Cardiac
Week 4 Cardiac Lecture I: Management of Cardiac Conditions and Pharmacology
Overview of Patient Care Management
Angina and Myocardial Infarction: Comprehensive management of patients experiencing these conditions, including initial assessment, pharmacological intervention, and potential revascularization strategies. Detailed management is covered in specific sections below.
Hemodynamic Shock: Management details are covered in a separate, dedicated lecture on shocks and hemodynamics. This includes various types of shock such as cardiogenic, hypovolemic, septic, and anaphylactic.
Electrical Conduction Disorders:
Focus on life-threatening dysrhythmias such as Ventricular Fibrillation (VFib), Pulseless Ventricular Tachycardia (pVT), and various degrees of heart block.
Treatment adheres to the latest ACLS (Advanced Cardiac Life Support) guidelines, as discussed in lectures, emphasizing rapid recognition and intervention.
Vascular Disorders (Life-Threatening): Specific attention to aneurysms, particularly aortic aneurysms (thoracic and abdominal), which involve a localized dilation of a blood vessel often due to weakening of the vessel wall.
Coagulation Disorders: Management of DIC (Disseminated Intravascular Coagulation), HIT (Heparin-Induced Thrombocytopenia), and ITP (Idiopathic Thrombocytopenic Purpura) is addressed in a separate lecture on shocks and hemodynamics, focusing on diagnosis and specific treatment protocols.
Surgical Interventions for Damaged Organs:
Coronary Artery Bypass Graft (CABG): Revascularization to improve blood flow to the heart muscle using grafts.
Aortic Valve Replacement (AVR): Replacement of a diseased aortic valve.
Aneurysm Repair: Surgical intervention to reinforce or replace a weakened arterial wall.
Heart Transplant: Replacement of a diseased heart with a healthy donor heart.
Advanced Therapeutic and/or Diagnostic Procedures: Designed to support cardiac output and tissue perfusion.
Electrocardiography (ECG/EKG): Non-invasive recording of the heart's electrical activity.
Hemodynamic Monitoring: Covered in a separate lecture with shocks, including arterial lines, central venous pressure (CVP), and pulmonary artery catheters.
Cardioversion and Defibrillation: Electrical therapies for dysrhythmias; details found in the EKG lecture outline.
Angiography: Imaging technique using contrast dye to visualize blood vessels.
Percutaneous Coronary Intervention (PCI): Non-surgical procedure to open narrowed coronary arteries.
PBG (Peripheral Bypass Graft): Surgical rerouting of blood around an occlusion in a peripheral artery.
Ventricular Assist Device (VAD): Mechanical pump implanted to support heart function and blood flow.
Pharmacology: Extensive review of essential cardiac medications (textbook recommended), including their mechanisms of action, indications, contraindications, and nursing considerations.
Antiarrhythmics
Vasopressors
Vasodilators
Adrenergic Agonists
Thrombolytics
Antiplatelets
Anticoagulants
Recommended Resources
EKG Practice: Use the
skillstat.com/tools/ecg-simulator/for a timed EKG game of common cardiac rhythms. This simulator is an excellent tool for developing rapid rhythm recognition skills crucial in emergency cardiac care. Click "LEARN" for educational content to reinforce understanding.Readings (from Course Point/Textbook):
All Quality and Safety Alerts from cardiac chapters, focusing on critical patient safety considerations.
Review tables on:
Common Medications Used to Treat Heart Failure, including dosages and side effects.
Medications Used in Cardiopulmonary Resuscitation, emphasizing ACLS protocols.
Summary of Antiarrhythmic Medications, detailing their classes and specific actions.
Common Serum Laboratory Tests and Implications for Patients with Cardiovascular Disease, such as cardiac biomarkers, electrolytes, and lipid panels.
Applying Electrodes: Proper technique for accurate ECG readings.
Nursing Research Profile - Electrode Placement, Skin Preparation, and Alarm Fatigue, highlighting evidence-based practice.
Patient Education - Self-Management After Cardiac Catheterization, including activity restrictions and wound care.
Risk Factors - Atrial Fibrillation, to guide prevention and patient teaching.
Assisting with External Defibrillation or Cardioversion, outlining nurse's role and safety measures.
Assessment - Assessing Angina, using PQRST mnemonic and associated symptoms.
Home Care Checklist - Managing Angina Pectoris, for continuity of care.
Assessment - Assessing for Acute Coronary Syndrome or Acute Myocardial Infarction, focusing on prompt recognition.
Treatment Guidelines for Acute Myocardial Infarction, including time-sensitive interventions.
Pharmacology - Administration of Thrombolytic (Fibrinolytic) Therapy, detailing indications and contraindications.
Pulmonary Artery Catheter and Pressure Monitoring Systems, for advanced hemodynamic assessment.
Postoperative Care of the Cardiac Surgical Patient, covering wound care, pain management, and complication monitoring.
Recommended Internet Sources: Reliable and evidence-based resources for continuous learning and professional development.
AACN (American Association of Critical Care Nurses): Offers resources for critical care nursing.
