PHYSIOLOGY MSGD6

TOPIC
LECTURER

OUTLINE I. GROSS ANATOMY – Discuss the Pericardium and

I. GROSS ANATOMY – Discuss the Pericardium and the Different Layers of the Different Layers of the Heart
the Heart
II. GROSS ANATOMY – Discuss the Chambers of the Heart, the Valves
Separating them, and the Normal Adult Circulation of Blood
III. GROSS ANATOMY – Discuss the surface anatomic relations of the
heart valves and the corresponding auscultatory areas
IV. GROSS ANATOMY - Describe the Blood Supply of the Heart
V. PHYSIOLOGY – Discuss the Different Phases of the Cardiac Cycle Using
Wigger’s Diagram
VI. PHYSIOLOGY – Discuss the Electrophysiology of the Cardiac
Conducting System
VII. PHYSIOLOGY – Differentiate the Properties of the Heart
(Chronotropism, Inotropism, and Dromotropism)
VIII. PHYSIOLOGY – Discuss the Effects of Preload, Afterload and Inotropy
on the Regulation of Stroke Volume
IX. BIOCHEMISTRY - Cross-reactivity to which component of the Group A • Sac that covers the heart
Streptococcal bacteria causes Rheumatic fever/Rheumatic Heart disease? • Covers also the great vessels of the heart (which is also
X. The Case! a major cardiac organ)
XI. CASE – Discuss the etiology and risk factors of RHD. Factors present
in the patient. • Bordered by the:
XII. CASE – Discuss the Pathogenesis of RHD ▪ Diaphragm inferiorly
XIII. CASE – What is the significance of elevated Anti-Streptolysin O Titer? ▪ Lungs and pleura laterally
XIV. CASE – Identify the Murmur being described in the patient
XV. CASE – Explain why the Patient’s Chest Pain is worse with coughing ▪ Sternum/rib cage anteriorly
and is relieved by leaning forward ▪ Clavicle superiorly
XVI. CASE – What are the other manifestations of Rheumatic Fever • Compose the middle mediastinum together with
XVII. CASE – What could have been done to lessen the risk of developing
RHD in the patient ascending aorta (carries the pericardium), pulmonary
XVIII. EXTRA – What is the immediate management needed for patients trunk and SVC
with RHD? • Protects the heart from sudden filling
XIX. EXTRA – What is the treatment (pharmacology, surgery or otherwise)
for RHD • Fibro-serous membrane
XX. Appendix • Parts
▪ Fibrous membrane
REFERENCES ▪ Continuous with the central tendon of the
• Hall JE. 2016. Guyton and Hall Textbook of Medical Physiology, 13/e. diaphragm (by the pericardial ligament),
Saunders Elsevier and tunica adventitia of the vessels
• Moore KL, Dalley AF, Agur AMR. 2014. Clinically Oriented Anatomy, 14/e. entering and leaving the heart.
Lippincott Williams and Wilkins ▪ Attaches anteriorly to the internal aspect of
• Grossman H, Porth CM. 2014. Porth’s Pathophysiology – Concepts of the sternum by the sternopericardial
Altered Health States, 9/e. Lippincott’s Williams and Wilkins
ligament
• Rubin R, Strayer DS. 2012. Rubin’s Pathophysiology
▪ Posteriorly bound by loose connective
Clinocopathological Foundations of Medicine, 6/e. Lippincott Williams
and Wiliins tissue in the posterior mediastinum
• Kasper DL, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo JL ▪ Serous membrane
(eds.). Harrison’s Principles of Internal Medicine, 19/e. 2015. McGraw- ▪ Composed of mesothelium (flattened cells
Hill. forming an epithelium lining) – 2 parts
• Devlin TM. 2011. Textbook of Biochemistry with Clinical Correlations, • Parietal membrane – lines the
7/e. John Wiley & Sons, Inc. fibrous membrane’s internal surface
• Trevor AJ, Katzung BG, Hall MK, Masters SB. 2013. Pharmacology • Visceral membrane – epicardium or
Examination and Board Review, 10/e. McGraw Hill.
outermost layer of the heart
• Kleigman RM, Stanton BF, St Geme III JW, Schor NF, Behrman RE. 2016.
o Aorta and pulmonary trunk –
Nelson Textbook of Pediatrics, 20/e. Elsevier Ltd.
• WebMD leaving the heart
• MedScape o SVC, IVC, and pulmonary
veins – entering the heart
• Pericardial cavity – space between the parietal and the
visceral membranes of the serous pericardium
• Transverse pericardial sinus
▪ Posterior to the aorta and the pulmonary trunk
▪ Anterior to the SVC and superior to atria
• Oblique pericardial sinus
▪ Posterior to the heart
Lecture Title: MSGD6 – Rheumatic Heart Disease
Transcribed by: MOLINA GASE
 ▪ Left atrium pericardial reflection (pulmonary
veins and IVC)

