L6_Circulatory system II.pdf

Circulatory System II Dr Emily Wong 1 Terminology When talking about action potentials and graded potentials we use these terms: depolarization, repolarization, hyperpolarization. These terms are all relative to the resting membrane potential (RMP). Depolarization is the potential moving from RMP to...

Circulatory System II Dr Emily Wong 1 Terminology When talking about action potentials and graded potentials we use these terms: depolarization, repolarization, hyperpolarization. These terms are all relative to the resting membrane potential (RMP). Depolarization is the potential moving from RMP to less negative values. Repolarization is the potential moving back to the RMP. Hyperpolarization is the potential moving away from the RMP in a more negative direction. 2 3 Heartbeat Coordination 4 Node Cells Node cells have automaticity and are found in the Sinoatrial node (SA), the Atrioventricular node (AV), the atrioventricular bundle, the Purkinje fibers (found in the walls of the ventricles), and AV bundle branches. In a healthy heart, the SA node is the pacemaker and controls the electrical impulses which cause contraction. Any damage to the SA node or to the heart walls can damage this circuit and cause problems. 5 Cardiac Cycle The cardiac cycle is all the events involved with the blood flow through the heart during one heart beat. Diastole is the relaxation phase. When chambers relax, they filled with blood. Systole is the contraction phase. When chambers contract, the blood is expelled. 6 7 Excitation of the Heart I At the beginning of cardiac cycle, the atrioventricular (AV) valves open. This allows blood to flow from atria into ventricles. At the same time, the pulmonary and aortic valves are closed, preventing blood in the pulmonary trunk and aorta from entering the ventricles i.e. prevents the backflow of blood. Ventricular filling is completed by atrial contraction. This contraction results from series of events starting from the excitation of SA node. 8 Excitation of the Heart II After the excitation of the SA node, depolarization is spread across the heart atrial walls and causes both atria to contract. This results in atrial depolarization which is represented by P wave on the ECG. Atrial depolarization initiates atrial systole (contraction) which is shown by the P-Q segment on the ECG. 9 Excitation of the Heart III Near the end of atrial systole, impulses from the SA node reach AV node. They are delayed for approximately 0.1 second. The purpose of this delay is for the full contraction of the atria in order to obtain a complete emptying of their contents. An additional amount of blood is then propelled into the ventricles. 10 Excitation of the Heart IV After passing by the AV node, the impulses travel further down to the AV bundles (also known as the Bundle of His) located within the septum of the heart. Signals are then passed to the AV bundle branches, which are split into the left and right bundle branches, for electrical conduction along the interventricular septum. Ultimately, the electrical impulses are sent towards the apex and to the rest of the heart via the Purkinje fibres, and trigger the ventricles to contract. It takes about 220 milliseconds in total for the impulses to travel from the SA node to the Purkinje fibres. In short, the sequence of excitation is as follows: SA node → atria → AV node → Bundle of His → AV bundle branches → Purkinje fibres → ventricles. 11 Excitation of the Heart V The activation of AV node results in ventricular depolarization, which is represented by the QRS complex on the ECG. The atria repolarize, the walls relax and remain in diastole for the rest of the cardiac cycle. The atrial repolarization is masked by the QRS complex. In ventricular systole, increased pressure in the ventricles forces the AV valves closed. The heart sound associated with closure of AV valves is known as S1 or “lub”. 12 Excitation of the Heart VI With continued contraction, ventricular pressure increases until they are higher than those in the pulmonary trunk and aorta. At this point, the pulmonary and aortic valves open and blood is ejected from the ventricles. Ventricular systole is represented by the S-T segment on the ECG. 13 Excitation of the Heart VII In ventricular diastole (relaxation), the ventricles repolarize. The T wave on the ECG represents ventricular repolarization. The blood in the pulmonary trunk and aorta flows back towards the semilunar valves, causing them to close. The heart sound associated with the closure of aortic and pulmonary valves is known as S2, often described as “dub”. 14 Sequence of Excitation 15 Clinical Issues Arrhythmias are the uncoordinated atrial and ventricular contractions caused by a defect in the conduction system. A fibrillation is a rapid and irregular (usually out of phase) contraction where the SA node is no longer controlling heart rate. An atrial fibrillation can cause clotting and inefficient filling of the ventricles. A ventricular fibrillation is more life threatening. The ventricles pump without filling and if the rhythm is not rapidly reestablished circulation stops and brain death occurs. Defibrillation is the application of an electrical stimulus to shock the heart back into a normal SA rhythm. For chronic conditions, “pacemakers” can be implanted. This is a device that delivers the electrical stimulus rather than the SA node. 16 Electrocardiogram A graphic record of the heart’s electrical activity. The leads must be placed correctly to get a proper reading. The reading is a composite of the electrical activity not a single action potential. 17 ECGs The P wave is the result of the depolarization wave from the SA node to the AV node. Atria contract 0.1 second after P wave starts. The QRS complex is the result of the ventricular depolarization and precedes ventricular contraction. The T wave is caused by ventricular repolarization. The atrial repolarization is obscured by the QRS complex. 18 Heart Sounds 19 Clinical Issues Abnormal heart sounds are called heart murmurs. Blood flow should be silent as long as it is smoothly flowing. If it hits anything that obstructs it, it will become turbulent and generate sound that can be heard with a stethoscope. Most causes of heart murmurs in adults are valve problems. If the valve is incompetent (doesn’t close correctly) then a swishing sound is heard. If the valve is stenotic (narrowed), a high pitched sound or a click can be heard. 