Cardiovascular Physiology

Electrophysiology of the Heart

• Action Potentials
• Conduction Pathways
• EKG’s
Autorhythmic Cardiac AP
•Phase 4 Depolarization
• only SA, AV, His/P
0 •I(f) - “Funny” current, now
3 thought to be inward Na+
4 •Phase 0 Depolarization
• due to Ca++ influx
•(L-type)
•Officially, no phase 1 or 2
•Phase 3 Repolarization
•Due to K+ permeability
Myocardial Action Potential
• 0 – Na+ influx
(voltage-gated)
• 1 – Na+ inactivation
and K+ (IK) outward
• 2 – slow inward Ca2+
ARP
• 3 – Ca2+ inactivation
RRP
and K+ outward (IK1)
EKG Waves and Intervals
QRS length

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
 EKG Reading
0.2 sec
0.04 sec

1.0 mV
Test pulse

HR = 1500/ small boxes between QRS complexes

 EKG Axis Determination

Late
Atrial Septal Apical Ventricular Repolarization
Depolarization Depolarization Depolarization Depolarization

Lead
I:
 Determining Mean Electrical Axis
• Use 2 different leads
• Measure the sum of the height and the negative depth of
the QRS complex
• Measure that vaule in mm onto the axis of the lead and
draw perpendicular lines
• The intersection is at the angle of the mean axis.
 Abnormalities
• Rate:
– Sinus bradycardia: <60 BPM at rest
– Sinus tachycardia: >100 BPM at rest
• A/V Heart Block:
– 1st degree: P/R interval > 0.2 sec (slow AV node)
– 2nd degree (Mobitz):
• Type 1 (Wenckebach): slowly increasing PR interval
until dropped QRS complex
• Type 2: Sudden dropped QRS
– 3rd degree (complete): no correlation between P
and QRS waves
 1st Degree AV Block- increased P-R interval

2nd Degree (Wenckebach)- increased P-R, then no QRS

2nd Degree (Mobitz II)- Isometric P-R, then no QRS

3rd Degree Preceded by Ventricular Escape

no block
 Caridac Pump Dynamics
• Cardiac Cycle
• Pressure
• Flow
• Resistance
• Elastance/Compliance
 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.
Length Tension Relationship
Operating
Range
Tension %

Active Resting
Tension Tension
100
Max

50

1.5 2.2 3.0

Sarcomere Length
m
 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.
 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1 agonists or cardiac glycosides (digoxin)

Increases inward Ca Inhibit Na/K ATPase

Causes PLB phosphorylation Decrease Ca export
Activates SERCA
 Measuring Contractility

Isovolumic LV
Pressure Adrenergic
Stimulation
120
120
mm Hg

Tension
Control
60
60 Acidosis

0
0
LV Volume

EDV
Time
Contractility Modified by:
ESV Time
Autonomic Nerves and
Neurohumors; Heart Rate;
Chemical Environment and
drugs
 Mechanisms of increased
contractility= regulation of [Ca++]
– The more crossbridges
between actin and myosin are
present, the higher the
contractility.
– PK-A phosphorylates the Ca
channels through which Ca
leaves the SR and enters the
myoplasm from the T-tubules..
This causes a greater amount PK-A
of Ca flux through the
channels and a greater net
calcium influx into the cell.
– As sarcomeres shorten, they
become less responsive to an More Ca++
increase in Ca++. So, positive avail. for
inotropic effects work best on later.
a heart that is working under
stress.
 LV pressure/volume loops
Normal Positive Inotropy

When does the

aortic valve open?
Increased Afterload
When is the 2nd heart
sound?
 Electrical-Pump
e Coupling Diagram
d
c
a. Atrial contraction
causes increased atrial
and ventricular
a b f
pressure.
b. Mitral valve closes (1st
heart sound),
isovolumetric
contraction begins.
c. Aortic valve opens,
aortic pressure equals
LV pressure.
d. Systolic pressure
e. Aortic valve closes
(second heart sound),
isovolumetric relaxation
begins
f. Mitral valve opens
PV Loop and Cardiac Cycle
Cardiac and vascular function Curves
Questions
Questions
Pulse Pressure