Walls of the Heart

• Epicardium – visceral layer of the serous pericardium
• Myocardium
▪ Composed of cardiac muscles (double helical
orientation cause of wringing motion of the heart)
▪ Anchored to the fibrous skeleton (anoli fibrosis)
• Endocardium – endothelium and subendothelium that
also covers the valves
Fibrous Skeleton

• Provides attachment for the leaflets and cusps

• Maintains the orifice of the atrioventricular (AV) and
semilunar (SL) valves, thus preventing overdistension
• Attachment for myocardium, which is uncoiled creates
a ventricular myocardial band
• Electric insulator by separating the myenterically
conducted impulses of the atria and ventricles
II. GROSS ANATOMY – Discuss the Chambers of the
Heart, the Valves Separating them, and the
Normal Adult Circulation of Blood
• Blood flow
▪ BODY  IVC  RA  RV  PA 
LUNGS  PV  LA  LV  BODY
Right Atrium
• Right border of the heart
• Left and right divided by atrial septum
• Fossa ovalis inside
• Receives venous blood from SVC and IVC
• Right auricle: ear-like cervical muscular part, add-on
room increasing its capacity as it overlaps the aorta
• Interior of RA
▪ Smooth or thin-walled posterior part
(sinus venosum) on which SVC and IVC,
as well as coronary sinus OPEN
▪ Rough muscle or Pectinate muscles that
are not significantly contractile
▪ Atriventricular (AV) orifice
• Separation of the smooth and rough muscles:
▪ Internally: crista terminalis
▪ Externally: sulcus terminalis
• Coronary sinus: majority of the blood will drain to the
coronary sinus
▪ Important anatomic structure in terms of
topography
▪ Forms border of tendon of Todaro:
important in location of triangle of Koch
(inside the triangle is AV node)
Lecture Title: MSGD 6 – Rheumatic Heart Disease
Transcribed by: MOLINA GASE
Figure 1: Right lateral view
Right Ventricle
• Crescent or half moon shaped
• Largest part of the anterior surface of the heart,
small part of the diaphragmatic surface, entire inferior
border of the heart
• Tapers into conus arteriosus (infundibulum), leading to
the pulmonary trunk.
• Trabeculae carnae - irregular muscular elevations
(interior)
• Supraventricular crest - separates the rigid wall of the
inflow part to the conus arteriosus.
• Tricuspid Valve
▪ attached to the fibrous ring
▪ contains 3 leaflets - anterior, posterior,
septal
▪ moderator band and septal band attaches
papillary muscles to ventricular wall,
helping the tricuspid valve to contract
• Chordae tendinae or tendinous cords - parachute like
cords attached to the anterior, posterior, and septal
cusps; attached to the adjacent sides of 2 cusps,
preventing separation, inversion, and prolapsing of the
cusps.
• Papillary muscles:
▪ Anterior papillary muscle – largest, most
prominent, attached to anterior wall of the
ventricle, holds the anterior and posterior
cusps
▪ Posterior papillary muscle – smaller than
anterior papillary muscle, arises from
inferior wall, attached to the septal and the
posterior cusps
▪ Septal papillary muscle – attached to the
interventricular septum, attached to the
septal and anterior cusps
• Interventricular septum (IVS) – muscle + membrane
parts; strong, oblique between right and left ventricles
▪ As thick as the remainder of the left
ventricle because it needs to resists high
amounts of pressure
▪ Fibrous skeleton form the membranous
part of the interventricular septum
Page 2 of 18
 ▪ Membranous part of the IVS is
the attachment site of the septal
cusps (inferiorly to the septal
cusp, it is an interventricular
septum; superiorly to the same
landmark tissue, it is part of the
atrioventricular skeleton.
• Septomarginal trabeculae – curved muscle of the right
ventricular chamber. It carries the right branch of the AV
node bundle. The right branch of the AV node bundle
allows coordinated contraction of the anterior papillary
muscle.
• Supraventricular crest – accommodates the 140
degree U-turn of blood; deflection of the inflow of the
blood to main cavity and outflow tract from the conus
arteriosus to the pulmonary orifice. Figure 3: Flap opened in posterolateral wall of left ventricle
• Pulmonary valve is located at the 3rd intercostal.
Left Ventricle
• Forms apex of heart, almost all its left surface and
border, most of the diaphragmatic surface.
• Shape: half-moon (crescent moon)
• Muscles with much contractile force
• Performs more work than the right ventricle.
• Interior contains:
▪ Walls 2x or 3x thicker than the right
ventricle.
▪ Covered with meshed trabeculae carnae
(finer and more numerous than the right
ventricle)
▪ Conical cavitiy, longer than that of the
right ventricle.
▪ Aortic vestibule leads to aortic orifice and
valve, smooth walled and non-muscular,
Figure 2: Opened right ventricle, anterior view and supero anterior outflow.
▪ Mitral valve – 2 leaflets: anterior and
Left Atrium posterior with anterior and posterior
papillary muscle bundles
• Most base of the heart
▪ Aortic orifice posterosuperior part, fibrous
• Not much contractile muscle as the right atrium
left and right cusps attached.
• Valveless left and right pulmonary vein enter this
▪ Aortic valve is located at the left
chamber.
side of the sternum, at the
• Has left auricle, trabeculae with pectinate muscle (this
second intercostal
is located at the superior border of the atrium, overlaps
the pulmonary trunk)
• Semilunar depression (interatrial septum location) –
serves as the floor of the oval fossa, and ridge
surrounding it is the valve of oval fossa)
• Interior of the Left Atrium:
▪ Larger smooth walled part and smaller
auricle
▪ 4 pulmonary veins entering it
▪ Thicker wall than right atrium
▪ Interatrial septum (slopes posteriorly and
to the right)
▪ Left AV orifice, discharge of oxygenated
blood

