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Jamk University of Applied Sciences

Sini Lällä

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heart anatomy cardiovascular system physiology human biology

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This document provides lecture material on the human heart, covering its anatomy, function, and regulation. The content details the various components of the heart, including the chambers, valves, and associated blood vessels, along with explanations of their role in circulation.

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The heart Jamk / Sini Lällä jamk Introduction The cardiovascular system consists of the blood, the heart, and blood vessels The heart is the pump that circulates the blood through an estimated 100,000 km (60,000 miles) of blood vessels Average mass 250-300...

The heart Jamk / Sini Lällä jamk Introduction The cardiovascular system consists of the blood, the heart, and blood vessels The heart is the pump that circulates the blood through an estimated 100,000 km (60,000 miles) of blood vessels Average mass 250-300 g (roughly the same size as a closed fist) The heart is located between the lungs in the mediastinum with about two-thirds of its mass to the left of the midline Because the heart lies between two rigid structures, the vertebral column and the sternum, external compression on the chest can be used to force blood out of the heart and into the circulation Jamk / Sini Lällä Apex - directed anteriorly, inferiorly and to the left Base - directed posteriorly, superiorly and to the right Heart Anterior surface - deep to the sternum and ribs orientation Inferior surface - rests on the diaphragm Right border - faces right lung Left border (pulmonary border) - faces left lung Base Apex Jamk / Sini Lällä Pericardium The pericardium is the membrane that surrounds and protects the heart It consists of an outer fibrous pericardium and inner serous pericardium, which is composed of a parietal and a visceral layer Between the parietal and visceral layers of the serous pericardium is the pericardial cavity, a space filled with pericardial fluid that reduces friction between the two membranes The fibrous pericardium prevents overstretching of the heart, provides protection, and anchors the heart in the mediastinum Jamk / Sini Lällä Layers of the heart wall The wall of the heart consists of three layers: The epicardium (external layer) Also called the visceral layer of the serous pericardium Thin transparent outer layer of the wall The myocardium (middle layer) Composed of cardiac muscle tissue Responsible for the pumping action of the heart The endocardium (inner layer) Provides a smooth lining for the chambers of the heart and covers the valves of the heart Jamk / Sini Lällä Chambers and sulci of the heart The heart has four chambers Two upper atria Blood receiving points Two inferior ventricles Pump blood to systemic and pulmonary circulation On the surface of the heart are series of grooves, called sulci, that contain coronary blood vessels and a variable amount of fat Jamk / Sini Lällä Right atrium Receives blood from three veins Superior vena cava Inferior vena cava Coronary sinus Blood passes from the right atrium into the right ventricle through a valve called the tricuspid valve Jamk / Sini Lällä Right ventricle Forms most of anterior surface of heart The cusps of the tricuspid valve are connected to tendonlike cords, the chordae tendineae, which, in turn are connected to cone-shaped trabeculae carneae called papillary muscles The right ventricle is separated from the left ventricle by a partition called the interventricular septum Blood passes from the right ventricle through the pulmonary valve into a large artery called the pulmonary trunk Jamk / Sini Lällä Left atrium Forms most of the base of the heart Receives blood from the lungs through four pulmonary veins Blood passes from the left atrium into the left ventricle through the bicuspid (mitral) valve Jamk / Sini Lällä Left ventricle Forms the apex of the heart Chordae tendineae anchor bicuspid valve to papillary muscles Blood passes from the left ventricle through the aortic valve into the largest artery of the body, the aorta Coronary arteries branch just above the aortic valve Jamk / Sini Lällä The thickness of the myocardium of the four Myocardial chambers varies according to each chamber’s function thickness and The atria walls are thin because they deliver blood to the ventricles function The ventricle walls are thicker because they pump blood greater distances The right ventricle walls are thinner than the left because they pump blood into the lungs, which are nearby and offer very little resistance to blood flow The left ventricle walls are thicker because they pump blood through the body where the resistance to blood flow is greater Jamk / Sini Lällä Valves open and close in response to pressure Heart valves and changes as the heart contracts and relaxes circulation of Each of the four valves help ensure the one- way flow of blood by opening to let the blood blood through and then closing to prevent the backflow of blood Jamk / Sini Lällä Atrioventricular (AV) valves (tricuspid and bicuspid valves) AV valves open and allow blood to flow from atria into