NURS 7053 Lecture Slides: Alterations of Cardiovascular Function I (PDF)

NURS 7053 ALTERATIONS OF CARDIOVASCULAR FUNCTION I Hypertension, Dyslipidemia, Atherosclerosis Learning Outcomes By the end of this module, you will be able to: 1.Explain the fundamental concepts of cardiovascular physiology relevant to hypertension, dyslipidemia, and atherosclerosis. 2.Ana...

NURS 7053 ALTERATIONS OF CARDIOVASCULAR FUNCTION I Hypertension, Dyslipidemia, Atherosclerosis Learning Outcomes By the end of this module, you will be able to: 1.Explain the fundamental concepts of cardiovascular physiology relevant to hypertension, dyslipidemia, and atherosclerosis. 2.Analyze the pathophysiological mechanisms underlying hypertension, dyslipidemia, and atherosclerosis, including their interrelationships. 3.Differentiate between the clinical manifestations of these conditions based on their underlying pathophysiology. 4.Evaluate diagnostic approaches and treatment strategies for hypertension, dyslipidemia, and atherosclerosis, justifying choices based on pathophysiological principles. Alt CV I HYPERTENSION  CASE INTRODUCTION In clinic today, you meet a 52-year-old parent of two who works as a corporate manager. They've come in because of persistent headaches and occasional dizziness that's been affecting their work. "I know my blood pressure isn't great," they tell you, pulling out a log showing repeated measurements around 162/94 mmHg. "But between the long hours at work and family commitments, I barely have time to eat, let alone cook. I practically live on coffee and fast food." You notice they appear fatigued and their BMI is 31. While reviewing their family history, they mention both their parent and sibling developed hypertension in their 50s. Classification (JACC, 2018) Hypertension  RETURNING TO OUR CASE In clinic today, you meet a 52-year-old parent of two who works as a corporate manager. Question: How They've come in because of persistent would you headaches and occasional dizziness that's been classify this blood affecting their work. "I know my blood pressure pressure? isn't great," they tell you, pulling out a log showing repeated measurements around 162/94 mmHg. "But between the long hours at work and family commitments, I barely have time to eat, let alone cook. I practically live on coffee and fast food." You notice they appear fatigued and their BMI is 31. While reviewing their family history, they mention both their parent and sibling developed hypertension in their 50s. Pathophysiology Review – Sympathetic nervous system stimulation Hypertension Pathophysiology Review – Sympathetic nervous system stimulation Hypertension Pathophysiology Review – Sympathetic nervous system stimulation – a1 effects High SVR Low SVR Hypertension Pathophysiology Review – Sympathetic nervous system stimulation – b1 effects b1 receptors in the SA node b1 receptors in the myocardium Hypertension Pathophysiology Review – Antidiuretic hormone (ADH)  BP  H2O BV & BP Release of ADH  osm reabsorption  osm Posterior pituitary Hypertension Pathophysiology Review – ANP & BNP Atrial/Ventricular stretch  ANP/BNP secretion  H2O & Na+ reabsorption  H2O & Na+ excretion  BV & BP Hypertension Pathophysiology Review – Thyroid hormone & cortisol Anterior Pituitary Thyroid Adrenal cortex Hypertension Pathophysiology Review – RAAS Angiotensinogen  BP Renin Angiotensin I ACE Arterial  SVR Angiotensin II vasoconstriction  BP Aldosterone  Na+ reabsorption  H2O reabsorption  BV  BP Hypertension Summary From 5th Ed text Pathophysiology Review – Vasoactive mediators that can affect SVR Endothelin (vasoconstrictor) Thromboxane (vasoconstrictor) High SVR Nitric oxide/ERDF (vasodilator) Prostaglandins (vasodilators and vasoconstrictors) Low SVR Hypertension Pathophysiology Proposed mechanisms – Increased SNS activity  increased secretion of catecholamines and/or increased receptor reactivity Hypertension Pathophysiology Proposed mechanisms – Over-expression of the RAAS leads to vasoconstriction and Na+/H2O retention Arterial  SVR Angiotensin II vasoconstriction  BP Aldosterone  Na+ reabsorption  H2O reabsorption  Blood Volume  Blood Pressure Hypertension Pathophysiology Proposed mechanisms – Mutation in genes that code for proteins in the renal tubules causing inappropriate Na+ reabsorption Na+ Reabsorption Na+ Na+ Filtration Schematic illustration of the glomerulus and proximal convoluted tubule Hypertension Pathophysiology Proposed mechanisms – Decrease in the production of