Skip to main content
UploadLanguage (EN)Support
BusinessMobileSocial MediaMarketingTechnologyArt & PhotosCareerDesignEducationPresentations & Public SpeakingGovernment & NonprofitHealthcareInternetLawLeadership & ManagementAutomotiveEngineeringSoftwareRecruiting & HRRetailSalesServicesScienceSmall Business & EntrepreneurshipFoodEnvironmentEconomy & FinanceData & AnalyticsInvestor RelationsSportsSpiritualNews & PoliticsTravelSelf ImprovementReal EstateEntertainment & HumorHealth & MedicineDevices & HardwareLifestyle
AU
Uploaded byAshish Umale
179 views

Hemodynamics & Electrophysiology of the Heart.pptx

Introduction to Cardiovascular Pharmacology Cardiovascular pharmacology is the branch of pharmacology that deals with drugs affecting the heart, blood vessels, blood pressure, and blood circulation. The primary objective of these drugs is to maintain adequate tissue perfusion and oxygen delivery by improving cardiac function or vascular function. Cardiovascular diseases such as hypertension, ischemic heart disease, heart failure, arrhythmias, and various disorders are among the leading causes of morbidity and mortality worldwide. Therefore, understanding the physiological basis of cardiac function is essential before studying the pharmacology of cardiovascular drugs. Hemodynamics explains how blood flows through the circulation, whereas electrophysiology explains how electrical impulses are generated and conducted through the heart to produce coordinated contraction. Hemodynamics of the Heart Definition of Hemodynamics Hemodynamics is the study of the movement of blood through the cardiovascular system and the forces that govern this movement. It includes the relationship between blood pressure, cardiac output, vascular resistance, venous return, and blood volume. The heart acts as a pump, and the blood vessels act as conduits (pathways) through which blood flows to all organs of the body. Cardiac Output Cardiac output is the volume of blood pumped by one ventricle per minute. It is determined by the product of heart rate and stroke volume. In a healthy adult, the normal cardiac output is approximately 5 liters per minute. Cardiac Output=Heart Rate×Stroke Volume Stroke Volume Stroke volume is the amount of blood ejected by a ventricle during one heartbeat. It depends on three major factors: preload, afterload, and myocardial contractility. Preload refers to the ventricular filling before contraction. Increased venous return increases preload and generally increases stroke volume through the Frank–Starling mechanism. Afterload refers to the resistance against which the ventricle must pump blood. Increased arterial pressure or peripheral resistance increases afterload and makes ejection more difficult. Contractility is the intrinsic ability of the myocardium to contract. Positive inotropic drugs enhance contractility and increase stroke volume. Electrophysiology of the Heart Introduction The heart possesses specialized conductive tissue capable of generating and conducting electrical impulses automatically. This property allows the heart to beat rhythmically without external stimulation. The electrical activity originates in the sinoatrial (SA) node and spreads through the atria, atrioventricular node, bundle of His, bundle branches, and Purkinje fibers before reaching the ventricles. Automaticity Automaticity is the ability of certain cardiac cells to generate spontaneous electrical impulses. The SA node has the highest rate of spontaneous depolarization and therefor

