Unit 6B: The Heart and Cardiac Output Flashcards

1
Q

The Heart

A

Muscular pump that moves the blood throughout the body
Heart muscle is called myocardium
Position:
- Sits posterior to sternum, left of body midline
- Between lungs in mediastinum
- Slightly rotated: right side more anterior than left
- Base, postero-superior surface
- Apex, inferior, conical end
- Projects slightly anteroinferiorly toward left side of body

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2
Q

The Heart is Enclosed in Three Tough Membranous Layers

The Pericardium

A

Fibrous pericardium: outermost covering
- Attaches to diaphragm and base of aorta, pulmonary trunk
- Anchors heart and prevents its overfilling
Parietal layer of serous pericardium
- Attaches to fibrous pericardium
Visceral layer of serous pericardium
- Attaches directly to heart
Two serous layers continuous and separated by pericardial cavity containing serous fluid which acts as a lubricant

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3
Q

Three Layers of the Heart

Heart Wall

A

Epicardium (viseral pericardium)
- Outermost heart layer
- Simple squamous epithelium and areolar connective tissue
Myocardium
- Middle layer of heart wall (thickest)
- Cardiac muscle tissue that contracts to pump blood
Endocardium
- Covers internal surface of heart and external surface of valves
- Simple squamous epithelium and areolar connective tissue
- Continuous with lining of blood vessels

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4
Q

Anatomy of the Heart - Chambers

Atria

A

Receive blood
- Right atrium - from systemic circulation (body’s organ systems)
- Left atrium - from pulmonary circulation (lungs)
- Separated by interatrial septum

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5
Q

Anatomy of the Heart - Chambers

Ventricles

A

Pump out blood
- Right ventricle - to pulmonary circulation
- Left ventricle - to systemic circulation
- Separated by interventricular septum

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6
Q

Heart Wall

A

Heart wall varies in thickness
- Ventricles (pumping chambers) have thicker walls than atria
- Left ventricle has thicker wall than right ventricle

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7
Q

Anatomy of the Heart - Great Vessels

Venae Cavae

A
  • Superior vena cava - drains blood from head, arms and upper torso
  • Inferior vena cava - drains blood from legs and lower torso
  • Both drain into right atrium
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8
Q

Anatomy of the Heart - Great Vessels

Pulmonary Trunk

A
  • Carries blood from right ventricle
  • Splits into right and left pulmonary arteries to lungs
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9
Q

Anatomy of the Heart - Great Vessels

Pulmonary Veins

A
  • Right and left pulmonary veins from lungs
  • Both sides feed straight into left atrium
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10
Q

Anatomy of the Heart - Great Vessels

Aorta

A
  • Carries blood from left ventricle to systemic circulation
  • Major arteries of the body branch off the aorta
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11
Q

Blood Supply to the Heart

A
  • The blood being pumped through the heart chambers does not exchange nutrients and metabolic end products with the myocardial cells
  • The arteries supplying the myocardium are the coconary arteries, and the blood flowing through them is referred to as coronary blood flow.
  • The coronary arteries exit from behind the ortic valve in the very first part of the aorta and lead to a branching network of small arteries, arterioles, capillaries, venules, veins like those in other organs
  • Most of the cardiac veins drain into a single large vein, the coronary sinus, which empties into the right atrium
  • Coronary blood vessels sit in grooves in the heart muscle called sulci
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12
Q

Anatomy of the Heart

Valves

A

Atria to Ventricles
- Atrioventricular valves (A-V valves) - right A-V valve or tricuspid valve - Left A-V valve, bicuspid valve, or mitral valve
Ventricles to lungs or organ systems
- Semilunar valves - Right: pulmonary semilunar valve (to lungs) (prevent backflow of blood into right ventricle - Left: aortic semilunar valve (to organ systems) (prevents backflow of blood into left ventricle)

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13
Q
A
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14
Q

Circulatory Pathways

A
  1. Superior or Inferior Vena Cava
  2. Right Atrium
  3. Right Atrioventricular Valve (Tricuspid Valve)
  4. Right Ventricle
  5. Pulmonary Semilunar Valve
  6. Pulmonary Trunk
  7. Pulmonary Arteries
  8. Pulmonary Arterioles
  9. Pulmonary Capillaries
  10. Pulmonary Venules
  11. Pulmonary Veins
  12. Left Atrium
  13. Left Atrioventricular Valve (Bicuspid Valve, Mitral Valve)
  14. Left Ventricle
  15. Aortic Semilunar Valve
  16. Ascending Aorta
  17. Aortic Arch
  18. Systemic Arteries
  19. Systemic Aterioles
  20. Systemic Capillaries
  21. Systemic Venules
  22. Systemic Veins
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15
Q

Autorhymicity of the Heart

Heart Contraction Involves Two Events

A
  • The conduction system initiates and propagates an action potential
  • Cardiac muscle cells initiate action potentials and contract
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16
Q

