Cardiovascular pharmacology
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Cardiovascular Pharmacology. Review of Cardiovascular Form and Function. Introduction and Background. Cardiovascular disease is the major cause of death in the US (>50% of all deaths) Cardiovascular function based on Cardiac pumping ability Pace-making electrical signals

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Cardiovascular pharmacology l.jpg

Cardiovascular Pharmacology

Review of Cardiovascular Form and Function

Introduction and background l.jpg
Introduction and Background

  • Cardiovascular disease is the major cause of death in the US (>50% of all deaths)

  • Cardiovascular function based on

    • Cardiac pumping ability

      • Pace-making electrical signals

      • Force of contraction

      • Height of ventricle discharge pressure

    • Integrity of vasculature

      • Presence of blockage

      • Muscular tone/structural integrity

      • Pressure drop needed to move blood to and through capillary beds

    • Blood volume/composition

      • Water, electrolyte, iron balances

      • Lipid and protein composition

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Major Cardiovascular Pathologies Requiring Pharmacological Intervention

  • Hypertension

  • Arrhythmia

  • Heart failure

  • Reduced vascular blood flow

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I. Background to Hypertension - InterventionRegulation of Blood Pressure

  • Arterial blood pressure due to combination of cardiac output (CO) and total peripheral resistance (TPR)

  • CO – regulated by heart rate and stroke volume (CO = HR x SV)

  • TPR function of

    • Viscosity of blood (hematocrit)

    • Length of blood vessels

    • Blood vessel luminal diameter (especially precapillary arterioles)

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Cardiac Output Intervention

  • Heart rate

    • Function of

      • sympathetic, vagal nervous activity

      • Neuro-hormonal substances

        • 1° angiotensin II

        • 2º vasopression (anti-diuretic hormone = ADH)

  • Stroke volume

    • Function of

      • Venous return (function of venous tone [contractile state] and circulating blood (vascular) volume)

        • Venous tone function of sympathetic activity (α1, α2 receptors)

        • Vascular volume depends on

          • Intake of fluids (thirst)

          • Output of fluids (urine, sweat, etc)

          • Distribution of fluids (Starling’s law)

      • Myocardial contractility (MC proportional to sympathetic tone [β1 receptors])

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Characteristics of some adrenoceptors (sympathetic nerves) Intervention

Tissues and effects


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Beat-to-Beat Modulation of Blood Pressure Intervention

Controlled by baroreceptor reflex arch

  • Baroreceptors located in aortic arch

  • Increased stretching due to higher aortic arch pressure  increased vagal nerve activity  decreased heart rate decreased cardiac output  decreased blood pressure

  • Fast acting

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Autonomic Regulation of Blood Pressure Intervention

  • Coordinates and integrates all regulators of cardiovascular function

  • Can regulate both cardiac output and blood vessel size via sympathetic and parasympathetic innervation of cardiovascular end-organs (heart, vasculature, kidneys, adrenal glands, etc)

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Autonomic Regulation of the Heart Intervention

  • Heart Rate

    • Parasympathetic input via vagus nerve causes decrease in HR (dominates)

    • Sympathetic input to sino-atrial node causes increase in HR (usually minor)

  • Heart contractility

    • Increased by sympathetic activity causing release of epinephrine, norepinephrine from adrenal gland

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II. Background to Arrhythmia - Rhythm of the Heart Intervention

  • Human heart is four-chambered

  • Chambers need to contract sequentially (atria, then ventricles) and in synchronicity

  • Also need relaxation between contractions to allow refilling of chambers

  • Above controlled electrically (Purkinje fibers allow rapid, organized spread of activation)

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Regulation of Heart Rate Intervention

  • Primarily accomplished by sinoatrial node (SA)

    • Located on right atrium

    • Receives autonomic input

    • When stimulated, SA signals atrial contractile fibers  atria depolarization and contraction (primes ventricles with blood)

  • Depolarization picked up by atrioventricular node (AV node)  depolarizes ventricles  blood discharged to pulmonary artery and dorsal aorta  eventually rest of body

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III. Background to Congestive Heart Failure Intervention Maintenance of Normal Heart Function

  • Normal cardiac output needed to adequately perfuse peripheral organs

    • Provide O2, nutrients, etc

    • Remove CO2, metabolic wastes, etc

    • Maintain fluid flow from capillaries into interstitium and back into venous system  if flow reduced or pressure increased in venous system  build up of interstitial fluid = edema

  • Because CO is a function of

    • Heart Rate – determined by pacemaker cells in the sinoatrial node

    • Stroke volume – determined by fill rate and contractile force

    • Atrial/ventricular/valvular coordination

      Any negative change on above can lead to inadequate perfusion and development of the syndrome of heart failure

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IV. Background to Reduced Vascular Blood Flow: Blood Vessel Anatomy and Function

  • Arterial blood vessels

    • Smooth muscle (slow, steady contraction)

    • elastic tissue (stretch on systole, recoil on diastole)

    • Contain about 10% of blood volume

    • Arterioles have sphincters which regulate 70% of blood pressure

  • Venous blood vessels

    • Highly distensible, some contractility

    • Contain over 50% of blood volume

  • Capillaries

    • Tiny but contain greatest cross-sectional area to allow high exchange rate

    • Contain precapillary sphincters to regulate blood flow

    • 5% of blood volume

      All vasculature under ANS and humeral control

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Quantification of Total Peripheral Resistance Anatomy and Function

TPR = _L · η_ for sum of all blood vessels

r4 (Poiseuille’s equation)

Where r = radius of blood vessel

L = length of blood vessel

η = viscosity of blood (function of hematocrit) hematocrit =

Therefore: change in blood vessel radius has greatest effect on TPR

Note: 70% of TPR produced/controlled by arterioles  target of drug treatment

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Humeral Regulation of Blood Pressure: Renin-Angiotensin-Aldosterone System

  • Renin:secreted by the kidney in response to reduced blood pressure or blood volume

  • Angiotensin:Renin converts Angiotensinogen  Angiotensin I

  • Angiotensin Converting-Enzyme (ACE): converts Angiotensin I  Angiotensin II in lung

  • Angiotensin II:

    • Actions:

      • Intense vasoconstriction  increase TPR

      • Causes release of Aldosterone from adrenal gland  promotes Na+ and water reabsorption in kidney  cause increased blood volume.

      • Regulatory negative feedback on the release of Renin.

      • CNS: Stimulate thirst in hypothalamus, stimulate sympathetic outflow.

        - All above designed to bring arterial blood pressure back up to normal set-point

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Autonomic regulation Renin-Angiotensin-Aldosterone Systemof the vasculature

  • Increased sympathetic activity  reduction in blood vessel opening (caliber)  increase in vascular resistance  etc.  etc  increase blood pressure

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Stop talking now and Renin-Angiotensin-Aldosterone Systemlet them go!

I’m outta’ here!