(1) The document provides an overview of cardiac anatomy and physiology, including the layers of the heart, chambers, valves, blood vessels, and the pumping action. (2) It describes the pericardium, myocardium, endocardium, atria, ventricles, valves, coronary arteries and veins, and how preload, contractility, afterload, and heart rate impact cardiac output. (3) Key concepts covered are the Frank-Starling mechanism, factors that increase or decrease preload, contractility, and afterload, and how systemic vascular resistance impacts cardiac output.

1. Cardiovascular Review: There’s
More Than Just a Beating Heart
Telemetry
Course
Natalie Bermudez, RN, BSN, MS
Clinical Educator for Cardiac Telemetry

2. The Human Heart
• Layers (3)
• Atria (2)
• Ventricles (2)
• Valves (4)
• Veins
• Arteries

3. Layers of the Heart
2) Pericardium
2) Myocardium
3) Endocardium

4. The Pericardium
• Double-walled serous sac surrounding the
heart
• Strengthened externally by a tough fibrous
connective tissue layer

5. The Pericardium: Three Layers
• Fibrous pericardium
(outer)
– Pericardiophrenic
ligament
• Blends with the outer
fibrous layer or adventitia
of all the great vessels
except the IVC
– Sternopericardial
ligaments
• Keeps heart in its place;
attaches to the sternum

6. The Pericardium: Three Layers
• Parietal Pericardium
– Lines the inner surface
of the fibrous
pericardium
• Visceral Pericardium
– Aka epicardium
– Serous fluid secreted
by these cells forms a
thin lubricating film in
the pericardial cavity
that provides a friction-
free environment for
the beating heart

7. Cardiac Tamponade
• It is a potentially fatal condition that occurs when
fluid rapidly accumulates in the pericardial cavity as
a result of trauma, aortic aneurysm, or cardiac
surgery.
• The increased fluid causes external compression of
the heart, which decreases venous return and CO.

8. The Myocardium
P Cells
• Pacemaker cells
– Responsible for generation of action
potentials
– electrical activity
Cardiomyocytes
• Myocardial Cells
– Contractile cells that generate force
– Mechanical activity

9. Myocardial Cardiac Cell Types
Fibroblasts
• Cells residing in the
extracellular mix
Endotehlial & Smooth
Muscle Cells
• Cells found in the blood
vessels

10. Atria & Ventricles
Right Atrium
Left Atrium
Right Ventricle
Left Ventricle

11. Heart Valves
Right:
Tricuspid
Pulmonic
Left:
Bicuspid (Mitral)
Aortic

12. Valvular Structures
Leaflets
AV Valves
(2 or 3)
Semilunar
(3)

13. Additional Valvular
Structures
Help to keep A-V valves closed during ventricular systole

14. Blood Vessels
Aorta (A & D)
SVC
IVC
Pulmonary Artery
Pulmonary Vein

15. Coronary Arteries
Anterior View

16. Coronary Arteries
Posterior View

19. Coronary Blood Flow
Coronary filling
occurs during
ventricular
Diastole

20. Coronary Blood Flow
An increase in
heart rate
shortens
diastole and can
decrease
myocardial
perfusion

21. Coronary Blood Flow
RCA Blood Supply:
(a) Originates behind the right
coronary cusp of the aortic valve
(b) Supplies
• Right atrium and Right ventricle
• SA Node and AV node
• Inferior-posterior wall of the LV
(in 90% of hearts)
• Inferior-posterior third of the
intraventricular septum

22. Coronary Blood Flow
LCA Blood Supply:
Divides into the Anterior Descending
Artery & Circumflex Artery
• Left atrium
• Most of the left ventricle
• Most of the
intraventricular septum

23. Coronary Blood Flow
Cardiac veins lie
superficially to the
arteries
The largest vein, the
coronary sinus
empties into to the
right atrium

24. Coronary Blood Flow
Most of the major
cardiac veins empty
into the coronary sinus
However, the anterior
cardiac veins empty
into the right atrium

25. Pumping Action of the Heart
Diastole:
Atrial Contraction
(ventricular muscle relaxation)
Pressure Greater in the Atria
A-V Valves Open
Ventricles Fill