Authorhythmicity of the Heart

Conduction System

A

Initiates and conducts electrical events to ensure proper timing of contactions Specialized cardiac muscle cells (pacemaker cells) that have action potentials but do not contract
- These cells are autorhythimc (contract cpontaneously)
Its activity is influenced by autonomic nervous system

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17
Q

Conuduction System

A

Sinoatrial (SA) node initiates heartbeat (pacemaker)
- Located high in posterior wall of right atrium
Atrioventricular (AV) node
- Located in floor of right atrium (near right AV valve)
Atrioventricular (AV) bundle (bundle of His)
- Extends from AV node though interventricular septum
- Divides into left and right bundles
Purkinje fibers
- Extend from left and right bundles at heart’s apex
- Course through walls of ventricles

18
Q

Autorhythmicity of the Heart

After Starting at SA Node the Action Potential Spreads:

A
  1. Action potential is distributed through atria, reaches node
    - Excitation travels via gap junctions and the two atria contract together
  2. Action potential is delayed at the AV node
    - AV nodal cells are slow because of small diameter and few gap juctions
    - Insulation of fibrous skeleton means AV node is bottleneck (only path)
    - Delay allows ventricles to fill before they contract
  3. Action potential travels through AV bundle to Purkinje fibers
    - AV node - AV bundle - Bundle branches - Purkinje fibers
  4. Action potential spreads through ventricles
    - Gap juctions allow impulse to spread through cardiac muscle fibers
    - Cells of the two ventricles contract nearly simultaneously, beginning to the apex
19
Q

Regulation of the Heart

A

The heart is autorhythmic, but it’s rate can be modifed by the brainstem
Cardiac center of medullar oblongata influences rate and force of the heart’s contractions
- Contains cardioacceleratory (sympathetic) and cardioinhibitory (parasympathetic) centres
- Receives signals from baroreceptors and chemoreceptors in aorta and carotid arteries
- Modifies (does not initiate) cardiac activity
Parasympathetic innervation decreases heart rate
- Starts at

20
Q

Development and Aging of Blood

Hematopiesis

A
  • Occurs in most bones in young children
  • Restricted to selected bones in axial skeleton in adulthood
  • Older red bone marrow replaced with fat as individuals age
  • Older individuals more likely to become anemic
  • May produce fewer and less active leukocytes
  • Certain types of leukemia more prevalent in elderly
21
Q

Fetal Circulation

After Birth

A

Foramen ovale closes
- Higher pressure on left side of heart pushes flaps of septum closed
- A remnant of the foramen is the fossa ovalis, a small depression
Ductus venosus ceases to be functional and constricts
- Becomes ligamentum venosum
Ductus arteriosus
- Closes within 10 to 15 hours of birth
- Becomes fibrous structure, ligamentum arteriosum
Umbilical vein and umbilical arteries become nonfunctional
- Umbilical vein becomes round ligament of the liver
- Umbilical arteries become medial umbilical ligaments

22
Q

Fetal Circulation

Before Birth

A

Fetus receiver oxygen and nutrients through placenta, while newborn’s cardiovascular system is independent
Fetal lungs nonfunctional
Blood pressure on right side of heart greater than left
Fetal vessels shunt blood to organs in need and away from immune organs (e.g. lungs)

23
Q

Fetal Circulation

First Breath

A

At birth, fetal circulation begins to change to adult pattern
With first breath
- Pulmonary arteries dilate and pulmonary resistence drops
- Pressure on right side of heart decreases
- Pressure now greater on left side of heart

24
Q

Development and Aging of the Cardiovascular System

A

Begins in third week with formation of two heart tubes from mesoderm in embryo
Heart tubes fuse, forming single primitive heart tube
Begins to beat by day 22
Bends and folds on itself in fourth week
Heart tube develops into named expansions
Weeks 5 to 8
- Single heart partitioned into four chambers
- Great vessels form
Common atrium abdivided into left and right atrium divided by interatrial spetum that contains an opening called the foramen ovale, which shunts blood from right atrium to left atrium through foramen (largely bypasses right ventricle and lungs)
Interventricular septum
- Partitions left and right ventricles
- Grows superiorly from floor of ventricles

25
Q

Factors Influencing Cardiac Output

Afterload

A

Resistance in arteries (esp. ascending aorta) to ejection of blood by ventricles
Pressure that must be exceeded before blood ejected
Hypertension increases afterload
Atherosclerosis (plaque in vessel linings) increases afterload
- Seen with aging
- Smaller arterial lumen exerts greater resistance to movement of blood
- Results in decreased stroke volume

26
Q

Factors Influencing Cardiac Output

Inotropic Agents Change Stroke Volume (Contractility)

A

Postive Inotropic Agents
- Increase contractility by increasing avaliable Ca 2+
- e.g. thyroid hormone, certain drugs such as digitalis
Negative Inotropic Agents
- Decrease contractility by decreasing avaliable Ca 2+
- e.g. electrolyte imbalances such as increased K+ or H+, certain drugs such as Ca 2+ channel-bloacking blood pressure drugs

27
Q

Factors Influencing Cardiac Output

Venous Return (cont..)

