2. OBJECTIVES
• Explain the physiology of circulation and
perfusion
• Describe the electrical and mechanical events
involved in the cardiac cycle.
• Discuss the factors that alter or impact the
electrical and mechanical events of the
cardiac cycle.
3. Definition
Cardiovascular physiology is the study
of the circulatory system. More
specifically, it addresses the
physiology of the heart ("cardio") and
blood vessels ("vascular").
4. HEART
(PUMP)
AUTOREGULATION
REGULATION
CARDIOVASCULAR
SYSTEM NEURAL
HORMONAL
VESSELS
(DISTRIBUTION SYSTEM) RENAL-BODY FLUID
CONTROL SYSTEM
7. Cardiac Pump Dynamics
• Overview on Anatomy of the heart.
• Electrophysiology of the heart
• Cardiac Cycle
• Pressure
8. Overview on Histo- Anatomy of the Heart:
• cardiac muscle fibers are relatively short, thick branched cells,
50-100 μm long
• striated myofibrils are highly ordered usually 1 nucleus per
cell and rather than tapering cells are bluntly attached to
each other by gap junctions (intercalated discs)
• myocardium behaves as single unit and atrial muscles
separated from ventricular muscles by conducting tissue
sheath (atria contract separately from ventricles)
• need constant supply of oxygen & nutrients to remain
aerobic and hence greater dependence on oxygen than
skeletal muscles
9. • cardiac muscle cells are not individually innervated like
skeletal muscle cells, they are self stimulating
• rhythmic beating of the heart is coordinated and maintained
by the heart conducting system
• heart has some specialized fibers that fire impulses to
coordinate contraction of heart muscle innervated by
autonomic NS
• sympathetic stimulation can raise rate
• parasympathetic stimulation can lower rate
10. Electrical cells Muscle (myocardial) cells
•Generate and conduct •Main function is
impulses rapidly contraction
Atrial muscle
•SA and AV nodes Ventricular muscle
Able to conduct electrical
•Nodal pathways
impulses
•Interventricular septum
•May generate its own
•No contractile Properties impulses with certain types
of stimuli
13. Overview on Nerve Terms
Resting state
• The relative electrical charges found on each
side of the membrane at rest
Net +ve charge on the outside
Net -ve charge on the inside
Action Potential
• Change in the electrical charge caused by
stimulation of a neuron
16. Summary of APs
Resting Depolarization Repolarization
Sodium stays The stimulus Sodium channels
outside of the cell hits the cell close
Potassium
Potassium Sodium channels Open-
mostly stays inside channels open up Potassium pours out
and sodium pours Allows for a quick
Massively in then the return to a resting
negative charges charges reverse: state
never leave the Positive inside
Negative outside Sodium is kicked
cell out of the cell- Active
transport Sodium-
potassium pump
17. OVERVIEW ON ECG
P wave = passage of current through atria from SA Node (conduction through
atria is very rapid)
QRS wave = passage of current through ventricles from AV Node – AV Bundle –
Purkinje Fibers (impulse slows as it passes to ventricles)
T wave = return to “resting” conditions
ECG is a record of the electrical activity of the conducting system.
