects: Arrhythmias imbalance Dehydration Hyperkalemia Acute kidney Fatigue Bronchospasm Hypotension Tachycardia Hypotension Kidney dysfunction injury Angioedema Hypotension Angina Digoxin toxicity Definition and Pathogenesis: Hypertensive Urgency Definition Pathogenesis A rapid increase in blood Caused by a variety of factors, pressure without immediate including stress, certain organ damage, often medications, or underlying associated with symptoms medical conditions. such as headache, nosebleed, or blurred vision. Hypertensive Urgency Elevated Blood Clinical Presentation Medical Assessment Urgent Care Required Pressure A rapid rise in blood Careful evaluation confirms Requires prompt medical Systolic blood pressure pressure without immediate no signs of end-organ attention and careful above 180 mmHg or organ damage, often damage, distinguishing it monitoring to prevent diastolic blood pressure presenting with headache from hypertensive progression to more severe above 120 mmHg, indicating and dizziness. emergency. complications. a serious condition requiring immediate attention.  Pharmacological Management Oral Medications 1 Clonidine: 0.1-0.2mg PO q1h (max 0.8mg/24h). Central α2-agonist for gradual BP reduction. Side effects: sedation, dry mouth, rebound hypertension Nifedipine: 10-20mg PO q4-6h. Calcium channel blocker for moderate BP control. Side effects: peripheral edema, headache, flushing Captopril: 25mg PO q1-2h. ACE inhibitor for BP reduction and RAAS modulation. Side effects: cough, hyperkalemia, angioedema Intravenous Medications 2 Nitroprusside: 0.3-10 mcg/kg/min IV. Vasodilator for rapid BP control. Side effects: cyanide toxicity, reflex tachycardia Labetalol: 10-20mg IV bolus q10min (max 300mg). Combined α/β-blocker for quick BP reduction. Side effects: bronchospasm, heart block Hydralazine: 10-20mg IV q4-6h. Direct vasodilator for immediate BP lowering. Side effects: lupus-like syndrome, tachycardia Key Considerations 3 Monitor BP q15-30min during initial treatment. Target 25% reduction in first hour, with gradual normalization over 24-48h. Avoid excessive rapid lowering to prevent organ hypoperfusion. Definitions and Pathogenesis: Valvular Disease Valvular heart disease encompasses structural and functional abnormalities of the heart's four valves (mitral, tricuspid, aortic, and pulmonic), compromising their critical role in maintaining unidirectional blood flow. These conditions can manifest through valve stenosis (pathological narrowing) or regurgitation (valvular incompetence leading to retrograde flow). Normal vs Diseased Valves Types of Valve Dysfunction Pathogenesis Factors Healthy cardiac valves ensure optimal hemodynamics through Stenotic valves demonstrate restricted leaflet mobility and The etiology of valvular disease is multifactorial, encompassing coordinated opening and closing during the cardiac cycle. reduced orifice area, increasing the transvalvular pressure congenital malformations (e.g., bicuspid aortic valve), Pathological changes in valve architecture or function can gradient and workload on the preceding chamber. Regurgitant degenerative processes (calcific changes), inflammatory disrupt this precise mechanism, leading to altered cardiac valves fail to form an adequate seal during closure, allowing conditions (rheumatic heart disease), infectious causes hemodynamics and potentially compensatory myocardial pathologic retrograde blood flow and volume overload. (endocarditis), and structural changes secondary to myocardial remodeling. dysfunction.  Valvular Disease Valvular Disease Pathological conditions affecting cardiac valves that disrupt normal blood flow, manifesting as either valve narrowing (stenosis) or improper closure causing backflow (regurgitation). Aortic Valve Critical three-leaflet valve that regulates unidirectional blood flow from the left ventricle into the ascending aorta during systole, preventing backflow during diastole. Mitral Valve Bicuspid valve consisting of two leaflets that ensures proper blood flow from the left atrium into the left ventricle during diastole, vital for maintaining left heart efficiency. Tricuspid Valve Three-leaflet valve separating the right atrium and ventricle, preventing blood backflow during right ventricular contraction and maintaining proper right heart function. Pulmonic Valve Semilunar valve with three cusps that regulates blood flow from the right ventricle into the pulmonary artery, essential for proper pulmonary circulation.  Aortic Stenosis and Regurgitation Aortic Stenosis Aortic Regurgitation A pathological narrowing of the aortic valve orifice that impedes left ventricular outflow. The restricted valve area A valvular dysfunction characterized by incomplete closure of the aortic valve cusps during diastole, causing (normally 3-4 cm²) creates increased afterload on the left ventricle, leading to compensatory hypertrophy. Early retrograde blood flow from the aorta into the left ventricle. The increased diastolic volume creates a progressive manifestations include exertional dyspnea and decreased exercise tolerance, progressing to the classic triad of volume overload, leading to eccentric left ventricular hypertrophy. Initial compensation maintains forward stroke angina, syncope, and heart failure. Left untreated, the compensatory mechanisms eventually fail, resulting in volume, but symptoms gradually develop including bounding pulses, widened pulse pressure, and exertional decompensated heart failure and increased mortality. dyspnea. Chronic regurgitation ultimately leads to ventricular dilation and systolic dysfunction.  