Cardiovascular Physiology
Physiological Anatomy of the Cardiac
Muscle
>Found in the heart
>Usually single nucleus
>prominent striations and branching
>muscles are connected to each other via
junctions called intercalated discs
>pacemaker cells control their contraction
which is involuntary
>Contraction is slow
Properties of Cardiac Muscles
>Excitation of the heart is triggered by
electrical impulse rather than neural
transmitters.
>Contraction of the heart is triggered by
elevation of intracellular calcium influx
> Myocytes depend heavily on oxygen & blood
supply.
> Not fatigued
> Excitability Cycle
Cardiac muscle as a syncytium
Two parts:
1. Syncytium- two atrias
2. Ventricular Syncytium- two ventricles
Role of a Long Refractory Period
1. Prevent ventricles from contracting at too
high rates so that enough time is allowed for
refill of the ventricles
2. Prevent retrograde excitation
Autorhythm
The heart can beat on its own without the need
for exogenous commands.
The heart generates electricity.
TERMINOLOGY
>Excitation- definition: generation of action
potentials; different from contraction
>Contraction- definition: shortening of muscle
cells; triggered by excitation
Refractory Period of Cardiac Muscle
Refractory period
Interval of time during which a normal cardiac
impulse cannot re-excite an already excited
area of cardiac muscles.
Normal refractory period of ventricle is 0.25 to
0.3 seconds, which is the duration of the action
potential.
Relative refractory period
additional 0.05 second
During which the muscle is more difficult than
normal to excite but nevertheless can be
excited.
Refractory period of atrial muscle (0.15 second)
shorter than the ventricles.
And the relative refractory period is another
0.03 seconds.
Excitation – Contraction - Coupling
Function of calcium ions and of the T-
tubules
>Diastole-Period of relaxation
>Systole-Period of contraction
Cardiac Cycle
Shows the mechanical and electrical events of a
single cardiac cycle.
7 phases
Use ECG as an event marker
Cardiac Cycle
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).

- preceded by the P-wave - aortic valve closes, followed by pulmonic valve

à Second Heart Sound (S2)
- Ventricular filling
- ventricular volume is constant because all the
- Filling of the ventricle by atrial systole causes valves are closed.
the Fourth Heart sound (S4)
- dicrotic notch or incisura
-A wave on the venous pulse curve
Cardiac Cycle
Atrial contraction
Rapid Ventricular Filling
Cardiac Cycle
- mitral valve is open and ventricular filling from
Isovolumetric ventricular contraction the atrium begins.

- 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)

- AV valves closure à First Heart Sounds (S1) - normal in children

- split sound Ventricular filling

- no blood leaves the ventricles during this Cardiac Cycle

phase because the Aortic Valve is closed.
Reduced ventricular Filling
Isovolumic Ventricular Contraction
- longest phase of the cardiac cycle.
Cardiac Cycle
- slower ventricular filling rate.
Rapid ventricular ejection
Hemodynamics
- ventricular pressure reaches its maximum
value during this phase. Poiseuille Equation

- most of the SV is ejected. - relationship of flow, pressure and resistance

- atrial filling begins. Q = P1 – P2

- the onset of T wave, which represents R

repolarization of the ventricles. Q – flow
Ventricular ejection P1 – upstream pressure
Cardiac Cycle P2 – downstream pressure
R – resistance of vessels between P1 and P2
Resistance vessel radius
- the most important factor
- inversely proportional to the fourth power of
the radius
- radius decreased by half, resistance increases
16-fold
- radius doubles, resistance decreases to 1/16
of the original vessel length
proportional to the amount of tension developed
and is increased by:
 increased afterload
 increased contractility
 increased size of heart
 increase HR
Fick Principle
>used to calculate blood flow through an organ

- the greater the length, the greater the Flow = Uptake

resistance
A–V
- if length doubles, resistance doubles
>pulmonary venous oxygen = systemic arterial
- length decreases by half, resistance decreases
by half >pulmonary arterial oxygen = systemic venous

