INTRODUCTION TO AND

OVERVIEW OF CVS DISORDERS

MULUALEM ALEMAYEHU ( MD,
INTERNIST, ASSISTANT PROFESSOR
OF MEDICINE)
 OUTLINE
• REVISION OF CVS ANATOMY & PHYSIOLOGY
• EPIDEMIOLOGY OF CARDIOVASCULAR
DISEASES
• APPROACH TO PATIENTS WITH CVS
DISORDERS
• DIAGNOSIS OF CARDIOVASCULAR DISORDERS
(DIAGNOSTIC MODALITIES)
REVISION OF CVS ANATOMY &
PHYSIOLOGY
THE BLOOD VESSELS
ENDOTHELIAL CELLS
GROSS ANATOMY OF THE HEART
GREAT VESSELS
VALVULAR ANATOMY
EPICARDIAC CORONARY ARTERIES
BLOOD SUPPLY TO THE HEART
THE ELECTRICAL CONDUCTION SYSTEM OF THE
HEART
THE ELECTRICAL CONDUCTION SYSTEM OF THE HEART

• There is a hierarchy of automaticity within the

tissue of the heart
• The tissue that possesses the greatest degree
of automaticity (e.g., has the fastest rate of
spontaneous depolarization) functions as the
dominant pacemaker
 MYOCYTE PHASES OF ACTION POTENTIAL (VENTRICLES, ATRIA ,
BUNDLE OF HIS, BUNDLE BRANCHES AND THE PURKINJE SYSTEM)
Phase 0: is the up stroke of the action potential and is
caused by a transient increase in Na+ conductance.
Phase 1: is a brief period of intial repolarization and is as a
result of movement of K+ ions out of the cell and a
decreased Na+ conductance.
Phase 2: is the plateau of the action potential and is
generated by a balance of repolarizing potassium currents and
depolarizing calcium current.
Phase 3: repolarization (Ca2+ conductance decreases and
K+ conductance increases)
Phase 4: the resting membrane potential (inward and out
ward currents are equal)
PHASES OF ACTION POTENTIAL (VENTRICLES, ATRIA , BUNDLE OF
HIS, BUNDLE BRANCHES AND THE PURKINJE SYSTEM)
PHASES OF ACTION POTENTIAL IN PACEMAKER CELLS (SA- AND AV- NODE)

• Phase 0: is the upstroke of the action potential

and is caused by an increase in Ca2+
conductance.
• Phase 3: is repolarization and is caused by
increased K+ conductance.
• Phase 4: is slow depolarization and accounts
for the pace maker activity of the SA node (is
caused by increased Na+ conductance via
funny currents/ If).
• Phase 1 and 2: absent
PHASES OF ACTION POTENTIAL (SINOATRIAL- AND AV- NODE)
PHASES OF ACTION POTENTIAL
DEFINITIONS OF CHRONOTROPIC AND DROMOTROPIC EFFECTS

• Cronotropic effect: change in heart rate

o A negative chronotropic effect es HR by
ing the firing rate of the SA node
o A positive chronotropic effect causes the
opposite
• Dromotropic effect: produce changes in
conduction velocity in the AV node
Cellular Basis of Cardiac Contraction
STEPS IN EXITATION- CONTRACTION COUPLING
• The action potential spreads from the cell membrane
into the T tubles
• During the pleatu of the action potential, Ca2+
conductance is increased and Ca2+ enters the cell
from the extracellular fluid
• This Ca2+ entry triggers the release of even more Ca2+
from the SR (Ca2+ -induced-Ca2+ release)
• Ca 2+ binds to troponin C , and tropomyosin is moved
out of the way, removing the inhibition of actin and
myosin binding
STEPS IN EXCITATION- CONTRACTION COUPLING
STEPS IN EXITATION- CONTRACTION COUPLING
• Actin and myosin bind, the thick and thin
filaments slide past each other, and the
myocardial cells contract.
• The magnitude of the tension that develops is
proportional to the intracellular concentration
of Ca2+
• Lowering of cytosolic [Ca2+] by the sarcoplasmic
reticulum (SR) cause this ion to dissociate from
troponin and relaxes the heart
Cross-Bridge Cycling
CARDIAC MUSCLE CONTRACTILITY
• It is the intrinsic ability of the cardiac
muscles to develop force at a given
muscle length.
• It is also called inotropism
• It is related to the intracellular Ca2+
concentration
• It can be estimated by the ejection
fraction
 POSITIVE INOTROPISM