vasodilators (NO, Pg, etc...) X Hypertension Pathophysiology Hemodynamic changes/consequences – Increase in SVR with normal CO Hypertension Pathophysiology Hemodynamic changes/consequences – Increased LV afterload  LV afterload LV hypertrophy Hypertension Pathophysiology Hemodynamic changes/consequences – Turbulence of blood causes shear stresses on vascular endothelium Vascular endothelium Hypertension Pathophysiology Vascular remodeling – Increased levels of angiotensin II causes hypertrophy, hyperplasia and reorganization of vascular smooth muscle leading to a narrowed lumen Vascular smooth muscle in tunica media Hypertension Pathophysiology Vascular remodeling – Degenerative changes in arterial wall From: http://www.nhlbi.nih.gov Vascular smooth muscle in tunica media Hypertension  RETURNING TO OUR CASE In clinic today, you meet a 52-year-old parent of two who works as a corporate manager. Question: Based on They've come in because of persistent this patient’s headaches and occasional dizziness that's been history, explain affecting their work. "I know my blood pressure which isn't great," they tell you, pulling out a log pathophysiological showing repeated measurements around mechanisms are 162/94 mmHg. "But between the long hours at likely contributing work and family commitments, I barely have to their time to eat, let alone cook. I practically live on hypertension coffee and fast food." You notice they appear fatigued and their BMI is 31. While reviewing their family history, they mention both their parent and sibling developed hypertension in their 50s. Risk Factors Genetics/family history Black race Older age Dietary factors Tobacco use Alcohol Obesity Hypertension Racial and Ethnic Disparities Racial and Ethnic Disparities in Hypertension Prevalence, Awareness, Treatment, and Control 90.00% 80.00% 70.00% 60.00% 50.00% 40.00% 30.00% 20.00% 10.00% 0.00% Hypertension Prevalence Hypertension Awareness Hypertension Treatment Hypertension Control White American Black Americans Hispanic Americans Asian Americans Racial and Ethnic Disparities Think-Pair-Share What do you believe are some of the factors contributing to racial and ethnic disparities in hypertension prevalence, management, and complications? What can be done to help reduce these disparities? – At an individual level – At a system level – At a national level  RETURNING TO OUR CASE In clinic today, you meet a 52-year-old parent of two who works as a corporate manager. Question: Which They've come in because of persistent risk factors can headaches and occasional dizziness that's been you identify in affecting their work. "I know my blood pressure this case? isn't great," they tell you, pulling out a log showing repeated measurements around 162/94 mmHg. "But between the long hours at Linking: How work and family commitments, I barely have might stress time to eat, let alone cook. I practically live on influence their coffee and fast food." You notice they appear sympathetic fatigued and their BMI is 31. While reviewing nervous system their family history, they mention both their activity? parent and sibling developed hypertension in their 50s. Clinical Consequences Atherosclerosis Hypertension Clinical Consequences Heart failure (diastolic)  LV afterload  Myocardial workload LV hypertrophy Hypertension Clinical Consequences Chronic kidney disease Hypertension Clinical Consequences Aneurysm Fig. 33-10 Page 1068 Hypertension Clinical Consequences Ocular changes From: http://www.doctorsvisioncenter.com Hypertension Clinical Consequences Metabolic syndrome Fig. 33-3 p. 1062 Hypertension One Minute Paper What surprises you about hypertension pathophysiology How does this discussion change your understanding of hypertension treatment? What questions remain unclear? DYSLIPIDEMIA  CASE INTRODUCTION A 45-year-old IT professional has come for follow- up after their recent type 2 diabetes diagnosis. They've been monitoring their blood glucose as recommended, but today's lipid panel results are concerning: total cholesterol 245 mg/dL, LDL 162 mg/dL, HDL 32 mg/dL, and triglycerides 200 mg/dL. "I spend most of my day at my computer," they explain. "I tried changing my diet when I got the diabetes diagnosis, but honestly, I'm confused about what I should be eating. Everything seems to affect my blood sugar." They work remotely and admit that some days they barely leave their desk. Types of Lipids Triglycerides Cholesterol Dyslipidemia Types of Lipoproteins Chylomicrons – Transport