1. Cardiovascular System: The Heart
Chapter 18

2. Heart Anatomy w/Review
Size of a fist
In the mediastinum
Obliquely situated
___?_____ to the diaphragm
___?_____ to the vertebral column
___?_____ to the sternum
Lungs are ___?_____ and slightly obscure it
Base is right and posterior, apex is point

3. Pericardium Serous membrane surrounding the heart
Protects, anchors, and prevents overfilling
Fibrous pericardium, collagen and elastic figure 8’s
Link all parts together while providing additional support
Limits AP spread
2 layers
Parietal layer covers the _____?_____
Visceral layer (epicardium) covers the _____?___
Pericardial cavity between w/ serous fluid

4. Heart Wall Epicardium (visceral pericardium) Myocardium Endocardium
Heart Wall
Epicardium (visceral pericardium)
Fatty layer
Myocardium
Cardiac muscle
Endocardium
Simple squamous epithelia
Continuous with blood vessels
Forms valves

5. Chambers of the Heart 2 superior atria 2 inferior ventricles
Interatrial septum
Coronary sulcus
2 inferior ventricles
Interventricular septum
Anterior and posterior ventricular sulcus
REMEMBER: directions for specimen/model NOT self

6. Atria of the Heart Receiving chambers Auricles to increase volume
Receiving chambers
Auricles to increase volume
Pectinate muscles internal, anterior walls
Fossa ovalis: remnant of fetal opening
Right entry (O2 poor from systemic)
Superior and inferior venae cavae
Coronary sinus
Left entry (O2 rich from pulmonary)
Right and left pulmonary veins

7. Ventricles of the Heart
Discharge chambers
Trabeculae carneae, folds of muscle
Papillary muscles
Right (anterior) exit
Pulmonary trunk
Right and left pulmonary arteries
Left (posterior) exit
Aorta

8. Heart Valves Keep single directional blood flow
Open/close due to pressure not contraction
Atrioventricular valves (AV)
Right is tricuspid
Left is bicuspid or mitral
Anchored to papillary muscles by
chordae tendineae ‘heart strings’
Semilunar valves (SL)
Aortic
Pulmonary

9. Valve Function AV
Returning blood to atria exerts pressure = valves open to ventricle
Ventricles contract = increase pressure = valves close
Chordae tendineae and papillary muscles prevent inward flip SL
Ventricles contract = increase pressure = valves open
Ventricles relax = blood flows back = close valves

10. Blood Flow Pathway Overview

11. Coronary Circulation Arterial supply in coronary sulcus
Right coronary splits
Marginal: lateral right myocardium
Posterior interventricular: heart apex and posterior ventricular walls (join for right atria and ventricle)
Left coronary splits
Circumflex: left atria and posterior wall of left ventricle
Anterior interventricular: interventricular septum and anterior ventricle walls (join for right atria and ventricle)
Actually varies between individuals
Venous supplies join in coronary sinus
Great cardiac in anterior interventricular sulcus
Middle cardiac in posterior interventricular sulcus
Small cardiac w/marginal artery

12. Cardiac Muscle Anatomy
Intercalated discs
Gap junctions: passage/exchange of ions
Desmosomes: stabilize and maintain structure
Heart behaves as a single unit
Other characteristics (review)
Nuclei #?
Control?
Structure?

13. Cardiac Muscle Contraction
Neural stimulation not needed = autorhythmicity
Can influence pace
Whole organ (not just motor units) contracts
Signals carried through gap junctions
Longer absolute refractory period
Regulates contraction rate
Prevents sustained contraction (tetanus)
Lots of mitochondria
Greater dependence on O2
Presence of fuel source more important than type

14. Autorhythmic Cells Initiate action potentials in the heart
Due to pacemaker potential or unstable resting period
Basic steps of an AP (review)
Changes
Continuous depolarization
to threshold (no flat line)
Ca 2+ channels open and Ca2+
rushes in
AP NOT triggered by Na+
Found in specific locations
Sinoatrial and atrioventricular nodes
Right and left bundle branches
Ventricular walls (Pukinje fibers)

