Cardiovascular Sys1

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The Cardiovascular System LORD IZON O. SANTOS, MDRN

The Cardiovascular System • A closed system of the heart and blood vessels • The heart pumps blood • Blood vessels allow blood to circulate to all parts of the body

• The function of the cardiovascular system is to deliver oxygen and nutrients and to remove carbon dioxide and other waste products Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.1

The Heart • Location • Thorax between the lungs • Pointed apex directed toward left hip

• About the size of your fist

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.2a

The Heart

Figure 11.1 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.2b

The Heart: Coverings • Pericardium – a double serous membrane • Visceral pericardium • Next to heart • Parietal pericardium • Outside layer

• Serous fluid fills the space between the layers of pericardium Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.3

The Heart: Heart Wall • Three layers • Epicardium • Outside layer • This layer is the parietal pericardium • Connective tissue layer

• Myocardium • Middle layer • Mostly cardiac muscle

• Endocardium • Inner layer • Endothelium

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.4

External Heart Anatomy

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Figure 11.2a

Slide 11.5

The Heart: Chambers • Right and left side act as separate pumps • Four chambers • Atria • Receiving chambers • Right atrium • Left atrium

• Ventricles • Discharging chambers • Right ventricle • Left ventricle Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.6

Blood Circulation

Figure 11.3 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.7

The Heart: Valves • Allow blood to flow in only one direction • Four valves • Atrioventricular valves – between atria and ventricles • Bicuspid valve (left) • Tricuspid valve (right)

• Semilunar valves between ventricle and artery • Pulmonary semilunar valve • Aortic semilunar valve Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.8

The Heart: Valves

• Valves open as blood is pumped through • Held in place by chordae tendineae (“heart strings”) • Close to prevent backflow

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.9

Operation of Heart Valves

Figure 11.4 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.10

The Heart: Associated Great Vessels • Aorta • Leaves left ventricle

• Pulmonary arteries • Leave right ventricle

• Vena cava • Enters right atrium

• Pulmonary veins (four) • Enter left atrium Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.11

Coronary Circulation • Blood in the heart chambers does not nourish the myocardium • The heart has its own nourishing circulatory system • Coronary arteries • Cardiac veins • Blood empties into the right atrium via the coronary sinus Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.12

The Heart: Conduction System

• Intrinsic conduction system (nodal system) • Heart muscle cells contract, without nerve impulses, in a regular, continuous way

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.13a

The Heart: Conduction System • Special tissue sets the pace • Sinoatrial node • Pacemaker • Atrioventricular node • Atrioventricular bundle • Bundle branches • Purkinje fibers Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.13b

Heart Contractions

• Contraction is initiated by the sinoatrial node • Sequential stimulation occurs at other autorhythmic cells

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.14a

Heart Contractions

Figure 11.5 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.14b

Filling of Heart Chambers – the Cardiac Cycle

Figure 11.6

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.15

The Heart: Cardiac Cycle • Atria contract simultaneously • Atria relax, then ventricles contract • Systole = contraction • Diastole = relaxation

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.16

The Heart: Cardiac Cycle • Cardiac cycle – events of one complete heart beat • Mid-to-late diastole – blood flows into ventricles • Ventricular systole – blood pressure builds before ventricle contracts, pushing out blood • Early diastole – atria finish re-filling, ventricular pressure is low Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.17

The Heart: Cardiac Output • Cardiac output (CO) • Amount of blood pumped by each side of the heart in one minute • CO = (heart rate [HR]) x (stroke volume [SV])

• Stroke volume • Volume of blood pumped by each ventricle in one contraction Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.18

Cardiac Output Regulation

Figure 11.7 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.19

The Heart: Regulation of Heart Rate • Increased heart rate • Sympathetic nervous system • Crisis • Low blood pressure • Hormones • Epinephrine • Thyroxine • Exercise • Decreased blood volume Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.21

The Heart: Regulation of Heart Rate •

Decreased heart rate

• Parasympathetic nervous system • High blood pressure / blood volume • Dereased venous return

Slide 11.22

Blood Vessels: The Vascular System • Taking blood to the tissues and back • Arteries • Arterioles • Capillaries • Venules • Veins Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.23

•BLOOD VESSEL: ANATOMY •Three layers (tunics) •Tunic intima •Endothelium •Tunic media •Smooth muscle •Controlled by sympathetic nervous system •Tunic externa •Mostly fibrous connective tissue

The Vascular System

Figure 11.8b Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.24

Differences Between Blood Vessel Types • Walls of arteries are the thickest • Lumens of veins are larger • Skeletal muscle “milks” blood in veins toward the heart • Walls of capillaries are only one cell layer thick to allow for exchanges between blood and tissue Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.26

Movement of Blood Through Vessels • Most arterial blood is pumped by the heart • Veins use the milking action of muscles to help move blood