Pulse Pressure = SP-DP

 Normal Pressures

– Right Atrium (Vena Cava)- 5 (systolic)/3

(diastolic) mmHg
– Left Atrium (Pulmonary veins) 10/8
– Right Ventricle – 28/3
– Left Ventricle –125/8
– Aorta- 120/70
Supine vs Standing
 Controlling Arterial Pressure
• Increasing TPR, SV, or HR increases Mean
Art. Pressure.
• Increasing Arterial compliance reduces MAP.
• Baroreceptors
– Aortic Arch, Carotid Body – sense drastic changes
in blood pressure, send impulse through CN IX and
X to depressor centers and cardiac inhibitory
centers
• Peripheral chemoreceptors
– Also in aorta and carotid - pO2 detectors increase
blood pressure in times of low pO2
 Central Chemoreceptors
pO2 pCO2 H+

Central Chemoreceptors

Sympathetic Outflow

Contractility, VR, Respiration,

Blood Pressure, etc
 Important Formulas
- CO=HR x SV = VR in most pts.
8l
Resistance 
 r 4

- Tension =(Pressure inside the chamber x radius)

(2 x wall thickness)
More generally, T ~ P x R
- Mean Art. P. = (1/3 Pulse P.) + Diast. P
- Stroke Volume=EDV-ESV
- Ejection Fraction= SV/EDV. Normal EF is 0.5-0.75
- Starling: J(mL/min) =K[(Pc-Pi)-(c-i)]
- Fick’s :CO = O2 Uptake / ([Arterial O2] - [Venous O2])
 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)
 Vasoactive Substances
• Local
– Metabolites (adenosine, K+, CO2)
– Neurotransmitters (1- constriction, 2-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
 Hyperemia
• Active Hyperemia: increased blood flow to
meet metabolic demands
– Exercising muscle
– Active neurons
• Reactive Hyperemia: Increased blood flow
occurring after a period of inadequate
blood flow
– Heart after contraction
– Transient Ischemic Attack
 Special Circulations
• Coronary: Mainly metabolic control.
– vessels narrow during systole due to mechanical compression
• Cerebral: Mainly metabolic.
• Muscle: Metabolic and sympathetic during
exercise, both symp and some para fibers
– muscular activity moves venous blood back to heart
• Skin: Sympathetic, Temperature regulated
– Cold- vasoconstriction of arterioles, AV shunts take over
– Warmth- vasodilation of arterioles
• Fetal: Anatomical Shunts
– Ductus Arteriosus, Foramen Ovale, Ductus Venosus
 Congestive Heart Failure
• Left Ventricle can’t pump blood properly
• Causes:
– HTN, CAD, Alcohol, others
– Lead to dilation of the chamber and thinning
of the ventricular walls
• Law of LaPlace- a dilated heart needs
more tension to generate a given pressure
• Symptoms: Pulmonary Congestion
(edema), dyspnea, orthopnea
 Acute Blood Loss/Hemorrhagic Shock
Decreased
Blood Loss
Ven. Return

CO, MAP
on Decrease Decompensa
Compensati ti on
Cardiac Hypoperfusion/Failure
Baroreceptor reflexes Decreased CO due to LV
arteriolar vasoconstriction ischemia

Chemoreceptor reflexes Acidosis

due to hypoxia Due to lactate buildup
Further depresses CO
Cerebral ischemic response
causes further symp. response CNS Depression
Medullary blood flow decrease
Increased capillary fluid leads to inhibition of CV centers
reabsorption
tissue fluid is re-absorbed Clotting Dysfunctions
Pro-coag during early shock
Endogenous vasoconstrictors Anti-coag during late shock
Epi, Ang II, Vasopressin

RAAS
Dec. renal perfusion activates
renin, increases ang II, aldo