WEEK 1: Coronary Artery Disease, Myocardial Ischemia & Acute Coronary Syndrome PDF

**WEEK 1: Coronary Artery Disease, Myocardial Ischemia & Acute Coronary Syndrome** **A Quick Review: Cardiac Anatomy & Physiology** **Wall of The Heart** - **Myocardium (Muscular layer, responsible for contracting)** - - - - **Coronary Circulation: Coronary Arteries** - - -...

**WEEK 1: Coronary Artery Disease, Myocardial Ischemia & Acute Coronary Syndrome** **A Quick Review: Cardiac Anatomy & Physiology** **Wall of The Heart** - **Myocardium (Muscular layer, responsible for contracting)** - - - - **Coronary Circulation: Coronary Arteries** - - - - - *Can you explain why the left ventricle is damaged with either right or left coronary artery occlusion?* *If there is RCA occlusion: not prefusing SA nodes are gonna be damaged; so the electric pulse wont signal the LCA to pump.* *Why does RIGHT sided coronary artery occlusion cause problems with BOTH the left and right side of the heart? Consider where the right coronary arteries are branching off to and what structures are on the right side of the heart..*  - - **Right & Left Coronary Arteries** Right - - Left - *what manifestations would you anticipate the client would have if their RCA was blocked? What about the LCA?* - **Collateral Circulation** New collateral vessels are formed through two processes 1\. **arteriogenesis** (**new** **artery** growth branching from **preexisting** arteries) 2\. **angiogenesis** (**growth** of **new** **capillaries** **within** a **tissue**) - - - - **Conduction System of The Heart** - **Normal Electrocardiogram (ECG) & Cardiac Electrical Activity**  - **Atherosclerosis: A Quick Review** **Progression of Atherosclerosis: A Review** Progression - - - - - - - - - **Progression of Atherosclerosis: The BIG Picture!** Result: partial or total occlusion of coronary artery  **Atherosclerosis & Coronary Artery Disease (CAD)** - - - - - - - **Modifiable Risk Factors For CAD & What To Do!** - - - - - - - - **Nonmodifiable Risk Factors For CAD** Major risk factors - - - - **Nontraditional Risk Factors For CAD** - - What Is CAD? - - - - - - -  **Pathophysiologic Continuum** - **Stable Angina** *(pain in the chest, not acute, chest pain is chronic, but stable (not triggered, doesnt happen at rest)* - - - **Acute Coronary Syndromes (ACS)** consist of: - - - **Unstable Angina (UA)** - - **Myocardial Infarction (MI)** - **NSTEMI- non ST elevation MI** - - **STEMI- ST elevation MI**, - - - **CAD Is Divided Into Two Types of Disorders** **Chronic Ischemic Heart Disease: stable** - - - **Acute Coronary Syndromes (ACS)- unstable** - - - *What is the difference between ischemia (partial) and infarction (complete)* **Stable Plaque Versus Unstable Plaque** **Two types of atherosclerotic lesions & their role in CAD/MI/ACS** **Stable plaque** - - - **Unstable plaque** - - - - - **Remember that a stable plaque may become unstable!** **It's A Balancing Act: Supply & Demand!** -  - - **Cycle of Myocardial Ischemic Events** - - - **Types of Transient Myocardial Ischemia** **Stable angina** chronic atherosclerotic coronary obstruction → recurrent predictable chest pain **Silent ischemia** *(poor perfusion but no symptoms)* myocardial ischemia that does not cause detectable symptoms **Prinzmetal angina** *(cold temp, stress,* abnormal **vasospasm** of coronary vessels → unpredictable chest pain **Stable Angina** - - - - - - - **Acute Coronary Syndromes (ACS)** - - - - - - - **Pathophysiology of ACSs**  - **Unstable Angina (UA) (**not relieved by rest, and a sign of MI coming/impending) - - - - - - - - - - **Pathogenesis of Unstable Plaques & Thrombus Formation** - **Evaluation & Treatment of Unstable Angina (EMERGENCY)** Evaluation - - Treatment - - - - - **What is a Myocardial Infarction (MI)?** - - **Plaque Disruption & Myocardial Infarction** **2 Major Types of MI** 1\. [Subendocardial infarction (referred to as a Non-ST-Segment Elevation MI (NSTEMI))] - - - [2. Transmural infarction (referred to as an ST-Segment Elevation MI (STEMI))] - - - **Individuals at highest risk for complications** - **Unstable Angina, NSTEMI & STEMI**  - - **What Causes Cellular Injury?