• Increased heart rate

• Sympathetic stimulation

• Cardiac glycosides (inhibits the Na +,K+-

ATPase)
Mechanisms Of Positive Intropic and Lusitropic Effects -
Adrenergic Stimulation
 NEGATIVE INOTROPISM

• Parasympathetic stimulation
Decreases the force of contraction in
the atria by decreasing the inward Ca2+
current during the pleatu of the
cardiac action potential.
 DETERMINANTS OF STROKE VOLUME

• PRELOAD

• AFTERLOAD

• MYOCARDIAL CONTRACTILITY
 PRELOAD
 It is equivalent to the length of the muscle at the onset
of contraction
 It determines the length of the sarcomeres at the onset of
contraction
o It also regulates the extent of activation of the contractile
system, i.e., its sensitivity to Ca2+
 This relationship forms the basis of Starling's law of the
heart, which states that, within limits, the force of
ventricular contraction depends on the end-diastolic
length of the cardiac muscle; in the intact heart the latter
relates closely to the ventricular end-diastolic volume.
FACTORS AFFECTING PRELOAD
 AFTERLOAD
 It is the tension that the muscle is called upon to
develop during contraction
 It is the load that opposes fiber shortening
o It is determined by the aortic pressure as well as
by the volume and thickness of the ventricular
cavity
o Laplace's law indicates that the tension of the
myocardial fiber is a function of the product of
the intracavitary ventricular pressure and
ventricular radius divided by the wall thickness
FACTROS AFFECTING AFTERLOAD
MYOCARDIAL CONTRACTILITY
CARDIAC PERFORMANCE
 CARDIAC METABOLISM
• Consumes 15 % of the total body O2
supply
• Most ATP production depends on the
oxidation of glucose and free fatty acids
(FFAs)
• In the fasted, resting state: circulating FFAs
are the principal sources of energy (~70%)
• In the fed state: glucose oxidation
.
EPIDEMIOLOGY OF CVS
DISORDERS
EPIDEMIOLOGY of Cardiovascular Diseases
2017
• Cardiovascular disease, listed as the underlying
cause of death, accounts for nearly 801,000 deaths
in the USA.
- That’s about 1 of every 3 deaths in the US.
• About 2,200 Americans die of cardiovascular
disease each day, an average of 1 death every 40
seconds.
• Cardiovascular diseases claim more lives each year
than all forms of cancer and Chronic Lower
Respiratory Disease combined.
 …cont
• About 92.1 million American adults are living with
some form of cardiovascular disease or the after-
effects of stroke.
• Direct and indirect costs of cardiovascular diseases
and stroke are estimated to total more than $316
billion; that includes both health expenditures and
lost productivity.
• Nearly half of all NH black adults have some form of
cardiovascular disease, 47.7 percent of females and
46.0 percent of males
ETIOLOGIES of Deaths attributable to CVS
disease in USA
1. Coronary Heart Disease is the leading cause
(45.1 percent) of deaths attributable to
cardiovascular disease in the US, followed by
2.stroke (16.5 percent),
3.Heart Failure (8.5 percent),
4.High Blood Pressure (9.1 percent),
5.diseases of the arteries (3.2 percent), and
6.other cardiovascular diseases
 Heart Disease
• Heart Disease (including Coronary Heart Disease,
Hypertension, and Stroke) remains to be the No. 1 cause of
death in the US.
• Coronary heart disease accounts for 1 in 7 deaths in the US,
killing over 360,000 people a year.
• About 790,000 people in the US have heart attacks each year.
- Of those, about 114,000 will die.
• The estimated annual incidence of heart attack in the US is
580,000 new attacks and 210,000 recurrent attacks.
- Average age at the first heart attack is 65.3 years for males
and 71.8 years for females.
 …cont.
• From 2004 to 2014, the annual death rate attributable to
coronary heart disease declined 35.5 percent – but the
burden and risk factors remain alarmingly high.
• The estimated direct and indirect cost of heart disease in
2012 to 2013 (average annual) was $199.6 billion.
• Heart attacks ($11.5 billion) and Coronary Heart Disease
($10.4 billion) were 2 of the 10 most expensive hospital
principal discharge diagnoses.
• Between 2013 and 2030, medical costs of Coronary Heart
Disease are projected to increase by about 100 percent
 GLOBAL DATA

