This document summarizes key concepts related to cardiovascular function and disorders of blood flow and blood pressure. It covers hemodynamics, regulation of blood pressure through the autonomic nervous system and renin-angiotensin system, and disorders such as hypertension and hyperlipidemia. The roles of the heart, blood vessels, and other components in maintaining blood flow and pressure are discussed, along with how drugs can affect these systems.
1. Control of Cardiovascular Function, Disorders of Blood Flow & Blood Pressure, Hyperlipidemia & Artherosclerosis
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3. Pulmonary and Systemic Circulation Baxter Corp. (1999)
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5. How does blood get back to the heart? Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p 461
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8. Resistance of a Tube Porth, Pathophysiology, Concepts of Altered Health States, 7 th ed., 2005, Lippincott, p. 452. Also see p 322, point 2 in Porth, Essentials Big factor!
9. Volume & Pressure Distribution Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 321. Arteriolar tone determines systemic vascular resistance
10. Same concept from Lehne Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p 461
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12. Resistance Arterioles Maintain Blood Pressure Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 338 Arteries have abundant smooth muscle. The diameter of the artery/arteriole is determined by the degree of contraction of the smooth muscle, which is mediated by the SNS (alpha receptors).
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17. Endothelial Cells Endothelial cells line all blood vessels. They are normally quite smooth and permit laminar blood flow. They also form a tight barrier in larger vessels, but in capillaries are more permissive of small molecules exiting and entering the vascular system.
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23. Functional Anatomy of the Heart Pericardium: Sac around heart Porth, 2007, Essential of Pathophysiology, 2 nd ed., Lippincott, p. 328. A “virtual space” which can become fluid or blood-filled (pericardial effusion).
25. Heart Valves Keep Blood Flow Unidirectional Semilunar valves: Control blood flow out of ventricles A ortic valve P ulmonic valve A-V valves : Control blood flow between atria & ventricles T ricuspid valve M itral valve Major function of heart valves: Forward direction of blood flow Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 329.
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32. Porth, 2007, Essential of Pathophysiology, 2 nd ed., Lippincott, p. 334. The Wiggers diagram
33. Ventricular Systole Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 334. Isovolumic (isometric) contraction Closure of AV valves (S1), all valves closed. No change in ventricular volume, ventricles contract. When ventricular pressures > aortic & pulmonary pressures, semilunar valves open, leading to the - Ejection period . Stroke volume ejected. Ventricles contract, then relax. Intraventricular pressures and become less than pressures in aorta & pulm. artery. Blood from large arteries flows back toward ventricles and aortic/pulmonic valves shut (S2).
34. Ventricular Diastole Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 334. Ventricular relaxation & filling. Isovolumic (isometric) relaxation: Semilunar valves closed, ventricles relax. No change in ventricular volume, but ventricular pressure until it’s less than atrial pressures. AV valves open, blood from atria enters ventricles -> Rapid filling period . Most ventricular filling in first third of diastole.(S3) During the last third, atria contract (atrial kick).
44. Effect of Afterload on CO Guyton, 2006, Textbook of Medical Physiology, 11th ed.,Saunders, p. 114.
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50. The Baroreceptor Reflex Baroreceptors in the aortic arch and carotid artery Autonomic centers in the brainstem Cardiac muscle, cardiac conduction system, and vascular smooth muscle.
51. The Sensory Components of the Baroreceptor Reflex – Chemo and Stretch Receptors Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 364.
52. ANS Regulation of BP – the Baroreceptor Reflex Be sure you know which receptors are where!!! McCance & Heuther, 2002, Pathophysiology: The Biologic Basis for Disease in Adults & Children, Mosby, p.961
53. Neurotransmitters Porth, Pathophysiology, Concepts of Altered Health States, 7 th ed., 2005, Lippincott, p. 1151.
56. Vasopressin (Antidiuretic Hormone (ADH)) Porth, Pathophysiology, Concepts of Altered Health States, 7 th ed., 2005, Lippincott, p. 756.
57. Porth, Pathophysiology, Concepts of Altered Health States, 7 th ed., 2005, Lippincott, p. 756. The ANS and RAAS systems work in concert.