Figure 4: Section through LA and LV with mitral valve cut away.

Lecture Title: MSGD 6 – Rheumatic Heart Disease Page 3 of 18

Transcribed by: MOLINA GASE
 III. GROSS ANATOMY – Discuss the surface
anatomic relations of the heart valves and the
corresponding auscultatory areas
Valves
Atrioventricular Valves

• Valves that guard the atrioventricular orifices

Tricuspid Valve
• Guards the orifice between the RA and the right
ventricle and prevents backflow (regurgitation) of blood
from RV to RA during systole
• Has 3 cusps that correspond to 3 papillary muscle
(anterior, posterior, and septal papillary muscles) that is
connected via the chordae tendinae (which prevents the
separation of the cusps during contraction)

Mitral Valve
• Guards the orifice between the LA and the LV and Figure 5: Erb's point: where S2 is best auscultated
prevents backflow (regurgitation) of blood from the LV
to RA IV. GROSS ANATOMY - Describe the Blood Supply of
• Has 2 cusps that receives the chordae tendinae from the Heart
more than 1 papillary muscle (provides support to mitral Vasculature of the Heart
valve to resist pressure developed during systole)
• Coronary arteries and cardiac veins
• The anterior and the posterior papillary muscles are
• Endocardium and subendocardium receive their
larger than in the right ventricle because the atrial
nutrients via diffusion
pressure is much higher in the systemic circulation
Coronary Arteries
Semilunar Valves
• Supply blood to myocardium and endocardium
• Valves that regulate the passage of blood through the
• Arise from aortic sinuses at proximal end, pass opposite
pulmonary and systemic circulation
sides of the pulmonary trunk
• Has 3 cusps and are concave when viewed superiorly
• Supplies atria and ventricles
• Do not have chordae tendinae to support them
• Has 2 main sources:
• Smaller in area than the cusps of the AV valves
▪ Left Coronary Artery (LCA)
because force exerted on them is less than half of that
▪ Right Coronary Artery (RCA)
exerted on the cusps of the AV valves