. Cardiovascular disease is the leading global cause

of death, accounting for more than 17.3 million
deaths per year in 2013, a number that is expected
to grow to more than 23.6 million by 2030.
• In 2013, cardiovascular deaths represented 31
percent of all global deaths.
• In 2010, the estimated global cost of cardiovascular
disease was $863 billion, and it is estimated to rise
to $1044 billion by 2030
 Symptoms of CVS
Three main symptoms:
1-Pulmonary Congestive Symptoms:
A-Dyspnea:
B- Orthopnea.
C- Paroxysmal Nocturnal Dyspnea (PND).
D- Cough with or without sputum.
E- Cardiac Asthma ( Wheezes).
F- Pulmonary Edema: Scanty, whitish frothy sputum.
 Symptoms of CVS
2-Systemic Congestive Symptoms:
A-Congested Neck Veins ( JVP).
C- Congested Liver: RT Hypochondrium pain.
D- Abdominal Swelling.
E- Bilateral Lower Limb Swelling.
 Symptoms of CVS
3-Low Output Symptoms:
A- To Brain: Guideness, Dizziness, Fainting
Attacks and Syncopal Attacks.

B-To Heart: Chest pain, Easy Fatigability.

* Palpitation: Awareness of Heart beat.
INVESTIGATION MODALITIES
DISORDERS OF THE
CARDIOVASCULAR SYSTEM
 ELECTROCARDIOGRAPHY
• The electrocardiogram (ECG or EKG) is a graphic
recording of electric potentials generated by the
heart
• The signals are detected by means of metal
electrodes attached to the extremities and chest wall
and are then amplified and recorded by the
electrocardiograph
• ECG leads actually display the instantaneous
differences in potential between these electrodes
 CLINICAL USES OF ECG
• Arrythmia
• Conduction disturbance
• Ischemia
• Life threatening metabolic disturbances
• Ventricular hypertrophy
• Increased susceptibility to sudden cardiac death
(e.g. QT prolongation syndromes)
• Guide reperfusion therapy
 ELECTRIC FIELDS
All electrical fields have two important associated
parameters:
Magnitude
Direction
The standard electrocardiogram is simply a
graphical representation of the direction and
magnitude of the electrical field of the heart as it
changes with time
Each lead looks at the electrical field of the
heart from a different angle
ELECTRICAL DIPOL
 ELECTRICAL DIPOL
• The direction of the dipole is simply the net direction of
the positive charge relative to the negative charge; this
corresponds to the direction of the wave front of
depolarization for the muscle strip
• The magnitude of the dipole is determined by the amount
of positive sodium ions that flow into the cell
• Since the heart is a complex three dimensional structure
consisting of millions of cells, the direction of the dipole
changes with time and is the result of a summation of all
the instantaneous dipoles
 VECTOR ANALYSIS
• Vector analysis illustrates a central concept of
electrocardiography-that the ECG records the complex
spatial and temporal summation of electrical potentials
from multiple myocardial fibers conducted to the surface of
the body
• Resultant vector is a force which reflects the
resultant electric activity of several synchronous
electrical vectors (forces) traveling in different
directions
• The mean QRS force is directed to the left ,inferiorly
and some what posteriorly
LIMB LEADS
 AUGMENTED LEADS
• Lead AVL is created by making the left arm
positive and the other limbs negative. Its angle
of orientation is -30°.
• Lead AVR is created by making the right arm
positive and the other limbs negative. Its angle
of orientation is -150°.
• Lead AVF is created by making the legs
positive and the other limbs negative. Its angle
of orientation is +90°.
HEXAXIAL REFERANCE SYSTEM
PRECORDIAL LEADS
 PLACEMENT OF PRECORDIAL LEADS
V1 — Fourth intercostal space to the right of the sternum