ACC (American College of Cardiology): Provides clinical guidelines and educational content for cardiovascular professionals.
AHA (American Heart Association) for professionals: Focuses on cardiovascular health, research, and emergency cardiac care.
HFSA (Heart Failure Society of America): Dedicated to advancing heart failure research and patient care.
Diagnostic Tests: General Rules and EKG Procedure
Nature of Tests: Can be invasive (e.g., cardiac catheterization) or noninvasive (e.g., ECG, blood tests). Registered nurses perform aspects of both (e.g., ECG, blood glucose testing) and are crucial in preparing patients and interpreting findings.
General Rules and Procedures for All Client Diagnostic Tests: These universal guidelines ensure patient safety, accurate results, and ethical practice.
Verification of the doctor's order for the specific test, ensuring the correct test is performed.
Verification and validation of client's identity using at least two unique identifiers (e.g., name and date of birth) to prevent errors.
Providing the client and/or significant others with a clear explanation of the diagnostic test (purpose, procedure, specific preparation like NPO after midnight) to ensure informed consent and cooperation.
Verification of the client's consent, as indicated, especially for invasive procedures.
Proper adherence to universal precautions, medical or surgical asepsis, to prevent infection.
Proper handwashing before and after each specimen collection and/or bedside diagnostic testing as a fundamental infection control measure.
Proper, complete, and accurate labeling of all nurse-obtained bedside specimens (minimally includes full name, date, and time of collection) to ensure correct identification.
Proper preservation (e.g., refrigeration, immediate transport) and timely transportation of the specimen to the laboratory with the correct requisition slip to maintain specimen integrity.
Use of the proper receptacle or container for the specific specimen, including necessary preservatives, chemicals, or anticoagulants, essential for accurate analysis.
Proper disposal of all used supplies and equipment following facility policies and biohazard protocols.
Performing a -Lead EKG Test: A -lead EKG provides a comprehensive view of the heart's electrical activity from different angles, crucial for diagnosing ischemia, infarction, and arrhythmias.
Assist the client into a comfortable supine position to minimize movement artifact.
Ask the client to remain as still as possible during the ECG to ensure clear signal acquisition.
Expose the client's chest, lower legs, and lower arms for electrode placement.
Cleanse the skin with alcohol and allow it to dry in the areas where leads will be placed to ensure good electrode contact and reduce impedance.
Secure the electrodes to flat areas on each extremity (above wrists and ankles) and on the chest according to anatomical landmarks.
Place the other six electrodes on the chest in the correct anatomical areas (V1-V6) for accurate readings of the precordial leads.
Run the ECG strip, ensuring proper machine calibration and speed.
Print the electrocardiogram data and place it into the client's medical record according to facility policy for review by the physician.
Notify the doctor of any unexpected or abnormal findings (e.g., ST elevation, new bundle branch block) immediately for prompt intervention.
Pharmacology in Cardiac Care
Key Drug Classes: These classes represent the primary pharmacological approaches to managing cardiac conditions, each with distinct mechanisms of action.
Antiarrhythmics: Restore normal heart rhythm.
Vasopressors: Increase blood pressure.
Vasodilators: Decrease blood pressure.
Adrenergic agonists: Mimic sympathetic nervous system effects.
Thrombolytics: Dissolve existing clots.
Antiplatelets: Prevent clot formation by inhibiting platelet aggregation.
Anticoagulants: Prevent clot formation by inhibiting clotting factors.
IV Vasopressors: These potent drugs are used to raise blood pressure in hypotensive states, often in critically ill patients.
Risk of tissue necrosis due to extravasation (leakage of drug into surrounding tissue), which can lead to severe tissue damage.
Central line access is preferred for administration due to the caustic nature of these drugs and to minimize extravasation risk.
Antidote for extravasation: Anticipate using of normal saline (NS) with of Phentolamine for local vasodilation. Phentolamine is an alpha-adrenergic blocker that counteracts the vasoconstrictive effects of the vasopressor, promoting blood flow to the affected area.
Adrenergic Receptors: These receptors mediate the effects of sympathetic nervous system neurotransmitters (epinephrine and norepinephrine) and vary in their physiological responses.
Alpha Adrenergic Receptors:
Agonists (e.g., Phenylephrine, Norepinephrine): Cause vasoconstriction, increased peripheral vascular resistance, and increased blood pressure.
Blockers/Antagonists (e.g., Prazosin, Phentolamine): Cause vasodilation, decreased peripheral vascular resistance, and decreased blood pressure.
Beta Adrenergic Receptors:
Agonists and Blockers/Antagonists.
Beta Adrenergic Receptor Sites: Primarily located in the heart. Stimulation causes tachycardia (increased heart rate) and increased myocardial contraction (e.g., Dopamine, Dobutamine).
Beta Adrenergic Receptors: Primarily located in the lungs and peripheral vasculature. Stimulation leads to bronchodilation and peripheral arterial vasodilation; they also relax smooth muscle and cause a slight increase in heart rate (e.g., Albuterol).