Resistance blood viscosity >lowest pO2 = pulmonary artery

- the greater the viscosity, the greater the Flow

resistance
Laminar Flow
- prime determinant of blood viscosity is
- flow in layers
hematocrit
- occurs throughout the entire cardiovascular
- anemia = decreased viscosity; polycythemia
system except heart
= increased viscosity
- highest velocity = center of the tube
Reynolds number
Turbulent Flow
- predicts whether blood flow will be laminar or
turbulent - nonlayered flow

Reynolds number = (diameter) (velocity) - creates murmurs (bruits); produces more

(density) resistance

viscosity - increased turbulence (increased Reynolds

number) : increased tube diameter, increasing
Cardiac Output
velocity, decreased blood viscosity, vessel
>considered as circulating blood volume branching and narrow orifice

>the product of heart rate (HR) and stroke Wall Tension

volume (SV)
Laplace Law T ∞ Pr
>at rest, HR is about 70 bpm, SV is 80 ml and
T = wall tension
CO is about 5.6 liters/min
P = pressure
>stroke work = stroke volume X aortic pressure
r = radius
>cardiac O2 consumption is directly
aorta = the artery with the greatest wall tension
(greatest pressure and radius)
Vessel Compliance
C=ΔV
ΔP
how easily a vessel is stretched (distensibility)
if easily stretched, a vessel is said to be a very
compliant vessel
stiff vessel – noncompliant vessel
Arterial Pressure
Systolic Pressure
- peak pressure during systole
- increase in SV, decrease in HR and vessel
compliance all causes an increased systolic
pressure
Diastolic Pressure
- lowest pressure at the end of diastole
- decrease in TPR, HR, SV and vessel
compliance all causes a decreased diastolic
pressure
Pulse Pressure
>difference between systolic and diastolic
pressure
>most important determinant of pulse pressure
is stroke volume
>Factors that increase (widen) pulse pressure:
• increased stroke volume (systolic
increases more than diastolic)
• decreased vessel compliance ( systolic
increases, diastolic decreases)
>compliant artery = small pulse pressure
>stiff artery = wide pulse pressure
Mean Arterial Pressure
average arterial pressure (more closer to
diastolic than systolic)
mean pressure = diastolic + 1/3 pulse
pressure
= 2/3
diastolic + 1/3 systolic
MAP = CO X TPR
Fast Response AP
Phase 0 – increased membrane conductance to
Na; fast Na channels open; Na influx
(depolarization)
Phase 1 – slight repolarization (voltage gated K
channels); closure of fast Na channels
Phase 2 – most important phase; slow Ca
channels open; Ca influx; K efflux through
ungated channels; voltage gated K channels are
closed
Phase 3 – slow Ca channels closed; voltage-
gated K channels open; large K efflux;
repolarization
Slow Response AP
to have a pacemaker potential or prepotential
all cells have an unstable phase 4 (slow gradual
depolarization towards threshold)
Phase 0 – increase in Ca conductance; Ca influx;
slow Ca spike
Phase 3 – repolarization; increased K
conductance; rapid K efflux
Phase 4 – slow gradual depolarization; increased
Na conductance; Na influx; automaticity
Excitability
the ability of the heart to initiate an AP
reflects the recovery of the channels that carry
the inward currents for the upstroke of the AP
absolute refractory period
- begins with upstroke and ends after the
plateau
- no AP can be elicited
relative refractory period
- the period after the absolute refractory period
when repolarization is almost complete
- an AP can be elicited, but not at full
magnitude
Ventricular Volumes
End-diastolic volume (EDV) : volume of blood in
the ventricle at the end of diastole
End-systolic volume (ESV) : volume of blood in
the ventricle at the end of systole
Stroke volume (SV) : volume of blood ejected by
the ventricle per beat
SV = EDV - ESV
Frank-Starling’s Law
systolic performance is determined by the
overall force generated by ventricular muscle
during systole (number of cross-bridge cycling)
greater number of cross-bridge cycling =
greater force of contraction
Factors that affect the number of cross-
bridge cycling:
>amount of preload on the muscle
>level of contractility
Preload
in skeletal muscle, the load on the muscle in a
relaxed state
the load or prestretch on ventricular muscle at
the end of diastole
best index of preload = LVEDV
contractility = a change in the force of
contraction at any given sarcomere length
(inotropism)
common clinical index of contractilty = EF
(SV/EDV)
loss of contractility is due to loss of functioning
sarcomere
Afterload
in skeletal muscle, the load on the muscle
during contraction
acceptable indices of afterload : mean aortic
pressure and peak left ventricular pressure
an acute increase in afterload reduces the
volume of blood ejected
blood not ejected remains in the LV and
increases preload in the next cycle
increased preload and increased force of
contraction restores SV
Heart Sounds
S1 – closure of AV valves (mitral, tricuspid)
S2 – closure of semilunar valves (aortic,
pulmonic)
S3 – early diastole in children, well-conditioned
athlete ( due to rapid ventricular filling) and
heart failure
S4 – occurs in late diastole when the atrium
contracts; as blood is propelled into
hypertrophied low-compliance ventricle
* valves on the right side of heart opens first,
but closes last
Ventricular Pressure Volume Loop
These are constructed by combining systolic
and diastolic pressure curves
The diastolic pressure curve is the relationship
between diastolic pressure and diastolic volume
in the ventricles.
The systolic pressure curve is corresponding
relationship between systolic and systolic
volume in the ventricles.
Steps in the cycle
BàC Isovolumetric Contraction)
CàD Ventricular Ejection of the heart -
increase contractility
DàA Isovolumetric Relaxation
CONTROL OF HEART RATE
AàB Ventricular Filling
intrinsic heart rate = 110/beats per minute
Pressure-Volume Loop
resting heart rate is lower than intrinsic HR
Cardiac and Vascular function Curve
Neural Influences
The Cardiac Output, or Cardiac Function Curve
parasympathetic : right vagus predominates in
The Venous Return, Vascular Function, curve SA node; left vagus in AV node
Venous Return sympathetic : stimulation causes tachycardia
Mean systemic pressure Bainbridge Reflex
Slope of the Venous Return Curve - stretch receptors in the right atrium (increase
Combining cardiac Output and Venous Return stretch = increase HR)

