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DRUGS USED IN DISORDERS OF THE
CARDIOVASCULAR SYSTEM
CVS Function, Regulation of the Heart
and Overview of Therapeutic Goals in CV
Disorders
Marc Imhotep Cray, M.D.
Photo: Photograph of chordae tendineae attached to papillary muscles of a ventricle. Seeley’s anatomy & physiology. 10th ed. New York, NY: McGraw-Hill 2010.
Marc Imhotep Cray, M.D.
Purpose of Presentation:
2
To provide an overview/review of the function of the
cardiovascular system, the regulation of the heart, the
pathophysiology of the most common cardiovascular diseases
and the therapeutic goals of each treatment strategy as a
prerequisite to learning and understanding each drug class.
Companion Notes: Core Principles in Cardiovascular Therapeutics.pdf
Marc Imhotep Cray, M.D.
Classification Schema:
CARDIOVASCULAR & RENAL AGENTS
3
Direct Vasodilators
Nitroglycerin
Nitroprusside
Nesiritide
Hydralazine
ACE Inhibitors, ARBs, & Renin
Inhibitors
Captopril
Losartan
Aliskiren
Inotropes & Pulmonary
Arterial Vasodilators
Digoxin
Milrinone
Sildenafil
Epoprostenol
Bosentan
Diuretics
Furosemide
Hydrochlorothiazide
Spironolactone
Eplerenone
Acetazolamide
Antiarrhythmics
Procamamide
Lidocaine
Flecainide
Amiodarone
Ibutilide
Adenosine
Calcium Channel
Blockers
Nifedipine
Verapamil
Diltiazem
Other antianginals
RanolazineMost Common Drugs (Classes) with Phonetic Pronunciations. pdf
Marc Imhotep Cray, M.D. 4
N.B. To best understand pharmacological approaches to
management of cardiovascular disorders, an overview of
the regulation of cardiovascular function is warranted.
Marc Imhotep Cray, M.D.
Overview of cardiovascular system
5
 The heart and circulatory system must provide continuous,
efficient, and reliable operation while adapting to short and
long-term physiologic changes
 Drugs that are used to treat cardiovascular disorders
constitute one of the largest categories of prescription drugs
used
Marc Imhotep Cray, M.D.
Overview of CVS (2)
6
 Two factors suggest that use of CV drugs will continue to
increase:
 An aging population and
 increasing use of drugs as prevention against future CVD
 Above 2 factors work synergistically:
 As preventive care increases average lifespan, population has a
greater risk of cardiovascular disease, and
 As life expectancy increases, greater emphasis is placed on earlier
preventive intervention
Marc Imhotep Cray, M.D.
Overview CVS (3)
7
Certain cardiovascular disorders, such as cardiac arrhythmias
and congestive heart failure (CHF), produce symptoms that are
readily apparent to person affected and have consequences long
known to necessitate treatment
Other conditions do not produce obvious symptoms  have become
recognized as health problems only as a result of epidemiologic studies
in relatively recent years
 For example, blood pressures that had been considered normal b/c they were
average (age-appropriate mean) are now widely considered to fall into
hypertension category and are now routinely treated w medication
 Cholesterol levels that were once deemed normal (or were even thought to be
so insignificant that they went unmeasured) are now routinely treated w
medications
Marc Imhotep Cray, M.D.
Overview of CVS (4) U.S. Epidemiology*
8
Dysfunction of CVS is the principal cause of death and disability in
middle-aged and elderly men and women in industrialized world
In United States in 2004, there were nearly 1 million deaths from
cardiovascular disease, representing approximately 36% of all deaths
Estimates of prevalence of cardiovascular disease in 2005 indicated
that more than
 70 million individuals had hypertension,
 16 million had coronary heart disease, and
 5 million had congestive heart failure
*Data from the American Heart Association
Marc Imhotep Cray, M.D.
Overview of CVS (5)
9
For many years, treatment of cardiovascular disorders primarily
targeted innervation of the heart and blood vessels by the 2
subdivisions of the ANS:
 Parasympathetic innervation of heart is principally via vagus nerve
(cranial nerve X) and is mediated by action of acetylcholine (ACh) at
muscarinic cholinergic receptors
 Sympathetic innervation of heart is mediated principally by action of
norepinephrine (NE) on β adrenoceptors (β1 subtype)
Marc Imhotep Cray, M.D.
