Perfusion_StudentCopy_Spring2024.pptx

Perfusion NRSG3301 CRYSTAL TREIGE MN NP Concept(s) & Exemplar(s) Concept(s): Perfusion Exemplar(s): Acute coronary syndrome (ACS) Myocardial infarction (MI) Heart failure Concept: Perfusion Perfusion refers to the flow of blood through arteries and capillaries delivering nutrients and oxyge...

Perfusion NRSG3301 CRYSTAL TREIGE MN NP Concept(s) & Exemplar(s) Concept(s): Perfusion Exemplar(s): Acute coronary syndrome (ACS) Myocardial infarction (MI) Heart failure Concept: Perfusion Perfusion refers to the flow of blood through arteries and capillaries delivering nutrients and oxygen to cells. Perfusion is a normal physiological process that requires the heart to generate sufficient cardiac output to transport blood through patent blood vessels for distribution in the tissues throughout the body. Thus, maintaining cardiovascular health is essential to optimal perfusion. CO (mls/min) = SV (mls/beat) X HR (beats/min) 5-6L/min avg. healthy adult (Giddens, 2018) Systemic & Pulmonary Circulation Acute Coronary Syndrome Acute coronary syndromes result from acute obstruction of a coronary artery. Consequences depend on degree and location of obstruction and range from unstable angina to non–ST-segment elevation myocardial infarction (NSTEMI), ST-segment elevation myocardial infarction (STEMI), and sudden cardiac death. Symptoms are similar in each of these syndromes (except sudden death) and include chest discomfort with or without dyspnea, nausea, and diaphoresis. Diagnosis is by electrocardiography (ECG) and serologic markers (Merck, 2023) Angina Pectoris Angina pectoris is the medical term for chest pain or discomfort due to coronary heart disease. It occurs when the heart muscle doesn't get as much blood as it needs. Occurs repeatedly (may or may not be predictable) This usually happens because one or more of the heart's arteries is narrowed or blocked, also called ischemia (American Heart Association, 2015) Angina Pectoris Most often caused by atherosclerosis (“the buildup of fats, cholesterol and other substances in and on the artery walls. This buildup is called plaque. The plaque can cause arteries to narrow, blocking blood flow. The plaque can also burst, leading to a blood clot” (MFMER, 2023) The decrease in blood flow -> decrease in oxygen to the myocardium ->pain (build up of metabolites) Can also be caused by the spasm of vascular smooth muscle  ANGINA: CLASSIFICATIONS STABLE ANGINA UNSTABLE ANGINA VARIENT Predictable and consistent Symptoms occur more (Variant angina/ pain that occurs on exertion frequently and last longer Prinzmetal’s angina) and is relieved by rest (5- than stable angina. The 15minutes) threshold for pain is lower, Pain at rest with and pain may occur at rest. reversible ST-segment Can last up to 30+ minutes. elevation; thought to May progress from stable to be caused by unstable angina. coronary artery vasospasm. Sudden & without warning. Types of Angina Angina: Risk Factors MODIFIABLE RISK FACTORS NON-MODIFIABLE RISK FACTORS Smoking Gender (males have increased risk) Diet (e.g. high cholesterol) Age Sedentary lifestyle Family history (e.g. high cholesterol, Excessive alcohol intake hypertension, history of CAD, etc.) Stress Diabetes Obesity Hypertension Diabetes Ethnicity Angina PPRECIPITATING FACTORS ATYPICAL CONSIDERATIONS Physical exertion Diabetes complication: do not always feel the pain because of neuropathy Exposure to cold Elderly: decreased in senses which may blunt pain response Eating a heavy meal Women: report pain differently Stress or an emotionally provoking Cognitive issues situation (release of catecholamines which increases HR) Angina: Symptoms Pain or discomfort that can spread to the chest, jaw, shoulders, arms (mostly the left arm) and back. Chest tightness, burning, heaviness, feeling of squeezing or not being able to breathe. Dizziness Dyspnea Diaphoresis Paleness Weakness Sometimes nausea and/or vomiting Angina: Diagnosis Vital signs EKG (may show reversible ischemic changes e.g. ST-segment depression) Stress test (not during immediate event) Lab testing (Troponin, CBC, INR, blood glucose, etc.) Echocardiogram (not during immediate event) Cardiac angiography *Angina does not result in death of myocardial tissue Angina Pharmacologic Interventions: Vasodilators (Nitroglycerin) nitrates are the main stay of treatment for angina pectoris – cause vasodilation Beta-Andrenergic Blocking Agents (Beta Blockers), e.g. – Metoprolol Calcium Channel Blocking Agents, e.g. – amlodipine and diltiazem Antiplatelet and Anticoagulant Medications - ASA, heparin, clopidogril Angina Bucher & Castellucci, 2014 Myocardial Infarction (MI) A myocardial infarction (MI) occurs as a result of sustained ischemia, causing irreversible myocardial cell death (Myocardial ischemia -> myocardial injury ->myocardial infarction) Myocardial Infarction (MI) Manifestations: Chest pain (may radiate to the neck, jaw, shoulder(s), left arm) Tachycardia, tachypnea Dyspnea, shortness