Cardiovascular System

Overview of Anatomy & Physiology

Assessment of CV Function

Ezra Oktaliansyah

Department of Anesthesiology & Reanimation Medical Faculty

Padjadjaran University / dr. Hasan Sadikin General Hospital
Bandung

Function of the heart:

pump oxygenated (saturated) blood into the
arterial system, which carries it to the cells
pump deoxygenated (desaturated) blood
back to the lungs via the veins for
reoxygenation

 heart size depends on the size of the person

approximately the size of the fist
encased in a thin, fibrous sac called the
pericardial sac or pericardium (2 layers)
composed of three layers:

inner layer - endocardium

middle layer - myocardium
outer layer - epicardium

Cardiac chambers:
Right atrium - receives deoxygenated blood
from the superior and inferior vena cava
(venous return)
Right ventricle - pumps blood against a low
resistance in the pulmonary artery (PVR) on
the way to the lungs where oxygenation
takes place

 Left atrium - receives oxygenated blood

from the lungs via 4 pulmonary veins
Left ventricle - pumps blood to the systemic
circulation via the aorta against a high
resistance (SVR)

Cardiac valves:
ensure one way flow of blood
two types:

atriovenricular valves
mitral (btw LA & LV)
tricuspid (btw RA & RV)

closed during V. systole and therefore prevent

backflow of blood to the atria during ventricular
contraction (systole)
open during ventricular relaxation (diastole)
allowing for filling of the ventricles

semilunar valves
pulmonic valve (btw RV & pul. artery)
aortic valve (btw LV & aorta)

closed during v. diastole and prevent backflow

into the ventricles during relaxation (ventricular
diastole)
unlike the AV valves, they are open during
contraction of the ventricles (ventricular
systole) allowing for emptying of the ventricles

Cardiac cycle
Heart muscle contracts & relaxes
rhythmically to assure proper circulation
one cardiac cycle=1 heart beat
two phases to the cardiac cycle:

systole
diastole

Systole
ventricles contract
blood ejected from the LVaorta and from
the RVpulmonary artery

Diastole
ventricles relax
pressure in the ventricle falls below that of
the atria
the AV valves open
blood which has been pooling in the atria
begins to flow into the ventricles

 as systole begins the AV valves (mitral &

tricuspid) close, S1 (lubb) produced
semilunar valves forced open, a silent event

 When ventricles are almost empty, pressure in

the ventricles drops, allowing the semilunar
valves (pulmonic and aortic) to close, S2
(dubb) produced
at this time atrial pressure higher, mitral &
tricuspid valves forced open, passively filling
the ventricles up to a certain point (if rapid
filling of dilated ventricle, S3 possible)

 to ensure that the blood remaining in the

atria is ejected, the atria contract (atrial
kick)
if there is any resistance to filling by the
ventricle, S4 possible

Electrical activity
An electrical conduction system is
responsible for the sequence of muscle
contractions that take place during the
cardiac cycle
in essence an electrical current stimulates
each contraction
under normal circumstances, this electrical
impulse originates in the SA node

 this property of the SA node to initiate an

impulse is known as automaticity
automaticity can be disturbed in MI (d/t
hypoxia), electrolyte imbalance, acid-base
imbalance, drugs, etc.
Non-automatic cell may become automatic
and subsequently cause dysrhythmias, (e.g.,
PACs, PJCs, PVCs, escape rhythms, etc.)

Normal conduction pathway

SA node via internodal tracts to AV node to the
Bundle of His
the Bundle of His then divides into the Right
Bundle Branch & the Left Bundle Branch
each branch terminates to form the Purkinge
fibers located in the ventricular myocardium,
where the ventricles, when stimulated, contract

Two electrical events

(recorded as waves on EKG):
depolarization - the spread of an electrical
impulse through the heart muscle
repolarization - the return of the heart muscle
to a resting state
the corresponding mechanical events are
contraction and relaxation, respectively
The ability of cardiac cells to respond to an
electrical impulse is called excitability

 The sequence of depolarization and

repolarization is called the cardiac action
potential.
It results when ions (charged particles such
as Na, K, & Ca) shift across the cell
membrane.

