Cardiology Week 2 Notes
Cardiology Week 2 Notes NSG 335
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This 5 page Class Notes was uploaded by Brieanna Phipps on Tuesday March 1, 2016. The Class Notes belongs to NSG 335 at University of North Carolina - Wilmington taught by Dr. Sauer in Spring 2016. Since its upload, it has received 27 views. For similar materials see Pathology and Pharmacology in Nursing and Health Sciences at University of North Carolina - Wilmington.
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Date Created: 03/01/16
Arteriosclerosis -chronic disease of the arterial system -abnormal thickening and hardening of the vessel walls Artherosclerosis -type of arteriosclerosis that occurs from build up of fats, cholesterol to form plagues on arteries which restricts blood flow. -plaque development -begins with injury to the endothelial cells -risk factors for injury: -smoking, HTN, diabetes, increased LDL, decreased HDL, autoimmunity -non-traditional risk factors: -elevated C-reactive protein, increased fibrinogen, insulin resistance, oxidative stress, periodontal disease, infection -progression: -inflammation fat streak fibrous plaque complicated plaque -results in: -inadequate perfusion, ischemia, necrosis Myocardial Ischemia -local, temporary cut off blood supply to the heart via the coronary arteries -ST changes when you are having ischemia -STEMI: ST elevation, more severe -non-STEMI: don’t see changes on EKG, but there are enzymes that have spilled from damaged cells -increased stress levels and hormones can increase ischemia -Stable Angina: progressive pain that exacerbates during exercise and subsides with rest -treat with long acting nitrates -Printzmetal’s Angina: vasospasm of coronary artery that doesn’t allow enough blood to pass -can progress to an MI if the spasm does not cease -treat with CCBs -Silent Ischemia: brought on by mental stress -more common in women -no traditional signs of ischemia -fatigue, back pain Unstable Angina -stable angina that does NOT stop with rest -same process as AMI -treatment for ANGINA-MONA -Morphine -dec RR, lower BP and HR, decrease pain and stress -Oxygen -helps save cells, 2-4L NC -Nitrates -vasodilates causing BP to go down -Aspirin -makes platelets more SLIPPERY to continue blood flow -325 mg, CHEW IT so it is more effective Chest Pain -injury to the cells begins after 8-10 seconds of decreased blood flow. That is when pain/angina starts: -chest pain -arm pain -jaw pain -indigestion -glycogen is depleted, becomes acidotic, oxygen imbalance leads to electrolyte imbalance, stimulation of PNS and SNS, increased glucose levels form SNS -angiotensin II is released with lack of blood flow- which causes vasoconstriction, fluid restriction, and release of catecholamines which causes vasospasms Cellular Death -cells release enzymes as they die (non-STEMI) -the muscle is stunned which decreases contractility -left side stunned, fluid will go to lungs and cause crackles -remodeling is mediated by angiotensin II (blocked by ACE or ARB) -clinical manifestations: -increased HR and BP, S3 sounds, crackles, peripheral vasoconstriction (skin cool and clammy) Medications for Ischemia -Nitrates -vasodilate -Beta Blockers -slow HR, increase diastolic filling time -Calcium Channel Blockers -relaxes muscles -works for ischemia or angina -for ANY spasm, use a CCB Medications for Angina/AMI -goal is to decrease the demand for oxygen. -increase oxygen or blood supply. -Aspirin decreases platelet aggregation -used indefinitely at 81-325mg/day Anticoagulants -Heparin -used to prevent clot from getting better -ADR: bleeding, Heparin-induced thrombocytopenia (HIT) -antidote: protamine sulfate -Warfarin -inhibits activity of vitamin K, which activates certain clotting factors -DVT treatment, embolization from A-fib or heart valve replacement, pulmonary embolism -antidote: vitamin K Interventions for AMI -Percutaneous Coronary Intervention (PCI) -punctures through femoral or radial artery -catheter through aorta to heart -PTCA (angioplasty) -Stents -bare metal -drug eluding- cephalosporin to decrease chance of rejection -Tissue Plasminogen Activator (TPA) -medication for patients who had S/S less than 3 hours before administration and PCI will be delayed for more than 2 hours -greatest risk is intracranial bleeding -contraindicated if S/S started more than 24 hours ago, scheduled for CABG, recent surgery or trauma, PUD, severe HTN, brain cancer -often results in reocclusion of the artery and failure to restore blood flow -used more in places where cardiac catheterization is not available Sinus Rhythms Originate with SA node Regular Sinus Bradycardia o Rate <60 o Causes: high fluid volume, MI, BB o Med: atropine Sinus Tachycardia o Rate 100-150 o Causes: exercise, anxiety, fever, low O2 o Identify the causes and treat it Atrial Rhythms Start in atria, but not SA node Atrial Tachycardia o Rate: 150-250 o Absent P wave o Can cause decreased coronary perfusion and ventricular filling o Meds: amiodarone, adenosine o Tx: Vagal manuevers, synchronized cardioversion Atrial Flutter o Rate varies o “saw-tooth” waves o No PR interval; One cell is being a bully and no letting SA node be in control o Meds: remove cause, BB, CCB, amiodarone, digoxin o Tx: synchronized cardioversion Atrial Fibrillation o Rate varies o Atria are quivering- no atrial kick o Meds: anticoagulant for potential clotting, CCB, BB, amiodarone o Tx: synchronized cardioversion Ventricular Rhythms Originate in ventricles Ventricular tachycardia o Can be with/without a pulse o Rate: >100 o No P wave o If there is a pulse: amiodarone, synchronized cardioversion o No pulse: defibrillation and CPR Ventricular Fibrillation o Rate: not measurable o No pulse o Will lead to asystole- must defibrillate, CPR Difference between Cardioversion and Defibrillation -Cardioversion -done to correct ventricular tachycardia (pulse) and atrial dysrhythmias -done under sedation, unless there is a threat of cardiovascular collapse -may cause serious dysrhythmias -may cause a transient elevation of ST segment -may cause pulmonary edema (rare) -Defibrillation -emergency life-saving procedure for ventricular tachycardia (no pulse), ventricular fibrillation and cardiac arrest -restarts the heart -no anesthesia is needed -may cause myocardial necrosis
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