Overview of CVS (6)
10
The vasculature is controlled in a site-dependent manner
 By parasympathetic subdivision mediated by ACh, which usually
causes vasodilation*, and
 By sympathetic subdivision mediated by NE, which generally
causes vasoconstriction
Hormones and local factors also contribute to overall vascular tone
*Remember: There are no cholinergic receptors in vascular
smooth muscle, however vascular smooth muscle
nonetheless responses to Ach causing vasodilation.
Marc Imhotep Cray, M.D.
Overview of CVS (7)
11
A major advance in treatment strategies for cardiovascular disorders
occurred as a result of recognition of significant contributions made by
other neurotransmitter and hormone systems to normal and pathologic
cardiovascular function
 Targeting these systems, such as renin-angiotensin-aldosterone system
(RAAS) , has led to a broader variety of treatment options
Cardiovascular drugs include some of oldest medications, discovered by
serendipity, and some of the newest, discovered by molecular modeling
and screening technology
 They include a wide variety of receptor agonists, receptor
antagonists, and enzyme inhibitors
Marc Imhotep Cray, M.D.
Cardiovascular function: Cardiac cycle
12
 To understand how cardiac function is regulated, one must
know the sequence of mechanical events during a complete
cardiac cycle and how these mechanical events relate to
electrical activity of heart
 Cardiac cycle diagram in next slide (sometimes called the
Wiggers diagram) depicts changes in left side of heart (left
ventricular pressure and volume, left atrial pressure, and
aortic pressure) as a function of time
Cardiac cycle / Wiggers diagram
Seven phases of cardiac cycle:
(1) atrial systole
(2) Isovolumetric contraction
(3) rapid ejection
(4) reduced ejection
(5) isovolumetric relaxation
(6) rapid filling
(7) reduced filling
14
Cardiovascular function: Anatomy
 Heart muscle pumps blood through circulatory
system
 Each day, heart beats 100,000 times and pumps
2000 gal of blood
 Heart is composed of 4 chambers (divisions):
o upper two, right and left atria
o lower two, the right and left ventricles
 Blood is pumped through chambers, in only 1
direction, via 4 valves:
o tricuspid, located between right atrium and
right ventricle
o pulmonary, between right ventricle and
pulmonary artery
o mitral, between left atrium and left ventricle and
o aortic, between left ventricle and aorta
15
CV function: Anatomy cont.
 Dark blood, low in oxygen, returns
from body tissues through veins
enters right atrium then flows to right
ventricle pulmonary artery and
lungs where it is oxygenated
 Blood returns by pulmonary veins to
left atrium and goes through mitral
valve into left ventricle which pumps
oxygen-rich, bright-red blood 
through aortic valve into aorta and
then into systemic circulation
Marc Imhotep Cray, M.D.
CV function: Definitions and Regulation
16
 Cardiac output (CO) is total blood volume pumped by ventricles per minute
 (CO=heart rate × stroke volume)
 Stroke volume (SV) is blood pumped by left or right ventricle per beat
 In a resting adult, SV averages 60 to 80 mL of blood
 The 3 determinates of SV are preload, contractility and afterload
 Systole is contraction phase of cardiac cycle ventricles pump stroke volumes
 Diastole is resting phase of cardiac cycle occurs between heartbeats
 End-diastolic volume (EDV) is blood volume in each ventricle at end of diastole:
 120 mL at rest
 End-systolic volume(ESV) is blood volume in each ventricle after contraction:
 50 mL at rest
Marc Imhotep Cray, M.D.
Definition of Terms and Regulation cont.
17
To maintain equal flow through pulmonary and systemic circuits,
left and right ventricles maintain same cardiac output
 resting CO is 4.8 to 6.4 L/min
CO increases (20-85%) during intense exercise to transport more
oxygen to muscles
 This greater blood flow is caused by higher blood pressure and
arteriolar vasodilation in muscles, which is due to smooth
muscle relaxation
Marc Imhotep Cray, M.D.
Functional Regulation of CVS:
18
 Function of cardiovascular system involves:
 autonomic nervous system (ANS)
 kidneys(RAAS)
 heart
 vasculature, and
 blood
N.B. B/C these systems represent an integrated network,
cardiovascular function can be affected by alterations at any point
A review of each system’s
main contribution follows.
Marc Imhotep Cray, M.D.
