2023 Lecture 1 Cardiac Assessment (1)
Page 1: Title Slide
- Assessment of Canadian Function
- Presenter: Shannon Bang
- Date: Fall 2005
Page 2: Learning Outcomes for Chapter 33
- Physiological Integrity
- Review cardiovascular anatomy and physiology (A&P): structures of the heart, blood flow, and relevant terms.
- Perform a focused physical assessment for patients with cardiovascular (CV) problems — collecting subjective and objective data.
- Identify assessment findings that suggest decreased cardiac output.
- Interpret laboratory test findings for patients with suspected or actual cardiovascular diseases and their clinical implications.
Page 3: Cardiovascular Anatomy and Physiology
- Overview of Circulation
- Capillaries - involved in gas exchange.
- Pulmonary circuit includes:
- Pulmonary arteries (carry deoxygenated blood to lungs)
- Pulmonary veins (carry oxygenated blood back to the heart)
- Heart chambers:
- Right atrium and ventricle for deoxygenated blood.
- Left atrium and ventricle for oxygenated blood.
- Vessels:
- Aorta to systemic arteries convey oxygenated blood.
- Systemic veins return deoxygenated blood to the heart.
Page 4: Cardiac Output
- Cardiac Output (CO): 4-7 L/min
- Formula: CO = Heart Rate (HR) x Stroke Volume (SV)
- Factors affecting cardiac output:
- Preload
- Afterload
- Contractility
- Questions for Discussion: What interventions can affect HR, preload, afterload, and contractility?
Page 5: Autonomic Nervous System
- Sympathetic Nervous System
- Release of catecholamines:
- Epinephrine
- Norepinephrine
- Results in the "fight or flight" response.
Page 6: Stress Response and Heart Rate
- Response Steps:
1. Stress triggers the brain to signal adrenal glands.
2. Adrenaline is released into the bloodstream.
3. Adrenaline acts on heart cells through receptors.
4. Result: Increased heart rate and fight-or-flight reactions.
Page 7: Sympathetic Nervous System Effects
- Beta Adrenergic Receptors:
- Beta 1 (Heart): Increases heart rate, contractility, conduction velocity, and automaticity.
- Beta 2 (Arteries/Vessels): Causes vasodilation and bronchodilation, stimulates renin release.
Page 8: Parasympathetic Nervous System
- Cholinergic System (Acetylcholine):
- Promotes non-stressful conditions.
- Decreases heart rate and force of heart contractions, decreases rate of breathing, and lowers blood pressure.
Page 9: Preload and Afterload
- Definitions:
- Preload: The volume of blood in the ventricles at the end of diastole.
- Afterload: The pressure the heart must generate to eject blood.
Page 10: Arteriolar Tone
- Vasoconstriction: Increased resistance and decreased flow.
- Caused by myogenic activity, increased oxygen, and sympathetic stimulation, among other factors.
- Vasodilation: Decreased resistance and increased flow.
- Triggered by metabolites (NO, histamine) and other factors.
Page 11: Contractility
- Contractility: Force of contraction.
- Higher contractility leads to increased cardiac output.
- Normal Ejection Fraction (EF): 50%-65%.
Page 12: Decreased Cardiac Output Symptoms
- Indicators:
- Altered Level of Consciousness (LOC)/Cognition: ranging from restlessness to unresponsiveness, disorientation, and syncope.
- Urinary output < 0.5 ml/kg/hr.
- Tachycardia.
- Decreased BP.
- Skin changes: pale, central cyanosis, cold/clammy/diaphoretic.
- Weak pulses.
Page 13: Pulse Sites
- Common Pulse Locations:
- Carotid
- Brachial
- Radial
- Ulnar
- Femoral
- Popliteal
- Posterior tibial
- Dorsalis pedis
Page 14: Blood Pressure (BP) Concepts
- Blood Pressure Equation: BP = CO x Afterload
- Systolic BP: Maximum pressure during ventricular contraction.
- Diastolic BP: Minimum pressure during ventricular relaxation.
- Discuss when BP is considered too low or high.
- Orthostatic Hypotension: Risks and prevention strategies.
Page 15: Blood Pressure Categories
- Classification (per AHA Guidelines 2017):
- Normal: SBP <120 mm Hg and DBP <80 mm Hg
- Elevated: SBP 120-129 mm Hg and DBP <80 mm Hg
- Hypertension: Stage 1: SBP 130-139 mm Hg, DBP 80-89 mm Hg; Stage 2: SBP ≥140 mm Hg, DBP ≥90 mm Hg.
