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1. Cardiac Anatomy & Physiology
IH Cardiac Services
Kelowna General Hospital
2020

2. Overview
• Blood Vessels
• Layers of the heart
• Pericardium
• Chambers of the heart
• Circulation:
– Pulmonary, systemic, coronary
• Heart Valves
• Conduction system
• Mechanical system
• Cardiac output

3. Blood Vessels
5 Types:
• Arteries- thick muscular walls to accommodate flow of
blood at high pressure and high speed
• Arterioles- thinner walls, they constrict or dialate to
control flow to capillaries
• Capillaries- walls made of only 1 layer of endothelial
cells
• Venules- receive blood from capillaries, walls are thinner
than arterioles
• Veins- thinner walls than arteries but larger diameters
because of the low blood pressure of venous return to
the heart

4. Arterioles

5. Internal Diameter, Wall Thickness &
Components of the Vessel
Circulatory System

6. The Heart
• Four-chambered, muscular organ
• Responsible for the vital transport of blood,
oxygen, nutrients, and byproducts to and
from the tissues.
• Average female heart is 9 ounces
• Average male heart is 10.5 ounces

7. Layers of the Heart
3 Layers:
• Epicardium: the outer layer, made up of scam epithelial
cells overlying connective tissue
• Myocardium: middle layer forms most of the heart wall, it
has striated muscle fibres that cause the heart to
contract
• Endocardium: hearts inner layer consists of enthral
tissue with small blood vessels and bundles of smooth
muscle

8. Pericardium
• Pericardium is the fibrous same that surrounds the heart
and the roots of the great vessels it consists of 2 parts
the fibrous and the serous pericardium. Confines and
stabilizes position of heart.
Pericardial Space
• Located between pericardium and
epicardium
• Contains pericardial fluid that acts as
lubricant

10. Chambers of the Heart
• 4 Chambers
– 2 Atria
– 2 Ventricles

11. Heart Valves
AV Valves
-Tricuspid (3 leaflets)
-Mitral (2 leaflets)
Semilunar Valves
-Aortic Valve (3 Leaflets)
-Pulmonary Valve (3 leaflets)

12. Thoracic Wall / Cavity

13. Circulation
• 3 Types: Pulmonary, Systemic, Coronary

14. 1. Pulmonary Circulation
• Blood travels to the lungs to pick up 02
and get rid of CO2. RV -> PA -> arterioles
->capillaries of the Lungs (exchange at the
alveoli) -> Venules ->PV -> LA

15. Cardiac Chambers and
StructuresRight-Sided Cardiac Chambers
• Receive deoxygenated, or venous, blood.
From there, it flows through the pulmonary
arteries to the lungs, where it becomes
oxygenated and releases carbon dioxide.
RA receives blood from 3 veins:
1. Inferior vena cava
2. Superior vena cava
3. Coronary sinus.
Venous blood is then pumped into
the pulmonary trunk from the RV.

16. Cardiac Chambers and
Structures
Left-Sided Cardiac Chambers
• Supply oxygenated (arterial) blood to the body.
LA receives blood from
the lungs via the
pulmonary veins.
LV pumps oxygenated
blood to body tissues
via the aorta.

17. 2. Systemic Circulation
• Blood pumped from LV and carries 02 and nutrients to the boys
cells and transport waste for excretion LV -> Aorta
• 3 branches for the upper body:
– Left common carotid - supplies blood to the brain
– Left subclavian artery supplies blood to left arm
– Innominate (brachiocephalic)- branches into the right common carotid (supplies
blood to the brain) and the right subclavian artery (supplies blood to right arm)
chest wall supplied by right innominate, right subclavian, left subclavian
• Lower Body: as the aorta descends it branches off to supply the
organs of GI/GU, spine, lower chest and muscles -then divides into
iliac arteries ->femoral

18. Blood flow pathway through the
heart

19. 3. Coronary Circulation
•The heart is supplied O2 and nutrients by
the right and left coronary arteries with arise
from the root of the aorta
LCA -> LAD & CX
RCA-> acute marginal & PDA

20. Coronary Arteries
Anterior & posterior views of theAnterior & posterior views of the
coronary artery circulationcoronary artery circulation

21. Left Coronary Artery (LCA)
• Left Main section of LCA also
referred to as “widow maker”
–Occlusion main vessel usually
results in immediate death
–Wipes out main pump of the
heart LV
• Divides into 2 branches
–Left anterior Descending
–Left Circumflex

22. Right Coronary Artery (RCA)
• Serves RA & RV in most people
• Supplies
– SA node (70%)
– AV node (90%)
– Portion of HIS bundle
– Poster 1/3 of septum
– RA & RV muscle
– Inferior posterior wall of LV
• Primary area of infarction
– Inferior wall
– Inferoposterior wall
– RV

23. Right vs Left Dominance
• In most people (85%) the distal RCA gives rise to the
posterior descending artery (PDA) which supplies the
inferior and posterior walls o f the ventricles and the
posterior 1/3 of the interventricular septum
• In 8 % of the population the PDA arises from the
circumflex artery instead (left dominance)
• The remaining population is balanced : dual supply from
RCA and Circumflex
– In a co-dominant heart a single or duplicated PDA supplied by
both RCA and LAD/LCx

27. Venous system
inter-twined
Less famous

28. Collateral Circulation
• Anastomotic channels known as collateral vessels can develop in the heart
as an adaptation to ischemia.
• Coronary collaterals can provide substantial blood flow to resting
myocardium, but are generally insufficient during increased demand
(exercise).
• Collaterals may: reduce infarct size after myocardial infarction (MI); reduce
post-MI complications such as rupture of a papillary muscle, myocardial free
wall, or interventricular septum; and reduce aneurysmal dilatation.
• The absence of collateral circulation to the infarct-related artery may be an
independent predictor of mortality in patients with an acute MI.
Reference: UpToDate (2020)

29. Normal Heart Conduction
• Electrical activation always precedes
mechanical activation, just by
milliseconds.
• Heartbeats occur as electrical
impulses move through the heart.
• The electrical side of the heart and its
contractions are at the core of how
the heart operates. This is what
constitutes a heartbeat.