INOTROPIC AGENTS CHANGE THE CARDIAC - afferent : vagus efferent : vagus

OUTPUT CURVE Chromotropic Effects
Positive Inotropics - on the heart rate
1. Beta -1 Stimulation - positive chromotropic effects = increases HR
2. Increase extracellular calcium concentration by increasing the firing rate of SA node

3. Decrease extracellular Na concentration - negative chromotropic effects = decreases HR

by decreasing the firing rate of SA node
4. Digitalis
Dromotropic
5. Increase in HR
- on conduction velocity in the AV node
Negative Inotropics
- positive dromotropic effects = increased
1. Heart failure conduction velocity at the AV node

2. Decrease pH - negative dromotropic effects = decreases

conduction velocity at the AV node
3. Decrease 02
Autonomic Effects
4. Increase C02
Regulation of Arterial Pressure
Stroke Work
Baroreceptor Reflex
>The work the heart performs on each beat
CONTROL OF BLOOD PRESSURE
Equals to FORCE x DISTANCE
Baroreceptor Reflex (short-term)
FORCE = Ao pressure x Stroke volume
Cerebral Ischemia
Cardiac 02 consumption increased by:
- when brain is ischemic, CO2 and H
- increased concentration in brain increases
afterload - increased size
- chemoreceptors respond by increasing both
sympathetic (increased contractility and TPR)
and parasympathetic (increased HR) outflow =
Cushing’s reaction
- blood flow to other organs are reduced to
preserve blood flow to the brain
Chemoreceptors
- located in bifurcation of common carotid
arteries and aortic arch
- very sensitive to hypoxia (decreased MAP)
Vasopressin
- located in atria
- receptors in atria respond to a decrease in
volume or pressure, cause the release of
vasopressin from posterior pituitary
- increases TPR (V1) and increases H2O
reabsorption in distal tubule of kidney and
collecting ducts (V2)
Atrial Natriuretic Peptide (ANP)
- increased atrial pressure = released of ANP in
atria
- causes vasodilation and decreased TPR
- increases salt and water excretion (decreased
blood volume)
- inhibits renin release
Inspiration
>intrapleural pressure becomes more negative
>increased systemic venous return
>increased right ventricular output causing
delay in closing of pulmonic valve (splitting of
heart sounds)
>volume of blood in pulmonary circuit increases
>decreased left ventricular output
Expiration
>intrapleural pressure becomes more positive
(increased)
>decreased systemic venous return
>decreased right ventricular output
>volume of blood in pulmonary circuit
decreases
>right atrium is compressed so blood pressure
increases causing a reflex decrease in heart rate
>increased left ventricular output
>Valsalva maneuver increase intrapleural
pressure and CVP; also decreases venous return
Microcirculation
>flow and pressure within the system is
controlled by varying the radius (resistance) of
the arterioles
vasodilation = increased flow and pressure
vasoconstriction = decreased flow and pressure
>capillaries are permeable to all dissolved
substances via simple diffusion except plasma
proteins
>the lymphatic system removes proteins in the
interstitial space
>filtration and reabsorption are the main
processes by which fluid moves between plasma
and interstitium due to pressure differences
(bulk flow)
FILTRATION
Capillary Hydrostatic Pressure
-increased by arterial dilation and venous
constriction
-decreased by arteriolar constriction (eg HPN)
Interstitial Oncotic Pressure
-increased by chronic lymphatic blockage
-increased capillary permeability (eg. burns)
REABSORPTION
Capillary Oncotic Pressure
-increased by dehydration due to excessive
sweating
-decreased by liver and renal disease
-decreased by saline infusion
Interstitial Hydrostatic Pressure
-clinically significant changes are seen in the
pulmonary circuit
-subatmospheric pressures will increase
pressure (eg. respiratory distress syndrome)
REGULATION OF BLOOD FLOW AT ORGAN
LEVEL
Autoregulation (Intrinsic)
- blood flow is regulated, not resistance