Aortic Valves
• Valve that connects the LV to the aorta (leads to
systemic circulation)

Pulmonary Valve
• Valve that connects the RV to the pulmonary artery
(leads to pulmonary circulation)

Figure 6: Coronary arteries

Left Coronary Artery (LCA)

• Arises from the left aortic sinus between the left auricle
and the left side of the pulmonary trunk, and proceeds
to the coronary sulcus. From the coronary sulcus, it
divides

Lecture Title: MSGD 6 – Rheumatic Heart Disease Page 4 of 18

Transcribed by: MOLINA GASE
 crux of the heart, and the posterior interventricular
branch (posterior descending artery) into the
intraventricular (IV) septum. The RCA supplies the
diaphragmatic surface of the heart.
• Locations supplied by the RCA:
▪ Right atrium
▪ Right ventricle
▪ Part of the left ventricle
▪ IV septum
▪ SA node

 (blockage in the branch supplying

this can cause heart block and the
heart will beat in an irregular rate,
requiring the person to use a
pacemaker)
▪ AV node
Cardiac Veins

Figure 7: LCA supplies left circumflex and anterior interventricular • The coronary sinus initially divides to the small
branch (left anterior descending). cardiac vein, which accompanies the right marginal
branch of the heart.
• The LCA supplies the • The great cardiac vein, being the main tributary of the
▪ Left atrium coronary sinus, gives rise to the anterior
▪ Left SA node interventricular vein that accompanies the anterior IV
▪ Most of Left ventricle branch of the LCA. It runs back to via the coronary
▪ Most inferior intraventricular muscles sulcus.
(anterior 2/3)
• The middle cardiac vein accompanies the posterior
▪ The atrioventricular bundle
interventricular branch (usually from RCA).
▪ SA node in 40% of people
• The oblique cardiac vein, small vein are unimportant
Right Coronary Artery postnatally, descends over the posterior wall and
• This artery arises from the right sinus of the aorta, merges with the great cardiac vein.
passing to the right side of the pulmonary trunk. This will • Anterior cardiac veins begin over the anterior surface
divide into: • Smallest cardiac vein are minute vessels that begin in
capillary beds

Figure 9: Cardiac veins

Innervation
Figure 8: RCA supplies the SA nodal branch, the AV nodal branch,
the right marginal branch and the posterior interventricular branch Sympathetic Nervous Stimulation
(posterior descending artery). • Causes tachycardia (increased heart rate and force of
contraction)
• After giving off the right marginal branch, it runs to the • β-receptors
left and back of the coronary sulcus to the posterior of
the heart. It will give rise to the AV nodal branch at the  Use β-blockers to control palpitations
Lecture Title: MSGD 6 – Rheumatic Heart Disease Page 5 of 18
Transcribed by: MOLINA GASE
 Parasympathetic Nervous Stimulation Cardiac Muscle Action Potential
• Causes bradycardia (decrease heart rate)

 Use epinephrine to increase heart rate

Figure 11: Phases of action potential in ventricular myocyte.

Phase 0

• Rapid depolarization
• Sudden Na+ influx
Figure 10: Innervations of the heart • Voltage-gated fast Na+ channels open
Phase 1
V. PHYSIOLOGY – Discuss the Different Phases of
the Cardiac Cycle Using Wigger’s Diagram • Initial rapid repolarization
• See appendix • Efflux of potassium
• Decrease in Na+ conductance
VI. PHYSIOLOGY – Discuss the Electrophysiology of
the Cardiac Conducting System Phase 2

Electrical Properties • Plateau – unique for cardiac AP

• Resting membrane potential = -90 mV • Due to voltage-gated slow Ca2+-Na+ channels
• Action potential • Efflux of K+ and unflux of Ca2+-Na+ at the same time
▪ presence of plateau in contrast to skeletal balances the polarity: no net change in voltage
muscle; Phase 3
▪ duration of action potential is LONGER
• Fast repolarization
• Large K+ efflux
Phase 4