CVS and the Autonomic Nervous System
19
 ANS innervates heart, blood vessels, kidney, and adrenal medulla
and has potential to modify cardiovascular function in a number of
different ways
(See CV physiology, Unit 4 string of MedPharm Digital Guidebook and NIP-associated graphics)
CO is amount of blood pumped by ventricles per unit time
 As stated previously, it is determined by volume of blood ejected
during each ventricular contraction (stroke volume [SV]) and how
frequently heart beats (heart rate [HR] ), expressed as CO = HR x SV
HR can be affected by a variety of factors but is principally under control
of ANS
 Beta blockers can reduce CO by decreasing HR and contractility
Marc Imhotep Cray, M.D.
The kidneys (RAAS)
20
 The kidneys adjust
excretion of Na+, other
ions and H2O to maintain
extracellular fluid and
volume fluid retention
by kidney is a modifiable
physiological parameter
that can result in changes
in blood pressure
Marc Imhotep Cray, M.D.
The heart
21
The heart, including
 rhythmic nature of its electrical signals
 force of contraction, and
 magnitude of discharge pressure
is responsible for pumping blood through pulmonary system
for oxygenation and delivering it through vasculature to organs
throughout body
Marc Imhotep Cray, M.D.
The circulation
22
 The circulation (both blood volume and composition) including
 H2O and electrolyte balances
 iron balances
 cholesterol and lipid composition
 capabilities for clot formation and lysis
 delivers O2 and nutrients to and carries away CO2 and waste
from all tissues
Marc Imhotep Cray, M.D.
Mathematical determinants of arterial
blood pressure (MAP)
23
Mean arterial pressure (MAP) is determined by:
 How much blood heart pumps into arterial system in a given time (CO)
and
 How much resistance arteries have to this input (total peripheral
resistance [TPR]) Mathematically, this is expressed as MAP = CO x TPR
o Consequently all drugs that lower blood pressure work by
affecting either CO or TPR (or both)
NB:
 The primary determinant of systolic blood pressure (SBP) is CO, whereas
 The primary determinant of diastolic blood pressure (DBP) is TPR
 b/c approximately one third of cardiac cycle is spent in systole and two
thirds in diastole, MAP can be calculated as MAP= 1/3 SBP + 2/3 DBP
Marc Imhotep Cray, M.D.
Cardiac output (CO) variables
24
 Stroke volume
 Contractility
 Myocardial oxygen demand
 Preload
 Afterload
 Ejection fraction
Marc Imhotep Cray, M.D.
CO variables: Stroke volume
25
 Stroke Volume is affected by Contractility, Afterload, and Preload
↑SV with:
 ↑ Contractility (e.g., anxiety, exercise)
 ↑ Preload (e.g., early pregnancy)
 ↓ Afterload
 A failing heart has ↓SV (systolic dysfunction)
Marc Imhotep Cray, M.D.
CO variables: Contractility
26
Contractility (and SV) ↑ with:
 Catecholamines (inhibition of
phospholamban  ↑ Ca2+ entry
into sarcoplasmic reticulum ↑
Ca2+-induced Ca2+ release)
 ↑intracellular Ca2+
 ↓ extracellular Na+ (↓activity of
Na+/Ca2+ exchanger)
 Digitalis (blocks Na+/K+ pump
↑intracellular Na+ 
↓Na+/Ca2+ exchanger activity
↑Intracellular Ca2+)
Contractility (and SV) ↓with:
 β1-blockade (↓ cAMP)
 HF with systolic dysfunction
 Acidosis
 Hypoxia/hypercapnia
(↓ pO2/ ↑ pCO2)
 Non-dihydropyridine Ca2+ channel
blockers (verapamil & diltiazem)
Marc Imhotep Cray, M.D.
CO variables: Myocardial oxygen demand
27
Myocardial O2 demand is↑ by:
 ↑ Contractility
 ↑ Afterload (proportional to arterial pressure)
 ↑ Heart Rate
 ↑ Diameter of ventricle (↑ wall tension)
Marc Imhotep Cray, M.D.
CO variables: Preload
28
 Preload approximated by ventricular EDV depends
on venous tone and circulating blood volume
 Venodilators (e.g., nitroglycerin) ↓preload
Marc Imhotep Cray, M.D.