- no nerves or circulating substances involved
- blood flow should be independent of blood
pressure
2 hypothesis:
>metabolic hypothesis – tissue produces a
vasodilatory metabolite that regulates flow
(eg CO2, H, K, lactate, adenosine)
>myogenic hypothesis – increased perfusion
pressure stretched the smooth muscle (arterial
wall) wherein the arteriole radius decreases with
no significant increase in flow (eg GIT)
Extrinsic Regulation
- tissues that are controlled by nervous and
humoral factors originating outside the organ
- cutaneous circulation and resting skeletal
muscles
- circulating epinephrine acts on β2 receptors
causing vasodilatation
- parasympathetic system does not affect
arterioles and has little or no effect on TPR
except the penis
LOCAL CONTROL OF BLOOD FLOW
Active Hyperemia
- blood flow is proportional to its metabolic
activity
Reactive Hyperemia
- an increase in blood flow occurs after a period
of occlusion of flow
- the greater the period of occlusion, the
greater the increase in blood flow above
preocclusion levels
Tissues least affected by nervous reflexes:
cerebral, coronary, renal, pulmonary and
skeletal muscle during exercise
SPECIAL CIRCULATIONS
Coronary Circulation
- controlled almost entirely by local metabolic
factors (hypoxia and adenosine) = flow equals
metabolism
- exhibits autoregulation; active and reactive
hyperemia
- during systole, mechanical compression of the
coronary vessels reduces blood flow causing
reactive hyperemia
Cutaneous Circulation
- has extensive sympathetic innervation
- temperature regulation is the principal
sympathetic innervation
Skeletal Muscle Circulation
-at rest, sympathetic control of blood flow
predominates
-during exercise, local metabolic control
overrides sympathetic control (sym has no
effect on flow)
-stimulation of α receptors = vasoconstriction
-stimulation of β receptors = vasodilatation
Cerebral Circulation
-the most important local vasodilator is arterial
PCO2 (or pH) regulating blood flow
-if arterial PCO2 is increased (hypoventilation;
pH decreased) = vasodilatation
-if arterial PCO2 is decreased (hyperventilation;
pH increased) = vasoconstriction
Renal and Splanchnic Circulation
- a small in blood pressure will invoke
autoregulatory mechanism to maintain renal
blood flow
- increased sympathetic activity (hypotension)
causes intially vsodilatation then
vasoconstriction, and a decreased blood flow
- venous PO2 is high in renal circulation
EFFECTS OF GRAVITY
-below heart level, there are equal increases in
systemic arterial and venous pressures
(assuming no muscular action)
-above heart level, systemic arterial pressures
progressively decrease
-surface veins above the heart cannot maintain
a significant pressure below atmospheric;
except deep veins in the cranium which
maintain a pressure that is significantly below
atmospheric
-a severed or punctured vein above heart level
has potential for introducing air into the system
due to negative intrathoracic pressure
Effects of supine to upright position:
-pressure in dependent vein increases
-blood volume in dependent veins increases
-circulating blood volume (cardiac output)
decreases
-stroke volume decreases
-arterial blood pressure decreases slightly (due
to reduction in CO)
Compensation via carotid sinus reflex will
include:
-total peripheral resistance increases
-heart rate increases
Basic Alterations During Exercise
-assuming that the person is in steady state,
performing moderate exercise at sea level
Pulmonary Circuit
>blood flow (cardiac output) - large increase
>pulmonary arterial pressure - slight increase
>pulmonary vascular resistance - large
decrease
>pulmonary blood volume - increase
>number of perfused capillaries - increase
>capillary surface area - increase (for gas
exchange)
BASIC ALTERATIONS DURING EXERCISE
Arterial System
• PO2 - no significant change
• PCO2 - no significant change