** - - - - - **After 20 minutes of ischemia, myocardial cells begin to die (necrosis). But the cells are viable if blood flow is restored within that 20 minutes!** **What Causes Cellular Injury?** - - - - - **Cellular Death** - - - **Structural & Functional Changes Associated With Acute Myocardial Ischemia** Prolonged ischemia causes irreversible damage to heart muscle (myocyte necrosis) - - - - - - - - Infarcted myocardium is surrounded by a zone of hypoxic injury, which may - - - **Structural and Functional Changes Associated With Acute Myocardial Ischemia** **Reperfusion Injury** - - - - - **Can add as much as 50% to overall infarct size** **Repair** - - - - **Complications of MI** - - - - - - - - - **Diagnostics: Electrocardiogram (ECG) Changes with MI** Affected area can be identified on a 12-lead ECG - - **ECG** changes **depend** on - - - **Ischemic/injured/infarcted tissue does not function like normal myocardial tissue**  **Electrocardiogram (ECG) Alterations**  Depolarization: positive Repolarization: negative, relaxation **What do the ST-segment depression (NSTEMI) and the ST-segment elevation (STEMI) ECGs tell us about the extent of heart damage?** **Diagnostics: Serum Biomarkers, FOR MUSCULAR DAMAGE (HEART)** - - - - **Diagnostics: Cardiac Specific Serum Biomarkers** *Are cardiac biomarkers released with NSTEMI? What about with STEMI?* *Troponin (cell death) is released by dead heart cells, so both will be released.* *Are cardiac biomarkers released with unstable angina (UA)?* *No, because it\'s not cell death, not done yet so you won\'t see cardiac biomarkers yet.* **Diagnostics: Non-Cardiac Specific Serum Biomarkers** Lactate dehydrogenase (LDH) - Myoglobin present in cardiac and skeletal muscle - - - - **Additional Labs** - - - *What causes all of these?* - **Symptoms/Assessment** - - - - - - - - - - - - - *What causes the pain and why does it radiate? WHY FEVER?* - **Treatments for MI**  - - - **Non-Pharmacological Treatment For ACS** - - - - **Coronary Artery Disease (CAD), Acute Coronary Syndrome (ACS) & Heart Failure (HF): How They Are All Related!\ ** **WEEK 1: Cardiac Pharmacotherapy** +-----------------------------------+-----------------------------------+ | **Classification** | **Drug** | +===================================+===================================+ | **Opioids** | **-morphine (see PAT201 | | | Pharmacology Key Concepts & | | | Pain)** | +-----------------------------------+-----------------------------------+ | **Calcium channel blockers | **-diltiazem** | | (selective for vessels)** | | | | **-amlodipine** | +-----------------------------------+-----------------------------------+ | **Vasodilators** | **-nitroglycerin** | +-----------------------------------+-----------------------------------+ | **β~1~-Adrenergic receptor | **-metoprolol (see PAT201 | | blockers** | Hypertension)** | +-----------------------------------+-----------------------------------+ | **ACE inhibitors** | **-enalapril (see PAT201 | | | Hypertension)** | +-----------------------------------+-----------------------------------+ | **Neprilysin inhibitor/ARB** | **-sacubitril & valsartan | | | (combination drug)** | +-----------------------------------+-----------------------------------+ | **Cardiac glycosides** | **-digoxin** | +-----------------------------------+-----------------------------------+ | **Antidysrhythmics | **-amiodarone** | | (antiarrhythmics)** | | +-----------------------------------+-----------------------------------+ | **Antiplatelets** | **-clopidogrel (see PAT201 | | | Atherosclerosis and Stroke)** | | | | | | **-ticagrelor** | +-----------------------------------+-----------------------------------+ | **Cyclooxygenase (COX) | **-acetylsalicylic acid (see | | inhibitors** | PAT201 Atherosclerosis and | | | Stroke)** | +-----------------------------------+-----------------------------------+ | **Thrombolytics** | **-tissue plasminogen activator | | | (tPA): alteplase (see PAT201 | | | Atherosclerosis and Stroke)** | +-----------------------------------+-----------------------------------+ | **Anticoagulants** | **-heparin** | | | | | | **-warfarin** | +-----------------------------------+-----------------------------------+ | **Antidote for heparin therapy** | **-protamine sulfate** | | | | | **Antidote for warfarin therapy** | **-vitamin K** | +-----------------------------------+-----------------------------------+ | **Low-molecular-weight heparins** | **-enoxaparin** | +-----------------------------------+-----------------------------------+ | **Direct thrombin inhibitors** | **-dabigatran** | +-----------------------------------+-----------------------------------+ | **Loop diuretics** | **-furosemide (see PAT201 | | | Hypertension)** | +-----------------------------------+-----------------------------------+ | **Thiazide diuretics** | **-hydrochlorothiazide (see | | | PAT201 Hypertension)** | +-----------------------------------+-----------------------------------+ | **Mineralocorticoid receptor | **-spironolactone** | | antagonists** | | +-----------------------------------+-----------------------------------+ **Factors Affecting Cardiac Performance** - - **Overall Pharmacological Goals** - - - - - **Pharmacological Goals For Client With Angina** **2 main goals** 1. 2. **4 different mechanisms** 1. 2. ↓ preload 3. 4. **Pharmacological Goals For Treatment of Acute MI** **5 main goals** 1\. Restore perfusion to damaged myocardium as quickly as possible - 2\. Reduce myocardial oxygen demand - - 3\. Control or prevent associated dysrhythmias - 4\. Reduce post-MI mortality - 5\. Control MI pain and associated anxiety - **Pharmacological Goals For Treatment of HF** 3 primary goals 1\. Reduction of preload 2\. Reduction of SVR (↓ afterload) - 3\. Inhibition of both the RAAS and vasoconstrictor mechanisms of SNS - **Pharmacotherapy: Analgesics** **Classification** **Drug** -------------------- ------------------------------------------------------------- **Opioids** **-morphine (see PAT201 Pharmacology Key Concepts & Pain)** **Opioids: Morphine** Indications - - Mechanisms of action - - - - Desired effects - - - - - - Adverse effects - - - - - But...how does morphine decrease preload and afterload? **Nursing Implications (things you need to assess for)** Assessments: - - - - - Monitoring: - - - - - Contraindications: - Administration considerations: - **Morphine** - **Pharmacotherapy: Drugs Affecting The Cardiovascular System** +-----------------------------------+-----------------------------------+ | **Classification** | **Drug** | +===================================+===================================+ | **Calcium channel blockers | **-diltiazem** | | (selective for vessels)** | | | | **-amlodipine** | +-----------------------------------+-----------------------------------+ | **Vasodilators** | **-nitroglycerin** | +-----------------------------------+-----------------------------------+ | **β~1~-adrenergic receptor | **-metoprolol (see PAT201 | | blockers** | Hypertension)** | +-----------------------------------+-----------------------------------+ | **ACE inhibitors** | **-enalapril (see PAT201 | | | Hypertension)** | +-----------------------------------+-----------------------------------+ | **Neprilysin inhibitor/ARB** | **-sacubitril & valsartan | | | (combination drug)** | +-----------------------------------+-----------------------------------+ | **Cardiac glycosides** | **-digoxin** | +-----------------------------------+-----------------------------------+ | **Antidysrhythmics | **-amiodarone** | | (antiarrhythmics)** | | +-----------------------------------+-----------------------------------+ **Calcium Channel Blockers (Selective for Vessels): Diltiazem** Indications - Mechanisms of action - - - - - Desired effects - Adverse effects - - **Nursing Implications** Assessment & Monitoring - - - - - - - - - Safety: - **Calcium Channel Blockers (Selective for Vessels): Amlodipine** Indications - Mechanisms of action - - Desired effects - - - - - Adverse effects - **Vasodilators: Nitroglycerin (short-acting)** Indications - Mechanisms of action - - Desired effects - - - Adverse effects - - - - **Nursing Implications** **Monitoring:** - **Administration Considerations:** Should be kept in a dark container **Use gloves when applying nitroglycerin paste, patch or ointment to prevent self-administration --** WHY? - - **Teaching:** - - - - **β1-Adrenergic Receptor Blockers ("olols"): Metoprolol** **Indications** - - - **Mechanisms of Action** - - **Desired effects** - **Adverse effects** - - - - - **Nursing implications** Monitor for : - - - - Safety: - Teach - Contraindications: - **ACE Inhibitors** - RECALL:\ What Does the ACE Normally Do?\ So, what happens...if we inhibit it? **ACE Inhibitors Block the RAAS**  - **ACE Inhibitors ("prils"): Enalapril** Indications - Mechanisms of Action - - Desired effects - - Adverse effects - - Caution with use of K+ sparing diuretics! **Nursing Implications** Assess: The client's current medications - avoid use with potassium supplements and potassium sparing diuretics -- - Monitor: - - - **Neprilysin Inhibitor /ARB: Sacubitril/Valsartan (combination drug)** Newer class (in 2015) called angiotensin receptor neprilysin inhibitors (ARNIs) Indications - Mechanisms of action - - - Desired effects - - Adverse effects - *Is this a maintenance drug or used in crisis? What would you monitor here?* **Cardiac Glycosides: Digoxin** Indications - - Mechanisms of action - - - - Desired effects - - - - - Adverse effects - - - - Nursing Implications Assessments: - - Monitor: - - Teaching: - - **Antidysrhythmics (Antiarrhythmics): Amiodarone** Indications - - - Mechanisms of action - Desired effects - - - Adverse effects - - - **Antidysrhythmics (Antiarrhythmics): Amiodarone** - - **Nursing Implications** Monitor: - - - - Teaching: - - **Pharmacotherapy: Coagulation Modifiers** +-----------------------------------+-----------------------------------+ | **Classification** | **Drug** | +===================================+===================================+ | **Antiplatelets** | **-clopidogrel (see PAT201 | | | Atherosclerosis and Stroke)** | | | | | | **-ticagrelor** | +-----------------------------------+-----------------------------------+ | **Cyclooxygenase (COX) | **-acetylsalicylic acid (see | | inhibitors** | PAT201 Atherosclerosis and | | | Stroke)** | +-----------------------------------+-----------------------------------+ | **Thrombolytics** | **-tissue plasminogen activator | | | (tPA): alteplase (see PAT201 | | | Atherosclerosis and Stroke)** | +-----------------------------------+-----------------------------------+ | **Anticoagulants** | **-heparin** | | | | | **Antidote for heparin therapy** | **-warfarin** | | | | | **Antidote for warfarin therapy** | **-protamine sulfate** | | | | | | **-vitamin K** | +-----------------------------------+-----------------------------------+ | **Low-molecular-weight heparins** | **-enoxaparin** | +-----------------------------------+-----------------------------------+ | **Direct thrombin inhibitors** | **-dabigatran** | +-----------------------------------+-----------------------------------+ **Mechanisms of Actions of Coagulation Modifiers**  **Antiplatelets** - - **The Adenosine Diphosphate (ADP) Receptor Blockers** - - - - - - **Antiplatelets: Clopidogrel** Indication - - - - Mechanisms of action - - Desired effects - - - - Adverse effects - - **Antiplatelets: Ticagrelor** **Nursing implications** - - - **Cyclooxygenase (COX) Inhibitors: Acetylsalicylic Acid** Indications - - - - - Mechanisms of Action - - Desired effects - - Adverse effects - - - - - - **ASA\ Nursing Implications** Monitor: - - - Safety: - **Thrombolytics** - - Main Goal is Reperfusion! - - - **Thrombolytics** - - - - *Thrombolytics are not the same as anticoagulants. Thrombolytics break down existing clots* **Blockage & Reperfusion Following MI**  **Thrombolytics: Tissue Plasminogen Activator (tPA): Alteplase\ **Indications - - Mechanisms of action - - - Desired effects - - - - Adverse effects - - - - - **Nursing Implications:** Monitoring: - - Contraindications: - - - Safety: - - Teaching: - **Anticoagulants & Antidotes** **Anticoagulants: Heparin**  - **Nursing Implications** Monitor: - - - Administration Considerations: - - - - - Should not be given with Aspirin and NSAIDs **Antidote For Heparin Therapy:\ Protamine\ Sulfate** **Anticoagulants: Warfarin** Indications - - - - - - Mechanisms of action - - - Desired effects - Adverse effects - - - **Nursing Implications** Educate - - Interactions: - Monitor: - - - Administration Considerations: - **Antidote for Warfarin Therapy: Vitamin K** **REVERSES ANTICOAGULANT ACTIVITY OF WARFARIN** - Indications - Mechanisms of action - Desired effects - Adverse effects - - **Warfarin: Dietary Requirements** Foods high in vitamin K may decrease warfarin's ability to prevent clots - Warfarin maintenance dose can fluctuate significantly depending on amount of vitamin K in diet - - - **Low-Molecular-Weight Heparins (LMWH): Enoxaparin** Indications - - - Mechanisms of action - Desired effects - - Adverse effects - **Nursing Considerations.** - **Direct Thrombin Inhibitors: Dabigatran** Indication - - - - Mechanisms of action - Desired effects - - Adverse effects - Extensively excreted by kidneys, so dose is dependent on kidney function **Nursing Implications** - - **Pharmacotherapy: Diuretics** **Classification** **Drug** -------------------------------------------- ---------------------------------------------------- **Loop diuretics** **-furosemide (see PAT201 Hypertension)** **Thiazide diuretics** **-hydrochlorothiazide (see PAT201 Hypertension)** **Mineralocorticoid receptor antagonists** **-spironolactone** - **Loop Diuretics Thiazide Diuretics Potassium-Sparing Diuretics**  **Loop Diuretics: Furosemide** Indications - - Mechanisms of action - - - Desired effect - - Adverse effects - - - - Nursing Implications: Furosemide Monitor: - - - Safety: - Interactions: - - **Thiazide Diuretics: Hydrochlorothiazide** **Nursing Implications** Monitor: - - Educate: - - Interactions: - - - - Administration: - **Mineralocorticoid Receptor Antagonists: Spironolactone** Indications - - Mechanisms of action - Desired effects - - - Adverse effects - - - - **Nursing Implications** Assess and Monitor: - - Education: - - **WEEK 2: Complications of MI and Alterations of** **Cardiovascular Function** **A Quick Review! Cardiopulmonary Circulation** Normal Blood Flow Through The Heart -  Know Normal to Understand Abnormal. Review *Cardio pulmonary circulation* - - **Heart Failure (HF)** **What Is HF?** *(not able to generate enough cardiac output, so its just in the heart, so our veins are not getting blood= hypotension)* - Heart is **unable** **to** **pump** enough **blood** to meet **body\'s metabolic needs** **What Are Some Causes of HF?** Associated with conditions including: ** coronary artery disease (CAD), MI** affects supply of O2 and nutrients to cardiac muscle ** chronic & sustained HTN** heart must pump more powerfully to eject blood - - ** diabetes mellitus** ** also associated with dyslipidemia** **Risk Factors For HF** - - - - - - - - - - - - **Prevention of HF** - - **Pathophysiology of HF** [Myocardium (this is the muscle, that contracts) becomes weak] So heart **cannot** **eject** **all** the **blood** **it** **receives** - [Left sided, right sided, or both sides] [Left sided HF (more common)] - - - [Right sided HF] - - **Inflammatory Cytokine Involvement** Inflammatory cytokines endothelial **hormones** RELEASED ** TNF-α** ** IL-6** **How HF is Classified** HF is Classified Based on: **⮚ systolic (contraction) failure vs diastolic (relaxation and refilling) failure** systolic -- decreased contractility leading to decreased ejection fraction (EF) diastolic -- normal contraction (normal EF) but abnormal relaxation ** location of failure** ** acute vs chronic** (degree of physical response) acute chronic **Systolic (contraction of ventricle and ejection) HF (HFrEF) = HF with reduced Ejection Fraction** ** EF \ - - - **Management** - - *What might the findings be?