CO variables: Afterload
29
 Afterload approximated by MAP
 ↑ afterload ↑ pressure  ↑wall tension per Laplace’s law
o LV compensates for ↑ afterload by thickening
(hypertrophy) in order to ↓wall tension
 Vasodilators (e.g., hydralazine) ↓Afterload (arterial)
 ACE inhibitors and ARBs ↓ both preload and afterload
 Chronic hypertension (↑MAP)  LV hypertrophy
Marc Imhotep Cray, M.D.
CO variables: Ejection fraction
30
 Left ventricular EF is an index of ventricular Contractility
normal EF is ≥ 55%
 EF ↓ in systolic HF(HFrEF)
 EF normal in diastolic HF(HFpEF)
Marc Imhotep Cray, M.D.
Strategies for Treating CV Diseases: Hypertension
31
Therapeutic Goal Pharmacologic Strategies
Reduce volume overload Diuretics decrease blood volume by increasing
volume of water excreted in the urine.
Reduce sympathetic outflow from
brain
Clonidine is an agonist at α2 receptors. It inhibits
release of NE and inhibits sympathetic outflow from
the brain
Block adrenergic receptors in heart Atenolol is a β1 adrenergic receptor antagonist that
reduces heart rate and myocardial work
Dilate blood vessels Prazosin blocks α1 adrenergic receptors causing
vasodilation
Nifedipine blocks calcium entry into smooth into
smooth cells of arterial walls, preventing contraction
Captopril reduces production of AT2 causing
vasodilation
Marc Imhotep Cray, M.D.
Strategies for Treating CV Diseases: Angina
Therapeutic Goal Pharmacologic Strategies
Reduce work of heart and improve
cardiac circulation =
Decrease myocardial O2 demand
Increase myocardial O2 supply
Stable Angina
Nitroglycerin reduces preload by venodilation
Atenolol decreases myocardial work (β1 antagonists)
Diltiazem decreases BP through vasodilation by blocking
calcium entry
Unstable Angina
β-Blockers reduce rate and myocardial work
Aspirin prevents platelet aggregation in myocardial
arteries
Heparin inhibits clotting in myocardial arteries
Nitroglycerin reduces preload
Eptifibatide or Tirofiban inhibit platelet aggregation
Marc Imhotep Cray, M.D.
Strategies for Treating CV Diseases:
Myocardial Infarction
33
Therapeutic Goal Pharmacologic Strategies
Reperfuse ischemic tissue Streptokinase converts plasminogen to
plasmin Plasmin digest fibrin and
fibrinogen, thus dissolving clots
Antianginals (see previous slide).
But not calcium channel blockers, which are
dangerous in setting of acute myocardial
infarction
Marc Imhotep Cray, M.D.
Strategies for Treating CV Diseases: Heart Failure
34
Therapeutic Goal Pharmacologic Strategies
Reduce workload
Improve myocardial
contractility
Diuretics decrease blood volume
Captopril causes vasodilation
Atenolol (β-blocker) reduces heart rate and work load
Nitroglycerin reduces venous tone (It also dilates
coronary arteries, enhancing blood delivery to heart)
Hydralazine and Nitroprusside relax arterioles
Digoxin increases calcium influx into myocardial cells
Amrinone inhibits cAMP degradation (cAMP is a
biochemical messenger that stimulates the heart)
Dobutamine increases cAMP production by stimulating
adrenergic receptors
Marc Imhotep Cray, M.D.
Strategies for Treating Cardiovascular
Diseases: Arrhythmias
35
Therapeutic Goal Pharmacologic Strategies
Restore synchronous
myocardial contraction
Several classes of agents
described in a subsequent
lecture, including:
Na+ Channel Blockers
K+ Channel Blockers
Ca+2 Channel Blockers
β-Blockers
Others agents
Marc Imhotep Cray, M.D.
Strategies for Treating Cardiovascular
Diseases: Vascular Occlusion
36
Therapeutic Goal Pharmacologic Strategies
Prevent coagulation Heparin and Warfarin inhibit coagulation
pathway
Prevent clot formation Aspirin inhibits platelet aggregation
Ticlopidine inhibits platelet binding to
fibrinogen
Destroy clots that have
already formed
Streptokinase converts plasminogen to
plasmin
Marc Imhotep Cray, M.D.