Education◦
Related topics:
B-Pharmacy• D-Pharmacy•
PREPARED BY Prof. ASHISH N. UMALE M. PHARM IN PHARMACOLOGY ASSISTANT PROFESSOR SHRADDHA INSTITUTE OF PHARMACY, WASHIM- 444505 PHARMACOLOGY-II
 Introduction to Cardiovascular Pharmacology Cardiovascular pharmacology is the branch of pharmacology that deals with drugs affecting the heart, blood vessels, blood pressure, and blood circulation.  The primary objective of these drugs is to maintain adequate tissue perfusion and oxygen delivery by improving cardiac function or vascular function.  Cardiovascular diseases such as hypertension, ischemic heart disease, heart failure, arrhythmias, and various disorders are among the leading causes of morbidity and mortality worldwide.  Therefore, understanding the physiological basis of cardiac function is essential before studying the pharmacology of cardiovascular drugs.  Hemodynamics explains how blood flows through the circulation, whereas electrophysiology explains how electrical impulses are generated and conducted through the heart to produce coordinated contraction.
 Hemodynamics of the Heart  Definition of Hemodynamics  Hemodynamics is the study of the movement of blood through the cardiovascular system and the forces that govern this movement.  It includes the relationship between blood pressure, cardiac output, vascular resistance, venous return, and blood volume.  The heart acts as a pump, and the blood vessels act as conduits (pathways) through which blood flows to all organs of the body.  Cardiac Output  Cardiac output is the volume of blood pumped by one ventricle per minute.  It is determined by the product of heart rate and stroke volume.  In a healthy adult, the normal cardiac output is approximately 5 liters per minute. Cardiac Output=Heart Rate×Stroke Volume
 Stroke Volume  Stroke volume is the amount of blood ejected by a ventricle during one heartbeat. It depends on three major factors: preload, afterload, and myocardial contractility.  Preload refers to the ventricular filling before contraction.  Increased venous return increases preload and generally increases stroke volume through the Frank–Starling mechanism.  Afterload refers to the resistance against which the ventricle must pump blood.  Increased arterial pressure or peripheral resistance increases afterload and makes ejection more difficult.  Contractility is the intrinsic ability of the myocardium to contract.  Positive inotropic drugs enhance contractility and increase stroke volume.
 Blood Pressure and Peripheral Resistance  Arterial blood pressure is determined by cardiac output and total peripheral resistance.  Blood Pressure=Cardiac Output × Peripheral Resistance  Vasoconstrictor substances such as angiotensin II and noradrenaline increase peripheral resistance and raise blood pressure.  Vasodilator drugs such as nitrates, hydralazine, and calcium channel blockers reduce peripheral resistance and lower blood pressure.  Venous Return and Central Venous Pressure  Venous return is the amount of blood returning to the heart through the veins.  Adequate venous return is essential for maintaining cardiac output.  Drugs such as nitrates reduce venous return by venodilation and are therefore useful in angina because they reduce the workload of the
Electrophysiology of the Heart Introduction  The heart possesses specialized conductive tissue capable of generating and conducting electrical impulses automatically.  This property allows the heart to beat rhythmically without external stimulation.  The electrical activity originates in the sinoatrial (SA) node and spreads through the atria, atrioventricular node, bundle of His, bundle branches, and Purkinje fibers before reaching the ventricles. Automaticity  Automaticity is the ability of certain cardiac cells to generate spontaneous electrical impulses.  The SA node has the highest rate of spontaneous depolarization and therefore acts as the natural pacemaker of the heart.  Drugs such as beta blockers decrease SA nodal firing and reduce heart rate.
Conductivity  Conductivity refers to the ability of cardiac tissue to transmit impulses from one cell to another.  The atrioventricular node conducts impulses more slowly than other parts of the conduction system.  Drugs such as verapamil, diltiazem, and digoxin further slow AV nodal conduction and are useful in supraventricular tachyarrhythmias (abnormally rapid heart rhythms (heart rate >100 beats/min))  Excitability  Excitability is the ability of cardiac cells to respond to a stimulus by generating an action potential.  Alterations in electrolyte concentrations, particularly potassium and calcium, significantly influence excitability and may predispose to arrhythmias. Contractility  Contractility is the strength with which the myocardium contracts.  Positive inotropic drugs such as digoxin increase contractility, whereas negative inotropic drugs such as certain calcium channel blockers and beta blockers reduce it.
The ventricular cardiac action potential consists of five phases. Phase 0 (Rapid Depolarization) This phase occurs due to the sudden opening of fast sodium channels and rapid influx of sodium ions. Class I antiarrhythmic drugs block these sodium channels and slow depolarization. Phase 1 (Initial Repolarization) A brief outward movement of potassium ions causes a slight fall in membrane potential. Phase 2 (Plateau Phase) Calcium enters the cell through L-type calcium channels while potassium continues to leave the cell. This phase is responsible for sustained contraction of the myocardium. Calcium channel blockers reduce calcium entry during this phase. Phase 3 (Repolarization) Potassium efflux predominates, and the membrane returns toward its resting potential. Class III antiarrhythmic drugs prolong this phase by blocking potassium channels. Phase 4 (Resting Phase) The resting membrane potential is maintained mainly by potassium permeability and the sodium-potassium ATPase pump. In pacemaker cells, gradual depolarization during phase 4 determines the heart rate.
Electrocardiogram and Pharmacological Significance The electrocardiogram records the electrical activity of the heart. Many cardiovascular drugs produce characteristic changes in the ECG. For example, digoxin shortens the QT interval and produces scooped ST segment, whereas potassium channel blockers such as amiodarone prolong the QT interval . ECG Component Physiological Event P wave Atrial depolarization PR interval Conduction through the AV node QRS complex Ventricular depolarization ST segment Ventricular plateau phase T wave Ventricular repolarization
Pharmacological Importance of Hemodynamics and Electrophysiology  The therapeutic actions of cardiovascular drugs are directly related to these physiological principles.  Antihypertensive drugs lower blood pressure by reducing cardiac output, peripheral resistance, or blood volume.  Antianginal drugs reduce myocardial oxygen demand by decreasing preload, afterload, or heart rate.  Drugs used in heart failure improve cardiac output by increasing contractility or reducing preload and afterload.  Antiarrhythmic drugs modify cardiac electrophysiology by altering impulse generation, conduction, or repolarization.  Diuretics decrease blood volume and reduce preload and blood pressure.
Clinical Relevance  Understanding hemodynamics and electrophysiology helps explain why cardiovascular drugs are selected in different diseases.  In hypertension, the goal is to reduce peripheral resistance or blood volume.  In angina pectoris, the aim is to decrease myocardial oxygen demand and improve coronary blood flow.  In heart failure, treatment focuses on improving cardiac output and reducing ventricular workload.  In arrhythmias, therapy aims to restore normal impulse formation and conduction.