ventricles when ventricular pressure is lower than atrial pressure The papillary muscles are relaxed, and the chordae tendineae are slack When the ventricles contract, the pressure of the blood drives the cusps upward until their edges meet and close the opening The papillary muscle are also contracting, which pulls and tightens the chordae tendineae  prevents the valve cusps from being forced to open in the opposite direction into the atria due to the high ventricular pressure Jamk / Sini Lällä Semilunar (SL) valves (aortic and pulmonary valves) Open when pressure in the ventricles exceeds the pressure in the arteries, permitting ejection of blood from the ventricles into the pulmonary trunk and aorta As the ventricles relax, blood starts to flow back toward the heart As the back-flowing blood fills the cusps, the semilunar valves close Jamk / Sini Lällä Valve function - summary When atria contract, AV valves When ventricles contract, SL valves open and allow blood to flow from open and allow blood to flow into atria into ventricles pulmonary trunk and aorta SL valves are closed AV valves are closed Jamk / Sini Lällä Systemic and pulmonary circulation With each beat, the heart pumps blood into two closed circuits The two circuits are arranged in series Systemic circulation The left side of the heart pumps blood throughout the body except for the air sacs of the lungs The left ventricle ejects blood into the aorta From the aorta, the blood divides into separate streams, entering progressively smaller systemic arteries that carry it to all organs throughout the body (except the air sacs of the lungs) In systemic tissues, arteries give rise to smaller- diameter arterioles, which finally lead into extensive beds of systemic capillaries Exchange of nutrients and gases occurs across the thin capillary walls Venules carry deoxygenated blood away from the tissues and merge to form larger systemic veins Ultimately the blood flows back to the right atrium Jamk / Sini Lällä Pulmonary circulation The right side of the heart is the pump for the Systemic and pulmonary circulation; it receives all the dark red, deoxygenated blood returning from the systemic pulmonary circulation circulation Blood ejected from the right ventricle flows into the pulmonary trunk, which branches into pulmonary arteries that carry blood to the right and left lungs Gas exchange occur in the pulmonary capillaries Oxygenated blood returns to the left atrium in pulmonary veins Jamk / Sini Lällä Diagram of blood flow Blue = deoxygenated blood Red = oxygenated blood ARTERIES CARRY BLOOD AWAY FROM THE HEART VEINS CARRY BLOOD BACK TO THE HEART Jamk / Sini Lällä Coronary circulation The coronary circulation provides blood flow to the myocardium Delivers oxygenated blood and nutrients to and removes carbon dioxide and wastes from the myocardium The coronary arteries branch from the ascending aorta and encircle the heart When the heart relaxes, the high pressure of blood in the aorta propels blood through the coronary arteries, into capillaries, and then into coronary veins Many anastomoses  connections between arteries supplying blood to the same region Provide alternate routes for blood if one artery becomes occluded Blockage in a coronary artery  the heart muscle lacks oxygen  may damage the tissue Coronary arteries The two coronary arteries branch from the ascending aorta Left coronary artery Circumflex branch In coronary sulcus, supplies left atrium and left ventricle Anterior interventricular artery Supplies both ventricles Right coronary artery Marginal branch In coronary sulcus, supplies right ventricle Posterior interventricular artery Supplies both ventricles Jamk / Sini Lällä Coronary veins After blood passes through the coronary arteries, it flows into capillaries, where it delivers oxygen and nutrients and collects carbon dioxide and wastes, and the into veins The deoxygenated blood drain into a large vascular sinus on the posterior surface of the heart, called the coronary sinus, which empties into the right atrium Jamk / Sini Lällä Myocardial ischemia and infarction Reduced blood flow through coronary arteries may cause ischemia (hypoxia  lack of oxygen) May weaken the myocardial cell Ischemia is often manifested through angina pectoris A complete obstruction of flow in a coronary artery may cause myocardial infarction (heart attack) Tissue distal to the obstruction dies and is replaced by scar tissue Jamk / Sini Lällä Autorhythmic fibers: the conduction system Cardiac muscle cells are autorhythmic cells because they are self-excitable They repeatedly generate spontaneous action potentials that then trigger heart contractions These cells act as a pacemaker to set the rhythm for the entire heart They form the conduction system, the route for propagating action potential (electrical impulse) through the heart muscle Jamk / Sini Lällä Conduction system of the heart – coordinates contraction of heart muscle Components of the conduction system are: Sinoatrial (SA) node Located in the right atrium Begins heart activity  triggers an action potential that spreads through both atria and stimulate them to contract Excitation spreads to AV node Atrioventricular (AV-node) Located in the septum between the two atria Delays the passage of action potential