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61. Disorders of Blood Pressure Regulation: Hypertension and Orthostatic Hypotension
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63. Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 374 Orthostatic Hypotension
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76. Lehne, 2009, Pharmacology for Nursing Care, 6 7h ed., Elsevier, p. 500 Sites of Action
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79. Algorithm for Treating Hypertension Lifestyle modifications Goal BP not met Stage 1 – thiazide diuretic /consider ACEI,ARB, beta blocker, CCB or combination Stage 2 – 2-drug combo (usually a thiazide + ACEI, ARB, beta blocker or CCB Goal BP not met Optimize dosage or add a drug from a different class Continue adding drugs from other classes until goal is achieved Goal BP not met Adapted from Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p. 507
80. Classes of Antihypertensive Drugs Recommended for Initial Therapy in Patients with High-Risk Comorbid Conditions Adapted from Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p. 508 Condition Drug Classes Recommended for Initial Therapy of HTN Diuretic Beta Blocker ACEI ARB CCB Aldosterone Antagonist Heart Failure X X X X X Post MI X X X Coronary Artery Disease Risk X X X X Diabetes X X X X X Chronic Kidney Disease X X Recurrent Stroke Prevention X X
81. Drugs That Affect BP: Diuretics Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p. 500
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83. Thiazides Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p. 445 Prevent re-absorption of sodium in the distal tubule.
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86. Loop Diuretics Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p. 445 Prevent the re-absorption of sodium from the ascending Loop of Henle.
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90. Potassium-Sparing Diuretics Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p. 445 Prevent the re-absorption of sodium from the collecting tubule and duct.
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95. Osmotic Diuretics -Mannitol Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p. 445 Prevents re-absorption of water from the proximal tubule.
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98. Drugs Acting on RAAS Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p. 500 Renin inhibitor
101. Porth, 2007, Essential of Pathophysiology, 2 nd ed., Lippincott, p. 365. ACE Inhibitors (ACEI) Captopril, lisinopril, enalapril, and others
102. Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p. 469
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106. Westra S and de Jager C. N Engl J Med 2006;355:295 A 75-year-old man presented to the emergency department with diffuse swelling of his tongue that had begun a few hours earlier. He had been taking 25 mg of captopril twice daily for the past 3 years because of hypertension. He was treated with epinephrine, corticosteroids, and antihistamines and the swelling resolved over a three-hour period. The angioedema was likely due to the angiotensin-converting enzyme inhibitor.
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109. Porth, 2007, Essential of Pathophysiology, 2 nd ed., Lippincott, p. 365. Angiotensin II Receptor Blockers (ARBs) Losartan, valsartan, candesartan, and others
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112. Porth, 2007, Essential of Pathophysiology, 2 nd ed., Lippincott, p. 365. Aldosterone Antagonists Spironolactone Eplerenone (Inspra) Potassium-sparing diuretics (covered previously as diuretics) Promote Na + & H 2 0 excretion in the collecting tubule & duct
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114. Drugs That Affect BP: Sympatholytics (Antiadrenergics) Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p. 500 Sites of Action
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117. Clinical Pharmacology of Some Beta Blockers Adapted from Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p. 167 Generic/trade name ISA Cardioselective (beta 1 > beta 2 ) Acebutolol/Sectal ® + Atenolol/Tenormin ® 0 Esmolol/Brevibloc ® 0 Metolprolol/Lopressor ® Slow release/Toprol XL 0 Nonselective (beta 1 = beta 2 ) Pindolol/Visken ® +++ Propranolol/Inderal ® Slow release/Inderal LA® 0 Nonselective alpha/beta blockers Carvedilol/Coreg ® 0 Labetolol/Normodyne ® or Trandate ® 0