Conductivity
Refers to the ability of the heart muscle
fibers to transmit electrical impulses along
and across cell membranes
can be enhanced or depressed by drugs,
ischemia, trauma

Contractility
Refers to the heart muscle fibers ability to
contract, or shorten, in response to an
electrical impulse (irrespective of volume)
can be impaired in MI, electrolye
disturbances, drugs, hypoxemia
decreased contractility results in a drop in the
stroke volume and ultimately leads to a drop
in cardiac output

Refractoriness
Refers to the hearts inability to respond to a
new stimulus while still in a state
depolarization from an earlier stimulus
this prevents the possibility of tetanic
contractions that would be fatal

Electrical activity &

corresponding waves on EKG
P wave - corresponds to the spread of the
impulse through the atria - atrial
depolarization
PR interval - conduction time through the
atria (.12-.20 sec.)
QRS complex - corresponds to spread of the
impulse through the ventricles - ventricular
depolarization

 QRS interval - conduction time through the

ventricles (.04-.12sec.)
ST segment & T wave - return of stimulated
ventricular muscle to a resting state ventricular repolarization**
QT interval - time it takes for the ventricles
to depolarize & repolarize

Coronary circulation
Heart muscle itself requires a supply of
oxygenated blood to meet its own metabolic needs
supplied through the coronary arteries which
branch off from the aorta just above the aortic
valve, encircle the heart, and penetrate the
myocardium
returned to right side of the heart via the coronary
veins

 Right Coronary Artery (RCA)

Left Main Coronary Artery (LCA):

Left anterior descending (LAD)

Circumflex artery

Collateral Circulation
The presence of more than one artery
supplying a muscle (a capacity present at
birth but not functional)
develops when the blood flow through an
artery progressively decreases and causes
ischemia to the muscle
extra blood vessels develop to meet
metabolic needs of the muscle

Cardiac Output
Volume of blood ejected by the heart/min.
(~ 4-8L)
Stroke volume X heart rate
cardiac index - a calculation that helps to
determine if CO is adequate in relation to
body size

CI=CO/BSA (Dubois scale) in L/min/m2

Stroke volume
Determined by:

preload
afterload
contractile state of the myocardium

Preload
Myocardial fiber length of the ventricle at end
diastole
also known as amount of stretch
Starlings law ( stretch force of
contraction) *
stretch determined by volume of blood in
ventricle
Preload = Venous Return

Afterload
The resistance against which the ventricle must
eject its volume
amount of pressure required by the LV to open
the aortic valve during systole and to eject
blood into the systemic circulation (SVR)
afterload for right side of the heart (PVR)
inversely related to stroke volume
related to BP ( systemic/pulmonary)

Contractile (inotropic) state

Refers to the vigor of contraction generated
by the myocardium regardless of its blood
volume (preload)
increased by SNS stimulation (epinephrine
endogenously or exogenously)
decreased by hypoxemia/acidosis

Regulation of CV system
involuntarily controlled by the ANS
the ANS plays a role in regulating

heart rate (chronotropic effect)

myocardial contractility (inotropic effect)
conduction velocity at the AV node
peripheral (systemic) vascular resistance
arteriole constriction and dilation

venous return
venule and vein constriction and dilation

 The two subdivisions of the ANS

(sympathetic & parasympathetic) generally
exert opposing influences and balance their
activities to promote cardiovascular
adaptation to internal and external demands

Parasympathetic nervous system

Mediated via the vagus nerve
when stimulated, parasympathetic nerve
endings release the neurotransmitter
acetylcholine, which produces inhibitory
effects
decreases the rate of SA node firing, thus
lowering HR
lessens atrial conductivity

