Group 1 ACS Arrhythmia CPS PDF

PHCLIN1 GROUP ONE Abellera, Borquel, Canaveral, Marquez, Pastor, Supsup  CONTENTS 1. Acute Coronary Disease/ Syndrome 2. Arrythmia 3. Cardiopulmonary Arrest 01 ACUTE CORONARY DISEASE/SYNDROME  Acute Coronary Syndrome  ACS, is one of the can’t-miss-diagnoses tha...

PHCLIN1 GROUP ONE Abellera, Borquel, Canaveral, Marquez, Pastor, Supsup  CONTENTS 1. Acute Coronary Disease/ Syndrome 2. Arrythmia 3. Cardiopulmonary Arrest 01 ACUTE CORONARY DISEASE/SYNDROME  Acute Coronary Syndrome  ACS, is one of the can’t-miss-diagnoses that must be ruled out when a patient presents with acute chest pain. ACS is caused by sudden decreased coronary blood flow, that also known as cardiac ischemia. TYPE OF ACS  STEMI stands for ST Elevation Myocardial Infarction. It is complete acute blockage of coronary artery which will lead to transmural infarct of the wall supplied by the artery.  NSTEMI or Non-ST-Elevation Myocardial Infarction is imbalance between myocardial oxygen supply and demand which will lead to non-trasmural subendocardial infarct.  Unstable Angina. It is imbalance between myocardial oxygen supply and demand which will lead to myocardial ischemia but not infarction.  PATHOPHYSIOLOGY  ACS is usually atherosclerosis, a condition where fatty deposits (plaques) accumulate in the coronary arteries. These plaques can rupture, leading to the formation of a blood clot that partially or completely obstructs the flow of blood to the heart muscle.  When the supply of oxygen to cells is too low,cells in the heart muscles can die. The death of cells results in damage to muscle tissues which will lead to heart attack.  POTENTIATING FACTORS MODIFIABLE RISK FACTOR NON- MODIFIABLE  Hypertension  Age  Hyperlipidemia (high cholesterol levels)  Family history  Smoking  Gender  Diabetes Mellitus  Obesity  Physical Inactivity  Excessive Alcohol Consumption CLINICAL MANIFESTATION SWEATING NAUSEA AND VOMITING FATIGUE AND PALPITATION WEAKNESS  LABORATORY AND DIAGNOSTIC TESTS 1. 12-Lead ECG - a graphical representation of the heart’s electrical activity, within 10 minutes of presentation to an ED with symptoms of ischemic chest discomfort, a 12-lead ECG should be obtained and interpreted. 2. Troponin I or T Test - is measured at presentation and repeated 2–3 times at 6- to 8- hour intervals to ascertain heart muscle damage. 3. Baseline complete blood count (CBC) and coagulation tests - should be obtained because most patients will receive antithrombotic therapy that increases the risk for bleeding 4. Serum Creatine (SCr) and Creatinine Clearance (CrCl) Test - to identify patients who may need dosing adjustments for medications, as well as those who are at high risk of morbidity and mortality.  LABORATORY AND DIAGNOSTIC TESTS 5. Echocardiogram - identify patients with EF less than or equal to 40% (0.40) who are at high risk of death following hospital discharge. 6. Stress test - a diagnostic procedure used to evaluate how well the heart functions under physical exertion. It often involves walking on a treadmill or riding a stationary bike while the heart is checked. 7. CT Scan - This test looks at the arteries that supply blood to the heart. It uses a powerful X-ray machine to create images of the heart and its blood vessels. 8. Myocardial perfusion imaging - This test shows how well blood flows through the heart muscle. A tiny, safe amount of radioactive substance is given by IV. A specialized camera takes pictures of the substance as it travels through the heart.  TREATMENT AND MANAGEMENT GENERAL APPROACH - Hospital Admission - Oxygen - Continuous multilead ST-segment monitoring - Frequent measurement of vital signs - Pain relief  TREATMENT AND MANAGEMENT Pharmacologic Therapy 1. Nitrates - promote the release of nitric oxide from the endothelium, which results in venous and arterial vasodilation. (eg. NTG or Nitroglycerin) 2. Aspirin - antiplatelet effects of ASA are mediated by inhibiting the synthesis of TXA2through an irreversible inhibition of platelet cyclooxygenase-1. 3. Platelet P2Y12 Inhibitors - block a subtype of ADP receptor (the P2Y12 receptor) on platelets, preventing binding of ADP to the receptor and subsequent expression of platelet GP IIb/IIIa receptors, reducing platelet aggregation. eg. Clopidogrel, Prasugrel, and Ticagrelor 4. Beta Blockers - helps relax the heart muscle and slow the heart rate. They decrease the oxygen demand on your heart and lower blood pressure. eg. Metoprolol, Propranolol, Atenolol  TREATMENT AND MANAGEMENT Pharmacologic Therapy 5. Angiotensin-converting enzyme (ACE) inhibitors - widen blood vessels and improve blood flow. This helps the heart to work better. eg. Lisinopril, Benazepril and others. 6. Statins - lower the amount of cholesterol in the blood. eg. Torvastatin, Simvastatin and others. 7. Thrombolytics: For an immediate breakdown of clots. This is an emergency medication. eg. Anistreplase, Reteplase, Streptokinase  TREATMENT AND MANAGEMENT Non-Pharmacologic Therapy 1. Maintain a healthy weight. Too much weight strains the heart. It also can lead to high cholesterol, high blood pressure, diabetes, heart disease and other conditions. 