Pulmonic Stenosis and Regurgitation Pulmonic Stenosis Pulmonic Regurgitation A valvular dysfunction characterized by incomplete closure of the pulmonic valve during A pathological narrowing of the pulmonic valve orifice that impedes blood flow from the diastole, resulting in pathologic backflow from the pulmonary artery into the right ventricle. right ventricle to the pulmonary artery. The increased resistance creates elevated right This abnormal flow pattern creates a chronic volume overload state, leading to ventricular pressure, triggering compensatory right ventricular hypertrophy. Initially, progressive right ventricular dilation and eventual dysfunction. While mild cases may patients may experience exertional dyspnea, chest pain, and easy fatigability. As the remain asymptomatic, significant regurgitation manifests as exercise intolerance, right condition progresses, manifestations can include peripheral edema, jugular venous ventricular enlargement, and peripheral edema. The condition can be particularly severe distention, and syncope during physical activity. Severe cases inevitably lead to right-sided when accompanied by pulmonary hypertension, accelerating the progression to right heart heart failure if left untreated. failure.  Tricuspid Stenosis and Regurgitation Tricuspid Stenosis Tricuspid Regurgitation A pathological narrowing of the tricuspid valve orifice that impedes diastolic blood flow between the right atrium A valvular dysfunction characterized by incomplete closure of the tricuspid valve leaflets during ventricular systole, and right ventricle. This obstruction results in increased right atrial pressure, leading to progressive right atrial resulting in pathologic retrograde blood flow into the right atrium. This abnormal hemodynamic pattern triggers enlargement and elevated systemic venous pressures. Early symptoms include easy fatigability and exercise progressive right atrial enlargement, elevated venous pressures, and systemic venous congestion. Clinical intolerance, progressing to peripheral edema, hepatic congestion, and prominent jugular venous distention. manifestations typically include hepatomegaly with pulsatile liver, peripheral edema, ascites, and pronounced Without intervention, severe cases can progress to reduced cardiac output, right-sided heart failure, and eventual jugular venous distention. The condition may be primary (due to inherent valve abnormalities or endocarditis) or systemic congestion. secondary (commonly resulting from right ventricular dilation or pulmonary hypertension). Mitral Stenosis and Regurgitation Mitral Stenosis Mitral Regurgitation A significant pathological narrowing of the mitral valve orifice that critically restricts blood flow from the left A complex valvular dysfunction where incomplete mitral valve leaflet coaptation during systole permits atrium to left ventricle during diastolic filling. This mechanical obstruction generates a substantial pressure pathologic retrograde blood flow from the left ventricle into the left atrium. This hemodynamic disturbance gradient, resulting in elevated left atrial pressure and subsequent pulmonary venous congestion. The creates a dual-chamber volume overload state, leading to progressive left atrial enlargement and eventual increased atrial wall stress frequently triggers atrial enlargement and fibrillation. Clinical manifestations left ventricular eccentric hypertrophy. Patients typically experience a gradual onset of symptoms, beginning progress from initial exertional dyspnea to orthopnea, paroxysmal nocturnal dyspnea, and in severe cases, with subtle exercise intolerance and progressing to marked dyspnea, fatigue, and palpitations. Without hemoptysis due to pulmonary venous hypertension and rupture of bronchial vessels. appropriate intervention, chronic volume overload ultimately leads to left ventricular systolic dysfunction and clinical heart failure. Valvular Disease: Pharmacology Management Medical Management Disease-Specific Pharmacotherapy 1 2 Anticoagulation options: Warfarin (target INR 2.5-3.5 for mechanical valves; Aortic regurgitation: Lisinopril (10-40mg daily, side effects: cough, hyperkalemia) monitor for bleeding). or Valsartan (80-320mg daily, side effects: hypotension). Rate control: Metoprolol (25-200mg/day, side effects: fatigue, bradycardia), Acute mitral regurgitation: IV Nitroglycerin (5-200 μg/min, side effects: Diltiazem (120-360mg/day, side effects: edema, hypotension). headache, hypotension), Furosemide (40-80mg IV, side effects: electrolyte Diuretics: Furosemide (20-80mg daily, side effects: electrolyte imbalance, Mitral valve prolapse: Propranolol (10-40mg TID, side effects: fatigue, disturbance). dehydration). bronchospasm). Endocarditis prophylaxis: Amoxicillin (2g single dose) or Clindamycin (600mg) Chronic aortic regurgitation: Nifedipine XL (30-90mg daily, side