* - - - **Diastolic HF (HFpEF) = HF with preserved Ejection Fraction (*filling thats the problem)*** decreased compliance (ability to expand and contract) of left ventricle & abnormal diastolic relaxation ventricle [cannot accept filling] with blood without significant resistance But EF is preserved **Pathophysiology of HF with Preserved ejection fraction (HFpEF)**  - - **Evaluation & Management of HFpEF** [Evaluation] - - - - [Management] - - - - **General Manifestations of HF** - - - **Left HF**  - - - **The Vicious Cycle of Left HF** - - - **Right HF** - Right ventricle unable to push bld into pulmonary circulation Causes conditions compromising pumping effectiveness of right ventricle left HF ** Clinical manifestations** ** jugular venous distension, peripheral edema** *(lower extremities)***, hepatosplenomegaly** - - **Manifestations of HF (Left vs Right)**  - - - - - - **HF Treatment Goals** - - - **Compensatory/Adaptive Mechanisms** *(to reach homeostasis)* **Compensatory Mechanisms: It\'s All About Maintaining Cardiac Output for Tissue/Organ Perfusion!** - - catecholamines - - - - - - **Compensatory Mechanisms** **SNS & RAAS Activation**  **Compensatory Mechanisms (cont'd)** [ADH (arginine vasopressin)] causes peripheral vasoconstriction & renal fluid retention BUT\...exacerbates hyponatremia & edema (preload) & afterload [Natriuretic peptides (NPs)] secreted in response to increased volume overload & dysfunction cause diuresis & reverse negative effects of SNS & RAAS on heart BUT\...chronic HF leads to depletion of NPs ** HF worsens!** **Compensatory Mechanisms (cont'd)** Frank-Starling law (rubber band analogy) increased preload (*stretching)* causes increased stretch of myocardial fibres force of each contraction is increased leading to increased CO BUT\...as preload continues to rise it causes repeated stretching of myocardium **Frank-Starling Law of The Heart** **Ventricular Remodeling** **When contractility decreases, SV falls, & left ventricular end-diastolic volume (LVEDV) increases** Increased PVR, causes resistance & increased workload for left ventricle **Afterload & Hypertrophy of Left Ventricle**  - **Pathophysiology of Ventricular Remodeling** **Disorders of The Myocardium** Cardiomyopathies (*disease of the cardiomyopathy)* **Types of Cardiomyopathies**  **Dilated Cardiomyopathy** - - Causes **Dilated Cardiomyopathy** **Hypertensive Hypertrophic Cardiomyopathy** Occurs due to increased resistance to ventricular ejection ** seen in HTN** Hypertrophy of myocytes attempts to compensate for increased myocardial workload Myocyte dysfunction develops over time **Hypertrophic Cardiomyopathy**  **Dysrhythmias** **A Quick Review: Normal Conduction In The Heart** - **Ischemic Events & Dysrhythmias: review from week 1**  **Premature Ventricular Contractions (PVCs)** **Common cause of irregular heart rhythms** not normally serious **unless** it occurs **at high frequency** **Effect** decreased cardiac output from loss of atrial contribution to ventricular preload for that beat **Ventricular Tachycardia** **Ventricular Fibrillation** [Complete disorganization of rhythm] ventricles pump little or no blood quickly starves tissues of oxygen [Ventricular fibrillation is considered cardiac arrest!] [Effect] **Heart Block** Also called atrioventricular (AV) conduction block Effect classified as first, second, or third degree **Deep Vein Thrombosis (DVT) & Pulmonary Embolism (PE)** **Deep Vein Thrombosis (DVT)** - flow & pressure are lower in veins than in arteries (have higher pressure) - thromboembolus can lead to PE - - - - **Pulmonary Embolism (PE)** PE is occlusion or partial occlusion of pulmonary artery or its branches by an embolus Risk factors for PE PE can cause infarction or occlusion PE can present with Tests **How Is MI Related to DVT & PE?** - - Thrombi associated with dysrhythmias -