Cardiovascular Disorders PDF

Cardiovascular Disorders Dr Ruth Hannon [email protected] Hypertension Definition / Hallmarks Elevated BP Normal Blood Pressure Most people at home, doctor’s office including chronic kidney disease Less than 140/90 mmHg People with diabetes Less than 130/80 mmHg Elderly (>80 yrs) Less than 160/90...

Cardiovascular Disorders Dr Ruth Hannon [email protected] Hypertension Definition / Hallmarks Elevated BP Normal Blood Pressure Most people at home, doctor’s office including chronic kidney disease Less than 140/90 mmHg People with diabetes Less than 130/80 mmHg Elderly (>80 yrs) Less than 160/90 mmHg Isolated systolic (systolic ≥ 140) “White coat” [ Product of CO & TPR ] Hypertension Canada’s Guidelines (2022) Regulation of BP McCance & Huether (2019) Figure 32.26 Pathology of Hypertension Power‐Kean, Zettel, El‐Hussein (2023) Figure 24.5 Complications of Hypertension Let’s not forget erectile dysfunction! Hammer & McPhee (2019) Figure 11.17 Hypertension TYPES 1. Primary HTN (essential / idiopathic) 2. Secondary HTN (5‐10%) Renal abnormalities Endocrine / adrenal disorders Vascular disorders Pregnancy Neurological disorders 3. Complicated HTN Endothelial dysfunction Insulin resistance Vascular disorders Catecholamines Inflammation 4. Malignant HTN (hypertensive crisis) Hypertension RISK FACTORS Age Ancestry Family History Lack of exercise Dietary factors Central obesity Insulin resistance / metabolic disorders Smoking Alcohol / Drugs Sleep apnea Mental Stress Power‐Kean, Zettel, El‐Hussein (2023) Figure 24.13 Primary Treatment Some general notes: Lifestyle modifications are the best way to treat & prevent Combination of changes often necessary: RNAO Nursing Management of Hypertension (2009) Table 4 DASH – Fruits, vegetables, low‐fat dairy, low salt See Supplemental Table S5 – Hypertension Canada Guidelines https://www.nhlbi.nih.gov/files/docs/public/heart/hbp_low.pdf Diuretics Thiazides Hydrochlorothiazide (HCTZ) Metalozone (Zaroxolyn) Loops Furosemide (Lasix) Ethracrynic acid (Edecrin) K+ sparing Hannon & Porth (2017) Figure 30.13 Amiloride Spironolactone (Aldactone) Combinations Aldactazide Moduretic Others Osmotic – Mannitol Carbonic anhydrase inhibitors – Acetazolamide (Diamox) ACE inhibitors / ARBs ACE inhibitors – – – – – – Captopril (Capoten) Enalapril (Vasotec) Fosinopril (Monopril) Perindopril (Coversyl) Quinapril (Accupril) Ramipril (Altace) Angiotensin Receptor Blockers – – – – – Candesartan (Atacand) Irbesartan (Avapro) Losartan (Cozaar) Telmisartan (Micardis) Valsartan (Diovan) Hannon & Porth (2017) Figure 23.4 Ca++ Channel Blockers Dihydropyridines – – – – Amlodipine (Norvasc) Felodipine (Plendil) Nifedipine (Adalat XL) Nimodipine Non‐Dihydropyridines – – Diltiazem (Cardizem SR, Tiazac) Verapamil (Isoptin SR) Ca++ ↑ Vasoconstric on ↑ Contrac lity eta Blockers Cardio‐selective (1) Atenolol (Tenormin) Bisoprolol (Monocor) Metoprolol (Lopressor) Non Cardio‐selective (1 & 2) Propranolol (Inderal) Nadolol Timolol  Adrenergics Alpha 1 Antagonists – Prazosin (Minipress) – Tamsulosin (Flomax) – Terazosin (Hytrin) Alpha 2 Agonists – Clonidine (Catapres) – Methyldopa (Aldomet) Alpha ‐ Beta Blockers – Carvedilol (Coreg) – Labetalol (Trandate) Other Antihypertensive Medications Vasodilators Hydralazine (Apresoline) Sodium Nitroprusside (Nipride) Nitrates Isosorbide dinitrate (Isordil) Nitroglycerin infusion (Tridil) Nitroglycerin spray, transdermal, sublingual ↑cGMP PKG ↓[Ca++]i Vasorelaxation NO Combination Medications Frequently done with thiazides, ACEIs, ARBs, and CCBs. Examples: ACEI + Diuretic ACEI + CCB ARB + Diuretic ARB + CCB Beta blocker + Diuretic Diuretic combos Others! Accuretic, Monopril HCT, Vaseretic Lotrel, Viacoram Atacand HCT, Diovan HCT, Micardis HCT Twynsta Lopressor HCT, Tenoretic, Viskazide Aldactazide, Moduretic, Dyazide Combipress, Apresazide, Minizide Treatment Compliance 20% of those treated for hypertension have their BP managed. Why? ‐ Compliance (“I feel well enough…”) ‐ Cost ‐ Side effects “The silent killer” Sites of Atherosclerosis Difference between arteriosclerosis and atherosclerosis? Hannon & Porth (2017) Figure 22.6 Atherosclerosis Disease Progression 1. 2. 3. 4. Endothelial injury Migration of inflammatory cells Smooth muscle cell proliferation and lipid deposition Development of atheromatous plaque with a lipid core Power‐Kean, Zettel, El‐Hussein (2023) Figure 24.8 Atherosclerosis Characteristics of the atherosclerotic lesion (1) (2) (4) (3) (5) Hansson, Robertson & Soderberg‐ Naucler (2006) Figure 1 Hammer & McPhee (2019) Figure 11.15 Atherosclerosis RISK FACTORS Dyslipidemia Diabetes mellitus Metabolic syndrome Hypertension Cigarette smoking Obesity Sedentary lifestyle Atherogenic diet Age Sex Heredity Hannon & Porth (2017) Figure 22.4 Atherosclerosis Complications Coronary artery disease Ischemic heart disease Myocardial infarction Thrombo‐emboli Aneurysms Treatment Aimed at minimizing complications of atherosclerosis Anticoagulants Vasodilators (CAD) Angioplasty CABG Vascular Pathologies 1. 2. 3. 4. 5. 6. 7. 8. Coronary artery disease (CAD) Myocardial infarction Peripheral artery disease (PAD) Deep vein thrombosis Varicosities Embolisms Aneurysms Dissections Coronary Artery Disease (CAD) Guyton & Hall (1996) Figure 21.3 & 21.4 Treatment includes: Beta blockers Vasodilators Anticoagulants Thrombolytics Angioplasty CABG Myocardial Infarction Hannon & Porth (2017) Figure 24.7 & 24.6 “Getting up can be hazardous to your health…” Types of MIs Type Clinical Situation Definition 1 Spontaneous MI related to ischemia from primary coronary event such as plaque rupture, erosion, fissuring, or dissection 2 Supply/Demand imbalance MI related to secondary ischemia due to myocardial oxygen supply/demand mismatch such as spasm, anemia, hypotension, arrhythmia 3 Sudden cardiac death Unexpected cardiac death, perhaps suggestive of MI, but occurring before blood samples can be obtained 4a PCI MI associated with PCI procedure 4b Stent thrombosis MI associated with stent thrombosis as seen on coronary angiogram or autopsy 5 CABG MI associated with CABG Based on Fourth Universal Definition of Myocardial Infarction (2018) Type 2 MIs Fourth Universal Definition of Myocardial Infarction (2018) Figure 5 Myocardial Infarction Healing Time Tissue Changes Stage of Healing 6-12 No gross changes, subcellular hours cyanosis with decreased temperature Not begun 18-24 Pale to grey-brown; slight pallor hours Inflammatory response, intercellular enzyme release 2-4 days Visible necrosis: yellow-brown in center and hyperemic around edges Proteolytic enzymes remove debris, elevation in glucose and FFA to help recovery from anaerobic state 4-10 days Area soft with fatty