to the ventricles Transmits signal to bundle of His Bundle of His The connection between atria and ventricles Divides into bundle branches which conduct the impulses toward the apex of the heart Purkinje fibers Large diameter fibers that rapidly conduct the action potential from the apex of the heart upward to the remainder of the ventricular myocardium  ventricles Jamk / Sini Lällä contract Rhythm of conduction system SA node fires spontaneously 90-100 times per minute SA node sets pace since it is the fastest AV node fires at 40-50 times per minute 100 msec delay at AV node due to smaller diameter fibers, allows atria to fully contract filling ventricles before ventricles contract If both nodes are suppressed, the heartbeat may still be maintained by autorhythmic fibers in the ventricles The pacing rate is so slow, only 20-40 times per minute, that blood flow to the brain is inadequate Artificial pacemaker needed if pace is too slow Extra beats forming at other sites than the SA node are called ectopic pacemakers Caffeine & nicotine increase activity Jamk / Sini Lällä Electrocardiogram (ECG or EKG) Impulse conduction through the heart generates electrical currents that can be detected at the surface of the body A recording of the electrical changes that accompany each cardiac cycle (heartbeat) is called an electrocardiogram (ECG or EKG) The ECG helps to determine if the conduction pathway is abnormal, if the heart is enlarged, and if certain regions are damaged In clinical practice, electrodes are positioned on the arms and legs and at six positions on the chest Jamk / Sini Lällä Electrocardiogram In a typical Lead II record, three clearly visible waves accompany each heartbeat P wave Atrial depolarization - spread of impulse from SA node over atria P-Q interval Conduction time from atrial to ventricular excitation QRS complex Ventricular depolarization - spread of impulse through ventricles S-T segment Time when the ventricles contract and pump blood to aorta and pulmonary trunk T wave Ventricular repolarization QT-interval Time from the ventricular depolarization to the ventricular repolarization Depolarization = change in resting membrane potential toward more Atrial repolarization occurs during the QRS complex, but it is not usually evident in an positive  heart contracts ECG because the larger QRS complex masks it Repolarization = recovery of the resting membrane potential  heart relaxes Jamk / Sini Lällä Jamk / Sini Lällä The cardiac cycle A single cardiac cycle includes all the events associated with one heartbeat A cardiac cycle consists of the systole (contraction) and diastole (relaxation) of both atria, rapidly followed by the systole and diastole of both ventricles In each cardiac cycle, the atria and ventricles alternately contract and relax, forcing blood from areas of higher pressure to areas of lower pressure When heart rate is 75 beats/min, a cardiac cycle lasts 0.8 sec The phases of the cardiac cycle are Atrial systole Ventricular systole Relaxation period Jamk / Sini Lällä Atrial systole Lasts about 0.1 sec The atria are contracting, the ventricles are relaxed Depolarization of the SA node causes atrial depolarization  P wave in the ECG Atrial depolarization causes atrial systole As atria contract, they exert pressure on the blood within, which forces blood through the open AV valves into the ventricles At the end of atrial systole (also the end of ventricular diastole), each ventricle contains about 130mL blood  end-diastolic volume (EDV) Jamk / Sini Lällä Ventricular systole Lasts about 0.3 sec The ventricles are contracting, the atria are relaxed (atrial diastole) The QRS complex in the ECG marks the onset of ventricular depolarization Ventricular depolarization causes ventricular systole Ventricles contract and increasing pressure forces the AV valves to close AV and SL valves are all closed (isovolumetric contraction) Pressure continues to rise and when left ventricular pressure surpasses aortic pressure (and right ventricular pressure rises above the pressure in pulmonary trunk), the SL valves open leading to ventricular ejection Each ventricle ejects about 70 mL of blood into the aorta (left ventricle) or pulmonary trunk (right ventricle) The amount of blood in each ventricle at the end of systole, about 60 mL, is the end-systolic volume (ESV) Stroke volume (SV) is the volume ejected per beat from each ventricle SV = EDV – ESV  130 mL – 60 mL = 70 mL Blood pressure in aorta is 120mmHg and 30mmHg in pulmonary trunk Differences in ventricle wall thickness allows heart to push the same amount of blood with more force from the left ventricle The T wave in the ECG marks the onset of ventricular repolarization Jamk / Sini Lällä Relaxation period Lasts about 0.4 sec The atria and the ventricles are both relaxed As the heart beats faster and faster, the relaxation period becomes shorter and shorter, whereas the durations of atrial systole and ventricular systole shorten only slightly Ventricular repolarization causes ventricular diastole Pressure in the ventricles fall and the SL valves close Brief time all four valves are closed  isovolumetric relaxation Pressure in the ventricles continues to fall, the AV valves open, and ventricular filling begins Jamk / Sini Lällä Heart sounds The