• pH - no change or decrease (lactic acid)
• MAP - slight increase
• Blood flow - large increase
• TPR - large decrease (dilation of skeletal
muscle beds)
• BP - minimal change (slight increase)
• CO - slight increase
Venous System
• PO2 - decrease
• PCO2 – increase
BASIC ALTERATIONS DURING EXERCISE
Exercising Skeletal Muscle
• blood flow increases (increased SV &
pulse pressure)
• vascular resistance decreases
• capillary pressure increases
• capillary filtration increases
• lymph flow increases
• venous PO2 decreases (to extremely low
levels)
• increased extraction of O2 (increased AV
O2 diff)
• decreased cutaneous blood flow, then
increases to dissipate heat
• increased coronary blood flow
• no change in cerebral blood flow
• decreased renal and splanchnic blood
flow
• light to moderate exercise, no increase in
preload; increased preload in heavy
exercise
Hemorrhage
-a decrease in blood volume decreases mean
systemic pressure resulting in decreased CO
and arterial pressure
-carotid sinus baroreceptors are activated,
increasing sympathetic and decreasing
parasympathetic outflow
-increased heart rate
-increased contractility
-increased TPR
-decreased unstressed volume and increased
stressed volume
-vasoconstriction occurs in skeletal, splanchnic
or cutaneous (except coronary or cerebral)
Hemorrhage
decreased PO2 (hypoxia) activates
chemoreceptors while decreased PCO2
activates central chemoreceptors increasing
sympathetic outflow
increased released of epi/NE by adrenal medulla
further increasing sympathetic outflow
increased released of RAA and ADH
arteriolar vasoconstriction decreases capillary
pressure favoring capillary reabsorption thus
increasing blood volume
ELECTROCARDIOGRAM
History
In 1790, using dissimilar metals like copper and
zinc, the resulting electrical current can
stimulate the frog’s legs to jump
In 1855, Kollicker and Mueller found that
when a motor nerve of a frogs leg was placed
over its isolated beating heart, the leg would
kick on every heartbeat
John Sanderson obtain a record of his patients
heartbeat through the skin using a Lippman
capillary electrometer coming from the idea of
Alexander Muirhead
History
Augustus Waller is the first to systematically
approach it in an electrical viewpoint still using
the same machine
In 1903, Willem Einthoven first used the string
galvanometer which is a large magnet
suspended in a silvered wire drilled 2 holes in
both poles of the magnet
Emmanuel Goldberger adds the augmented
limb leads to Einthoven six chest leads
Electrocardiogram (12 Lead)
ECG or EKG
-Records the electrical activity of the heart as
well as valuable function about the hearts
function and structure
-In resting situation, the muscle cells of the
heart are polarized (negatively charge), and
when they are depolarized, they contract
Consists of 6 limb leads and 6 precordial leads
ECG Tracing Paper
Principles
Action potentials on cardiac muscles create
extracellular voltages
The thorax acts as a volume conductor so that
voltages generated by the cells are conducted
to the body surface
Deflections in the ECG corresponds to electrical
activity or events on the heart
Can be recorded using an active or exploring
electrodes connected to an electrode either via
bipolar or unipolar leads
Bipolar Leads
Used before unipolar leads are developed
It uses two active electrodes
The limb leads forms the points of what is
known as the Einthovens triangle
Current flows only in the body fluids, the records
obtained are those that would be obtained if the
electrodes were at the points of attachment of
the limbs, no matter where on the limbs the
electrodes are placed
Einthoven Triangle
Lead I
- is the voltage between the (positive) left arm
(LA) electrode and right arm (RA) electrode
Lead II
- is the voltage between the (positive) left leg
(LL) electrode and the right arm (RA) electrode
Lead III
- is the voltage between the (positive) left leg