Always check if a drug is an Agonist (stimulates the receptor) vs. Antagonist (blocks the receptor) to understand its therapeutic effect.
Antiarrhythmics: Medications used to suppress abnormal heart rhythms, classified by their primary mechanism of action.
Classes: I (sodium channel blockers - IA, IB, IC), II (beta-blockers), III (potassium channel blockers), IV (calcium channel blockers).
Examples: Quinidine (Class IA), Amiodarone (Class III), Sotalol (Class II/III), Procainamide (Class IA), Lidocaine (Class IB), Flecanide (Class IC), Encainide (Class IC), Tcainaide (Class IC), Propafenone (Class IC), Adenosine (miscellaneous, slows AV conduction).
Class II (Beta-blockers): Esmolol, Metoprolol, Propranolol; reduce heart rate and contractility by blocking beta-adrenergic stimulation.
Class IV (Calcium Channel Blockers): Diltiazem and Verapamil; slow AV conduction and reduce myocardial contractility.
Vasopressors: Drugs that induce vasoconstriction and thereby elevate mean arterial pressure, used in states of severe hypotension.
Epinephrine, Norepinephrine, Vasopressin, Phenylephrine, Giapreza (Angiotensin II drug).
Vasodilators: Medications that relax and widen blood vessels, leading to decreased vascular resistance and increased blood flow.
Drips: Nipride (Nitroprusside) and Nitroglycerine (NTG).
Nipride requires a brown bag for light protection as it is light-sensitive. It necessitates close monitoring for neuro changes indicative of cyanide toxicity, especially with prolonged use or high doses. Cyanide is a metabolite of nitroprusside.
Calcium Channel Blockers (Arterial Vasodilators): Clevidipine (Cleviprex) and Nicardipine (Cardene); reduce peripheral vascular resistance.
ACE Inhibitors: Enalapril (Vasotec); block the conversion of angiotensin I to angiotensin II, leading to vasodilation.
Alpha Adrenergic Blockers: Labetalol (blocks alpha and beta receptors) or Phentolamine (Regitine), which dilate both arteries and veins.
Adrenergic/Sympathetic Drugs: Medications that mimic or modify the effects of the sympathetic nervous system.
Epinephrine (Epi): Acts as a partial adrenergic agonist (beta-2 bronchodilation) and partially non-adrenergic (alpha-1 vasoconstriction in high doses). It is a potent vasoconstrictor and cardiac stimulant.
Albuterol: Primarily a beta-2 adrenergic agonist, causing bronchodilation. It can also lower serum potassium by promoting the intracellular shift of potassium.
Adrenergic Agonists:
Alpha : Phenylephrine, Oxymetazoline (nasal decongestant); cause vasoconstriction.
Alpha : Clonidine, Methyldopa; inhibit sympathetic outflow, leading to vasodilation and reduced BP.
Beta : Dopamine (at high doses); increases myocardial contractility and heart rate.
Beta : Albuterol; causes bronchodilation.
Cholinergic (Parasympathetic): Acetylcholine: The primary neurotransmitter of the parasympathetic nervous system, generally producing opposite effects to adrenergic drugs (e.g., slowing heart rate).
Chronotropic Agents: Affect heart rhythm/rate (e.g., positive chronotropes increase heart rate, negative chronotropes decrease it).
Antagonists/Beta Blockers: Esmolol: A short-acting beta-1 selective blocker used for rapid heart rate control.
Thrombolytics or Fibrinolytics: Drugs that dissolve existing blood clots, crucial in acute occlusive events.
Mechanism: Work by converting plasminogen to plasmin, an enzyme that breaks down fibrin in clots.
Examples: Alteplase (TpA), Streptokinase, TNKase (Tenecteplase).
Uses: Acute Ischemic Stroke, Myocardial Infarction (MI), Pulmonary Embolism (PE), Deep Vein Thrombosis (DVT), blocked central lines or dialysis catheters.
TNKase is specifically used for stroke and MI due to its fibrin specificity and ease of administration.
Contraindications: Include active bleeding, recent surgery, hemorrhagic stroke, severe uncontrolled hypertension, and known bleeding disorders.
Antiplatelets: Prevent platelet aggregation, which is the initial step in thrombus formation, helping to prevent arterial clots.
Anticoagulants: Prevent clot formation or extension by interfering with the coagulation cascade, primarily targeting venous clots but also used for arterial prevention in certain conditions.
Examples: Apixaban (Eliquis - DOAC), Dabigatran (Pradaxa - DOAC), Edoxaban (Savaysa - DOAC), Enoxaparin (Lovenox - Low Molecular Weight Heparin), Heparin (unfractionated), Rivaroxaban (Xarelto - DOAC), Warfarin (Coumadin - Vitamin K antagonist).
Resource:
medlineplus.gov/bloodthinners.htmlfor comprehensive patient information.
Inotropic Drugs (for Cardiogenic Shock): These drugs enhance myocardial contractility, thereby increasing cardiac output, which is vital in conditions like cardiogenic shock where the heart's pumping ability is severely impaired. This is known as a positive inotropic effect.
