Cardiovascular Physiology

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Cardiovascular Physiology
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Electrophysiology of the Heart

• Action Potentials
• Conduction Pathways
• EKGs

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Autorhythmic Cardiac AP

• Phase 4 Depolarization
• only SA, AV, His/P
• I(f) - Funny current, now thought to be inward
  Na
• Phase 0 Depolarization
• due to Ca influx
• (L-type)
• Officially, no phase 1 or 2
• Phase 3 Repolarization
• Due to K permeability

0
3
4
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Myocardial Action Potential

• 0 Na influx (voltage-gated)
• 1 Na inactivation and K (IK) outward
• 2 slow inward Ca2
• 3 Ca2 inactivation and K outward (IK1)

ARP
RRP
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EKG Waves and Intervals
QRS length
R
T
P
Q
S
Normal PR interval 0.12-0.2 sec QRS length
lt0.10 sec QT interval 0.3-0.4
sec Abnormalities in QRS ventricular
depolarizaton problems P-R interval A/V
conduction problems
P-R interval
Q-T interval
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EKG Reading
0.2 sec
0.04 sec
1.0 mV Test pulse
HR 1500/ small boxes between QRS complexes
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EKG Axis Determination
Late Ventricular Depolarization
Atrial Depolarization
Septal Depolarization
Apical Depolarization
Repolarization
Lead I
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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.

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Abnormalities

• Rate
• Sinus bradycardia lt60 BPM at rest
• Sinus tachycardia gt100 BPM at rest
• A/V Heart Block
• 1st degree P/R interval gt 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

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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
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Caridac Pump Dynamics

• Cardiac Cycle
• Pressure
• Flow
• Resistance
• Elastance/Compliance

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Starlings 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.

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Length Tension Relationship
Operating Range
Tension Max
Active Tension
Resting Tension
100
50
2.2
1.5
3.0
Sarcomere Length mm
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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.

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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 b1 agonists or cardiac glycosides (digoxin)

Inhibit Na/K ATPase Decrease Ca export
Increases inward Ca Causes PLB phosphorylation Act
ivates SERCA
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Measuring Contractility
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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 of Ca
  flux through the channels and a greater net
  calcium influx into the cell.
• As sarcomeres shorten, they become less
  responsive to an increase in Ca. So, positive
  inotropic effects work best on a heart that is
  working under stress.

PK-A
More Ca avail. for later.
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LV pressure/volume loops
Normal
Positive Inotropy
When does the aortic valve open? When is the 2nd
heart sound?
Increased Afterload
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Electrical-Pump Coupling Diagram
e
d
c

• Atrial contraction causes increased atrial and
  ventricular pressure.
• Mitral valve closes (1st heart sound),
  isovolumetric contraction begins.
• Aortic valve opens, aortic pressure equals LV
  pressure.
• Systolic pressure
• Aortic valve closes (second heart sound),
  isovolumetric relaxation begins
• Mitral valve opens

b
f
a
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PV Loop and Cardiac Cycle
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Cardiac and vascular function Curves
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Questions
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Questions
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Pulse Pressure
Pulse Pressure SP-DP
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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

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Supine vs Standing
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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

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Central Chemoreceptors
pO2
pCO2
H
Central Chemoreceptors
Sympathetic Outflow
Contractility, VR, Respiration, Blood Pressure,
etc
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Important Formulas

• - COHR x SV VR in most pts.
• - 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 VolumeEDV-ESV
• - Ejection Fraction SV/EDV. Normal EF is
  0.5-0.75
• - Starling J(mL/min) K(Pc-Pi)-(pc-pi)
• - Ficks CO O2 Uptake / (Arterial O2 -
  Venous O2)

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Resistance

• Parallel
• Most vascular beds
• Lower total Resistance
• Independent control
• Series
• Sequential pressure drops
• Portal circulations(Hepatic, Hypothalamic
  Hypophyseal, etc)

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Vasoactive Substances

• Local
• Metabolites (adenosine, K, CO2)
• Neurotransmitters (a1- constriction, b2-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

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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

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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

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Congestive Heart Failure

• Left Ventricle cant 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

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Acute Blood Loss/Hemorrhagic Shock
Blood Loss
Decreased Ven. Return
CO, MAP Decrease
Compensation
Decompensation
Cardiac Hypoperfusion/Failure Decreased CO due
to LV ischemia Acidosis Due to lactate
buildup Further depresses CO CNS Depression
Medullary blood flow decrease leads to
inhibition of CV centers Clotting Dysfunctions
Pro-coag during early shock Anti-coag during
late shock
Baroreceptor reflexes arteriolar
vasoconstriction Chemoreceptor reflexes due to
hypoxia Cerebral ischemic response causes
further symp. response Increased capillary fluid
reabsorption tissue fluid is
re-absorbed Endogenous vasoconstrictors Epi,
Ang II, Vasopressin RAAS Dec. renal perfusion
activates renin, increases ang II, aldo