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Cardiovascular
Cardiovascular
Cardiovascular
>pacemaker cells control their contraction Interval of time during which a normal cardiac
which is involuntary impulse cannot re-excite an already excited
area of cardiac muscles.
>Contraction is slow
Normal refractory period of ventricle is 0.25 to
Properties of Cardiac Muscles 0.3 seconds, which is the duration of the action
potential.
>Excitation of the heart is triggered by
Relative refractory period
electrical impulse rather than neural
transmitters. additional 0.05 second
>Contraction of the heart is triggered by During which the muscle is more difficult than
normal to excite but nevertheless can be
elevation of intracellular calcium influx
excited.
> Myocytes depend heavily on oxygen & blood
Refractory period of atrial muscle (0.15 second)
supply.
shorter than the ventricles.
> Not fatigued
And the relative refractory period is another
> Excitability Cycle 0.03 seconds.
The heart can beat on its own without the need Cardiac Cycle
for exogenous commands.
Ventricular systole -
isovolumic contraction - Reduced Ventricular Ejection
ejection
-slower ventricular ejection of blood.
Ventricular diastole -
isovolumic relaxation - rapid - atrial filling continues.
filling Cardiac Cycle
- atrial contraction Isovolumetric Ventricular Relaxation
Cardiac Cycle - Repolarization of the Ventricles is now
Atrial Systole complete (T-wave).
- after the onset of the QRS wave, which - rapid flow of blood from the atria into the
represents electrical activation of ventricles. ventricles causes the Third heart Sound (S3)
>compliant artery = small pulse pressure reflects the recovery of the channels that carry
the inward currents for the upstroke of the AP
>stiff artery = wide pulse pressure
absolute refractory period
- begins with upstroke and ends after the (SV/EDV)
plateau
loss of contractility is due to loss of functioning
- no AP can be elicited sarcomere
- the period after the absolute refractory period in skeletal muscle, the load on the muscle
when repolarization is almost complete during contraction
- an AP can be elicited, but not at full acceptable indices of afterload : mean aortic
magnitude pressure and peak left ventricular pressure
Vasopressin Microcirculation
- increases TPR (V1) and increases H2O vasoconstriction = decreased flow and pressure
reabsorption in distal tubule of kidney and >capillaries are permeable to all dissolved
collecting ducts (V2) substances via simple diffusion except plasma
Atrial Natriuretic Peptide (ANP) proteins
- increased atrial pressure = released of ANP in >the lymphatic system removes proteins in the
atria interstitial space
- causes vasodilation and decreased TPR >filtration and reabsorption are the main
processes by which fluid moves between plasma
- increases salt and water excretion (decreased and interstitium due to pressure differences
blood volume) (bulk flow)
>intrapleural pressure becomes more negative -increased by arterial dilation and venous
constriction
>increased systemic venous return
-decreased by arteriolar constriction (eg HPN)
>increased right ventricular output causing
delay in closing of pulmonic valve (splitting of Interstitial Oncotic Pressure
heart sounds)
-increased by chronic lymphatic blockage
>volume of blood in pulmonary circuit increases
-increased capillary permeability (eg. burns)
>decreased left ventricular output
Expiration
REABSORPTION
>intrapleural pressure becomes more positive
(increased) Capillary Oncotic Pressure
-increased by dehydration due to excessive Active Hyperemia
sweating
- blood flow is proportional to its metabolic
-decreased by liver and renal disease activity
- tissues that are controlled by nervous and -at rest, sympathetic control of blood flow
humoral factors originating outside the organ predominates
- cutaneous circulation and resting skeletal -during exercise, local metabolic control
muscles overrides sympathetic control (sym has no
effect on flow)
- circulating epinephrine acts on β2 receptors
causing vasodilatation -stimulation of α receptors = vasoconstriction
Renal and Splanchnic Circulation -assuming that the person is in steady state,
performing moderate exercise at sea level
- a small in blood pressure will invoke
autoregulatory mechanism to maintain renal Pulmonary Circuit
blood flow >blood flow (cardiac output) - large increase
- increased sympathetic activity (hypotension) >pulmonary arterial pressure - slight increase
causes intially vsodilatation then
vasoconstriction, and a decreased blood flow >pulmonary vascular resistance - large
decrease
- venous PO2 is high in renal circulation
>pulmonary blood volume - increase
Compensation via carotid sinus reflex will BASIC ALTERATIONS DURING EXERCISE
Exercising Skeletal Muscle decreased PO2 (hypoxia) activates
chemoreceptors while decreased PCO2
• blood flow increases (increased SV & activates central chemoreceptors increasing
pulse pressure) sympathetic outflow
• increased coronary blood flow In 1855, Kollicker and Mueller found that
when a motor nerve of a frogs leg was placed