dietary lipids from the small intestine to other regions of the body Chylomicrons VLDL – Transport endogenous triglycerides and cholesterol to the tissues Triglycerides VLDL LDL Tissue capillary Dyslipidemia Types of Lipoproteins IDL – Degraded VLDL, used to form LDL LDL – Transport endogenous cholesterol in the plasma to the tissues Triglycerides VLDL LDL Tissue capillary Dyslipidemia Types of Lipoproteins HDL – Transport lipids from the tissues to the liver to be metabolized Cholesterol/Phospholipids HDL Tissue capillary Additional Functions: Participates in endothelial repair Reduces clot formation Dyslipidemia Risk Factors Genetic predisposition Dietary factors Obesity Lack of exercise Hyperinsulinemia/diabetes mellitus Dyslipidemia  RETURNING TO OUR CASE A 45-year-old IT professional has come for follow- up after their recent type 2 diabetes diagnosis. Question: How They've been monitoring their blood glucose as does this recommended, but today's lipid panel results are patient’s diabetes concerning: total cholesterol 245 mg/dL, LDL 162 affect their lipid mg/dL, HDL 32 mg/dL, and triglycerides 200 profile at a mg/dL. "I spend most of my day at my molecular level? computer," they explain. "I tried changing my diet when I got the diabetes diagnosis, but honestly, I'm confused about what I should be eating. Everything seems to affect my blood sugar." They work remotely and admit that some days they barely leave their desk. Physiology of LDL Metabolism First step of cholesterol production requires the enzyme HMG-CoA reductase In the hepatocytes, cholesterol and varying amount of other lipids bind to an apolipoprotein to form VLDL VLDL is excreted into the bloodstream by exocytosis, then converted to IDL and eventually LDL To uptake LDL into its cytoplasm a cell must have (or synthesize) LDL- receptors Dyslipidemia Physiology of LDL Metabolism From: http://www.nature.com/nrg/journal/v10/n2/fig_tab/nrg2481_F1.html Dyslipidemia  RETURNING TO OUR CASE A 45-year-old IT professional has come for follow- up after their recent type 2 diabetes diagnosis. Discussion: They've been monitoring their blood glucose as Explain how this recommended, but today's lipid panel results are patient’s concerning: total cholesterol 245 mg/dL, LDL 162 metabolic status mg/dL, HDL 32 mg/dL, and triglycerides 200 affects LDL mg/dL. "I spend most of my day at my metabolism computer," they explain. "I tried changing my diet when I got the diabetes diagnosis, but honestly, I'm confused about what I should be eating. Everything seems to affect my blood sugar." They work remotely and admit that some days they barely leave their desk. Laboratory Evaluation Elevated LDL-C and/or VLDL Low HDL-C Elevated cholesterol Elevated triglycerides Dyslipidemia  RETURNING TO OUR CASE A 45-year-old IT professional has come for follow- up after their recent type 2 diabetes diagnosis. Question: Which They've been monitoring their blood glucose as lipid values are recommended, but today's lipid panel results are abnormal? Why concerning: total cholesterol 245 mg/dL, LDL 162 might they be out mg/dL, HDL 32 mg/dL, and triglycerides 200 of normal range? mg/dL. "I spend most of my day at my computer," they explain. "I tried changing my diet when I got the diabetes diagnosis, but honestly, I'm confused about what I should be eating. Everything seems to affect my blood sugar." They work remotely and admit that some days they barely leave their desk. ATHEROSCLEROSIS  CASE INTRODUCTION Your next patient is 60 years old and has been having chest pain that comes and goes, especially when climbing the stairs at work where they're a housekeeper. "It's probably nothing," they say, "but my daughter insisted I come in." They've had high blood pressure and cholesterol for years but stopped taking medications because they were too expensive. You notice the distinct smell of cigarette smoke, and they acknowledge smoking a pack a day for the past 30 years. During the exam, they need to stop and catch their breath after minimal activity. They're worried about missing work for appointments but are becoming increasingly concerned about their symptoms. Definition & Causes Chronic disease of the arteries characterized by abnormal thickening and hardening of the vessel wall. caused by Endothelial Injury and Dyslipidemia Atherosclerosis Risk Factors Hypertension Tobacco use Diabetes mellitus Infection Autoimmune disease/immune reactions Mechanisms Increased LDL levels Decrease in the release of Hyperhomocystinemia