of breath Nausea and vomiting (common) Anxiety and an impending sense of doom Diaphoresis or sweating Cool, mottled skin; diminished peripheral pulses Hypotension or hypertension Palpations, dysrhythmias Signs of left heart failure Decreased level of consciousness Coronary Arteries Myocardial Infarction Myocardial Infarction: EKG Myocardial Infarction: EKG Myocardial Infarction (MI) STEMI = ST-segment elevation myocardial infarction Non-STEMI = Non–ST-segment elevation myocardial infarction ACS Signs & Symptoms of MI Chest pain (crushing substernal radiating to jaw, arm, back, etc.). Women may present differently with back, arm pain, etc.) Dyspnea Diaphoresis (clammy, cool skin) Anxiety Nausea and/or vomiting Heartburn Dizziness ***Fatigue Myocardial Infarction (MI) Immediate treatment goals for pt dx. With MI include: **EKG within 10 minutes of presentation Relieve chest pain Reduce the extent of myocardial damage Maintain cardiovascular stability Decrease cardiac workload Prevent complications ** ‘Time is muscle’  recommendation for the initiation of percutaneous coronary intervention (PCI) within 60 minute of medical contact Bucher & Castellucci, 2014 Ddiagnostics EKG Vital signs Labs: Troponin I  elevated 2-4 hrs; peaks 24-36 hrs; lasts 7-10 days Troponin T  elevated 2-4 hrs; peaks 24-36 hrs; lasts 10-14 days CK-MB  elevated at 4-8 hrs, peaks 18-24 hrs; lasts 72 hrs C-reactive protein inflammatory CBC, INR, blood glucose, etc. Stress test, cardiac echo, angiography, etc. Coronary Angioplasty Treatment: Medication FIBRINOLYTICS- TNK, Streptokinase ASAP: rule out contraindications Morphine may/may not be considered Oxygen Nitroglycerine ASA Angiotensin-converting enzyme (ACE inhibitors), e.g. – enalapril *Also reduce mortality with MI HEART FAILURE (HF) Heart Failure Heart Failure is a condition in which the heart is unable to pump enough blood into circulation to meet the body’s needs (maybe acute or chronic) The inability of the heart to: Fill with enough blood AND/OR Pump with enough force to meet the metabolic demands. CO= HR x SV (4-8 L/min some sources 5-6L/min) Causes MI, coronary artery disease (CAD) Hypertension (including pulmonary hypertension) Fluid overload Atrial fibrillation (A-fib) – upper chambers of the heart (atria) beat at an irregular rhythm Valve issues (incomplete closure) Infection Substance use disorder Congenital Hypermetabolic states Heart Failure RIGHT SIDED LEFT SIDED Systemic Pulmonary Edema Peripheral Edema EF50% (Ejection fraction measures the amount of blood the left ventricle of the JVP increase heart pumps out to your body with each heartbeat) Weight gain (2/day or 5/wk) Crackles Hepatomegaly Orthopnea Lethargic PND Nocturia Dyspnea, cough Weight gain Heart Failure: Manifestations (Abdel-Bassett et al., 202 Heart Failure Diagnostic Testing: B natriuretic peptide (BNP) 300, >600 mod., >900 severe CXR (cardiomyopathy, fluid) ECG Echocardiogram Serum electrolytes Urinalysis, blood urea nitrogen (BUN), serum creatinine Liver function tests (LFT’s) Arterial blood gas (ABG’s) Dantino-Bouffard, 2014 Pharmacology Angiotensin-Converting Enzyme Inhibitors - Perindopril Angiotensin II-Receptor Blockers - Atacand (candesartan) Beta-Blockers Diuretics, Vasodilators Antiarrhythmics Positive Inotropic Agents (dig) Heart Failure: Treatment Approach Interrelated Concepts Referenc es Bermudez, N. (2012). ACS: A triad of troubles sets the stage for MI, Nursing Made Incredibly Easy, 10(6), 14-17. Bucher, L. & Castellucci, D. (2014). Chapter 36: Nursing management: Coronary artery disease and acute coronary syndrome. In S. Lewis, S. Dirksen, M. Heitkemper, L. Bucher, & I. Camera (Eds.). Medical-Surgical Nursing in Canada: Assessment and Management of Clinical Problems (3rd Cdn. ed.) (pp. 891-927) (M. Barry, S. Goldworthy, D. Goodridge, Cdn. Adpt.). Toronto, ON: Elsevier Canada. Buckler, L. (2009). Managing heart failure, Nursing Made Incredibly Easy, 7(3), 12-21 Crowther, M. (2012). Heart failure readmissions: Can hospital care make a difference?, Nursing Made Incredibly Easy, 10(2), 1-3. Dantino-Bouffard, , L. (2014). Chapter 37: Nursing management: Heart failure. In S. Lewis, S. Dirksen, M. Heitkemper, L. Bucher, & I. Camera (Eds.). Medical-Surgical Nursing in Canada: Assessment and Management of Clinical Problems (3rd Cdn. ed.) (pp. 928-949) (M. Barry, S. Goldworthy, D. Goodridge, Cdn. Adpt.). Toronto, ON: Elsevier Canada. Herman, A. (2013). Coronary artery disease: The plaque plague. Nursing Made Incredibly Easy, 11(2), 34-43. Kirwan, M. (2009). An eye for MI. Nursing Made Incredibly Easy, 7(1), 5-10. Markaity, M. (2012). Congestive heart failure: An 'F' isn't an option. Nursing Made Incredibly Easy, 10(2), 13-23. Trakalo, K.., Horowitz, L., & McCulloch, A., (Eds.) (2015). Nursing: A concept-based approach to learning. (Vol. 1& 2). Boston, MA: Pearson Education. Wilson, S. (2017). Chapter 18: Perfusion. In J. Giddens (Ed.), Concepts for nursing practice, 2nd edition (pp. 179-187). St. Louis, MO: Elsevier.