Page 16: Cardiac Cycle
- Heart Sounds:
- S1: AV valve closure during systole; best heard at the mitral area.
- S2: Semilunar valve closure; best heard at Erb's point.
- AV valves: Tricuspid/Mitral; Semilunar: Pulmonic/Aortic.
Page 17: Heart Sounds Auscultation
- Auscultation Sites:
- Aortic Area: Right 2nd ICS
- Pulmonic Area: Left 2nd ICS
- Erb's Point: Left 3rd ICS
- Tricuspid Area: Left lower sternal border
- Mitral Area: Left 5th ICS, medial to MCL.
Page 18: Patient Care Overview
- Focus on Patients with Acute Coronary Syndrome (ACS)
- Refer to Chapter 38 for detailed guidelines.
Page 19: Learning Outcomes for Chapter 38
- Health Promotion and Maintenance:
- Differentiate between modifiable and non-modifiable risk factors for coronary artery disease (CAD).
- Develop patient teaching plans for cardiovascular risk modification.
- Psychosocial Integrity:
- Assess responses to acute coronary events, especially myocardial infarction (MI).
- Physiological Integrity:
- Compare stable vs. unstable angina and MI manifestations.
- Interpret assessment findings in CAD patients.
- Prioritize nursing care for chest pain patients.
- Teach about drug therapy for CAD.
Page 20: Statistics on Heart Disease
- Heart disease: Leading cause of death in the US for both genders.
- Death occurs every 38 seconds.
- 20% mortality within one year post-myocardial infarction (MI).
- High rates of undiagnosed CAD among those experiencing MI; 47% of cardiac deaths occur prior to hospital arrival.
Page 21: Coronary Artery Anatomy
- Right Coronary Artery (RCA):
- Supplies blood to the right atrium and ventricle, bottom portion of the left ventricle, and back of the septum.
- Left Coronary Artery:
- Splits into circumflex artery and left anterior descending artery (LAD). Supplies blood to the left atrium, and front/bottom of the left ventricle.
Page 22: Coronary Artery Disease (CAD)
- Pathophysiology:
- Hardening, inflammation, narrowing, and clot development leading to ischemia.
- Arteriosclerosis: Hardened arteries; Atherosclerosis: Plaque development causing narrowing and inflammation, leading to loss of oxygen (ischemia).
Page 23: Plaque Development Process
- Fatty Streaks:
- Development in arterial walls; triggers white blood cells and plaque formation.
- Potential for thrombosis when plaque ruptures.
Page 24: Non-Modifiable Risk Factors for CAD
- Includes:
- Family history of cardiovascular disease
- Advancing age (>45 for men, >55 for women)
- Gender and race.
Page 25: Modifiable Risk Factors for CAD
- Includes:
- Smoking
- Hyperlipidemia
- Hypertension
- Physical inactivity
- Obesity
- Diabetes (Metabolic Syndrome)
- Stress/Depression
Page 26: Assessment Questions
- Key Questions for Nurses:
- Which modifiable risk factors will be assessed for patient teaching?
- A. Older age
- B. Tobacco use
- C. Gender
- D. High-fat diet
- E. Family history
- F. Obesity
Page 27: Cholesterol Overview
- Cholesterol: A waxy substance found in blood and all body cells; needed for hormone production and cell membrane formation.
- Sources: Diet and liver.
Page 28: Lipoproteins
- LDLs (Low-Density Lipoproteins): Stick to artery walls and contribute to plaque buildup.
- HDLs (High-Density Lipoproteins): Carry LDLs to the liver for breakdown; higher HDL levels are protective against heart disease.
Page 30: Medications Affecting Lipoprotein Metabolism
- Interventions Include:
- Diet and exercise (fruits, vegetables, whole grains)
- Niacin: flushing as a side effect.
- Omega-3 fatty acids (fish)
- Statins: dosing instruction and side effects (GI upset, liver damage).
Page 32: Angina Pectoris
- Definition: Chest pain due to cardiac origin; results from ischemia of myocardium.
- Symptoms may radiate to arm and jaw, with associated shortness of breath, anxiety, or nausea.
Page 33: Assessment of Angina
- Differences:
- Stable angina vs. unstable angina; assessing pain characteristics between both types.