(LL) electrode and the left arm (LA) electrode
Unipolar Leads
Consists of the augmented limb leads (aVF, aVR,
aVL) and the 6 precordial leads (V1-V6)
The augmented limb leads are derived from
leads I, II and III in which the recording on one
limb is augmented by 50%
The augmented limb leads plus leads I, II, and III
forms the hexaxial reference system (frontal
plane)
Precordial leads views the horizontal plane of
the heart (Z axis)
Unipolar Leads
Lead augmented vector right (aVR) has the
positive electrode (white) on the right arm. The
negative electrode is a combination of the left
arm (black) electrode and the left leg (red)
electrode, which "augments" the signal strength
of the positive electrode on the right arm.
Lead augmented vector left (aVL) has the
positive (black) electrode on the left arm. The
negative electrode is a combination of the right
arm (white) electrode and the left leg (red)
electrode, which "augments" the signal strength
of the positive electrode on the left arm.
Lead augmented vector foot (aVF) has the
positive (red) electrode on the left leg. The
negative electrode is a combination of the right
arm (white) electrode and the left arm (black)
electrode, which "augments" the signal of the
positive electrode on the left leg.
Hexaxial Reference System
Normal axis:
-30o to +90o
Left axis deviation: -30o to -90o
Right axis deviation: +90o to +180o
Extreme axis deviation: -90o to -180o
Normal ECG
P wave
- atrial depolarization (SA node to AV node)
PR interval
- initial depolarization of the ventricle
QRS complex
- ventricular depolarization and atrial
repolarization
QT interval
- entire period of depolarization and
repolarization of the ventricle
ST segment
- entire ventricle is depolarized (isoelectric);
the plateau or initial phase of repolarization
T wave
- ventricular repolarization
Precordial Leads
V1 - In the fourth intercostal space (between
ribs 4 & 5) just to the right of the sternum
(breastbone).
V2 - In the fourth intercostal space (between
ribs 4 & 5) just to the left of the sternum.
V3 - Between leads V2 and V4.
V4 - In the fifth intercostal space (between ribs
5 & 6) in the mid-clavicular line (the imaginary
line that extends down from the midpoint of the
clavicle (collarbone).
V5 - Horizontally even with V4, but in the
anterior axillary line. (The anterior axillary line is
the imaginary line that runs down from the point
midway between the middle of the clavicle and
the lateral end of the clavicle; the lateral end of
the collarbone is the end closer to the arm.)
V6 - Horizontally even with V4 and V5 in the
midaxillary line. (The midaxillary line is the
imaginary line that extends down from the
middle of the patient's armpit.)
Normal 12 Lead ECG
INTERPRETATION OF ECG
• Rate
• Rhythm
• Axis
• Hypertrophy
• Infarction
Rate
The SA node generates a Sinus Rhythm at a
range of 60 to 100 beats per minute
Tachycardia = > 100 beats per minute
Bradycardia = < 60 beats per minute
Rate can be determine either by observation
alone or when bradycardic, via computation
Automaticity Foci (Ectopic Foci)
These are other potential pacemakers which has
inherent ability to pace if normal SA node
pacemaking fails
Rhythm
On ECG, there is a consistent equal distance
(duration) between similar waves during a
normal regular cardiac rhythm
The automacity of the SA node precisely
maintains a constant cycle duration between
the pacing impulses it generates
And because the sequence of depolarization is
the same in each repeating cycle, there is a
predictable pattern of regularity in the waves
Rhythm
Sinus Arrythmia
A normal physiological mechanism that is
related to phases of respiration
Not a true arrythmia
>Inspiration = stimulates sympathetic action on
the SA node causing a slight increase in HR
>Expiration = stimulates parasympathetic
action on the SA node causing a slight decrease
in HR
Sinus Arrythmia Premature Beats