vasodilatory mediators Increased tendency for the blood to clot Atherosclerosis  RETURNING TO OUR CASE Your next patient is 60 years old and has been having chest pain that comes and goes, Discussion: Identify the especially when climbing the stairs at work modifiable and non- where they're a housekeeper. "It's probably modifiable risk factors and nothing," they say, "but my daughter insisted explain their I come in." They've had high blood pressure pathophysiological and cholesterol for years but stopped taking significance medications because they were too expensive. You notice the distinct smell of cigarette smoke, and they acknowledge smoking a pack a day for the past 30 years. During the exam, they need to stop and catch their breath after minimal activity. They're worried about missing work for appointments but are becoming increasingly concerned about their symptoms. Pathophysiology Overview Fig. 33-12 Page 1072 Atherosclerosis Pathophysiology Endothelial injury Fig. 33-12 A Page 1072 Atherosclerosis Pathophysiology Endothelial injury Endothelium stops making normal antithrombotic and vasodilatory substances Abnormal vasoconstriction Ischemia Fig. 33-13 Page 1072 Atherosclerosis Pathophysiology Endothelial injury Endothelium stops making normal antithrombotic and vasodilatory substances Macrophages adhere and migrate below the injured endothelium Fig. 33-12 A Page 1072 Atherosclerosis Pathophysiology Endothelial injury Growth factors are released which stimulates smooth muscle hyperplasia Abnormal vasoconstriction Ischemia Atherosclerosis Pathophysiology Endothelial injury Inflammation Macrophages adhere and migrate below the injured endothelium Fig. 33-12 A p. 1072 Atherosclerosis Pathophysiology Endothelial injury Inflammation Macrophages adhere and migrate below the injured endothelium Release of enzymes and oxygen free radicals Fig. 33-12 A Page 1072 Atherosclerosis Pathophysiology Hyperlipidemia LDLs migrate below the endothelium Oxidation of LDL by the macrophages Fig. 33-13 Page 1072 Formation of the fatty streak Fig. 33-12 B Page 1072 Atherosclerosis Pathophysiology Formation of the fatty streak Progressive damage to vessel wall Scar tissue deposition & formation of fibrous plaque Plaque calcifies Fig. 33-12 C Page 1072 Atherosclerosis Pathophysiology Formation of the fatty streak Progressive damage to vessel wall Scar tissue deposition & formation of fibrous plaque Plaque calcifies Rough plaque surface promotes clot formation Obstruction worsens Fig. 33-12 D Page 1072 Atherosclerosis  RETURNING TO OUR CASE Your next patient is 60 years old and has been having chest pain that comes and goes, Discussion: Describe especially when climbing the stairs at work how this patient’s where they're a housekeeper. "It's probably risk factors nothing," they say, "but my daughter insisted contribute to I come in." They've had high blood pressure endothelial injury and cholesterol for years but stopped taking medications because they were too expensive. You notice the distinct smell of cigarette smoke, and they acknowledge smoking a pack a day for the past 30 years. During the exam, they need to stop and catch their breath after minimal activity. They're worried about missing work for appointments but are becoming increasingly concerned about their symptoms. Laboratory Evaluation Evidence of dyslipidemia – High cholesterol, triglycerides, LDL/VLDL – Low HDL Evidence of atherosclerosis – High hs-CRP Other – High fasting glucose – High HbA1c Atherosclerosis  LOOKING AHEAD Your next patient is 60 years old and has been having chest pain that comes and goes, Discussion: Based on the especially when climbing the stairs at work pathophysiology we’ve where they're a housekeeper. "It's probably discussed, explain the nothing," they say, "but my daughter insisted mechanisms behind this I come in." They've had high blood pressure patient’s symptoms and cholesterol for years but stopped taking medications because they were too expensive. You notice the distinct smell of cigarette smoke, and they acknowledge smoking a pack a day for the past 30 years. During the exam, they need to stop and catch their breath after minimal activity. They're worried about missing work for appointments but are becoming increasingly concerned about their symptoms.  3-2-1 REFLECTION CONNECTING THE DOTS 3 List three new things you learned today 2Identify two interesting concepts you'd like to learn more about 1 Write down one question that remains unclear