changes in centre, Debris cleared, collagen matrix regions of hemorrhage in infarcted laid down area 10-14 Weak, fibrotic scar tissue with days beginning revascularization 6-8 wks Scarring usually complete Healing continues but area very mushy, vulnerable to stress Tough inelastic scar replaces necrotic myocardium Angioplasty (PCI) Crowley (2004) Figure 13.34 CABG Crowley (2004) Figure 13.32 Left Internal Mammary Artery (LIMA) Hannon & Porth (2017) Figure 24.10 Peripheral Artery Disease (PAD) Ankle brachial index (ABI) Neurovascular assessment – Pain, Pulse, Pallor, Paresthesia, Paralysis, Poikilothermia Medications – Antiplatelets Aspirin, clopidogrel/plavix – Anticoagulants Heparin LMWH DOACs – Factor Xa or thrombin inhibitors Warfarin – Thrombolytics Alteplase, tenecteplase, streptokinase Vascular Flow Disorders DVT – Virchow’s triad Varicosities Embolisms Thromboembolism Air Amniotic fluid Bacterial Fat Foreign matter Stasis of Blood Endothelial Injury DVT Hypercoagulability of Blood Aneurysms Price (2003) Figure 34.11 Power‐Kean, Zettel, El‐Hussein (2023) Figure 24.7a Aortic Dissections Crowley (2004) Figure 13.45 A = Adventitia, M = Media, I = Intima, T = Intimal tear, FL = False lumen, TL = True lumen Treatment Heart Failure Definition Failure of the heart to pump enough blood to satisfy the needs of the body. – Complex, Progressive – Cardiac remodelling Manifestations Decrease in cardiac output and/or Damming of blood in pulmonary or systemic circuit Complications Pulmonary edema Cardiogenic shock DEATH NYHA Classification Class I No symptoms with ordinary activity Class II Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, dyspnea, or angina Class III Marked limitation of physical activity. Comfortable at rest, but less than ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain Class IV Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency may be present even at rest Determinants of Cardiac Output Contractility Afterload Preload Stroke Volume Synergistic LV Contraction Wall Integrity Valvular Competence Heart Rate Cardiac Output Heart Failure Causes: Essentially any factor that reduces the hearts’ pumping ability / capacity: 1. Mechanical 2. Myocardial (muscular) 3. Increased pressure or volume load Obstruction to ventricular filling Tamponade Endocardial restriction Ventricular aneurysm Primary (cardiomyopathies, myocarditis, toxicity) Secondary (CAD, metabolic abnormalities, inflammation, systemic disease, COPD) Altered cardiac conduction sequence Standstill, fibrillation, extreme tachy or brady, asynchrony The Vicious Cycle LV Dysfunction ↑ cardiac workload (↑ preload and afterload) ↑ Cardiac Output (via ↑contrac lity and heart rate) ↑ Blood Pressure (via vasoconstric on and ↑BV) ↓ Cardiac Output and ↓ Blood Pressure Frank‐Starling Mechanism Remodelling Neurohormonal activation Heart Failure Types or ways to classify HF: Acute or chronic (duration) Compensated or decompensated (progression) High or low output (clinical manifestations) Left‐sided or right‐sided (ventricle affected) Backward or forward (mechanism) Systolic or diastolic dysfunction (cardiac cycle) Latest Definitions – – – – HFrEF (reduced, LVEF ≤ 40%) Bozkurt, et al. (2021) Figure 1 HFmrEF (mildly reduced, LVEF 41‐49%) HFpEF (preserved, LVEF ≥ 50%) [HFimpEF (improved, LVEF was ≤ 40%, then 2nd measurement > 40%)] Heart