26. Pumping Action of the Heart
Atrial Contraction → 10% to 20%
left ventricular filling
Pulmonary Veins passively fill left
ventricle while mitral valve is open

27. Pumping Action of the Heart
In elevated heart rates Atrial
Contraction → 40% left ventricular
filling
A.K.A. Atrial Kick

28. Pumping Action of the Heart
End-Diastolic Volume (EDV)
Amount of blood in ventricular
volume right before systole occurs
Left Ventricular EDV is
approximately 120 ml

29. Aortic Valve Opens Aortic Valve Closes
AV AV
Valve S1 S2 Valve
Closes Opens

30. Pumping Action of the Heart
Ventricular Contraction
Systole:
(relaxation of atrial muscles)
Pressure Greater in Ventricles than
Aortic & Pulmonic Blood Vessels
Aortic & Pulmonic Valves Open
Blood Ejected into Vessels

31. Pumping Action of the Heart
Stroke Volume
The amount of blood ejected by the left or
right ventricle at each heartbeat.
The amount varies with age, sex, and exercise
but averages 60 to 80 ml.
EDV = LVEDV - LVESV
(Taber’s Medical On-line Dictionary)

32. Pumping Action of the Heart
Cardiac Output
The amount of blood discharged
from the left or right ventricle per
minute.
(Taber’s Medical On-line Dictionary)

34. Pumping Action of the Heart
Ejection Fraction
The percentage of the blood emptied
from the ventricle during systole
The left ventricular ejection fraction
averages 60% to 70% in healthy hearts
(Taber’s Medical On-line Dictionary)
Normal LV EF = 50% to 75%
EF = Ventricular EDV/EDV x 100

35. Pumping Action of the Heart
Cardiac Output is
determined by:
Preload
Contractility
Afterload
Heart Rate
(Core Curriculum for Progressive Care Nurses, p. 138)

36. Pumping Action of the Heart
Preload
Stretching of the muscle fibers in the
ventricle. Results from blood volume in
the ventricles at diastole (EDV).
(Comerford & Mayer, 2007, p. 15)
…Refers to the degree of stretch of the
cardiac muscle fibers at the end of
diastole
(Smeltzer et al, 2008, p. 786)

37. Frank-Starling Mechanism
Preload is described by the
Frank-Starling Mechanism
A.K.A.
Frank-Starling Law of the Heart
or
Starling’s Law

38. Frank-Starling Mechanism
In the intact heart, this means that
the force of contractions will increase
as the heart is filled with more blood
and is a direct consequence of the
effect of an increasing load on a
single muscle fiber.

39. Frank-Starling Mechanism
The Rubber Band Effect
The farther a rubber band is
stretched, the farther it will go!!

40. Preload
Increased Preload Occurs With:
• Increased circulating volume
• Venous constriction (decreases venous pooling
and increases venous return to the heart)
• Drugs: Vasoconstrictors

41. Preload
Decreased Preload Occurs With:
• Hypovolemia
• Mitral stenosis
• Drugs: Vasodilators
• Cardiac Tamponade
• Constrictive Pericarditis

42. Pumping Action of the Heart
Contractility
Refers to the inherent ability of the
myocardium to contract normally
It is directly influenced by preload
The greater the stretch, the more
forceful the contraction
(Comerford & Mayer, 2007, p. 15)

43. Contractility
Increased Contractility Occurs With:
• Drugs: Positive inotropic agents
– digoxin, milrinone, epinephrine, dobutamine
• Increased heart rate
– Bowditch’s phenomenon
• Sympathetic stimulation
– via ß1-receptors

44. Contractility
Decreased Contractility Occurs With:
• Drugs: Negative inotropic agents
– Type 1A antiarrhythmics, ß-Blockers, CCBs,
barbituates
• Hypoxia
• Hypercapnia
• Myocardial ischemia
• Metabolic acidosis

45. Pumping Action of the Heart
Afterload
Refers to the pressure that the
ventricular muscles must generate to
overcome the higher pressure of the
aorta to the blood out of the heart
(Comerford & Mayer, 2007, p. 15)