THE END
37
Marc Imhotep Cray, M.D. 38
Lectures/discussions to follow:
2. Hypercholesterolemia and Atherosclerosis
3. Angina
4. Heart Failure
5. Arrhythmias
6. Hypertension
7. Peripheral Vascular Disease
Further study (SDL):
Online resource center: Medical Pharmacology Cloud Folder
Companion Notes: Cardiovascular Pharmacology

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CVS Function, Regulation of the Heart and Overview of Therapeutic Goals in CV Disorders

  • 1. DRUGS USED IN DISORDERS OF THE CARDIOVASCULAR SYSTEM CVS Function, Regulation of the Heart and Overview of Therapeutic Goals in CV Disorders Marc Imhotep Cray, M.D. Photo: Photograph of chordae tendineae attached to papillary muscles of a ventricle. Seeley’s anatomy & physiology. 10th ed. New York, NY: McGraw-Hill 2010.
  • 2. Marc Imhotep Cray, M.D. Purpose of Presentation: 2 To provide an overview/review of the function of the cardiovascular system, the regulation of the heart, the pathophysiology of the most common cardiovascular diseases and the therapeutic goals of each treatment strategy as a prerequisite to learning and understanding each drug class. Companion Notes: Core Principles in Cardiovascular Therapeutics.pdf
  • 3. Marc Imhotep Cray, M.D. Classification Schema: CARDIOVASCULAR & RENAL AGENTS 3 Direct Vasodilators Nitroglycerin Nitroprusside Nesiritide Hydralazine ACE Inhibitors, ARBs, & Renin Inhibitors Captopril Losartan Aliskiren Inotropes & Pulmonary Arterial Vasodilators Digoxin Milrinone Sildenafil Epoprostenol Bosentan Diuretics Furosemide Hydrochlorothiazide Spironolactone Eplerenone Acetazolamide Antiarrhythmics Procamamide Lidocaine Flecainide Amiodarone Ibutilide Adenosine Calcium Channel Blockers Nifedipine Verapamil Diltiazem Other antianginals RanolazineMost Common Drugs (Classes) with Phonetic Pronunciations. pdf
  • 4. Marc Imhotep Cray, M.D. 4 N.B. To best understand pharmacological approaches to management of cardiovascular disorders, an overview of the regulation of cardiovascular function is warranted.
  • 5. Marc Imhotep Cray, M.D. Overview of cardiovascular system 5  The heart and circulatory system must provide continuous, efficient, and reliable operation while adapting to short and long-term physiologic changes  Drugs that are used to treat cardiovascular disorders constitute one of the largest categories of prescription drugs used
  • 6. Marc Imhotep Cray, M.D. Overview of CVS (2) 6  Two factors suggest that use of CV drugs will continue to increase:  An aging population and  increasing use of drugs as prevention against future CVD  Above 2 factors work synergistically:  As preventive care increases average lifespan, population has a greater risk of cardiovascular disease, and  As life expectancy increases, greater emphasis is placed on earlier preventive intervention
  • 7. Marc Imhotep Cray, M.D. Overview CVS (3) 7 Certain cardiovascular disorders, such as cardiac arrhythmias and congestive heart failure (CHF), produce symptoms that are readily apparent to person affected and have consequences long known to necessitate treatment Other conditions do not produce obvious symptoms  have become recognized as health problems only as a result of epidemiologic studies in relatively recent years  For example, blood pressures that had been considered normal b/c they were average (age-appropriate mean) are now widely considered to fall into hypertension category and are now routinely treated w medication  Cholesterol levels that were once deemed normal (or were even thought to be so insignificant that they went unmeasured) are now routinely treated w medications
  • 8. Marc Imhotep Cray, M.D. Overview of CVS (4) U.S. Epidemiology* 8 Dysfunction of CVS is the principal cause of death and disability in middle-aged and elderly men and women in industrialized world In United States in 2004, there were nearly 1 million deaths from cardiovascular disease, representing approximately 36% of all deaths Estimates of prevalence of cardiovascular disease in 2005 indicated that more than  70 million individuals had hypertension,  16 million had coronary heart disease, and  5 million had congestive heart failure *Data from the American Heart Association
  • 9. Marc Imhotep Cray, M.D. Overview of CVS (5) 9 For many years, treatment of cardiovascular disorders primarily targeted innervation of the heart and blood vessels by the 2 subdivisions of the ANS:  Parasympathetic innervation of heart is principally via vagus nerve (cranial nerve X) and is mediated by action of acetylcholine (ACh) at muscarinic cholinergic receptors  Sympathetic innervation of heart is mediated principally by action of norepinephrine (NE) on β adrenoceptors (β1 subtype)
  • 10. Marc Imhotep Cray, M.D. Overview of CVS (6) 10 The vasculature is controlled in a site-dependent manner  By parasympathetic subdivision mediated by ACh, which usually causes vasodilation*, and  By sympathetic subdivision mediated by NE, which generally causes vasoconstriction Hormones and local factors also contribute to overall vascular tone *Remember: There are no cholinergic receptors in vascular smooth muscle, however vascular smooth muscle nonetheless responses to Ach causing vasodilation.