Failure Pathophysiology During heart failure, several compensatory mechanisms interact: Heart Failure Pathophysiology During heart failure, several compensatory mechanisms interact Frank Starling’s Law of the Heart Myocardial hypertrophy / remodelling Sympathetic nervous system R‐A‐A System Inflammatory processes Others Heart Failure LEFT versus RIGHT Causes S&S Diagnostics Hannon & Porth (2017) Figure 26.2 Heart Failure HIGH CO – normal or high CO, yet insufficient for tissue needs Causes: Severe anemia Beriberi heart disease (Vitamin B1/thiamine) Sepsis Thyrotoxicosis (Graves’ disease) Atrioventricular defect Power‐Kean, Zettel, El‐Hussein (2023) Figure 24.40 Heart Failure Goals of Treatment Decrease workload of the heart (↓ cardiac VO2 max) Conserve myocardial tissue Accomplished through: ↑ contrac lity ↓ preload and/or afterload ↓TPR ↓BV ↓SNS (↓HR, ↓O2 demand, ↑ventricular filling, ↑EF, ↓remodelling) Enhancing pumping efficiency (cardiac resynchronization) Treatments for Heart Failure Treatments Digoxin (digitalis) Diuretics Aldosterone antagonists ACEIs, ARBs, & ARNIs  ‐blockers Others – Cardiac resynchronization (ICD) – Left Ventricular Assist Device (LVAD) – Heart transplant (“the Gold Standard”) Possible anticoagulation for all (CAD or AF) Digoxin Treatments Digoxin (digitalis) Diuretics Aldosterone antagonists ACEIs, ARBs, & ARNIs  ‐blockers Others Positive inotropy (↑contrac lity) Long term use: ↓ symptoms ↑ exercise tolerance Negative chronotropy (↓SNS, ↓ AV conduc on) ↓risk of HF progression Does not improve survival Diuretics Treatments Digoxin (digitalis) Diuretics Aldosterone antagonists ACEIs, ARBs, & ARNIs  ‐blockers Others Notes: Facilitates use of other drugs (never alone) Electrolyte depletion common Higher doses ↑ mortality rate Relieve fluid retention (↓ Blood Volume) ↑ exercise tolerance Dosing changes with weight Aldosterone Antagonists Treatments Digoxin (digitalis) Diuretics Aldosterone antagonists ACEIs, ARBs, & ARNIs  ‐blockers Others Notes: Well tolerated Reserved for NYHA Class III‐IV Spironolactone, Eplerenone ↓ morbidity & mortality Side effects: hyperkalemia, gynecomastia (spironolactone) ACEI / ARBs Treatments Digoxin (digitalis) Diuretics Aldosterone antagonists ACEIs & ARBs  ‐blockers Others Inhibit Ang‐II prod. Blocks Ang‐II effects Hannon & Porth (2017) Figure 23.4 Notes: Recommended for all ↓ symptoms ↑ exercise tolerance ↓disease progression ↓ risk of death Beneficial effects take time (1‐2 months) ARNIs (Angiotensin receptor neprilysin inhibitors) Treatments Digoxin (digitalis) Diuretics Aldosterone antagonists ARNIs (Entresto)  ‐blockers Others Docherty, et al. (2020) Figure 1 Notes: Recommended for all HFrEF Must be able to tolerate ACI or ARB first ↓ hospitaliza ons and risk of death Beneficial effects take time (1‐2 months) eta Blockers Treatments Digoxin (digitalis) Diuretics Aldosterone antagonists ACEIs, ARBs, & ARNIs  ‐blockers Others Long term use: ↓ symptoms Combination with other meds: ↓ morbidity & mortality ↓risk of HF progression Hannon & Porth (2017) Fig 23.2 Blocks SNS Short term ↓ contrac lity Long term ↑ EF (1‐3 months) Implantable Cardioverter Defibrillator Indications SCD is a significant risk factor for NYHA Class II‐III Arrhythmia (VT/VF) is the predominant cause 12% CHF Other NYHA II Sudden Death n = 103 24% 12% Other Cardiac Cause 64% 26% 59% NYHA