ECG is NOT a record of heart contractions
18. EKG Waves and Intervals
QRS length
R
T
P
Q S
Normal: PR interval: 0.12-0.2 sec
P-R QRS length: <0.10 sec
interval
QT interval: 0.3-0.4 sec
Q-T interval
Abnormalities in:
QRS – ventricular
depolarizaton problems
P-R interval – A/V
conduction problems
19. Pediatric Vs Adult ECGs
• Pediatric ECGs findings that may be normal:
• HR >100BPM
• Shorter PR, QT Int and QRS Duration
• Inferior and Lateral small Q waves
• RV Larger than LV in neonates, so:
RAD
Large Precordial R Waves
Upright T Waves
20. ECG Recordings (QRS Vector pointing leftward, inferiorly
& posteriorly)
3 Bipolar Limb Leads:
RA LA
I = RA vs. LA (+)
LL
21. ECG Recordings (QRS Vector pointing leftward, inferiorly
& posteriorly)
3 Bipolar Limb Leads:
RA LA
I = RA vs. LA (+)
II = RA vs. LL (+)
LL
22. ECG Recordings (QRS Vector pointing leftward, inferiorly
& posteriorly)
3 Bipolar Limb Leads:
RA LA
I = RA vs. LA (+)
II = RA vs. LL (+)
III = LA vs. LL (+)
LL
23. ECG Recordings (QRS Vector pointing leftward, inferiorly
& posteriorly)
3 Bipolar Limb Leads:
RA LA
I = RA vs. LA (+)
II = RA vs. LL (+)
III = LA vs. LL (+)
3 Augmented Limb Leads:
LL
aVR = (LA-LL) vs. RA(+)
24. ECG Recordings (QRS Vector pointing leftward, inferiorly
& posteriorly)
3 Bipolar Limb Leads:
RA LA
I = RA vs. LA (+)
II = RA vs. LL (+)
III = LA vs. LL (+)
3 Augmented Limb Leads:
LL
aVR = (LA-LL) vs. RA(+)
aVL = (RA-LL) vs. LA(+)
25. ECG Recordings (QRS Vector pointing leftward, inferiorly
& posteriorly)
3 Bipolar Limb Leads:
RA LA
I = RA vs. LA (+)
II = RA vs. LL (+)
III = LA vs. LL (+)
3 Augmented Limb Leads:
LL
aVR = (LA-LL) vs. RA(+)
aVL = (RA-LL) vs. LA(+)
aVF = (RA-LA) vs. LL(+)
27. ECG Recordings: (QRS vector---leftward, inferiorly and posteriorly
3 Bipolar Limb Leads
I = RA vs. LA(+)
II = RA vs. LL(+)
III = LA vs. LL(+)
3 Augmented Limb Leads
aVR = (LA-LL) vs. RA(+)
aVL = (RA-LL) vs. LA(+)
aVF = (RA-LA) vs. LL(+)
6 Precordial (Chest) Leads: Indifferent electrode (RA-LA-LL) vs.
chest lead moved from position V1 through position V6.
29. THE HEART AS A PUMP
• REGULATION OF CARDIAC OUTPUT
– Heart Rate via sympathetic & parasympathetic
nerves
– Stroke Volume
• Frank-Starling “Law of the Heart”
• Changes in Contractility
• MYOCARDIAL CELLS (FIBERS)
– Regulation of Contractility
– Length-Tension and Volume-Pressure Curves
– The Cardiac Function Curve
30. Autoregulation
(Frank-Starling “Law of the Heart”)
CARDIAC OUTPUT = STROKE VOLUME x HEART RATE
Contractility
Sympathetic
Nervous System
Parasympathetic
Nervous System
31. THE CARDIAC CYCLE
LATE DIASTOLE
DIASTOLE
ISOMETRIC
VENTRICULAR
RELAXATION ATRIAL
SYSTOLE
VENTRICULAR
EJECTION ISOMETRIC VENTRICULAR
CONTRACTION
33. D
HEART
SE ITY
EA IL
CR ACT SYSTOLIC PRESSURE CURVE
IN TR
N
CO
Isotonic (Ejection) Phase
After-load
Isovolumetric
PRESSURE
Phase
Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE
End Systolic Volume End Diastolic Volume
34. D
HEART
ASE ITY
C RE CTIL SYSTOLIC PRESSURE CURVE
DE TRA
N
CO
Isotonic (Ejection) Phase
After-load
Isovolumetric
PRESSURE
Phase
Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE
End Systolic Volume End Diastolic Volume
35. HEART
IN ED
LL S
SYSTOLIC PRESSURE CURVE
FI EA
G
CR
IN
Isotonic (Ejection) Phase
After-load
Isovolumetric
PRESSURE
Phase
Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE
End Systolic Volume End Diastolic Volume
36. Influences of the Cardiac Cycle
Master controller: the medulla
Incoming input
• Chemoreceptors- Sense changes in pH, PaCO2
and PaO2
• Baroreceptors- Sense changes in arterial
pressure
Response of the medulla
• Stimulate the autonomic nervous system
37. Autonomic Nervous System
Sympathetic Nervous System- Extensively
innervates the SA node and ventricular cells
Increase in heart rate
Increase in conduction and contractility in the
ventricles
Parasympathetic Nervous System- Innervates
the SA and AV nodes
• Decreases heart rate
• Decreases conduction times through the AV node
38. Hormones
• Epinephrine & Norepinephrine
– From the adrenal medulla
• Renin-angiotensin-aldosterone
– Renin from the kidney
– Angiotensin, a plasma protein
– Aldosterone from the adrenal cortex
• Vasopressin (Antidiuretic Hormone-ADH)
– ADH from the posterior pituitary
39. Determination of Stroke Volume
Preload
• Amount of blood delivered to the chamber
• Depend upon venous return to the heart
• Also dependent upon the amount of blood delivered
to the ventricle by the atrium
Contractility
• The efficiency and strength of contraction
• Frank Starling’s Law
Afterload
• Resistance to forward blood flow by the vessel walls
40. Preload and Afterload
• Preload: Wall tension at EDV (analogous to EDV or
EDP
– As Preload increases, so does Stroke Volume. This is a
regulatory mechanism.