Dobutamine: A beta-1 agonist, maximum dose is .
Milrinone: A phosphodiesterase inhibitor, dose range is .
Key Points for Cardioversion and Defibrillation
Electric Cardioversion in Atrial Fibrillation (AFib): A Transesophageal Echocardiogram (TEE) may be performed prior to the procedure to evaluate for possible atrial thrombi. This is crucial to prevent embolic stroke if a clot is present.
Defibrillation Pad Placement: Pads should not touch the patient's clothing or bed linen. Also, avoid placing pads near medicine patches (e.g., nitroglycerine, nicotine) due to potential burns, or in the direct flow of oxygen due to fire risk.
Defibrillator Synchronization: The synchronized part on the defibrillator must always be OFF for defibrillation (delivering an unsynchronized shock to terminate VFib/VTach) and ON for cardioversion (delivering a synchronized shock to avoid the T-wave and prevent VFib).
Pads on Large-Breasted Women: Defibrillation pads should NOT be placed above the breast tissue or directly on the clavicle. Proper placement ensures optimal current delivery across the heart while minimizing skin impedance and discomfort.
Case Study: Deborah and Coronary Heart Disease
Patient Profile: Deborah, years old, smokes half a pack of cigarettes daily, and is overweight. Her father died of an acute MI at age . Annual physical revealed LDL , HDL , and total cholesterol . This profile indicates multiple significant risk factors for cardiovascular disease.
. Deborah's Known Risk Factors for Coronary Heart Disease:
Age (over years old, a non-modifiable risk factor).
Being overweight (contributes to dyslipidemia, hypertension, and insulin resistance).
Smoking (causes endothelial damage, increases oxidative stress, and decreases HDL).
Family history of heart disease (father's MI at a young age is a strong genetic predisposition).
Low serum HDL levels ( is below optimal, reducing protective cholesterol transport).
High serum LDL levels ( is significantly elevated, increasing atherogenic plaque formation).
. Necessity of Diet Modification for Lipid Control: Diet plays a critical role in managing lipid profiles and preventing atherosclerosis.
Excessive caloric intake, particularly from refined carbohydrates and unhealthy fats, lowers HDL levels and contributes to triglyceride elevation.
Elevated serum cholesterol is affected by both dietary cholesterol and a diet high in saturated fats, which impairs LDL receptor function and increases hepatic cholesterol synthesis.
Hypercholesterolemia leads to increased VLDL (very-low-density lipoprotein) and LDL levels in the blood, promoting plaque formation.
Trans fat is a potent atherogenic lipid, directly raising LDL and lowering HDL. Limiting its dietary intake is critical for managing at-risk patients and reducing cardiovascular risk.
. Impact of Smoking and Exercise on Atherosclerosis and Lipids: Lifestyle choices are powerful modifiers of cardiovascular health.
Smoking: Contributes to oxidative processes in the vessel lumen (endothelial damage). It magnifies existing endothelial dysfunction in predisposed individuals, decreases circulating HDL levels, and increases platelet aggregation and carbon monoxide levels, leading to reduced oxygen-carrying capacity.
Exercise: Increases serum HDL levels, which has a protective effect. High HDL levels are inversely related to atherosclerosis and coronary artery disease development. HDL clears cholesterol from atheromatous plaques and transports it to the liver for excretion (reverse cholesterol transport), and is believed to inhibit cellular uptake of LDL.
Cardiac Questions for Review (Answers provided)
Sign of Ischemia on EKG: T-wave inversions and ST depression (subendocardial ischemia).
Sign of Infarction on EKG: NSTEMI (Non-ST-Elevation Myocardial Infarction), also known as USA (Unstable Angina), and STEMI (ST-Elevation Myocardial Infarction). Q-waves can also develop after a STEMI, indicating transmural infarction and myocardial cell death.
Variant Angina: Prinzmetal's angina, caused by coronary artery spasm, often occurring at rest and typically responsive to calcium channel blockers.
Complications of an MI: Cardiogenic shock, Ventricular Septal Rupture (VSR), Thromboembolism, Dysrhythmias, Pericarditis, Papillary muscle dysfunction/rupture.
Diagnostic Studies for MI Management: ECG, CXR (to rule out aortic dissection and acute pericarditis), Radionuclide studies (perfusion imaging), MRI/MRA (Magnetic Resonance Angiography), CT/Angiography, Coronary Angiography (gold standard for CAD), Stress testing (pharmacological or exercise).
Pharmacotherapy for MI Management: Oxygen, Sublingual Nitroglycerine (SL NTG) ( every as needed), Daily Aspirin (ASA), Heparin drip (or LMWH), ACE inhibitors (to preserve Ejection Fraction (EF) and prevent ventricular remodeling), Magnesium (if needed for dysrhythmias), Insulin (to maintain blood sugar control, which is critical in MI), Nitrate therapy, Beta-adrenergic blockers.
Most Important Assessment on Nitroglycerine Drip: Blood Pressure (BP), to monitor for hypotension.