III n = 103 MERIT‐HF Study Group. LANCET (1999) 353:2001 15% 88% Arrhythmic Cause Albert CM. Circulation (2003) 107:2096 Remember … Cardiac excitation Marieb & Hoehn (2019) Fig 18.13 Implantable Cardioverter Defibrillator Dual Chamber ICD Pacing ↑ pumping efficiency Ventricle VT prevention / pacing Cardioversion Defibrillation Atrium & Ventricle Bradycardia sensing / pacing ADDENDUMS… Courtesy of Laurene Long, 2007 Ventricular Resynchronization Intraventricular activation Organized / coordinated sequence Improved pumping efficiency Left Ventricular Assist Device LVAD Mechanical pump ↓ LV workload Bridge till transplant Complications Blood clots Infection TRANSPLANT Some considerations: MHC class Transplant rejection (immunosuppression) Endothelial damage (MI) http://www.chfpatients.com/implants/lvads.htm Marieb (2007) p707 Cardiomyopathies “A disease of the myocardium associated with cardiac dysfunction” WHO (1995) Genetic ‐ Hypertrophic (obstructive) ‐ Arrhythmogenic Right Ventricular Dysplasia (ARVD) ‐ Channelopathies Mixed ‐ Dilated (congestive) ‐ Restrictive Acquired ‐ Inflammatory (myocarditis) ‐ Takotsubo (stress) ‐ Peripartum Power‐Kean, Zettel, El‐Hussein (2023) Figure 24.25 Primary vs Secondary Cardiomyopathies Daughenbaugh (2007) Table 2 Newer Drugs For HF Camzyos (mavacamten) Newer Drugs For HF Verquov (vericiguat) Role endothelial cGMP: ‐ ↓ BP ‐ Regulates vascular tone ‐ Regulates endothelial permeability ‐ Inhibits platelet aggregation ARVD Arrhythmogenic Right Ventricular Dysplasia (ARVD) Leading cause of SCD in young individuals Largely hereditary (>50%) Pathology Loss/replacement of RV myocytes with fatty/fibrofatty tissue Results in reentrant ventricular tachyarrhythmias Treatment Antiarrhythmics (?) Ablation (?) ICD Transplant (rare) Channelopathies Channel + Pathology = Channelopathy Diseases due to mutation(s) in an ion channel or channels Types LQTS (torsades de pointes) Brugada Syndrome (SUNDS) CPVT SQTS Valvular Diseases Screening Etiology: Congenital Acquired Damage to heart valves causing: Stenosis Regurgitation (insufficiency) Damage: Degradation (incompetent) Fusion (scarring, calcification) Hannon & Porth (2017) Figure 21.6 Valvular Diseases Types Aortic stenosis Aortic insufficiency Acute / Chronic Mitral stenosis Mitral prolapse Mitral insufficiency Acute / Chronic Hannon & Porth (2017) Figure 24.19 Valvular Diseases Treatment Repair – – Percutaneous Mitral Balloon Valvotomy Commissurotomy PMBV Replacement – – Mechanical Tissue http://www.cardiosmart.org/uploadedImages/Heart _Disease/CTT_Pages/Balloon_Valvuloplasty.jpg Mechanical 1. Caged Ball Noisy No central flow 2. Tilting Disk Clots Improves central flow 3. Bileaflet Excellent flow Not full closure ↓ clots Strut damage Well tolerated http://cape.uwaterloo.ca/che100projects/heart/files/testing.htm Tissue (Bioprosthetic) Human Homograft Autograft – Ross procedure Animal (Xenograft) Porcine Bovine [Equine] http://cape.uwaterloo.ca/che100projects/heart/files/testing.htm Complications Summary ‐Remodelling Power‐Kean, Zettel, El‐Hussein (2023) Figure 24.35 Congenital Heart Disease Types 1. Atrial septal defect 2. Ventricular septal defect 3. Tetralogy of Fallot 4. Tricuspid Atresia 5. Transposition of the great arteries 6. Coarctation of the Aorta Coarctation of the Aorta http://www.pediatriccardiacinquest.mb.ca/diagrams/2_09.jpg