Chapter 15: The Cardiovascular System
1

The thickness of the myocardium of the four chambers varies according to the function of each chamber.
The atria walls are thin because they deliver blood to the ventricles.
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.
2

Posterior to sternum medial to lungs
Anterior to vertebral column
Base lies beneath 2 nd rib
Apex at 5 th intercostal space
Lies upon diaphragm

4

5

6

• Right Atrium
• receives blood from
• inferior vena cava
• superior vena cava
• coronary sinus
• Right Ventricle
• receives blood from right atrium
• Left Atrium
• receives blood from pulmonary veins
• Left Ventricle
• receives blood from left atrium
7

Anterior View
8

Posterior View
9

• Receives blood from 3 sources
– superior vena cava, inferior vena cava and coronary sinus
• Interatrial septum partitions the atria
• Fossa ovalis is a remnant of the fetal foramen ovale
• Tricuspid valve
– Blood flows through into right ventricle
– has three cusps composed of dense CT covered by endocardium
10

• Forms most of anterior surface of heart
• Papillary muscles are cone shaped trabeculae carneae
(raised bundles of cardiac muscle)
• Chordae
TENDINAE : cords between valve cusps and papillary muscles
• Interventricular septum: partitions ventricles
• Pulmonary semilunar valve: blood flows into pulmonary trunk
11

• Forms most of the base of the heart
• Receives blood from lungs- 4
Pulmonary VEINS
• (2 right + 2 left) Red blood in a vein? Weird!
• Bicuspid valve: blood passes through into left ventricle
– has two cusps
– to remember names of this valve, try the pneumonic
LAMB
• Left Atrioventricular, Mitral, or Bicuspid valve 12

• Forms the apex of heart
• Chordae tendineae anchor bicuspid valve to
PAPILLARY muscles (also has trabeculae carneae like right ventricle)
• Aortic semilunar valve:
– blood passes through valve into the ascending aorta
– just above valve are the openings to the coronary arteries
13

14

• A-V valves open and allow blood to flow from atria into ventricles when ventricular pressure is lower than atrial pressure
– occurs when ventricles are relaxed, chordae tendineae are slack and papillary muscles are relaxed
15

• A-V valves close preventing backflow of blood into atria
– occurs when ventricles contract, pushing valve cusps closed, chordae tendinae are pulled taut and papillary muscles contract to pull cords and prevent cusps from everting
16

• SL valves open with ventricular contraction
– allow blood to flow into pulmonary trunk and aorta
• SL valves close with ventricular relaxation
– prevents blood from returning to ventricles, blood fills valve cusps, tightly closing the SL valves
17

Atria contract, blood fills ventricles through A-V valves
Ventricles contract, blood pumped into aorta and pulmonary trunk through SL valves
18

Dense CT rings surround the valves of the heart, fuse and merge with the interventricular septum
Support structure for heart valves
Insertion point for cardiac muscle bundles
Electrical insulator between atria and ventricles prevents direct propagation of AP ’ s to ventricles
19

20

21

Atrial Systole /Ventricular Diastole Atrial Diastole /Ventricular Systole https://www.youtube.com/watch?v=waOSUpEHPQs
22

• Atrial Systole/Ventricular Diastole
• blood flows passively into ventricles
• remaining 30% of blood pushed into ventricles
• A-V valves open/semilunar valves close
• ventricles relaxed
• ventricular pressure increases
23

Ventricular Systole/Atrial diastole
• A-V valves close
• chordae tendinae prevent cusps of valves from bulging too far into atria
• atria relaxed
• blood flows into atria
• ventricular pressure increases and opens semilunar valves
• blood flows into pulmonary trunk and aorta
24

Lubb
• first heart sound
• occurs during ventricular systole
• A-V valves closing
Dupp
• second heart sound
• occurs during ventricular diastole
• pulmonary and aortic semilunar valves closing
Murmur
– abnormal heart sound
25

26

Cardiac muscle fibers form a functional syncytium
• group of cells that function as a unit
• atrial syncytium
• ventricular syncytium
27