V2 — Fourth intercostal space to the left of the sternum

V3 — Midway between V2 and V4

V4 — Fifth intercostal space at the midclavicular line

V5 — Anterior axillary line at the level of V4

V6 — Midaxillary line at the level of V4

PLACEMENT OF PRECORDIAL LEADS
ELECTRIC ACTIVITY OF ECG LEADS
ARBITRARY ORIENTATION OF DIFFERENT LEADS

1. Inferior leads: II, III and aVF

2. Left latteral wall: I and aVL
3. Cavitory: aVR
4. Anterior wall of the heart: V1 to V6
 Anteroseptal leads: V1 to V4
 Apical leads: V5 to V6
 Together, the frontal and horizontal plane
electrodes provide a three-dimensional report
of cardiac electrical activity.
 Each lead can be likened to a different video
camera angle "looking" at the same dynamic
events (atrial and ventricular depolarization
and repolarization) from different spatial
orientations
GENERATION OF THE P-WAVE
 VENTRICULAR DEPOLARIZATION
• In both ventricles, the overall endocardial excitation
pattern begins on septal surfaces and sweeps down
and around the free walls to the posterior and basal
regions in an apex to base direction
• The activation fronts then move from endocardium
to epicardium.
• Excitation of the endocardium begins at sites of
Purkinje–ventricular muscle junctions and proceeds
by muscle cell to muscle cell conduction in an
oblique direction toward the epicardium
 VENTRICULAR DEPOLARIZATION
 Step 1 (Septal depolarization): activation of
the ventricles begin with endocardial region
of the mid portion of interventricular septum
from left spreading transversly to the right.
 Step 2: Dominance of the left ventricle and
activation of both ventricles
 Step 3: Activation of posterobasal portions of
the heart, pulmonary conus and the upper
most part of the interventricular septum
GENERATION OF THE QRS COMPLEX
 VENTRICULAR REPOLARIZATION
• Repolarization follows depolarization and is a
complex event that remains poorly
understood
• In the normal adult,ventricular repolarization
results isoelectric ST segment and a mean T
wave vector oriented to the left, inferiorly
(between 0 and +900 in the frontal plane), and
is slightly anteriorly
ECG WAVE FORMS AND INTERVALS
 PR INTERVAL
• It measures the time between the onset of
atrial and ventricular depolarization
• This includes the physiologic delay imposed
by stimulation of cells in the AV junction
• Normal Value: 0.12 to 0.20 sec
 QRS INTERVAL
The QRS interval (normally <= 0.10 sec) is a measure of the
duration of ventricular depolarization.
The QRS complex is subdivided into specific deflections or
waves
If the initial QRS deflection in a given lead is negative, it is termed a
Q wave.
The first positive deflection is termed an R wave.
A negative deflection after an R wave is called an S wave.
Subsequent positive or negative waves are labeled R' or S',
respectively.
Lower case letters (q, r, or s) are used for relatively small amplitude
waves of less then 0.5 mV (less than 5 mm with standard
calibration).
An entirely negative QRS complex is called a QS wave
 QT- and R-R INTERVALS
• The QT interval begins with the onset of the QRS
complex and ends at the end of the T-wave
• It involes both ventricular depolarization and repolarization
times, and varies inversely with the heart rate.
• A rate-related (or corrected) QT interval (QTc) can be
calculated from:
• QTc = QT interval ÷ square root of the RR interval
• The upper limit of the normal value for the QTc is
approximately 0.44
• R-R interval
GRID LINES AND STANDARDIZATION OF THE ECG
NORMAL ECG FROM A HEALTHY SUBJECT
VENTRICULAR ACTION POTENTIAL AND QRS-T CYCLE
CHEST RADIOGRAPHY (PA)
CHEST RADIOGRAPHY (LEFT LATTERAL)
CHEST RADIOGRAPHY (LEFT LATTERAL)
ECHOCARDIOGRAPHY
2D ECHO STILL-FRAME IMAGES (NORMAL STUDY)
2D ECHO STILL-FRAME IMAGE (ABNORMAL STUDY)
DOPPLER ECHO
CARDIAC ENZYMES
BNP
 NUCLEAR CARDIOLOGY
• Planar Myocardial Perfusion Imaging

• Radionuclide Angiography or Ventriculography

• Single-photon emission computed tomography

(SPECT)

• Positron Emission Tomography (PET) scan

MRI (MAGNETIC RESONANCE IMAGING)
COMPUTED TOMOGRAPHIC IMAGING
SELECTION OF NON-INVASIVE IMAGING MODALITIES
 OTHERS
• Stress ECG
• Holter Monitor
• Event recorder
• Conventional Angiography
END OF LECTURE 1