20 Cardiac Output Cardiac output is the amount of blood pumped out of each ventricle in one minute. It is the product of heart rate (HR) and stroke volume (SV). CO = HR x SV Normal cardiac output is about 5.25 L/min. In a healthy system SV is fairly constant. If blood volume drops or if the heart weakens, then SV declines and CO is maintained by increasing HR. 21 Stroke Volume SV is the difference between the end diastolic volume and the end systolic volume. SV= EDV-ESV So with every beat the heart pumps about 60% of the blood in its chambers or 70 mL. This is important to preload, afterload and contractility of the heart. 22 Regulation of Heart Rate Things that increase HR are positive chronotropic factors. Things that decrease HR are negative chronotropic factors. Heart rate is also controlled by the input from the nervous system: SNS increases heart rate; PSNS decreases heart rate. 23 Control of Heart Rate 24 Preload and Afterload Preload is the degree to which the cardiac muscle cells are stretched before they contract. Afterload is the pressure that the ventricles must overcome to force open the aortic and pulmonary valves. Anything that increases systemic or pulmonary arterial pressure can increase afterload. (ex. Hypertension) 25 Stroke Volume Anything that increases EDV or increases the force of the ventricular contraction can increase SV. The ventricles are never completely empty of blood, so a more forceful contraction will expel more blood with each pump. Extrinsic controls of SV include: − Sympathetic drive to ventricular muscle fibers − (NE at the Beta 1 receptors in cardiac muscle cells) − Hormonal control − (Thyroid hormones can increase the force of contraction) 26 Control of Stroke Volume 27 Measurement of Cardiac Function Human cardiac output can be measured by a variety of methods. Echocardiography: Echocardiography is a noninvasive technique that uses ultrasonic waves. This technique can detect the abnormal functioning of cardiac valves or contractions of the cardiac walls, and can also be used to measure ejection fraction. Cardiac angiography: requires the temporary threading of a thin, flexible tube called a catheter through an artery or vein into the heart. A liquid containing radio-opaque contrast material is then injected through the catheter during high-speed x-ray videography. This technique is useful for evaluating cardiac function and for identifying narrowed coronary arteries. 28 The Vascular System The vascular system contains the “pipes” that carry the blood. The arteries and veins both have vascular smooth muscle cells, and endothelial cells but the amount of each varies. The types of structures involved are: Arteries ‒ Arterioles ‒ Capillaries Veins ‒ Venules 29 The Vascular System 30 Arteries Compliance = Δvolume/Δ pressure The higher the compliance of a structure, the more easily it can be stretched. Arteries are often called pressure reservoirs because of the elastic recoil. They are not as compliant as veins. Venous compliance is approximately 30 times larger than arterial compliance. 31 Pulse Pressure The difference between systolic pressure and diastolic pressure (120 – 80 = 40 mmHg in the example) is called the pulse pressure. It can be felt as a pulsation or throb in the arteries of the wrist or neck with each heartbeat. The most important factors determining the magnitude of the pulse pressure are: (1) Stroke volume (2) Speed of ejection of the stroke volume (3) Arterial compliance A decrease in arterial compliance occurs in arteriosclerosis (stiffening of the arteries). 32 Arterioles These are the smallest arteries. Their function is controlled by neural, hormonal, and local chemicals. They control minute-to-minute blood flow into the capillary beds. If they contract, blood flow is diverted away from their tissues; if they dilate, then blood flow to the tissue increases. The smaller ones, which directly lead into the capillary beds, are usually just a single layer of smooth muscle which spirals around the endothelium. Changes in the diameter of these vessels has an impact on blood pressure. 33 Flow – Pressure Relationship F = ΔP/R So, if you increase resistance by vasoconstriction and keep pressure the same, then flow to a tissue decreases. If you need to increase flow to a tissue, then you either increase the pressure or vasodilate to decrease resistance. 34 Extrinsic Controls 35 Capillaries 36 Capillaries are the smallest blood vessels. This is where gas and nutrient exchange happens by diffusion out of the blood into the tissues (or back into the blood). Velocity of Capillary Blood Flow Velocity is slowest in the capillary beds because they have a greater cross-sectional area. 37 Veins 38 Venous System Venules vary in structure as they progress away from the capillaries. Veins have all three distinct layers (tunics). The walls are thinner than arteries, so they often appear collapsed in histological slides. Veins also have less smooth muscle and more elastin than arteries. Veins are highly distensible, so they are called capacitance vessels that act as blood reservoirs. 39 Varicose Veins Remember that veins have one-way valves that prevent the backflow of blood. Varicose veins are veins that have become dilated and tortuous because of incompetent (leaky) valves. About 15% of adults suffer from this condition, mainly in the lower limbs. 40 Venous Pressure Blood pressure in veins is ~15 mm Hg. This is not sufficient to move blood back to the heart. So there are the “pumps”: 1. Respiratory pump: Pressure changes in the central cavity due to the pressure changes due to breathing. This helps to propel blood back to the heart. 2. Muscular pump: When muscles contract they squeeze the veins. This results in blood moving forward and being prevented from backflow by the veins. This moves blood toward the heart. The smooth muscle in the veins is under SNS control and contracts when stimulated, similar to the arterial smooth muscle. This causes contraction and a narrowing of the lumen. 41 42 Determinants of Venous Pressure 43