Sympathetic nervous system

Mediated by Beta receptors
when stimulated, the nerve endings release the
neurotransmitter norepinephrine and produce
the following effects:

increase in heart rate

increase in conduction speed through the AV node
increased atrial and ventricular contractility
peripheral vasoconstriction (? result)

Hormonal & other influences on

CO
ADH
renin-angiotensin-aldosterone mechanism
exercise, anger, fear, pain, anxiety, excitement
can augment the SNS effects
drugs

2 adrenergic agonists - stimulate SNS (HR)

blockers - Block SNS (HR)
cardioselective blockers (block only 1 receptors)

Blood pressure
Expressed as systolic blood pressure/diastolic
blood pressure
SBP-peak pressure exerted against arteries
when heart contracts (measure of contractile
function)
DBP-residual pressure during relaxation of
the heart (er in atherosclerosis)
BP=COxSVR

Important receptors
Changes in sympathetic and
parasympathetic activity occur in response
to messages sent from sensory receptors in
various parts of the body
for cardiovascular function, the important
receptors are: arterial baroreceptors, stretchsensitive cardiopulmonary receptors of the
atria and veins, and chemoreceptors

Baroreceptors
Stretch sensitive nerve endings affected by changes
in art. BP
located in the walls of the aortic arch and carotid
sinuses
stimulated by an in art. BP, a vagal response
results in in heart rate and art. BP
with BP, less stretch, fewer impulses, see
sympathetic mediated in HR and vasoconstriction

Cardiopulmonary stretch
receptors
located in vena cava & atria
respond to length changes, reflective of circulatory
volume status
with in BP in vena cava and RA due to
hypovolemia, stretch receptors send fewer impulses
than usual to the CNS
result is a sympathetic response to kidney to
enhance Na and water retention & release of ADH
(hypervolemia produces the opposite)

Chemoreceptors
Found in the aortic arch and carotid bodies
sensitive to CO2 and arterial pH
(acidemia) and secondarily sensitive to
hypoxemia
when such changes occur, they send
impulses to the CNS to increase HR

Some factors affecting BP

cardiac output/blood volume
systemic vascular resistance
elasticity of blood vessels
blood viscosity
age
weight
emotion
exercise

Assessment of CV function
History
Physical Examination

inspection
palpation
percussion
auscultation

Lab & Diagnostic Tests

Present History
Chief complaint & symptom analysis
(PQRST)

chest pain
dyspnea (DOE, othopnea, PND)
cough (hemoptysis)
palpitations
skipped beats
dizziness, fainting, syncope

fatigue/weakness
weight gain
peripheral skin changes (e.g., edema, PVD)
leg pain

Past History
Hypertension
Diabetes
Rheumatic fever/Rheumatic heart disease
Elevated homocysteine levels (homocysteine,
an amino acid produced in the body, is
considered to be a contributing risk factor and
is associated with B12, folic acid, and B6
deficiencies)

Lifestyle
May constitute modifiable risk factors for
heart disease

smoking
elevated cholesterol levels/high fat diet (esp.
saturated fats)
sedentary activity/physical inactivity
obesity
stress

Physical Examination
Inspection

color
presence of clubbing
capillary refill
edema
vital signs
peripheral pulses
level of consciousness (LOC)

 Inspection contd

JVP
urine output
PMI
xanthelasma
arcus senilus
ear lobe creases

 Percussion
Palpation

thrill
heave/lift
abdomen
liver (including the hepatojugular reflex)

 Auscultation

normal heart sounds (S1, S2)

abnormal heart sounds
Gallops (S3, S4)
pericardial friction rub
murmurs

bruit
lung sounds

Lab & Diagnostic Tests

Chest x-ray
EKG & cardiac monitoring
Stress test (ETT)
Electrophysiological studies
Cardiac catheterization
Angiography

 Echocardiogram
Intra-arterial pressure monitoring
Hemodynamic monitoring (CVP, PA )

 CBC (Hgb, Hct, WBC, Platelets)

Serum lipids
Cardiac enzymes
Blood coagulation
Serum electrolytes
BUN & Cr
Drug levels