30. Electrical System
• The hearts pacemaker cells have 3 unique
characteristics:
-Automaticity: ability to generate an impulse
automatically
-Conductivity: the ability to pass the impulse to the
next cell
-Contractility: the ability to shorten the fibres in the
heart when receiving the impulse

31. Electrical System
• The SA node is the pacemaker of the
heart. If it fails the AV node or the Bundle
branches can take over.
Rates
• SA Node 60-100
• AV Node 40-60
• Bundle Branches 20-40

32. Cardiac Innervation
Sympathetic nerves
– Innervate the SA node, AV node, myocardium and vasculature
– Sa node (b1) fibres increase pace making activity (chronotropy) -
cardiac muscle fibres increase contractility (inotropy ) to help
increase CO
– Stimulation of b1 and B2 in the skeletal and coronary circulation
causes vasodilation
Para sympathetic nerves
– Innervate the SA node, AV node, atrial myocardium but few
vascular beds
– Basal vagal tone dominates the tonic Sympathetic stimulation of
the SA node and AV node resulting in slowing of pacemaker
activity and conduction parasympathetic have little impact on
total PVR

33. Conduction Pathway

34. Conduction System in Action
• Steps of conduction:
– Impulse Formation at the SA Node
– Depolarization of the Left and Right Atrium
– Delay at the AV Node
– Conduction at The Bundle Branches
– Conduction Through the Purkinje Fibers
– The Mechanical Contraction of the Ventricle, or
Systole
– The Mechanical Relaxation of the Ventricle, or
Diastole

37. Mechanical System
• For the cardiac cycle to work properly it
needs electrical stimulation with a
mechanical response
• Cardiac cycle has 2 phases:
– Systole
– Diastole

38. Cardiac Cycle
Systole
• Ventricles contract at the beginning of systole Increasing
pressure in the ventricles forces the MV and TV to close
and the AV and PV to open as the ventricles contract,
the pressure buildup in the ventricles, once the pressure
overcomes the pressure in the PA and blood in the aorta
blood is ejected out

39. Cardiac Cycle
Diastole
• When the ventricles empty and relax the Ventricular
pressure falls below the pressure in the PA and Aorta At
the beginning of diastole the AV and PV valve close to
prevent the back flow of blood into the Ventricles and the
MV and TV open allowing blood to flow into the
ventricles from the atria When the ventricles become full
(near the end of this phase) the atria contract to send the
remaining blood to the ventricles

40. S1 occurs
S2 occurs

41. Right vs. Left Ventricle
• Differ markedly in size & energy
consumption – CO equivalent.
• RV 1/6 muscle mass & performs 1/4 of
the work of the LV
• RV can pump an equivalent CO due to
low resistance in pulmonary vasculature
• Pulmonary VR 10% of Systemic VR
• RV thin walled with low O2 demand so
quicker recovery if pure RV MI
(Carter & Ellis (2005). Right ventricular Infarction Critical Care Nurse,
April, 25 (2))

42. Cardiac Output =
Heart Rate X
Stroke Volume

43. Heart Rate = Autonomic
Nervous System (Sympathetic
& Parasympathetic) and
Medications

44. Stroke Volume =
Preload, Contractility,
Afterload

46. Preload
• The stretching of muscle fibers in the
ventricles
• Volume of blood in ventricle
@ end-diastole (EDV)

47. What affects Preload?
• Blood Volume status
• Ventricular Compliance
• Venous Tone (skeletal muscle movement)
• Medications (i.e. nitro, diuretics…)

48. Contractility (Inotropy)
• Ability of heart muscle
fibers (sarcomeres) to
shorten when stimulated
(contract). Influenced by
preload- the greater the
stretch the more forceful
the contraction
• Positive inotropic
medications 
e.g. Dobutamine
Dopamine
• Negative inotropic
medications 
e.g. Beta-blocker

49. What affects Contractility?

50. What affects Afterload?
• The Pressure the heart has to work
against
• Forces are:
– valve stenosis,
– blood viscosity,
– hypertensive conditions,
– systemic vascular resistance (size of lumens
of the arteries)

51. FIGURE 7-5 Determinants of cardiac output. (Adapted from
Michaelson CR: Congestive heart failure, St Louis, 1983, Mosby.)

52. Pressure vs. Volume
↑Pressure Volume Overload

53. References
DuManoir, C. (2010) 12/15 Lead ECG: What do you see? Powerpoint
presentation.
Hall, J. & Premji, A. (2015). Toronto Notes (31st Ed.). Toronto,ON:
Toronto Notes for medical Students, Inc.
Lilly, L. (2016). Pathophysiology of Heart Disease (6th Ed.).
Philadelphia, PA: Wolters Kluwer.
Mclaughlin, M (2014). Cardiovascular Care Made incredibly easy (3rd
Ed.) Philadelphia, PA: Wolters Kluwer.
Rawnsley, D. (2015). Cardiac Anatomy and Physiology. PowerPoint
presentation.