2. Manage stress. Getting more exercise, practicing mindfulness and connecting with others in support groups are some ways to ease stress. 3. Control your blood pressure. Have your blood pressure checked regularly by your health care provider. 4. Check your cholesterol. Have your blood cholesterol levels checked regularly at a medical office. 5. Eat a heart-healthy diet. Choose fruits, vegetables and whole grains. Limit low-fat dairy products and lean meats.  THERAPEUTIC OUTCOME Restoration of blood flow to the infarct-related artery Prevention of death and other MI complications Prevention of coronary artery reocclusion Relief of ischemic chest discomfort Resolution of ST segment and T-wave changes on the ECG. Relieve pain and distress Enhanced quality of life 02 ARRYTHMIA  PATHOPHYSIOLOGY PRIMARY PACEMAKERS Sino atrial node (SA Node): Cells found in the wall of the right atrium that spontaneously create an action potential (60-100 bpm) LATENT PACEMAKERS Atrioventricular node (AV Node): Impulse arrival at the AV node is briefly delayed to allow the completion of atrial contraction and ventricular filling before the ventricle’s contraction begins BUNDLE OF HIS This is the muscle fiber after the AV node where the impulse continues to travel along the left and right bundle branch located at the septum. PURKINJE FIBERS are special ventricular fibers extending from the bundle branches that receive signals and propagate this impulse to the ventricular muscle causing ventricular contraction.  PATHOPHYSIOLOGY NORMAL AND ABNORMAL CARDIAC CONDUCTION AND ELECTROPHYSIOLOGY The heart functions via both mechanical and electrical activity. Mechanical activity of the heart refers to atrial and ventricular contraction, the mechanism by which blood is delivered to tissues. When circulated blood returns to the heart via venous circulation, blood enters the right atrium. Mechanical activity of the heart (contraction of the atria and ventricles) occurs as a result of the electrical activity of the heart. The heart possesses an intrinsic electrical conduction system The ventricular action potential depicting the flow of specific ions responsible for each phase. The phases of the action potential that correspond to the absolute and relative refractory periods are portrayed, and the relationship between phases of the action potential and the electrocardiogram (ECG).  PATHOPHYSIOLOGY *The P wave reflects atrial depolarization *The PR interval represents the spread of impulses from the atria through the Purkinje fibers. *The QRS complex reflects ventricular depolarization. *The ST segment represents phase 2 of the action potential- the absolute refractory period (part of ventricular repolarization). *The T wave shows phase 3 of the action potential-ventricular repolarization.  PATHOPHYSIOLOGY *The P wave reflects atrial depolarization *The PR interval represents*The the spread P waveof impulses from the reflects atrial atria through the Purkinje fibers. depolarization *ThePR *The QRS complex interval reflects ventricular represents the spreaddepolarization. of impulses from the atria through the Purkinje fibers. *The ST segment represents phase *The QRS 2 of the complex action potential- reflects ventricularthe depolarization. absolute refractory period (part of ventricular repolarization). *The ST segment represents phase 2 of the action potential- the absolute refractory period (part *The T wave shows phase 3 of theofaction potential-ventricular ventricular repolarization. repolarization). *The T wave shows phase 3 of the action potential-ventricular repolarization.  PATHOPHYSIOLOGY  Mechanisms of Cardiac Arrhythmias Abnormal Impulse Initiation Abnormal initiation of electrical impulses occurs as a resultof abnormal automaticity. If SA node automaticity decreases, this results in a reduced rate of impulse generation and a slow heart rate (sinus bradycardia). Conversely, if SA node automaticity increases, this results in an increased rate of generation of impulses and a rapid heart rate (sinus tachycardia). If other cardiac fibers become abnormally automatic, such that the rate of spontaneous impulse initiation exceeds that of the SA node, or premature impulses are generated, other tachyarrhythmias may occur. Many cardiac fibers possess the capability for automaticity, including atrial tissue, the AV node, the Purkinje fibers, and the ventricular tissue.  PATHOPHYSIOLOGY Abnormal atrial automaticity may result in premature atrial contractions or may precipitate atrial tachycardia or atrial fibrillation. Abnormal automaticity in the ventricles may result in ventricular tachycardia (VT) or ventricular fibrillation (VF). Abnormal Impulse Conduction -Impulse fails to die out after normal activation of the heart and persists as a result of continuous activity around the circuit to re-excite  PATHOPHYSIOLOGY An irregular hearbeats including abnormalities of impulse formation Arrhythmias are grouped by the speed of the heart rate: Tachycardia = >100 bpm Bradycardia =