118. Therapeutic Uses Adapted from Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p.168 A – approved; I - investigational Drug HTN Angina Dysrrhy-thmias MI Migraine Stage Fright Heart Failure Cardioselective Acebutolol A I A Atenolol A A I A I I Esmolol I A Metolprolol A A I A I A Nonselective Pindolol A I I Propranolol A A A A A I Nonselective alpha/beta blockers Carvedilol A I A A Labetolol A
119. Sympatholytics - Alpha-1 antagonists Sites of Action Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p. 500
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121. Centrally Acting Alpha-2 Agonists Sites of Action Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p. 500
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124. Lehne, 2009, Pharmacology for Nursing Care, 7 th ed., Elsevier, p. 481 Calcium Channels in the Heart
140. Five Types of Lipoproteins Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 348. -Of the five, LDLs and HDLs are the most important - As the density of the lipoprotein increases, the proportion of triglycerides decreases and the proportion of cholesterol increases
141. Lipoprotein Synthesis & Transport Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 349. Synthesis in small intestine, liver Liver important in LDL metabolism; removes LDL via LDL receptors
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144. LDL Receptors in Liver Remove LDLs from the Blood Robbins & Cotran Pathologic Basis of Disease (7th ed), 2005, Elsevier, p.158
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147. Classification of LDL, Total, and HDL Cholesterol Cholesterol Level (mg/dL) Classification Total <200 Optimal 200-239 Borderline high > 240 High LDL cholesterol <100 Optimal 100-129 Above optimal 130-159 Borderline high 160-189 High > 190 Very high Adapted from Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 350. Cholesterol Level (mg/dL) Classification HDL cholesterol <40 Low > 60 High
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151. Atheromatous Plaque Porth, 2007, Essential of Pathophysiology, 2 nd ed., Lippincott, p. 353 Plaque Complicated Lesion
156. Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 352. Atheromas tend to develop at sites of turbulent flow – near branch points As the artheroma develops, it creates more of a constriction, which produces more turbulent flow. See Figure 17.8 in Porth!
157. Laminar & Turbulent Flow Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 323.
173. Bile Acid Sequestrants Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 349. Prevent the absorption of cholesterol in the intestine
174. Bile acid reabsorption (GI) synthesis in liver need for cholesterol LDL receptors Robbins & Cotran Pathologic Basis of Disease (7th ed), 2005, Elsevier, p.158
181. Nicotinic Acid (Niacin) [Niacor, Niaspan] Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 349. Decreases production of VLDLs by inhibiting lipolysis in adipose tissue LDL
Lehne pg 492-494 : Re-iterate that thiazides do not affect VSM!
Lehne pg 500
Lehne 501 - 502
Lehne pg 439
Lehne pg 441
Lehne pg 443
Lehne 439: mechanism of action
Lehne pg 439
Lehne p 440 - incorporate pt/family teaching into these adverse effects
Lehne pg 443; compare mechanism of action here for Aladatone and triamterone (p.443 and 444)
Lehne pg 443
Lehne pg 444
Lehne pg 444
Lehne pg 444
Porth pg 364
Lehne pg 464
Lehne pg 464-466
Lehne pg 464-465
Lehne pg 466-467
Lehne pg 467
Lehne pg 467-468
Lehne pg 468
Lehne pg 468
Lehne pg 469
Lehne 495
Lehne pg 495-496
Lehne pg 498
Lehne pg 498;include pt teaching about sedation and no driving, don’t stop med quickly
Lehne pg 474
Lehne p475
Lehne pg 476
Lehne pg 477
Lehne pg 478
Lehne 484-5
Lehne pg 485
Porth pg 347
Porth pg 347
Porth pg 348
Lehne pg 558
Porth 349, 350
Porth pg 350
Porth pg 352
Porth 352
N98-305 Pathophys ACS 11/02/11 12:10 PM Histologic studies have characterized the progression of atherosclerotic lesion types. The earliest lesions (from the first decade on) are characterized histologically by isolated foam cells or fatty streaks in the vessel wall. Lesion growth at this stage occurs mainly by lipid accumulation. Intermediate lesions, which may be associated with small extracellular lipid pools, progress to atheroma, which has a core of extracellular lipid. These lesions may be seen starting in the third decade. Starting in the fourth decade, lesions may progress to the fibrous plaque stage, which is characterized by accelerated increases in smooth muscle and collagen. Complicated lesions are characterized by thrombosis, fissure, and hematoma formation. 2 Atherosclerosis Timeline 2 Stary HC, Chander AB, Dinsmore RE, et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. Circulation. 1995;92:1355–1374. Slide 2
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