– Factors that increase venous return, or preload:
• the muscular pump (muscular action during exercise compresses
veins and returns blood to the heart), an increased venous tone,
and increased total blood volume.
• Afterload: A sum of all forces opposing ventricular
ejection. Roughly measured as Aortic Pressure.
– As Afterload increases, stroke volume decreases.
41. Starling’s Law of the Heart
• The heart adjusts its pumping rate to the rate of
blood return. How?
– More blood returning stretches the atria and ventricles
more.
– Stretching heart SA node muscle causes faster rhythmicity.
– Stretching heart muscle causes faster conduction.
– Stretching heart muscle causes stronger, more complete
contraction.
42. Contractility
• Increased by increasing myocardial Ca++
• Means greater shortening of fibers at a given
fiber length.
• Increased contractility = Increased CO (SV)
– Positive Inotropy:
• Increased HR (more Ca++ in the cell)
• using β1 agonists or cardiac glycosides (digoxin)
Increases inward Ca Inhibit Na/K ATPase
Causes PLB phosphorylation Decrease Ca export
Activates SERCA
43. CARDIAC FUNCTION CURVE
THE FRANK- STARLING “LAW OF THE HEART”
15-
10-
CARDIAC OUTPUT (L/min)
Pressure
5-
Volume
-4 0 +4 +8
RAP mmHg
44. CARDIAC FUNCTION CURVE
THE FRANK- STARLING “LAW OF THE HEART”
15-
Inc
Co rease
ntr
act d
ilit
y
10-
CARDIAC OUTPUT (L/min)
5-
-4 0 +4 +8
RAP mmHg
45. CARDIAC FUNCTION CURVE
THE FRANK- STARLING “LAW OF THE HEART”
15-
De
c
Co reas
ntr e d
act
ilit
y
10-
CARDIAC OUTPUT (L/min)
5-
-4 0 +4 +8
RAP mmHg
46. CARDIAC FUNCTION CURVE
THE FRANK- STARLING “LAW OF THE HEART”
15-
Inc
He rease
art d
Ra
te
10-
CARDIAC OUTPUT (L/min)
5-
-4 0 +4 +8
RAP mmHg
47. CARDIAC FUNCTION CURVE
THE FRANK- STARLING “LAW OF THE HEART”
15-
De
c
He reas
art ed
Ra
te
10-
CARDIAC OUTPUT (L/min)
5-
-4 0 +4 +8
RAP mmHg
50. Flow
• Blood circulates by going down a pressure
gradient
• to understand circulation we must understand
blood pressure
51. Blood Pressure
Blood Pressure is created by
1. The force of the heart beat
• the heart maintains a high pressure on the
arterial end of the circuit
2. Peripheral resistance
• back pressure, resistance to flow
• eg atherosclerosis inhibits flow so raises
blood pressure
52. Control of Blood Pressure
• Baroreceptor
• Baroreflex
• Renin-angiotensin system
– Renin
– Angiotensin
• Juxtaglomerular apparatus
• Aortic body and carotid body
• Autoregulation
53. MOTOR CORTEX
HYPOTHALAMUS Sympathetic
Chemosensitive Area Nervous
System
VASOMOTOR CENTER
PRESSOR AREA
Glossopharyngeal DEPRESSOR AREA
Nerve
CARDIOINHIBITORY AREA
Vagus
Baroreceptors
Carotid Sinus
Aortic Arch HEART
Arterioles
Veins
Chemoreceptors Adrenal
Carotid Bodies
Aortic Bodies Medulla
Bainbridge Reflex (↑ Heart Rate)
Atrial Receptors Volume Reflex (↑ Urinary OUTPUT)
a. ↓ Vascular Sympathetic Tone
b. ↓ ADH Secretion
c. ↓ Aldosterone Secretion
54. Veins
• Pressure inside is 35 to 15 mmHg
• 60-70 % of the blood is in veins
• Transport of blood to heart for oxygenation
55. Flow in Veins
• Flow of blood in veins is due to way valves and
venous pumps
Way valves
• prevent backflow
• most abundant in veins of limbs