Morphine for Chest Pain: IV every as needed for persistent chest pain, also acts as a venodilator.
Difference Between Stable and Unstable Angina (USA):
Stable Angina: Chest pain relieved by rest and Nitroglycerine; predictable pattern related to exertion.
Unstable Angina (USA): Chest pain occurs at rest, is more prolonged and severe than stable angina, or has a different pattern, indicating a worsening of CAD and increased risk of MI.
Causes of Heart Failure:
Impaired Function (Systolic or Diastolic Dysfunction): Cardiomyopathies (dilated, hypertrophic, restrictive), Myocarditis, MI, Valvular disease (stenosis or regurgitation), Congenital Heart defects, Constrictive pericarditis.
Excess Demand (High-Output Failure or Increased Workload): Systemic Hypertension (HTN), Pulmonary Hypertension, Thyrotoxicosis, Pulmonary Edema, Anemia, Fluid Overload.
Heart Failure Management at Home: Sodium (Na) restriction (<2 ext{ g/day), avoidance of alcohol, regular prescribed exercise, and diligent monitoring of daily weights (report gain of in or in a week). Medications include ACE inhibitors (block renin-angiotensin-aldosterone system to reduce afterload), Digoxin (positive inotrope, negative chronotrope), loop diuretics (furosemide), Spironolactone (potassium-sparing diuretic, aldosterone antagonist), beta blockers, and Calcium Channel blockers (in specific cases).
Management for Acute Heart Failure: Hemodynamic monitoring (e.g., arterial line, PA catheter), Intubation and mechanical ventilation, Diuresis (IV loop diuretics), Devices to increase Cardiac Output (CO) (e.g., IABP, VAD), Inotropes (e.g., Dobutamine, Milrinone), Vasodilators (e.g., IV Nitroglycerine, Nesiritide).
Biomarker for Heart Failure Exacerbation: Brain Natriuretic Peptide (BNP), elevated levels indicate ventricular stretch and fluid overload.
Hypertensive Crisis:
Definition: Acute elevation of BP >180/120 ext{ mmHg} that can be a hypertensive urgency (no acute organ damage) or emergency (with acute target organ damage).
Important Assessments: For cardiovascular (MI, heart failure, aortic dissection), cerebrovascular (stroke, encephalopathy), acute renal damage, and retinal damage.
MAP Reduction: Reduce Mean Arterial Pressure (MAP) by no more than within the first hour to prevent hypoperfusion and ischemic events. An arterial line (A-line) may be needed for continuous, accurate BP monitoring.
Medications: Nitroglycerine (NTG), Nipride (Sodium Nitroprusside), Hydralazine, Labetalol, Esmolol, Nicardipine.
Aortic Aneurysms (AA) vs. Aortic Dissection:
Aortic Aneurysm (AA): Dilation of the aorta to times its normal size. Can be thoracic (TAA) and/or abdominal (AAA). Often asymptomatic until rupture. Requires aortic surgical repair for larger sizes (>5.5 ext{ cm}) or rapid expansion.
Aortic Dissection: A tear in the intimal layer of the aortic wall, allowing blood to flow between the layers, creating a false lumen. Often seen with uncontrolled hypertension. Patients present with sudden, severe, ripping or tearing pain in the back or chest, often with fainting, which can indicate dissection of the aorta and potentially cardiac tamponade. Management includes aggressive BP and pain control, and urgent surgery for dissections greater than in length or affecting the ascending aorta.
Cardiac Ischemia Pain vs. Pericarditis Pain:
Pericarditis: Chest pain relieved when leaning forward, increased with deep breathing (pleuritic pain). May be accompanied by fever, chills, and a pericardial friction rub.
Ischemia: Chest pain (angina) increases with activity or exercise, and is typically relieved by rest or nitroglycerine.
Widespread Chest Pain: Aggravated with coughing or palpation typically indicates musculoskeletal pain, not cardiac.
Common Valvular Diseases: Affect the heart's ability to effectively pump blood. Mitral and Aortic Stenosis (narrowing of valve opening) or Insufficiency/Regurgitation (incomplete valve closure). Management involves medical therapy for symptoms and, for severe cases, valve repair or valve replacement (using mechanical or biological/tissue valves).
Myocarditis vs. Myocardial Ischemia:
Myocarditis: Inflammation of the heart muscle, characterized by non-specific ST and T changes on EKG. Caused by viral infections (most common), bacterial infections, or related to medications (e.g., phenothiazines or tricyclic antidepressants), or autoimmune diseases. Managed with supportive care, steroids, immunosuppressive drugs, or in severe cases, heart transplant.
Cor Pulmonale (Right-sided Heart Failure) vs. Left-sided Heart Failure:
Cor Pulmonale: Right-sided heart failure caused by Pulmonary Hypertension or other pulmonary disease (e.g., COPD), leading to increased afterload on the right ventricle.
Left-sided Heart Failure: Results from left ventricle failure, leading to pulmonary congestion (e.g., pulmonary edema) and reduced cardiac output to the systemic circulation.
Types of Cardiomyopathies: Diseases of the heart muscle, affecting its ability to pump blood effectively.