effects: for penicillin-allergic patients. peripheral edema, dizziness). Surgical Management Indications Post-Intervention Management 3 4 Pre-operative optimization: Beta-blockade with Metoprolol (25-100mg BID, side Mechanical valves: Warfarin (INR goal 2.5-3.5, side effects: bleeding). effects: fatigue, bradycardia). Bioprosthetic valves: Aspirin (81mg daily, side effects: bleeding, gastric Bridge anticoagulation: Enoxaparin (1mg/kg BID, side effects: bleeding risk, Heart failure therapy: Carvedilol (3.125-25mg BID, side effects: dizziness, irritation). thrombocytopenia). fatigue), Spironolactone (25-50mg daily, side effects: hyperkalemia, Post-operative pain management: Hydromorphone (0.5-2mg q4-6h PRN, side gynecomastia). effects: sedation, respiratory depression). Endocarditis prophylaxis: Amoxicillin (2g single dose) or Clindamycin (600mg) for penicillin-allergic patients.. Definition and Pathogenesis: Endocarditis Definition Pathogenesis Inflammation of the Bacteria or fungi can enter the endocardium, the inner lining bloodstream and attach to of the heart, commonly damaged heart valves, leading affecting the heart valves. to inflammation and infection.  Endocarditis Endocarditis 1 Inflammation of the inner lining of the heart, typically affecting heart valves. Valve Damage 2 Inflammation can damage heart valves, leading to leakage (Regurgitation) or narrowing (Stenosis) Infective Endocarditis 3 Caused by bacteria or fungi that infect the heart valves. Nonbacterial Thrombotic Endocarditis 4 Caused by non-infectious factors, such as cancer or autoimmune disorders.  Pharmacological Management Blood Culture Protocol Common Pathogens IV Antibiotic Obtain at least 2 separate blood cultures Three most common infectious agents: Treatment 4-6 weeks pathogen-directed therapy: from different venous sites before Staphylococcus Ampicillin + gentamicin + antibiotics Streptococcus flucloxacillin/oxacillin Repeat cultures when indicated to ensure Alternative: Vancomycin + gentamicin (if Enterococci bacterial treatment plan is effective penicillin allergy) Based on: The American Heart Association 2015 Adult Infective Endocarditis guidelines and European Society of Cardiologists 2015 management of infective endocarditis guidelines Definition and Pathogenesis: Myocarditis What is Myocarditis? Viral Trigger Disease Progression Inflammation of the myocardium (heart Viral infection triggers an immune The immune response leads to muscle), visible as swelling and response in the heart tissue. inflammation and damage of the heart damage to the muscle tissue. Noted also autoimmune, and muscle tissue. congenital causes Myocarditis Myocarditis Viral Infection Muscle Damage Heart Failure Inflammation of the heart Commonly caused by Inflammation can damage In severe cases, myocarditis muscle, often caused by a viruses such as the heart muscle, leading to can progress to heart failure. viral infection. coxsackievirus or weakened pumping ability. adenovirus. Pharmacological Management of Myocarditis Antiviral Medications Anti-inflammatory Medications Heart Failure Medications Acyclovir: 5-10 mg/kg IV q8h Ibuprofen: 400-800 mg PO q6-8h Lisinopril (ACE inhibitor): 2.5-40 Indication: Herpes virus Indication: Mild inflammation mg daily Indication: Reduced myocarditis Side effects: Renal Side effects: GI upset, bleeding risk ejection fraction Side effects: dysfunction, nausea, headache Cough, hyperkalemia Ganciclovir: 5 mg/kg IV q12h Prednisone: 1-2 mg/kg/day Metoprolol (Beta-blocker): Indication: Cytomegalovirus Indication: Severe inflammation 12.5-200 mg daily Indication: myocarditis Side effects: Side effects: Fluid retention, Heart rate control Side effects: Neutropenia, thrombocytopenia hyperglycemia Fatigue, bradycardia Furosemide (Diuretic): 20-80 mg daily Indication: Fluid overload Side effects: Electrolyte imbalance Definition and Pathogenesis: Pericarditis Definition Pathogenesis Inflammation of the Often caused by viral pericardium, the sac that infections, but can also be encloses the heart. triggered by bacterial infections, autoimmune disorders, or trauma.  Pericarditis Pericarditis Definition Common Causes Primary Symptoms Clinical Signs Acute inflammation of the Primarily triggered by viral Characterized by sharp, Distinguished by a pericardium, the infections (especially stabbing chest pain that characteristic pericardial double-layered protective coxsackievirus, echovirus, typically worsens when lying friction rub - a scratching, sac that encases the heart and influenza), but can also flat or taking deep breaths. grating sound heard through and major blood vessels. result from bacterial Pain may improve when a stethoscope during infections, autoimmune sitting up and leaning heartbeats, indicating conditions, or heart attack. forward. inflammation between pericardial layers.  Pharmacological Management Nonsteroidal Anti-inflammatory Corticosteroids Colchicine Drugs (NSAIDs) Reserved for severe cases or Particularly effective for preventing First-line treatment for acute pericarditis NSAID-refractory patients. recurrence. pain and inflammation. Prednisone: Initial Dosing: 0.5-0.6mg twice daily Ibuprofen: 600-800mg every 8h (max 0.25-0.5mg/kg/day (≥70kg); once daily (