• no change in cerebral blood flow over its isolated beating heart, the leg would
kick on every heartbeat
• decreased renal and splanchnic blood
flow John Sanderson obtain a record of his patients
heartbeat through the skin using a Lippman
• light to moderate exercise, no increase in capillary electrometer coming from the idea of
preload; increased preload in heavy Alexander Muirhead
exercise
History
Hemorrhage
Augustus Waller is the first to systematically
-a decrease in blood volume decreases mean approach it in an electrical viewpoint still using
systemic pressure resulting in decreased CO the same machine
and arterial pressure
In 1903, Willem Einthoven first used the string
-carotid sinus baroreceptors are activated, galvanometer which is a large magnet
increasing sympathetic and decreasing suspended in a silvered wire drilled 2 holes in
parasympathetic outflow both poles of the magnet
-increased heart rate Emmanuel Goldberger adds the augmented
limb leads to Einthoven six chest leads
-increased contractility
Electrocardiogram (12 Lead)
-increased TPR
ECG or EKG
-decreased unstressed volume and increased
stressed volume -Records the electrical activity of the heart as
well as valuable function about the hearts
-vasoconstriction occurs in skeletal, splanchnic
function and structure
or cutaneous (except coronary or cerebral)
-In resting situation, the muscle cells of the
Hemorrhage
heart are polarized (negatively charge), and Consists of the augmented limb leads (aVF, aVR,
when they are depolarized, they contract aVL) and the 6 precordial leads (V1-V6)
Consists of 6 limb leads and 6 precordial leads The augmented limb leads are derived from
leads I, II and III in which the recording on one
ECG Tracing Paper limb is augmented by 50%
Principles The augmented limb leads plus leads I, II, and III
Action potentials on cardiac muscles create forms the hexaxial reference system (frontal
extracellular voltages plane)
The thorax acts as a volume conductor so that Precordial leads views the horizontal plane of
voltages generated by the cells are conducted the heart (Z axis)
to the body surface Unipolar Leads
Deflections in the ECG corresponds to electrical Lead augmented vector right (aVR) has the
activity or events on the heart positive electrode (white) on the right arm. The
Can be recorded using an active or exploring negative electrode is a combination of the left
electrodes connected to an electrode either via arm (black) electrode and the left leg (red)
bipolar or unipolar leads electrode, which "augments" the signal strength
of the positive electrode on the right arm.
Bipolar Leads
Lead augmented vector left (aVL) has the
Used before unipolar leads are developed positive (black) electrode on the left arm. The
negative electrode is a combination of the right
It uses two active electrodes arm (white) electrode and the left leg (red)
electrode, which "augments" the signal strength
The limb leads forms the points of what is
of the positive electrode on the left arm.
known as the Einthovens triangle
Lead augmented vector foot (aVF) has the
Current flows only in the body fluids, the records
positive (red) electrode on the left leg. The
obtained are those that would be obtained if the
negative electrode is a combination of the right
electrodes were at the points of attachment of
arm (white) electrode and the left arm (black)
the limbs, no matter where on the limbs the
electrode, which "augments" the signal of the
electrodes are placed
positive electrode on the left leg.
Einthoven Triangle
Hexaxial Reference System
Lead I
Normal axis:
- is the voltage between the (positive) left arm
-30o to +90o
(LA) electrode and right arm (RA) electrode
Left axis deviation: -30o to -90o
Lead II
Right axis deviation: +90o to +180o
- is the voltage between the (positive) left leg
(LL) electrode and the right arm (RA) electrode Extreme axis deviation: -90o to -180o
Lead III Normal ECG
- is the voltage between the (positive) left leg P wave
(LL) electrode and the left arm (LA) electrode
- atrial depolarization (SA node to AV node)
Unipolar Leads
PR interval • Rhythm
The hearts response to a pause in pacing Could either be a sinus block, AV block, bundle
branch block or hemiblock (block of anterior or
Caused by an unhealthy SA node when it fails to posterior fascicle of LBB
emit a pacing stimulus
1. Partial (First-Degree) Block
Sick Sinus Syndrome
- slowed conduction to AV node
A wastebasket of arrhythmias caused by SA
node dysfunction with unresponsive or - prolonged PR interval (>220msec)
dysfunctional supraventricular automaticity foci
that can’t employ their normal escape 2. Second Degree Block
mechanism - some impulses not transmitted thru AV node
Most often seen in elderly patients with heart - 2 types: Mobitz I and Mobitz II
disease
Heart Block
Young healthy individuals (athletes) often have
excessive parasympathetic hyperactivity at rest, Mobitz I (Wenckebach)
have some signs of SSS (pseudo Sick Sinus
Syndrome) - PR interval progressively lengthens
Mobitz II
- no lengthening of PR interval
Axis
Hypertrophy
Infarction