46. Afterload
Increased Afterload Occurs With:
• Aortic stenosis
• Peripheral arteriolar vasoconstriction
• Hypertension
• Polycythemia
• Drugs: Arterial vasoconstrictors

47. Afterload
Decreased Afterload Occurs With:
• Hypovolemia
• Sepsis
• Drugs: Arterial vasodilators

48. Heart Rate
Influenced By Many Factors:
• Blood volume status
• Sympathetic & Parasympathetic Tone
• Drugs
• Temperature
• Respiration
• Dysrhythmias
• Peripheral Vascular Tone
• Emotions
• Metabolic Status (includes hyperthyroidism)

49. Heart Rate
Determinant of Myocardial O2 Supply
& Demand:
• Increased heart rates increase myocardial
oxygen demand
• Fast heart rates (> 150 bpm) decrease diastolic
coronary blood flow (shorter diastole)

50. Ventricular Function Curve

52. Pumping Action of the Heart
Systemic Vascular Resistance
Also affects cardiac output…
The resistance against which the left
ventricle must pump to move blood
throughout systemic circulation
(Comerford & Mayer, 2007, p.13)

53. Pumping Action of the Heart
Systemic Vascular Resistance
Can be affected by:
• Tone and diameter of the blood vessels
• Viscosity of the blood
• Resistance from the inner lining of the
blood vessels
(Comerford & Mayer, 2007, p.13)

54. Pumping Action of the Heart
Systemic Vascular Resistance
SVR has an inverse relationship to CO
If SVR decreases, CO increases
If SVR increases, CO decreases
SVR = mean arterial pressure – central venous pressure x 80
cardiac output
(Comerford & Mayer, 2007)

55. Pumping Action of the Heart
Systemic Vascular Resistance
Conditions that cause an increase in SVR:
• Hypothermia
• Hypovolemia
• Pheochromocytoma
• Stress response
• Syndromes of low CO

56. Pumping Action of the Heart
Systemic Vascular Resistance
Conditions that cause a decrease in SVR:
• Anaphylactic and neurogenic shock
• Anemia
• Cirrhosis
• Vasodilation

57. Blood Vessels
• About 60,000 miles of
arteries, aterioles, capillaries,
venules, and veins keep blood
circulating to and from every
functioning cell in the body!
• There is approximately 5
liters of total circulating
blood volume in the adult body

58. Blood Vessels
Five Types:
Arteries
Arterioles
Capillaries
Venules
Veins

59. Arteries
• Strong, compliant elastic-walled
vessels that branch off the aorta,
carry blood away from the heart,
and distribute it to capillary beds
throughout the body
• A high-pressure circuit
• Able to stretch during systole
and recoil during diastole
because of the elastic fibers in
the arterial walls

60. Arterial Baroreceptors
• These are receptors that
are sensitive to arterial wall
stretching
• Located in the aortic arch
and near the carotid
sinuses
• Responsible for modulation
of vascular resistance and
heart rate in order to
maintain appropriate BP
• Keep MAP constant

61. Arterial Baroreceptors
Vasomotor Center:
• In high blood pressures,
the aortic arch and carotid
sinus stretch
• When stretching is sensed,
a message is sent via the
vagus nerve (aortic arch)
and the glossopharyngeal
nerve (carotid sinus)

62. Arterial Baroreceptors
• Inhibition of SNS outflow to
the peripheral blood vessels
& Stimulates the PNS
• Blood Pressure Decrease by:
– Vasodilation of peripheral
vessels
– Decrease in HR & contractility
– Decrease SVR

63. Arterial Baroreceptors
• Responsible for short-term
adjustment of BP
• Respond to abrupt
fluctuations in BP (postural
changes)
• Less effective in long-term
regulation of BP
– Reset or become insensitive
when subjected to prolonged
elevated BP

64. Arterial Baroreceptors
In low blood pressures:
• SNS is stimulated & PNS is
inhibited
• Blood Pressure Increased by:
– Increased HR & Contractility
– Peripheral Arterial & Venous
Constriction
• Preserves blood flow to the brain &
heart