Coarctation of the Aorta Power‐Kean, Zettel, El‐Hussein (2023) Figure 25.3 McCance & Huether (2019) Figure 34.13 Infectious Diseases Types 1. Rheumatic Fever 2. Endocarditis 3. Pericarditis Rheumatic Fever Recurrent episodes of rheumatic fever can lead to damage of heart muscle and valves Group A –hemolytic streptococcus (S. pyogenes) Autoimmune (molecular mimicry) Mitral and Aortic valves http://microbewiki.kenyon.edu/index.php Endocarditis Bacterial infection of the endocardium (acute, subacute, and chronic) At risk individuals have: Damaged / prosthetic valves History of endocarditis Hypertrophic CM Heart transplant ICD / LVAD Characterized by: Heart murmur Prolonged fever Bacteremia Splenomegaly Embolic phenomena* Power‐Kean, Zettel, El‐Hussein (2023) Figure 24.33 Pericarditis Inflammation of the pericardium Causes Infection (viral, bacterial, fungal) Trauma (surgery) Malignant neoplastic disease Uremia MI Collagen disease (SLE) Idiopathic http://www.aurorahealthcare.org Treatment Pericardiocentesis Pericardial window Pericardiectomy Antibiotics / antifungals / NSAIDs Power‐Kean, Zettel, El‐Hussein (2023) Figure 24.22 References Bozkurt, B., et al. (2021). Universal definition and classification of heart failure. Journal of Cardiac Failure, 27(4), 387-413. Brieler, J., Breeden, M.A., & Tucker, J. (2017). Cardiomyopathy: An overview. American Family Physician, 96 (10), 640-646. Chojnowski, D. (2004). Putting together the pieces of cardiomyopathy. Nursing Made Incredibly Easy, 2 (3), 18-28. Crowley, L. (2004). Introduction to human disease (6th ed.). Jones and Bartlett Publishers, Inc. Daughenbaugh, L. (2007). Cardiomyopathy: An overview. Journal of Nurse Practitioners, 3, 248-258. Docherty, K.F., Vaduganathan, M., Solomon, S.D., & McMurray, J.J.V. (2020). Sacubitral/Valsartan, neprilysin inhibition 5 years after PARADOGM-HR. JACC: Heart Failure, 8(10), 800-810. Ezekowitz, J.A., O’Meara, E., McDonald, M.A., Abrams, H., Chan, M., Ducharme, A., Giannetti, N., Grzeslo, A., Hamilton, P.G., Heckman, G.A., Howlett, J.G., Koshman, S.L., Lepage, S., McKelvie, R.S., Moe, G.W., Rajda, M., Swiggum, E., Virani, S.A., Zieroth, S., … Sussex, B. (2017). Comprehensive update of the Canadian Cardiovascular Society guidelines for the management of heart failure. Canadian Journal of Cardiology, 33 (11), 1342-1433. References Hammer, G., & McPhee, S. (2019). Pathophysiology of disease (8th ed.). McGrawHill Companies. Hannon, R., & Porth, C. (2017). Porth pathophysiology – Second Canadian Edition. Lippincott Williams & Wilkins. Heart and Stroke Foundation of Ontario and RNAO. (2009 revised). Nursing management of hypertension. RNAO. Marieb, E., & Hoehn, K. (2019). Human Anatomy and Physiology (11th ed.). Pearson Education Inc. McCance, K., & Huether, S. (2019). Pathophysiology (8th ed.). Mosby, Inc. Mulvihill, M., Zelman, M., Holdaway, P., Tompary, E., & Turchany, J. (2001). Human diseases a systemic approach (5th ed.). Prentice Hall Inc. Power-Kean, K., Zettel, S., & El-Hussein, M.T. (2023). Huether and McCance’s understanding pathophysiology (2nd Canadian ed.). Elsevier. Price, S., & Wilson, L. (2003). Pathophysiology (6th ed.). Mosby, Inc. Rabe, T., & Ruiz, A. (2003). Inside your outside! Random House. Thygesen, K., et al. (2018) Fourth universal definition of myocardial infarction. Circulation, 138(20), e618-e651.