A

Venous Pressure Gradient
- BP is 20 mmHg in venules, almost 0 in vena cava - small difference, but it keeps blood flowing from higher to low pressure
Skeletal Muscle Pump
- Assists venous return from limbs
- As muscle contracts, veins are squeezed
- Blood is pushed and valves prevent backflow
- Blood is moved more quickly during exercise
- Blood pools in legs veins with prolonged inactivty
Respiratory Pump assists venous return in the thorax
- In inspiration: diaphragm contracts, so abdominal pressure increases and thoracic pressure decreases
- Blood in abdominal veins is driven toward thoracic cavity
- Increases in breathing rate facilitate blood movement

28
Q

Factors Inflencing Cardiac Output

Venous Return

A

Volume of blood returned to the heart
Determines end-diastolic volume (EDV)
Volume determines preload
- Pressure stretching heart wall before shortening
- The more stretching during preload, the more forceful the contraction
Venous return may be increased by increased venous pressure or increased time to fill
- Venous pressure increases during exercise as muscles squeeze veins
- Time to fill increases with slower heart rate (e.g. in high-caliber athletes with strong hearts)
- Decreases with low blood volume (e.g. with hemorrhage) or high heart rate

29
Q

Factors Influencing Cardiac Output

Heart Rate

A

Chronotropic Agents change heart rate
- Postive chronotropic agents increase heart rate (e.g. thyroid hormone, caffeine, nicotine, cocaine)
- Negative chronotropic agents decrease heart rate (e.g. betablocker drugs)

30
Q

Factors Influencing Cardiac Output

Stroke Volume

A

Venous Return - amount of blood retuning to heart
Intropic Agents - affect force of contraction
Afterload - blood pressure in aorta (resists ventricular ejection)

31
Q

Cardiac Output

Cardiac Reserve

A

Capacity to increase cardiac output above rest level
HR accelerates and stoke volume increases during exercise
- Gives measure of level of exercise an individual can pursue
- e.g. CO can increase four-fold in healthy, nonathlete and up to seven-fold in athlete

32
Q

Application: Heart Rate

Bradycardia

A
  • Persistently low resting heart rate in adults
  • Below 60 beats/minute
  • Normal change in athletes
  • Abnormal due to: hypothyroidism, electrolyte imbalance, and congestive heart failure
33
Q

Application: Heart Rate

Tachycardia

A
  • Persistently high resting heart rate
  • Over 100 beats/minute
  • Casued by heart disease, fever, and anxiety
34
Q

Cardiac Output

A

Amount of blood pumped by a single ventricle in one minute
- Measured in litres per minute
Measure of effectiveness of cardiovascular system
Increases in healthy individuals during exercise
Determined by heart rate (beats per minute) and stroke volume (amount of blood ejected per beat)
- HR x SV = CO
- e.g. 75 beats/min x 70 ml/beat = 5.25 L/min
CO must meet tissue needs
- Individuals with smaller hearts have smaller stroke volume and so must have faster heart rate (e.g. women and children)
- Individuals with stronger hearts have larger stroke volume and slower heart rate (e.g. endurance athletes have thicker heart walls and stronger)

35
Q

The Cardiac Cycle

Ventricular Balance

A
  • Equal amounts of blood are pumped by left and right sides of the heart
  • Left heart pumps blood farther and so must be stronger (thicker)
  • But ejected blood volumes must be the same or edema (swelling) can occur
36
Q

The Cardiac Cycle

End Diastolic Volume (EDV)

A
  • Volume of blood in the ventricles at the end of diastole
  • maximum volume the heart holds during a cardiac cycle
37
Q

The Cardiac Cycle

End Systolic Volume (ESV)

A
  • Volume of blood in the ventricles after their contraction ends
  • Ventricles are never completely empty
38
Q

The Cardiac Cycle

Cardiac Cycle

A

All events in heart from the start of one heart beat to start of the next
- Includes both systole (contraction of ventricles) and diastole (relaxation of ventricles)
Contraction increases pressure; relaxation decreases it
- Blood moves down its pressure gradient (high to low)
- Valves ensure that flow is forward (closure prevents backflow)
Ventricular activity is most important driving force
- Ventricular contraction raises ventricular pressure - AV valves pushed closed, smeilunar valves pushed open and blood ejected to artery
- Ventricular relaxation lowers ventricular pressure - semilunar valves close, AV valves open

39
Q

Electrocardiogram (ECG/EKG)

Waves

A

P wave
- Reflects electrical changes of atrial depolarization
QRS complex
- Electrical changes associated with ventricular depolarization
- Atria also simultaneously repolarizing
T wave
- Electrical change associated with ventricular repolarization

40
Q

Electrocardiogram (ECG/EKG)

Segments

A
  • Two segments between waves correspond to plateau phases of cardiac action potentials (no electrical change)
    P-Q segment
  • Associated with atrial cells’ plateau (atria are contracting)
    S-T segment
  • Associated with ventricular plateau (ventricles are contracting)