65. Arterioles
• Control systemic vascular
resistance and thus arterial
pressure
• Lead directly into capillaries
• Have strong smooth
muscle walls innervated by
the ANS

66. Arterioles
Autonomic Nervous System
• Adrenergic (Stimulatory) System
– 2 Neurotransmitters
• Epinephrine: stimulates β-receptors which increases
heart rate and contractility and causes arteriolar
vasodilation
• Norepinephrine: stimulates α-receptors which
results in vasoconstriction

67. Arterioles
Autonomic Nervous System
• Cholinergic (Inhibitory) System
– 1 Neurotransmitter
• Acetylcholine: Decreases heart rate; releases nitric
oxide causing vasodilation

68. Capillaries
Microscopic
Walls are composed of only a single layer of
endothelial cells

69. Capillaries
Capillary pressure is extremely low
to allow for exchange of
nutrients, oxygen, and carbon
dioxide with body cells

70. Sphincters
At the ends of the arterioles and beginning
of capillaries
• Dilate to permit blood flow
• Constrict to increase blood pressure
• Close to shunt blood

71. Venules
Gather blood
from capillaries
Walls are thinner
than those of
arterioles

72. Veins
Thinner walls than
arteries
Large diameters
because of the
low blood
pressure of
venous return to
the heart

73. Veins
Valves prevent backflow
Pooled blood in each valve
segment is moved toward
the heart by pressure
from the moving volume
of blood in the previous
valve segment

74. Veins
Most veins
return blood
to the right
atrium of the
heart

75. Blood pressure
regulation is
maintained via
vasodilation or
vasoconstriction
of the arterial
vessels

76. Function of Blood Vessels
What is the function of blood vessels???
• Distribution of blood throughout the body
– Supplies all cells w/ O2 & nutrients
– Removes metabolic waste & CO2
• Provides a conduit for hormones, cells of the
immune system, & regulation of body
temperature
FYI – The lymphatic system is a parallel circulatory
system that functions to return excess
interstitial fluid to the heart

77. Blood Pressure Regulation
Resistance Vessels
Dilation of arteries (resistance vessels) =
decrease in cardiac afterload
Arteriolar dilators reduce cardiac workload
while causing cardiac output and tissue
perfusion to increase

78. Blood Pressure Regulation
Capacitance Vessels
Dilation of veins (capacitance vessels) =
reduced force of blood return to the
heart thus decreasing preload
Results in decreased force of ventricular
contraction and oxygen consumption,
decreased cardiac output and tissue
perfusion

79. Renin-Angiotensin-Aldosterone
System
Blood Pressure Regulatory
Mechanism

80. R-A-A-S
Renin
a.k.a. angiotensinogenase
Converts angiotensinogen to
angiotensin I

81. R-A-A-S
Angiotensin I
Has no biological activity
Exists solely as a precursor to
angiotensin II

82. R-A-A-S
Angiotensin II
Angiotensin I is converted into
angiotensin II by the angiotensin-
converting enzyme
Potent vasoconstrictor
Also acts on the adrenal cortex in
releasing aldosterone

83. R-A-A-S
Aldosterone
Regulates sodium and potassium in
the blood – retain sodium &
excrete potassium
Release triggered by increased
levels of angiotensin II, ACTH,
and potassium

84. References
Comerford, K.C., & Mayer, B.H. (Eds.). (2007). Hemodynamic
monitoring made incredibly visual. Ambler, PA: Lippincott,
Williams, and Wilkins.
Donofrio, J., Haworth, K., Schaeffer, L., & Thompson, G. (Eds.).
(2005). Cardiovascular care made incredibly easy. Ambler, PA:
Lippincott, Williams, and Wilkins.
Smeltzer et al. (2008). Brunner and suddarth’s textbook of
medical-surgical nursing, (11th ed.). Philadelphia, PA: Lippincott
Williams and Wilkins.
Woods, S. L., Froelicher, E. S., Underhill Motzer, S., & Bridges, E.
J. (2005). Cardiac nursing, (5th ed.). Philadelphia, PA: Lippincott
Williams & Wilkins.