28

29

• Cardiac muscle fibers swirl diagonally around the heart in interlacing bundles
30

• recording of electrical changes that occur in the myocardium
• used to assess heart ’ s ability to conduct impulses
P wave
– atrial depolarization
QRS wave
– ventricular depolarization
T wave – ventricular repolarization
31

• 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.
• Figure 20.12 shows a typical ECG.
32

• EKG
– Action potentials of all active cells can be detected and recorded
• P wave
– atrial depolarization
• P to Q interval
– conduction time from atrial to ventricular excitation
• QRS complex
– ventricular depolarization
• T wave

34

• In a typical Lead II record, three clearly visible waves accompany each heartbeat It consists of:.
•
P wave ( atrial depolarization - spread of impulse from SA node over atria)
•
QRS complex ( ventricular depolarization - spread of impulse through ventricles)
• T wave (ventricular repolarization).
• Correlation of ECG waves with atrial and ventricular systole (Figure 20.13)
35

• As atrial fibers depolarize, the P wave appears.
• After the P wave begins, the atria contract (atrial systole).
Action potential slows at the AV node giving the atria time to contract.
• The action potential moves rapidly through the bundle branches, Purkinje fibers, and the ventricular myocardium producing the QRS complex.
• Ventricular contraction after the QRS complex and continues through the ST segment.
• Repolarization of the ventricles produces the T wave.
• Both atria and ventricles repolarize and the P wave appears.
36

Additional Factors that Influence HR
• physical exercise
• body temperature
• concentration of various ions
• potassium
• calcium
• parasympathetic impulses decrease heart action
• sympathetic impulses increase heart action
• cardiac center regulates autonomic impulses to the heart
37

•
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 = SV X HR
•
Cardiac reserve is the ratio between the maximum cardiac output a person can achieve and the cardiac output at rest.
38

• CO = SV x HR
– at 70ml stroke volume & 75 beat/min----5 and 1/4 liters/min
– entire blood supply passes through circulatory system every minute
• Cardiac reserve is maximum output/output at rest
– average is 4-5x while athlete ’ s is 7-8x
39

• Preload (affect of stretching)
– Frank-Starling Law of Heart
– more muscle is stretched, greater force of contraction
– more blood more force of contraction results
• Contractility
– autonomic nerves, hormones, Ca+2 or K+ levels
• Afterload
– amount of pressure created by the blood in the way
– high blood pressure creates high afterload
40

41

• According to the Frank-Starling law of the heart , a greater preload (stretch) on cardiac muscle fibers just before they contract increases their force of contraction during systole.
– Preload is proportional to EDV.
– EDV is determined by length of ventricular diastole and venous return.
• 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.
42

•
Myocardial contractility , the strength of contraction at any given preload, is affected by positive and negative inotropic agents .
– Positive inotropic agents increase contractility
– Negative inotropic agents decrease contractility.
• For a constant preload, the stroke volume increases when positive inotropic agents are present and decreases when negative inotropic agents are present.
43

• The pressure that must be overcome before a semilunar valve can open is the afterload.
• In congestive heart failure , blood begins to remain in the ventricles increasing the preload and ultimately causing an overstretching of the heart and less forceful contraction
– Left ventricular failure results in pulmonary edema
– Right ventricular failure results in peripheral edema.
44

• Heart rate affected by hormones
(epinephrine, norepinephrine, thyroid hormones).
• Cations (Na + , K + , Ca +2 ) also affect heart rate.
•
Other factors such as age, gender, physical fitness, and temperature also affect heart rate.
45

Artery
• thick strong wall
• endothelial lining
• middle layer of smooth muscle and elastic tissue
• outer layer of connective tissue
• carries blood under relatively high pressure
Arterioles
• thinner wall than artery
• endothelial lining
• some smooth muscle tissue
• small amount of connective tissue
• helps control blood flow into a capillary
46

47

• smallest arterioles only have a few smooth muscle fibers
• capillaries lack muscle fibers
48

• smallest diameter blood vessels
• extensions of inner lining of arterioles
• walls are endothelium only
• semipermeable
• sinusoids – leaky capillaries
49