  • 11. Marc Imhotep Cray, M.D. Overview of CVS (7) 11 A major advance in treatment strategies for cardiovascular disorders occurred as a result of recognition of significant contributions made by other neurotransmitter and hormone systems to normal and pathologic cardiovascular function  Targeting these systems, such as renin-angiotensin-aldosterone system (RAAS) , has led to a broader variety of treatment options Cardiovascular drugs include some of oldest medications, discovered by serendipity, and some of the newest, discovered by molecular modeling and screening technology  They include a wide variety of receptor agonists, receptor antagonists, and enzyme inhibitors
  • 12. Marc Imhotep Cray, M.D. Cardiovascular function: Cardiac cycle 12  To understand how cardiac function is regulated, one must know the sequence of mechanical events during a complete cardiac cycle and how these mechanical events relate to electrical activity of heart  Cardiac cycle diagram in next slide (sometimes called the Wiggers diagram) depicts changes in left side of heart (left ventricular pressure and volume, left atrial pressure, and aortic pressure) as a function of time
  • 13. Cardiac cycle / Wiggers diagram Seven phases of cardiac cycle: (1) atrial systole (2) Isovolumetric contraction (3) rapid ejection (4) reduced ejection (5) isovolumetric relaxation (6) rapid filling (7) reduced filling
  • 14. 14 Cardiovascular function: Anatomy  Heart muscle pumps blood through circulatory system  Each day, heart beats 100,000 times and pumps 2000 gal of blood  Heart is composed of 4 chambers (divisions): o upper two, right and left atria o lower two, the right and left ventricles  Blood is pumped through chambers, in only 1 direction, via 4 valves: o tricuspid, located between right atrium and right ventricle o pulmonary, between right ventricle and pulmonary artery o mitral, between left atrium and left ventricle and o aortic, between left ventricle and aorta
  • 15. 15 CV function: Anatomy cont.  Dark blood, low in oxygen, returns from body tissues through veins enters right atrium then flows to right ventricle pulmonary artery and lungs where it is oxygenated  Blood returns by pulmonary veins to left atrium and goes through mitral valve into left ventricle which pumps oxygen-rich, bright-red blood  through aortic valve into aorta and then into systemic circulation
  • 16. Marc Imhotep Cray, M.D. CV function: Definitions and Regulation 16  Cardiac output (CO) is total blood volume pumped by ventricles per minute  (CO=heart rate × stroke volume)  Stroke volume (SV) is blood pumped by left or right ventricle per beat  In a resting adult, SV averages 60 to 80 mL of blood  The 3 determinates of SV are preload, contractility and afterload  Systole is contraction phase of cardiac cycle ventricles pump stroke volumes  Diastole is resting phase of cardiac cycle occurs between heartbeats  End-diastolic volume (EDV) is blood volume in each ventricle at end of diastole:  120 mL at rest  End-systolic volume(ESV) is blood volume in each ventricle after contraction:  50 mL at rest
  • 17. Marc Imhotep Cray, M.D. Definition of Terms and Regulation cont. 17 To maintain equal flow through pulmonary and systemic circuits, left and right ventricles maintain same cardiac output  resting CO is 4.8 to 6.4 L/min CO increases (20-85%) during intense exercise to transport more oxygen to muscles  This greater blood flow is caused by higher blood pressure and arteriolar vasodilation in muscles, which is due to smooth muscle relaxation
  • 18. Marc Imhotep Cray, M.D. Functional Regulation of CVS: 18  Function of cardiovascular system involves:  autonomic nervous system (ANS)  kidneys(RAAS)  heart  vasculature, and  blood N.B. B/C these systems represent an integrated network, cardiovascular function can be affected by alterations at any point A review of each system’s main contribution follows.