Dilated Cardiomyopathy: Most common type, characterized by ventricular dilation and impaired systolic function. Both right and left ventricular sizes are increased, affecting the tricuspid and mitral valves, leading to insufficiency (regurgitation). Systolic function (pumping ability) is decreased. Lab results often show elevated BNP. Management focuses on treating the cause, addressing arrhythmias, and controlling heart failure symptoms with medications like ACE inhibitors, beta-blockers, and diuretics.
Hypertrophic Cardiomyopathy: Characterized by abnormal thickening of the ventricular wall, particularly the septum. The septum is stiff, affecting diastolic (resting/filling) function, so the heart cannot relax and fill properly. Can cause sudden death from ventricular arrhythmias, often without symptoms, especially in young athletes. Management includes beta-blockers, calcium channel blockers, and in some cases, surgical myectomy or alcohol septal ablation.
Restrictive Cardiomyopathy: Least common type. Characterized by severe stiffness and impaired ventricular filling (diastolic dysfunction) due to fibrosis or infiltration of the myocardium (e.g., amyloidosis, sarcoidosis). Symptoms include heart failure (especially right-sided), arrhythmias, fatigue, weakness, and potential early death due to rigid ventricular walls. Management is primarily symptomatic and aimed at treating the underlying cause.
Cardiac Lecture II: Management of Angina/Myocardial Infarction
Coronary Artery Disease (CAD)
Definition: Narrowing or occlusion of the coronary arteries, typically due to atherosclerosis, which restricts blood flow to the myocardium.
Assessment: A thorough assessment is crucial for early detection and management.
History: Hypertension (HTN), Diabetes Mellitus (DM), Stroke, Rheumatic Fever (Rh.fever), Asthma, Renal disease, and previous cardiac events are significant indicators.
Medications: Current use of vasoconstrictors, HTN medications, cholesterol-lowering drugs (statins), and DM medications provides insight into co-morbidities and current treatment.
Psychosocial Events: Any relevant psychosocial stressors (e.g., chronic stress, depression) can contribute to CAD progression.
Risk Factors: Non-modifiable: Gender (males > females; risk equalizes post-menopause), heredity, age. Modifiable: Smoking, high cholesterol (dyslipidemia), HTN, DM, sedentary lifestyle, obesity/overweight.
Pain Assessment (PQRST): Essential for characterizing chest pain.
Provocation/Palliative: What causes or relieves the pain? (e.g., exertion, rest, nitroglycerine).
Quality: Describe the pain (e.g., crushing, sharp, dull, squeezing, burning, heavy).
Region/Radiation: Where is the pain located and does it spread (e.g., jaw, left arm, back)?
Severity: Rate the pain on a scale (e.g., ); assess impact on daily activities.
Timing/Treatment: When did it start, how long has it lasted, and what has been done to treat it? (e.g., onset, duration, remedies tried).
Diagnostics: Comprehensive evaluation helps confirm CAD and assess its severity.
EKG, Holter monitor (for arrhythmias), Stress test (exercise or pharmacological), Chest X-ray (CXR - to assess heart size and pulmonary congestion), Echocardiogram (Echo - assess heart structure and function), Transesophageal Echocardiogram (TEE - detailed view of heart valves and chambers), Heart scan (e.g., cardiac CT for calcification), Cardiac Catheterization (invasive, gold standard for CAD visualization), MRI, Electrophysiological Studies (EPS - for complex arrhythmias).
CAC (Coronary Artery Calcium) Test: Measures arterial calcium (calcium score) to indicate plaque burden and predict future heart attack risk (AHA, ). A higher score indicates a greater risk.
Labs: Crucial for diagnosis and monitoring.
Electrolytes: Potassium (K+), Calcium (Ca++), Magnesium (Mg++) are vital for cardiac function; imbalances can cause arrhythmias.
Cardiac Enzymes (Biomarkers): Elevated levels indicate myocardial damage.
Troponin I (TNI): Normal value <0.5 ext{ mcg/L}. Highly specific to cardiac muscle. Elevates within hours of MI onset, peaks hours after chest pain onset, and remains elevated for up to days.
Creatine Kinase (CK): Total CK is specific to skeletal muscles, brain, and heart.
Creatine Kinase-MB (CKMB): An isoenzyme specific to cardiac muscle. Increases in hours and returns to baseline in hours. Useful for detecting reinfarction due to its shorter elevation time.
Troponin T (TNT): Normal value <0.1 ext{ mcg/L}. Similar kinetics to Troponin I.
Myoglobin: Elevates within minutes of MI, making it an early, but non-specific, marker. Normal value <72 ext{ ng/mL}. Returns to normal within hours.
CKMB to CK Ratio: Normal is (Reference Interval). A ratio greater than indicates a cardiac source, and greater than indicates MI when total CK is elevated.
Nursing Diagnosis: Common nursing diagnoses for CAD patients.
Pain (Acute Chest Pain related to myocardial ischemia).
Anxiety (related to fear of death, recurrent pain, or diagnostic procedures).