Arrythmias Originates in an irritable automaticity focus that

fires spontaneously producing a beat
-Irregular Rhythms
Irritability is a result of increase sympathetic
-Escape stimulation, presence of stimulants like caffeine,
-Premature Beats ampethamines or coccaine, excess digitalis,
hyperthyroidism or low O2
-Tach-arrythmias
Premature Beats
-Heart blocks
Tachy-arrythmias
-Wandering Pacemaker
Rapid rhythms originating in very irritable
-A irregular rhythm produce by the pacemaker automaticity foci
activity of the atrial foci
Easily recognized by rate alone
-Normal rate range (>100, it’s called Multifocal
Atrial Tachycardia) Paroxysmal Tachycardia

-MAT’s are usually seen in COPD and toxicity Flutter

with digitalis meds Fibrillation
-Wandering Pacemaker Heart Blocks
Atrial Fibrillation An unhealthy SA node misses one or more
An irregular ventricular rhythm cycles, and usually resumes pacing but the
pause may evoke and “escape” response from
An erratic atrial spikes from multiple atrial foci an ectopic focus
( no P waves seen)
Blocks electrical conduction that prevent (or
Escape delay) the passage of depolarizing stimuli

The hearts response to a pause in pacing
Caused by an unhealthy SA node when it fails to
emit a pacing stimulus
Sick Sinus Syndrome
A wastebasket of arrhythmias caused by SA
node dysfunction with unresponsive or
dysfunctional supraventricular automaticity foci
that can’t employ their normal escape
mechanism
Most often seen in elderly patients with heart
disease
Young healthy individuals (athletes) often have
excessive parasympathetic hyperactivity at rest,
have some signs of SSS (pseudo Sick Sinus
Syndrome)
Could either be a sinus block, AV block, bundle
branch block or hemiblock (block of anterior or
posterior fascicle of LBB
1. Partial (First-Degree) Block
- slowed conduction to AV node
- prolonged PR interval (>220msec)
2. Second Degree Block
- some impulses not transmitted thru AV node
- 2 types: Mobitz I and Mobitz II
Heart Block
Mobitz I (Wenckebach)
- PR interval progressively lengthens
Mobitz II

- no lengthening of PR interval

3. Complete (Third-Degree) Block

- No impulses conducted through atria to

ventricle (beats independently)

- No correlation of P waves to QRS complexes

Axis

Refers to the direction of the movement of

depolarization, which spreads throughout the
hart to stimulate the myocardium to contract

In patients with ventricular hypertrophy, the

mean QRS vector points towards the area of
hypertrophy

For example, in patients with myocardial

infarction, there is dead or necrotic area of the
heart and does not depolarize. So the mean QRS
vector moves away from the infarct

Hypertrophy

Hypertrophy or increase in muscle mass of the

heart can be diagnosed using an ECG

Right Atria = diphasic wave, initial larger

Left Atria = diphasic wave, terminal larger

Right Ventricle = large R wave, V1

Left Ventricle = large S, V1 and large R, V5 (sum

should be > 35mm)

Infarction

Refers to the complete occlusion of a coronary

artery wherein it becomes non-viable and
neither depolarizes nor contracts

Ischemia = inverted T waves; ST segment

depression

Injury = elevated ST segment

Subendocardial infarct = ST segment

derpression

Infarction = presence of Q wave (>.04 sec); ST

segment elevation