act of listening to sounds within the body is called auscultation, and it is usually done with a stethoscope The sound of a heartbeat comes primarily from the turbulence in blood flow caused by the closure of the valves, not from the contraction of the heart muscle The first heart sound (lubb) is created by blood turbulence associated with the closing of the atrioventricular (AV) valves soon after ventricular systole begins The second heart sound (dupp) Auscultation sites represents the closing of the semilunar (SL) valves at the beginning of ventricular diastole Jamk / Sini Lällä Cardiac output Cardiac output (CO) is the volume of blood ejected from the left ventricle (or the right ventricle) into the aorta (or pulmonary trunk) each minute Cardiac output equals the stroke volume (the volume of blood ejected by the ventricle with each contraction) multiplied by the heart rate (the number of beats per minute) CO (ml/min) = SV (ml/beat) x HR (beats/min) CO = 70 ml x 75 beats/min = 5250 ml/min  5 liters/min The entire blood volume flows through the pulmonary and systemic circulations each minute When body tissues use more or less oxygen, cardiac output changes to meet the need Cardiac reserve is the difference between person’s maximum cardiac output and cardiac output at rest Four to five times the resting value is average Top endurance athletes may have cardiac reserve seven or eight times their resting CO People with severe heart disease may have little or no cardiac reserve, which limits their ability to carry out even the simple tasks of daily living Jamk / Sini Lällä Changing heart rate is the body’s principal mechanism of short-term control over cardiac output and blood pressure Several factors contribute to regulation of heart rate: Autonomic regulation Nervous control from the cardiovascular center in the medulla oblongata Sympathetic impulses increase heart rate and force of contraction Parasympathetic impulses decrease heart rate Regulation Baroreceptors (pressure receptors) detect change in blood pressure and chemoreceptors, which monitor chemical changes in the blood, send info of heart rate to the cardiovascular center Located in the arch of the aorta and carotid arteries Chemical regulation Hormones Epinephrine, norepinephrine, thyroid hormones  enhances cardiac contractility and increase heart rate Ions (Na+, K+, Ca2+) Crucial for the production of action potentials Other factors Age, gender, physical fitness, and temperature Jamk / Sini Lällä Nervous system control of the heart Jamk / Sini Lällä Three factors regulate stroke Jamk / Sini Lällä volume and ensure that the left and right ventricles pump equal volumes of blood Preload  the degree of Regulation stretch on the heart before it contracts of stroke Contractility  the forcefulness of contraction of volume individual ventricular muscle fibers Afterload  the pressure that must be exceeded before ejection of blood from the ventricles Preload (affect of stretching) Frank-Starling Law of Heart: A greater preload (stretch) on cardiac muscle fibers prior to contraction increases their force of contraction (the more heart fills with blood during diastole the greater the force of contraction during systole) Preload is proportional to end-diastolic volume (EDV) Two key factors determine EDV: The duration of ventricular diastole When heart rate increases, the duration of diastole is shorter Less filling time means a smaller EDV Venous return (the volume of blood returning to the right ventricle) When venous return increases, a greater volume of blood flows into the ventricles and the EDV is increased The Frank Starling law of the heart equalizes the output of the right and left ventricles and keeps the same volume of blood flowing to both the systemic and pulmonary circulations Jamk / Sini Lällä Contractility and afterload Myocardial contractility, the strength of contraction at any given preload, is affected by positive and negative inotropic agents Positive inotropic agents increase contractility For example, stimulation of the sympathetic division of the autonomic nervous system (ANS), hormones such as epinephrine and norepinephrine Negative inotropic agents decrease contractility For example, inhibition of the sympathetic division of the ANS, acidosis For a constant preload, the stroke volume increases when positive inotropic agents are present and decreases when negative inotropic agents are present Afterload The pressure that must be overcome before a semilunar valve can open An increase in afterload causes stroke volume to decrease Afterload is increased for example when the blood pressure is elevated Jamk / Sini Lällä Factors that increase cardiac output Jamk / Sini Lällä Extra material: Anatomy of the heart 1 Jamk / Sini Lällä Extra material: Anatomy of the heart 2 Jamk / Sini Lällä Superior right point at the superior border of the 3rd right Extra material: costal cartilage Superior left point at the inferior border of the 2nd left surface projection costal cartilage 3cm to the left of midline of the heart Inferior left point at the 5th intercostal space, 9 cm from Jamk / Sini Lällä the midline Inferior right point at superior border of the 6th right costal cartilage, 3 cm from the midline

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