  • 19. Marc Imhotep Cray, M.D. CVS and the Autonomic Nervous System 19  ANS innervates heart, blood vessels, kidney, and adrenal medulla and has potential to modify cardiovascular function in a number of different ways (See CV physiology, Unit 4 string of MedPharm Digital Guidebook and NIP-associated graphics) CO is amount of blood pumped by ventricles per unit time  As stated previously, it is determined by volume of blood ejected during each ventricular contraction (stroke volume [SV]) and how frequently heart beats (heart rate [HR] ), expressed as CO = HR x SV HR can be affected by a variety of factors but is principally under control of ANS  Beta blockers can reduce CO by decreasing HR and contractility
  • 20. Marc Imhotep Cray, M.D. The kidneys (RAAS) 20  The kidneys adjust excretion of Na+, other ions and H2O to maintain extracellular fluid and volume fluid retention by kidney is a modifiable physiological parameter that can result in changes in blood pressure
  • 21. Marc Imhotep Cray, M.D. The heart 21 The heart, including  rhythmic nature of its electrical signals  force of contraction, and  magnitude of discharge pressure is responsible for pumping blood through pulmonary system for oxygenation and delivering it through vasculature to organs throughout body
  • 22. Marc Imhotep Cray, M.D. The circulation 22  The circulation (both blood volume and composition) including  H2O and electrolyte balances  iron balances  cholesterol and lipid composition  capabilities for clot formation and lysis  delivers O2 and nutrients to and carries away CO2 and waste from all tissues
  • 23. Marc Imhotep Cray, M.D. Mathematical determinants of arterial blood pressure (MAP) 23 Mean arterial pressure (MAP) is determined by:  How much blood heart pumps into arterial system in a given time (CO) and  How much resistance arteries have to this input (total peripheral resistance [TPR]) Mathematically, this is expressed as MAP = CO x TPR o Consequently all drugs that lower blood pressure work by affecting either CO or TPR (or both) NB:  The primary determinant of systolic blood pressure (SBP) is CO, whereas  The primary determinant of diastolic blood pressure (DBP) is TPR  b/c approximately one third of cardiac cycle is spent in systole and two thirds in diastole, MAP can be calculated as MAP= 1/3 SBP + 2/3 DBP
  • 24. Marc Imhotep Cray, M.D. Cardiac output (CO) variables 24  Stroke volume  Contractility  Myocardial oxygen demand  Preload  Afterload  Ejection fraction
  • 25. Marc Imhotep Cray, M.D. CO variables: Stroke volume 25  Stroke Volume is affected by Contractility, Afterload, and Preload ↑SV with:  ↑ Contractility (e.g., anxiety, exercise)  ↑ Preload (e.g., early pregnancy)  ↓ Afterload  A failing heart has ↓SV (systolic dysfunction)
  • 26. Marc Imhotep Cray, M.D. CO variables: Contractility 26 Contractility (and SV) ↑ with:  Catecholamines (inhibition of phospholamban  ↑ Ca2+ entry into sarcoplasmic reticulum ↑ Ca2+-induced Ca2+ release)  ↑intracellular Ca2+  ↓ extracellular Na+ (↓activity of Na+/Ca2+ exchanger)  Digitalis (blocks Na+/K+ pump ↑intracellular Na+  ↓Na+/Ca2+ exchanger activity ↑Intracellular Ca2+) Contractility (and SV) ↓with:  β1-blockade (↓ cAMP)  HF with systolic dysfunction  Acidosis  Hypoxia/hypercapnia (↓ pO2/ ↑ pCO2)  Non-dihydropyridine Ca2+ channel blockers (verapamil & diltiazem)
  • 27. Marc Imhotep Cray, M.D. CO variables: Myocardial oxygen demand 27 Myocardial O2 demand is↑ by:  ↑ Contractility  ↑ Afterload (proportional to arterial pressure)  ↑ Heart Rate  ↑ Diameter of ventricle (↑ wall tension)
  • 28. Marc Imhotep Cray, M.D. CO variables: Preload 28  Preload approximated by ventricular EDV depends on venous tone and circulating blood volume  Venodilators (e.g., nitroglycerin) ↓preload
  • 29. Marc Imhotep Cray, M.D. CO variables: Afterload 29  Afterload approximated by MAP  ↑ afterload ↑ pressure  ↑wall tension per Laplace’s law o LV compensates for ↑ afterload by thickening (hypertrophy) in order to ↓wall tension  Vasodilators (e.g., hydralazine) ↓Afterload (arterial)  ACE inhibitors and ARBs ↓ both preload and afterload  Chronic hypertension (↑MAP)  LV hypertrophy