Page 34: Electrocardiography (ECG)
- Purpose:
- Evaluates heart rhythm and identifies non-perfused heart regions (myocardial infarction).
Page 35: Stress Testing
- Objective:
- Assess changes in ST segments or dysrhythmias through stress (treadmill/stationary bike or medication-induced).
Page 37: Nursing Implications for Stress Testing
- Preparation:
- Fasting 2 hours prior, avoiding stimulants.
- Hold beta blockers and calcium channel blockers.
- Comfortables clothing and shoes
- Post-test monitoring for 15 minutes.
Page 38: Cardiac Catheterization
- Description:
- Invasive procedure to diagnose heart disease via injected dye and imaging.
- Assess pressures, EF, and extent of atherosclerosis.
Page 39: Catheterization Setup
- Components:
- Brachial artery for access; introducer sheath either in groin or arm.
Page 40: Angiography Procedure
- Process:
- Dye injected into coronary arteries to visualize blockage sites via X-ray images.
Page 41: Coronary Angioplasty Process
- Pre-Stenting and Post-Stenting Comparison:
- 99% proximal LAD stenosis followed by stenting procedure.
Page 42: Nursing Care Before Procedure
- Prerequisites:
- Assess for allergies and obtain consent; establish IV for heparin.
- Monitor kidney function and manage Metformin usage pre and post.
Page 43: Complications from Cardiac Procedures
- Possible Complications:
- Include dysrhythmias, bleeding, dye reactions, ischemia, renal failure, myocardial infarction, and stroke.
Page 44: Post-Angiogram Care
- Post-Procedure Protocols:
- Keep patient leg flat for 2-6 hours, monitor the site, and vital signs.
- Ensure hydration to flush out dye.
Page 45: Nursing Diagnoses for Angina
- Priority Nursing Diagnoses: Address differences between angina and myocardial infarction.
- Common goal: Increase blood supply and decrease demand.
Page 46: Interventions for Angina
- Focus on:
- Reducing heart demands (rest), increasing oxygen supply (medications).
- Monitoring and modifying risk factors.
Page 47: Platelet Aggregation Inhibitors
- Key Medications:
- Aspirin: daily use, with precautions for GI bleeding and contraindications in asthma.
- ADP receptor inhibitors (e.g., Clopidogrel) associated with bleeding risks.
Page 48: Nitrates for Angina Management
- Mechanism:
- Dilates veins and arteries to increase coronary blood flow and reduce blood pressure.
- Available in various forms (sublingual, spray, IV, topical).
Page 49: Nitrate Side Effects
- Common Adverse Effects:
- Hypotension, orthostatic hypotension, headache, and tolerance requiring careful administration.
Page 50: Patient Teaching for Nitrates
- Administration Guidance:
- Must wet mouth before taking.
- Recommended dosing and safety precautions.
Page 51: Beta Blockers Information
- Overview:
- Block epinephrine, reducing HR and BP; various types, including cardiac selective.
- Key Side Effects:
- Bradycardia, bronchoconstriction, hypotension, potential blood sugar influence.
Page 54: Myocardial Infarction Clinical Manifestations
- Subjective Signs:
- Chest pain unrelieved by typical interventions, fatigue, dyspnea, and anxiety.
Page 55: Objective Clinical Findings in MI
- Indicators:
- Altered general appearance: pallor, cool, clammy skin and diaphoresis.
- ST segment changes and increased cardiac enzymes.
Page 56: Cardiac Enzymes
- Markers for Muscle and Myocardial Damage:
- CK (Creatine Kinase), Myoglobin, and Troponin; indicative of muscle and myocardial injuries.
Page 57: Chest Pain Protocol
- Emergency Response:
- Rapid response team activation; immediate EKG and definitive measures for suspected STEMI.
Page 58: Nursing Process for MI
- Key Considerations:
- Determine primary nursing diagnosis, anticipated outcomes, and potential complications following MI.
Page 59: Anticoagulants Overview
- Function and Side Effects:
- Prevent clot formation; includes Heparin and monitoring protocols prior.
Page 60: Heparin Protocols for Angina/NSTEMI
- Dosage Management:
- Specific weight-based protocols with careful monitoring for dosing errors and anticoagulant activity.
Page 61: Patient Self-Management Recommendations
- Focus Areas:
- Medications (aspirin, statins, beta blockers), lifestyle changes (diet, smoking cessation), and cardiac rehabilitation.