Figure 11.9 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.27

Capillary Beds • Capillary beds consist of two types of vessels • Vascular shunt – directly connects an arteriole to a venule

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Figure 11.10

Slide 11.28a

Capillary Bed Diffusion at Capillary Beds • True capillaries – exchange vessels

• Oxygen and nutrients cross to cells • Carbon dioxide and metabolic waste products cross into blood Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Figure 11.10

Slide 11.28b

Major Arteries of Systemic Circulation

Figure 11.11 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.30

Major Veins of Systemic Circulation

Figure 11.12 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.31

Arterial Supply of the Brain

Figure 11.13 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.32

Hepatic Portal Circulation

Figure 11.14 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.33

Circulation to the Fetus

Slide 11.34

Highly oxygenated blood from the placenta enters the fetus via the umbilical vein. A large proportion of this blood passes into the liver to supply the hepatic sinusoids. The remainder bypasses the liver in the ductus venosus, drains into caudal vena cava and mixes with poorly oxygenated blood returning from the fetal body. The blood in the caudal vena cava, which, although mixed is still well oxygenated, drains into the right atrium of the heart. Most of the blood entering the right atrium from the caudal vena cava is directed through the foramen ovale into the left atrium where it is mixed with a small amount of deoxygenated blood returning from the lungs. The contents of the left atrium enter the left ventricle and are expelled from the heart into the aorta.

The contents of the right atrium (which consist of some well oxygenated blood from the caudal vena cava and poorly oxygenated blood returning from the head and forelimbs via the cranial vena cava) enter the right ventricle and are expelled from the heart via the pulmonary artery. Only approximately 5 -10% of the blood in the pulmonary artery enters the lungs in the fetus due to the high resistance of their collapsed, non-aerated state. The remainder enters the ductus arteriosus which is a shunt linking the pulmonary artery and the aorta. The convergence of the poorly oxygenated pulmonary blood and the well-oxygenated aortic blood occurs after the main supply to the head and forelimbs have branched off the aortic arch. This ensures that the blood richest in oxygen reaches the developing brain. The abdominal aorta supplies the rest of the body and gives off two umbilical arteries (branches of the internal iliac arteries) which carry poorly oxygenated blood back to the placenta.

Changes at birth At birth the lungs can inflate and perform their true function meaning that the fetal bypass systems are no longer required. •Umbilical vein - Constricts to form the ligamentum teres, which extends from the umbilicus to the liver. The mesentery that surrounded the umbilical vein becomes the falciform ligament. Ductus venosus - A sphincter in the ductus venosus constricts so that all blood entering the liver passes through the hepatic sinusoids. Foramen ovale - Due to aeration of the lungs, pulmonary resistance decreases and pulmonary blood flow increases.

The increase in pulmonary blood flow causes the pressure in the left atrium to raise above that of the right which results in the valve of the foramen ovale being pushed against the septum secundum. This closes the foramen ovale and its vestge is known as the fossa ovale. Ductus arteriosus - The change in the partial pressure of oxygen in the blood once the lungs become functional controls the constriction of the ductus arteriosus. Closure of the duct is usually complete soon after birth and its remnant is known as the ligamentum arteriosus. Umbilical arteries - The intra-abdominal portions of the umbilical arteries constrict. Some parts remain patent supplying the urinary bladder and these are contained within the lateral vesicle ligaments which are vestiges of the mesetery surrounding the umbilical arteries.

Pulse • Pulse – pressure wave of blood • Monitored at “pressure points” where pulse is easily palpated Figure 11.16 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.35

Blood Pressure • Measurements by health professionals are made on the pressure in large arteries • Systolic – pressure at the peak of ventricular contraction • Diastolic – pressure when ventricles relax

• Pressure in blood vessels decreases as the distance away from the heart increases Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.36

Blood Pressure: Effects of Factors • Neural factors • Autonomic nervous system adjustments (sympathetic division)

• Renal factors • Regulation by altering blood volume • Renin – hormonal control

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.39a

Blood Pressure: Effects of Factors • Temperature • Heat has a vasodilation effect • Cold has a vasoconstricting effect

• Chemicals • Various substances can cause increases or decreases

• Diet Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.39b

Factors Determining Blood Pressure

Figure 11.19 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.40

Variations in Blood Pressure • Human normal range is variable • Normal • 140–110 mm Hg systolic • 80–75 mm Hg diastolic • Hypotension • Low systolic (below 110 mm HG) • Often associated with illness • Hypertension • High systolic (above 140 mm HG) • Can be dangerous if it is chronic Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.41

Developmental Aspects of the Cardiovascular System • A simple “tube heart” develops in the embryo and pumps by the fourth week • The heart becomes a four-chambered organ by the end of seven weeks • Few structural changes occur after the seventh week Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Slide 11.44

Heart Attack (Myocardial Infarction) Description This image shows clearly the damage caused by a heart attack. To the right of the image, you can see the back wall of the left ventricle where there is an extensive area of dead tissue (infarct). The central part of the infarct shows the yellow appearance of dead tissue (necrosis), and bordering on this is an outer reddish area which suggests partial healing by early scar tissue. The front wall of the left ventricle (on the left of the image) appears normal. Where the reddish area curves around the yellow dead tissue at the top, you can see the right coronary artery, which is considerably narrowed due to artherosclerosis (hardening of the artery walls). A blood clot has formed in this narrowed area and was responsible for the heart attack.