• quiet standing can cause blood to pool in veins
and may cause
56. venous pumps
Muscular pump (=skeletal muscle pump)
• during contraction veins running thru muscle are
compressed
• and force blood in one direction (toward heart)
Respiratory pump
Inspiration:
• creates pressure gradient in Inferior Vena Cava to
move blood toward heart
Expiration:
• increasing pressure in chest cavity forces thoracic
• blood toward heart
57. CAPILLARIES
• Pressure inside is 35 to 15 mmHg
• 5% of the blood is in capillaries
• exchange of gases, nutrients, and wastes
• flow is slow and continuous
59. Capillary Beds
•Capillaries ( usually 10 –100) are organized into capillary beds
•Functional groupings of capillaries functional units of
circulatory system
•Arterioles and venules are joined directly by metarterioles
(become thoroughfare channels after capillaries branch off)
•Capillaries branch from metarterioles 1-100/bed cuff of smooth
muscle surrounds origin of capillary branches = precapillary
sphincter
Amount of blood entering a bed is regulated by:
a. vasomotor nerve fibers
b. local chemical conditions
60. VASOMOTION = Intermittent flow due to constriction-
relaxation cycles of precapillary shpincters
or arteriolar smooth muscle (5 - 10/min)
AUTOREGULATION OF VASOMOTION:
1. Oxygen Demand Theory (Nutrient Demand Theory)
O2 is needed to support contraction (closure)
2. Vasodilator Theory
Vasodilator substances produced (via ↓ O2)
e.g. Adenosine → Heart
CO2 → Brain
Lactate, H+, K+ → Skeletal Muscle
3. Myogenic Activity
61. Vasoactive Substances
• Local
– Metabolites (adenosine, K+, CO2)
– Neurotransmitters (α1- constriction, β2-dilation)
– Hormones (Histamine, Bradykinin)
• General
– Renin-Angiotensin-Aldosterone System – conserves
water and salt, constricts arterioles
– ADH (Vasopressin) – vasoconstrictor and water conservation
– ANP (Atrial Natriuretic Peptide) – arteriolar dilator and
increased salt/water excretion
62. Resistance
1 1 1 1
• Parallel = +
R R1 R2
+ ⋅⋅⋅ +
Rn
– Most vascular beds
– Lower total Resistance
– Independent control
• Series R = R1 + R2 + ⋅ ⋅ ⋅ + Rn
– Sequential pressure drops
– Portal circulations(Hepatic, Hypothalamic
Hypophyseal, etc)
63. Name of % of cardiac Autoregu
Perfusion Comments
circulation output lation
pulmonary 100%
Vasoconstriction in response to hypoxia
circulation (deoxygenated)
Fixed volume means intolerance of high
cerebral circulation 15% high under-perfused pressure. Minimal ability to use
anaerobic respiration
Minimal ability to use anaerobic
respiration. Blood flow through the left
coronary artery is at a maximum during
coronary circulation 5% high under-perfused
diastole (in contrast to the rest of
systemic circulation, which has a
maximum blood flow during systole.)
Splanchnic
15% low Flow increases during digestion.
circulation
Part of portal venous system, so oncotic
hepatic circulation 15%
pressure is very low
renal circulation 25% high over-perfused Maintains glomerular filtration rate
skeletal muscular Perfusion increases dramatically during
17%
circulation exercise.
Cutaneous Crucial in thermoregulation. Significant
2% over-perfused
circulation ability to use anaerobic respiration