  • 30. Marc Imhotep Cray, M.D. CO variables: Ejection fraction 30  Left ventricular EF is an index of ventricular Contractility normal EF is ≥ 55%  EF ↓ in systolic HF(HFrEF)  EF normal in diastolic HF(HFpEF)
  • 31. Marc Imhotep Cray, M.D. Strategies for Treating CV Diseases: Hypertension 31 Therapeutic Goal Pharmacologic Strategies Reduce volume overload Diuretics decrease blood volume by increasing volume of water excreted in the urine. Reduce sympathetic outflow from brain Clonidine is an agonist at α2 receptors. It inhibits release of NE and inhibits sympathetic outflow from the brain Block adrenergic receptors in heart Atenolol is a β1 adrenergic receptor antagonist that reduces heart rate and myocardial work Dilate blood vessels Prazosin blocks α1 adrenergic receptors causing vasodilation Nifedipine blocks calcium entry into smooth into smooth cells of arterial walls, preventing contraction Captopril reduces production of AT2 causing vasodilation
  • 32. Marc Imhotep Cray, M.D. Strategies for Treating CV Diseases: Angina Therapeutic Goal Pharmacologic Strategies Reduce work of heart and improve cardiac circulation = Decrease myocardial O2 demand Increase myocardial O2 supply Stable Angina Nitroglycerin reduces preload by venodilation Atenolol decreases myocardial work (β1 antagonists) Diltiazem decreases BP through vasodilation by blocking calcium entry Unstable Angina β-Blockers reduce rate and myocardial work Aspirin prevents platelet aggregation in myocardial arteries Heparin inhibits clotting in myocardial arteries Nitroglycerin reduces preload Eptifibatide or Tirofiban inhibit platelet aggregation
  • 33. Marc Imhotep Cray, M.D. Strategies for Treating CV Diseases: Myocardial Infarction 33 Therapeutic Goal Pharmacologic Strategies Reperfuse ischemic tissue Streptokinase converts plasminogen to plasmin Plasmin digest fibrin and fibrinogen, thus dissolving clots Antianginals (see previous slide). But not calcium channel blockers, which are dangerous in setting of acute myocardial infarction
  • 34. Marc Imhotep Cray, M.D. Strategies for Treating CV Diseases: Heart Failure 34 Therapeutic Goal Pharmacologic Strategies Reduce workload Improve myocardial contractility Diuretics decrease blood volume Captopril causes vasodilation Atenolol (β-blocker) reduces heart rate and work load Nitroglycerin reduces venous tone (It also dilates coronary arteries, enhancing blood delivery to heart) Hydralazine and Nitroprusside relax arterioles Digoxin increases calcium influx into myocardial cells Amrinone inhibits cAMP degradation (cAMP is a biochemical messenger that stimulates the heart) Dobutamine increases cAMP production by stimulating adrenergic receptors
  • 35. Marc Imhotep Cray, M.D. Strategies for Treating Cardiovascular Diseases: Arrhythmias 35 Therapeutic Goal Pharmacologic Strategies Restore synchronous myocardial contraction Several classes of agents described in a subsequent lecture, including: Na+ Channel Blockers K+ Channel Blockers Ca+2 Channel Blockers β-Blockers Others agents
  • 36. Marc Imhotep Cray, M.D. Strategies for Treating Cardiovascular Diseases: Vascular Occlusion 36 Therapeutic Goal Pharmacologic Strategies Prevent coagulation Heparin and Warfarin inhibit coagulation pathway Prevent clot formation Aspirin inhibits platelet aggregation Ticlopidine inhibits platelet binding to fibrinogen Destroy clots that have already formed Streptokinase converts plasminogen to plasmin
  • 37. Marc Imhotep Cray, M.D. THE END 37
  • 38. Marc Imhotep Cray, M.D. 38 Lectures/discussions to follow: 2. Hypercholesterolemia and Atherosclerosis 3. Angina 4. Heart Failure 5. Arrhythmias 6. Hypertension 7. Peripheral Vascular Disease Further study (SDL): Online resource center: Medical Pharmacology Cloud Folder Companion Notes: Cardiovascular Pharmacology