Atherosclerosis is responsible for the majority of deaths in our society. It is also responsible for a huge amount of morbidity. If one studies insurance tables, atherosclerosis causes a large contribution to years of potential life lost. Atherosclerosis is predominantly a disease of arteries – both large and medium-sized. It affects elastic and muscular vessels. Atherosclerosis may also involve veins when they become vein grafts and are exposed to arterial pressure.

Risk factors for atherosclerosis include those, which are modifiable, and those, which are not.     

 

                                                       

Age - in general, atherosclerosis increases with age. The earliest lesions of atherosclerosis are present after the age of 10 years old and some believe that this is a disease present since infancy Gender – atherosclerosis is present more in males, however females catch up after menopause. Some old dated thinking regarded females as having less atherosclerosis than males. However, it is recognized now that females do develop significant atherosclerosis. Estrogen is protective as it has multiple effects including effects on lipids, nitric oxide, vascular tone and antioxidant properties.

Smoking causes multiple malignancies and accelerates and initiates atherosclerosis. Many effects on the endothelial cell including poor vascular tone with vasoconstriction, oxidation, and prothrombotic products. Inactivity and obesity Diabetes – affects endothelium and lipids Hypertension - accelerates the development of atheroma Hyperlipidemia Family history – probably multifactorial based on many of the above factors

ARTERIOSCLEROSI S OF THE EXTREMITIES

Arteriosclerosis of the extremities is a disease of the peripheral blood vessels that is characterized by narrowing and hardening of the arteries that supply the legs and feet. The narrowing of the arteries causes a decrease in blood flow. Symptoms include leg pain, numbness, cold legs or feet and muscle pain in the thighs, calves or

S1 S2

closure of AV valves (lub) closure of SL valves (dup)

S3 & S4

diastolic filling sound

S3 is heard after S2, if present

suspect CHF

S4 is heard prior to S1,

if present suspect noncompliant ventricles although this is common among elderly

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Thromboangitis obliterans Buerger’s  disease • Obstructive inflammatory process affecting the  peripheral arteries • male, 20 to 40 years old • intermittent claudication, numbness and  tingling, thrombophlebitis • may require amputation of the affected digits

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Coronary artery disease (CAD) is caused by a

narrowing or constriction of the arteries that supply the heart muscle with blood. This narrowing is a result of atherosclerosis—the buildup of cholesterol and other fatty substances in the arteries. When the arteries narrow, blood flow is reduced. The reduced blood flow (ischemia) causes the heart muscle to receive less oxygen in certain areas. If the blood flow is completely cut off, a heart attack (myocardial infarction) will occur, and the heart muscle will be permanently damaged.

•ANGINA •Duration of pain – In general, anginal pain lasts for only a few minutes and is relieved by rest or nitroglycerin. •MYOCARDIAL INFARCTION (HEART ATTACK) •Heart attack pain is usually more severe than anginal pain, and may last longer, often 15 minutes or more. •Pain that lasts less than 30 seconds and goes away with a few deep breaths or a change in position is usually not angina.

•External factors – •Anginal pain is often brought on by exercise or activity, emotional tension, dreams, cold or windy weather, low blood sugar, or even eating. •Your symptoms can subside when you alter the behavior or environmental trigger. •Heart attack pain will usually not subside with rest and may be accompanied by other symptoms such as shortness of breath, nausea, or sweating. •The elderly or people with diabetes may have less typical or more subtle symptoms signaling angina or heart attack. Some people may have “silent ischemia” and experience no symptoms.

Types of Angina There are three primary types of angina: •Stable angina – The attacks are predictable, and the triggers that cause them can be identified. They do not occur when you are resting or relaxed, and symptoms will usually disappear after a few minutes of rest. •Unstable angina – The symptoms are less predictable. Chest pain may occur while resting or even sleeping (nocturnal angina), and the discomfort may last longer and be more intense. Stable angina becomes unstable when symptoms occur more frequently, last longer, or are precipitated more easily. You should call your doctor immediately if you experience symptoms at rest, or a worsening pattern of symptoms.

Variant or Prinzmetal's angina – This is usually caused by the spasm of a coronary vessel. It occurs when you are at rest, and often in the middle of the night. It can be quite severe. It may indicate that you have one of the following conditions: •Coronary artery disease •Extremely high blood pressure •Hypertrophic cardiomyopathy (disease of the heart muscle) •Diseases of the heart valves

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