Knowledge Deficit (regarding disease process, risk factors, or treatment plan).
Health Seeking Behaviors (readiness to improve health behaviors).
Management of Care for CAD: Focuses on modifying risk factors and comprehensive medical treatment.
Medical Interventions: Address cholesterol and triglycerides (both fat substances; cholesterol is vital for hormones/cell function and cell membrane integrity, triglycerides store excess calories and are a source of energy).
Antilipemics (Statins): HMG-CoA reductase inhibitors that reduce cholesterol synthesis. Lovastatin (Altocor, Mevacor), Atorvastatin (Lipitor), Fluvastatin (Lescol), Pravastatin (Pravachol), Rosuvastatin (Crestor), Simvastatin (Zocor).
Other Antilipemics: Cholestyramine (Questran - bile acid sequestrant), Colesevelam (Welchol - bile acid sequestrant), Colestipol (Colestid - bile acid sequestrant), Nicotinic acid (Niacin - vitamin B3, reduces VLDL and LDL, increases HDL), Gemfibrosil (Lopid - fibrate, reduces triglycerides), Fenofibrate (Tricor - fibrate).
Prevent Platelet Adhesion and Aggregation: Antiplatelet drugs reduce the risk of clot formation in arteries.
Clopidogrel (Plavix - typically if patient cannot take aspirin, or as dual antiplatelet therapy after stent placement), Ticlopidine (Ticlid), Dipyridamole (Persantine), Aspirin (inhibits COX-1, reducing thromboxane A2 production).
Angina
Definition: Pain or discomfort resulting from myocardial ischemia, an imbalance between myocardial oxygen supply and demand.
Types:
Unstable Angina (USA) or Acute Coronary Syndrome (ACS): New onset, occurring at rest, or worsening pattern.
Stable Angina (SA): Predictable, occurs with exertion, relieved by rest or nitroglycerine.
Silent Angina: Ischemia without chest pain; often detected by EKG changes.
Variant Angina (Prinzmetal's): Caused by coronary artery spasm, often at rest.
Assessment: Similar to CAD assessment, with detailed chest pain evaluation using the PQRST mnemonic, and associated symptoms like dyspnea, diaphoresis, nausea, or lightheadedness.
Diagnostics: EKG (may show ST changes), Labs (cardiac enzymes, Hemoglobin/Hematocrit (H/H) to rule out anemia, cholesterol, triglycerides), Stress testing, Cardiac Catheterization.
Nursing Diagnosis: Acute Chest Pain, Knowledge Deficit (regarding angina management), Activity Intolerance (due to pain or dyspnea), Anxiety.
Management of Care for Angina (Medical for ACS): Rapid intervention to restore oxygen supply-demand balance and prevent progression to MI.
Oxygen administration: To improve myocardial oxygenation, especially if O saturation is below .
Aspirin ( chewable non-enteric coated): To rapidly inhibit platelet aggregation.
Nitroglycerine (SL, spray, topical, or IV): Causes vasodilation, reducing preload and afterload, and increasing coronary artery blood flow.
Isosorbide (oral nitrate): Longer-acting nitrate for sustained vasodilation.
Morphine: Administer only if needed after NTG, as it can reduce antiplatelet effects and cause hypotension; used for pain relief and anxiolysis.
Beta-blockers: Metoprolol, Carvedilol, Propranolol, Labetalol; reduce myocardial oxygen demand by decreasing heart rate, contractility, and blood pressure.
Calcium Channel Blockers: Nifedipine (Procardia), Diltiazem (Cardizem), Verapamil; cause vasodilation and can reduce myocardial oxygen demand, particularly useful for vasospastic angina.
Anticoagulants: Aspirin, Clopidogrel (Plavix), Dipyridamole (Persantine), Ticlopidine, Heparin, Enoxaparin (Lovenox); prevent clot formation and propagation.
ACE Inhibitors: Enalapril (Vasotec), Moexipril (Monopril), Captopril; reduce ventricular remodeling and improve outcomes post-MI.
Glycoprotein IIb/IIIa Inhibitors: Abciximab (Reopro), Tirofiban (Aggrastat), Eptifibatide (Integrilin); potent antiplatelet agents used in PCI or high-risk ACS. They block the final common pathway of platelet aggregation.
Advanced Therapeutic and/or Diagnostic Procedures to Support Cardiac Output
Angiography and PCI (Percutaneous Coronary Intervention): Invasive procedures used to visualize and treat coronary artery blockages.
PCI for Angina: Performed in the Cardiac Catheterization Lab (Cath Lab) to open stenotic or occluded coronary arteries.
Procedures:
Stent placement: A mesh tube inserted to keep the artery open.
Drug-Eluting Stents (DES): Stents coated with antiproliferative agents (e.g., sirolimus, everolimus, zotarolimus, paclitaxel, biolimus) to prevent restenosis.
Angioplasty: Balloon inflation to compress plaque against the arterial wall.
PCI Sites: Brachial, Radial, or Femoral artery; preferred site may vary based on patient anatomy and operator preference.