15. Beating to It’s Own Drum
Sinoatrial (SA) node or ‘pacemaker’
Depolarization rate is fastest
Impulse ~75 times/min
Atrioventricular (AV) node delays impulse
Bundle of His electrically connects chambers
Bundle branches to apex
Pukinje fibers to contractile fibers in ventricles

16. Extrinsic Heart Control
Cardiac centers in medulla
Cardioacceleratroy center
Sympathetic NS
Pre- from T1-T5 up
Post- through cardiac plexus to SA and AV nodes & arteries
Cardioinhibitory center
Parasympathetic NS
Pre- from vagus to heart
Post- to SA and AV nodes

17. Electrocardiogram (ECG or EKG)
Records all electrical autorhythmic cell activity
Distinguishable waves
P wave: SA node depolarizes atria
Atria contracts
Drop from AV node delay
QRS complex: ventricle depolarization
Ventricle contracts
Masks atrial repolarization
T wave: ventricle repolarization

18. Heart Sounds ‘Lub’ when AV valves close ‘Dup’ when SL valves close
Ventricular systole (contraction) begins
Bicuspid (mitral) before tricuspid
‘Dup’ when SL valves close
Ventricular diastole (relaxation)
begins
Aortic before pulmonary
Listen to 4 regions for
differences

19. Cardiac Cycle Ventricular filling Ventricular systole (contraction)
Relaxed chambers creates low pressure  allows passive blood flow in
Atria contract, ‘topping off’ ventricles = end diastolic volume (EDV)
Ventricular systole (contraction)
Ventricles contract increasing pressure (isovolumetric contraction phase)
AV valves close and SL valves open
End systolic volume (ESV) remains
Early diastole
Ventricles relax decreasing pressure (isovolumetric relaxation phase)
SL valves close

20. Cardiac Output (CO) Amount of blood pumped by each ventricle
CO (ml/min) = HR (beats/min) x SV (ml/beat)
Stroke volume (SV) is amount of blood per ventricular contraction
Variable and increases with demand
Max CO – rest CO = cardiac reserve
Athletes have higher

21. Regulating Stroke Volume
SV = EDV – ESV
EDV is amount of blood in ventricle during diastole
ESV is amount of blood in ventricle after systole
Affecting factors
EDV by preload: degree of cardiac stretch pre-contraction in ventricles
Slow HR increases volume of return
Exercise increases speed of return
ESV by contractility: contractile force of cardiac cells
SNS innervation, Ca2+ entry, and hormones increase
More blood leaves = decrease in ESV
Ca2+ blockers, increased extracellular K+ , and acidosis decrease
ESV by afterload: pressure needed to eject blood
High BP  more difficult to eject blood = increased ESV

22. Regulating Heart Rate ANS Chemical controls Other factors
SNS stimulates with stress, excitement, or exercise
PNS stimulates with ACh and opposes SNS
Majority of autonomic stimuli; slows heart rate
Chemical controls
Hormones: epinephrine, norepinephrine, and thyroxine increase
Ions
Other factors
Temperature
Age and exercise

23. Homeostatic Imbalances
Pericarditis: inflammation of pericardium roughens serous membrane
Cardiac tamponade: heart is compressed by fluid in pericardial cavity
Angina pectoris: deficient blood flow to myocardium
Myocardial infarction: prolonged coronary blockage; heart attack
Incompetent valves: valves fail to close allowing blood backflow
Stenosis: valves are stiff or obscure opening; heart must work harder
Ischemia: depriving tissue of oxygen
Arrhythmia: uncoordinated atrial/ventricular contractions
Fibrillation: rapid, out of phase contraction
Heart block: AV node damage; ventricles contract on own
Heart murmurs: blood swooshing; valves fail to close
Tachycardia: abnormally fast HR; stress, drugs, or temp cause
Bradycardia: abnormally slow HR; drugs, endurance training, or PNS