• water and other substances leave capillaries because of net outward pressure at the capillaries ’ arteriolar ends
• water enters capillaries ’ venular ends because of a net inward pressure
• substances move in and out along the length of the capillaries according to their respective concentration gradients
50

• Venule
• thinner wall than arteriole
• less smooth muscle and elastic tissue than arteriole
• Vein
• thinner wall than artery
• three layers to wall but middle layer is poorly developed
• some have flaplike valves
• carries blood under relatively low pressure
• serves as blood reservoir
51

52

53

54

Blood Pressure – force the blood exerts against the inner walls of the blood vessels
Arterial Blood Pressure
• rises when ventricles contract
• falls when ventricles relax
• systolic pressure – maximum pressure
• diastolic pressure – minimum pressure
55

56

If blood pressure rises, baroreceptors initiate the cardioinhibitory reflex, which lowers the blood pressure
57

Dilating arterioles helps regulate blood pressure
58

• not a direct result of heart action
• dependent on
• skeletal muscle contraction
• breathing
• venoconstriction
59

• cells of alveolar wall are tightly joined together
• the high osmotic pressure of the interstitial fluid draws water out of them
60

• heart enlargement
• death of cardiac muscle cells
• increase in fibrous connective tissue of the heart
• increase in adipose tissue of the heart
• increase in blood pressure
• decrease in resting heart rate
61

• MI = myocardial infarction
– death of area of heart muscle from lack of O
2
– replaced with scar tissue
– results depend on size & location of damage
• Blood clot
– use clot dissolving drugs streptokinase or t-PA & heparin
– balloon angioplasty
• Angina pectoris----heart pain from ischemia of cardiac muscle
62

• Coronary artery disease ( CAD ), or coronary heart disease ( CHD ), is a condition in which the heart muscle receives an inadequate amount of blood due to obstruction of its blood supply. It is the leading cause of death in the United States each year. The principal causes of obstruction include atherosclerosis, coronary artery spasm, or a clot in a coronary artery.
• Risk factors for development of CAD include high blood cholesterol levels, high blood pressure, cigarette smoking, obesity, diabetes, “ type A ” personality, and sedentary lifestyle.
63

• Atherosclerosis is a process in which smooth muscle cells proliferate and fatty substances, especially cholesterol and triglycerides (neutral fats), accumulate in the walls of the medium-sized and large arteries in response to certain stimuli, such as endothelial damage (Figure 20.18).
• Diagnosis of CAD includes such procedures as cardiac catherization and cardiac angiography.
• Treatment options for CAD include drugs and coronary artery bypass grafting (Figure 20.19).
64

• Risk factors in heart disease:
– high blood cholesterol level
– high blood pressure
– cigarette smoking
– obesity & lack of regular exercise.
• Other factors include:
– diabetes mellitus
– genetic predisposition
– male gender
– high blood levels of fibrinogen
– left ventricular hypertrophy
65

• Risk factor for developing heart disease is high blood cholesterol level.
– promotes growth of fatty plaques
– Most lipids are transported as lipoproteins
• low-density lipoproteins (LDLs)
• high-density lipoproteins (HDLs)
• very low-density lipoproteins (VLDLs)
– HDLs remove excess cholesterol from circulation
– LDLs are associated with the formation of fatty plaques
– VLDLs contribute to increased fatty plaque formation
• There are two sources of cholesterol in the body:
– in foods we ingest & formed by liver
66

• TC (total cholesterol) under 200 mg/dl
• LDL under 130 mg/dl
• HDL over 40 mg/dl
• Normally, triglycerides are in the range of 10-
190 mg/dl.
• Among the therapies used to reduce blood cholesterol level are exercise, diet, and drugs.
67

• Heart muscle receiving insufficient blood supply
– narrowing of vessels-
--atherosclerosis, artery spasm or clot
– atherosclerosis-smooth muscle & fatty deposits in walls of arteries
• Treatment
– drugs, bypass graft, angioplasty, stent
68

69

70