Post-Procedure Care: Critical for preventing complications and ensuring patient recovery.
Check insertion site for hematoma, bleeding, or ecchymosis.
Monitor for retroperitoneal bleeding if femoral site was used (indicated by flank pain, dropping BP, tachycardia, rigid abdomen).
Instruct patient not to bend the groin if femoral site was used (maintain leg straight) to prevent re-bleeding or hematoma expansion.
Perform pulse checks (posterior tibial, pedal) in the affected extremity (distal to the insertion site) to assess for arterial occlusion.
Monitor Blood Pressure (BP) closely for hypotension or hypertension.
Post-Cath Lab Arrhythmias: Ventricular Tachycardia (VTach), Atrial Fibrillation (AFib), AV blocks, Reperfusion PVCs (Premature Ventricular Contractions), STEMI (due to procedure-related complications).
CABG (Coronary Artery Bypass Graft): A surgical revascularization procedure where healthy blood vessels (grafts) are used to bypass blocked coronary arteries, commonly using the saphenous vein from the leg or the internal mammary artery (IMA) from the chest wall.
Acute Myocardial Infarction (MI) Management
Best Practice: Patients should be transported from the ED or ambulance directly to the Cardiac Cath Lab if personnel are available, to minimize time to treatment (door-to-PCI time) and limit myocardial damage.
Definition: Death (necrosis) of myocardial tissue resulting from prolonged severe ischemia, typically due to persistent occlusion of a coronary artery.
Pathophysiology: Imbalance between myocardial oxygen supply and demand, with supply severely reduced or cut off, leading to cellular anoxia and death.
Terminology: Older terms like Q-wave vs. Non-Qwave MI are no longer common; current terms are USA (Unstable Angina), STEMI (ST-Elevation Myocardial Infarction), and NSTEMI (Non-ST-Elevation Myocardial Infarction), all falling under ACS (Acute Coronary Syndrome). STEMI denotes a full thickness (transmural) infarction.
Assessment: Signs and symptoms (chest pain, dyspnea, nausea, diaphoresis), plus fulfilling out of criteria for MI: Chest Pain (CP) consistent with ischemia, elevated Troponin I (TNI) or CKMB, and ST elevation on EKG (for STEMI).
Diagnosis: EKG (ST elevation or depression, T wave inversion, Q waves), Cardiac Enzymes (elevated Troponin and CKMB), and Cath Lab findings (identification of culprit lesion).
Nursing Diagnosis: As listed for CAD/Angina, often including Decreased Cardiac Output, Risk for Impaired Spontaneous Ventilation, and Risk for Dysrhythmias.
Complications: Heart Failure, Arrhythmias (life-threatening VT/VF), Death, Wall rupture (ventricular or papillary muscle), Thromboembolism (due to mural thrombi), Pericarditis (Dressler's syndrome).
Medical Management: Time-sensitive interventions to limit infarct size and manage complications.
Pain Relief, Oxygen, Antiarrhythmics, Prevention of platelet aggregation, Fibrinolytic therapy (if PCI not available).
Fibrinolytic Therapy: Door-to-needle time of ; indicated if symptom onset is hours and no contraindications are present (e.g., active bleeding, prior hemorrhagic stroke).
Cath Lab (PCI): Door-to-PCI time of (ideally from first medical contact for STEMI). This is the preferred reperfusion strategy.
Surgical Revascularization: CABG (using saphenous vein or Internal Mammary Artery (IMA) grafts), Transmyocardial Revascularization (TMR) or Transmyocardial Laser Revascularization (TMLR - creating channels in heart muscle for blood flow).
ACLS Management of ACS
EMS Assessment: Initial critical actions by emergency medical services.
ABCs (Airway, Breathing, Circulation).
CPR and defibrillation if needed per ACLS guidelines.
Administer Aspirin, Oxygen (if hypoxemic), Nitroglycerine, and Morphine (if needed for pain; MONA protocol).
Obtain a -Lead EKG. If ST-Elevation (STE) is present, notify the hospital immediately. Note the time of symptom onset and first medical contact. Transfer directly to the ED or Cath Lab per protocol for rapid reperfusion.
If fibrinolytics are being considered, use a checklist to rule out contraindications.
ED/Cath Lab Assessment (<10 ext{ minutes}): Rapid and focused assessment upon arrival to the emergency department or cath lab.
Declare ACS (STEMI or NSTEMI) based on EKG and initial assessment, and activate the Cath Lab if STEMI is confirmed.
Confirm patient identity and obtain quick history (chief complaint, risk factors, medications, allergies).
Perform a focused physical exam (heart sounds, lung sounds, peripheral pulses).
Obtain IV access and draw blood for cardiac biomarkers (Troponin I/T, CKMB), CBC, electrolytes, coagulation studies.
Provide ongoing monitoring for vital signs, oxygen saturation, and cardiac rhythm.
Prepare for reperfusion therapy (PCI or fibrinolytics) based on diagnosis and facility protocols, ensuring consent is obtained and all necessary preparations are made for rapid treatment.