• The resting membrane potential

• Period in which inward and outward current are equal
and the membrane potential approaches K+ equilibrium
potential

 The initial depolarization is due to Na+ influx through

rapidly opening Na+ channels (phase 0).
 The inactivation of Na+ channels contributes to the rapid
repolarization phase (phase 1).
 Ca2+ influx through more slowly opening Ca2+ channels
produce the plateau phase (phase 2).
 Repolarization is due to net K+ efflux through multiple
types of K+ channels (phase 3 and 4)

Lecture Title: MSGD 6 – Rheumatic Heart Disease Page 6 of 18

Transcribed by: MOLINA GASE
 Refractory Period
• Atria – 0.15 seconds
• Ventricles – 0.25 to 0.30 seconds
• Action potential in skeletal muscle – 1.5 msec
• Action potential in cardiac muscle – 300 msec

Figure 13: Calcium pumps in cardiac muscle

Movement of Calcium Ions in Cardiac Muscle

AP enters from adjacent cell

Voltage gated calcium channel opens and allows Ca2+ to enter

Figure 12: Comparison of AP and contractile response of a

mammalian cardiac muscle fiber in a typical ventricular cell. Ca2+ induces Ca2+ release through RYR channels

• The cardiac myocyte cannot be excited in the absolute

refractory period (ARP). Local release of Ca2+ spark
• The cardiac myocyte can be excited to a minimal extent
during the relative refractory period (RRP) if enough
stimulation is reached; that is – a stimulation that is Summed Ca2+ spark creates a Ca2+ signal
stronger than the previous one.
• During phases 0 to 2 and about half of phase 3 (until the
Ca2+ ions bind to troponin to initiate contraction
membrane potential reaches approximately -50 mV
during repolarization) cardiac muscle is at ARP.
• It remains RRP during phase 4
Relaxation occurs when Ca2+ unbinds from troponin
• Duration of heart muscle contraction is almost as long
as the AP. Refractory period is also almost as long as
the AP. Ca2+ is brought back into the SR for storage by SERCA
• Importance of refractory period – it gives the heart
enough time to fill with blood
Ca2+ is exchanged with Na+
Excitation-Contraction Coupling
• Electrical stimulus is converted to mechanical
contraction Na+ gradient is maintained by the Na-K ATPase

Action potential
Pacemaker Tissue

AP passes through muscle membrane - T-tubule

• Have self-generating AP
• Baseline potential or RMP is -60mV
• Meaning some channels are already activated
Influx of Ca2+ ions from the wider T-tubules (ECF) • Depolarizing current is carried by relatively slow Ca 2+
currents instead of by fast Na+ currents
Influx of Ca2+ also activates SR release of Ca2+ ions 1. SA node – main pacemaker of the heart (fastest
firing rate of impulses (80 to 100)
2. AV node – secondary to SA node around 60
Activation of actin-myosin sliding filament
3. Bundle of His
4. Bundle branches
5. Purkinje fibers – tertiary node

Lecture Title: MSGD 6 – Rheumatic Heart Disease Page 7 of 18

Transcribed by: MOLINA GASE
 • ICa(L) – when membrane depolarizes to -40 mV, a
second type of Ca2+ channel opens called long-lasting,
or L-type Ca2+ channels.
• Opening of these channels causes more Ca2+ to enter
the cell and to further depolarize the cell until an action
potential threshold is reached (usually between -40 and
-30 mV)

 Rhythmically discharging cells have a membrane

potential that, after each impulse, declines to the firing
level. Thus, this prepotential or pacemaker potential
(Figure 16B) triggers the next impulse. At the peak of
each impulse IK then declines, and a channel
permeable to both Na+ and K+ is activated. Because this
channel is activated following hyperpolarization, it is
referred to as “h” channel (Ih); however because of its
unusual (funny) activation it has also been dubbed an
“f” channel (If).
 As Ih increases, the membrane begins to depolarize,
forming the first part of the prepotential. Ca2+ channels
then open. These are of two types in the heart, the T
(for transient channels) and the L (for long-lasting)
channels. The calcium current (ICa) due to the opening
of the T channels completes the preopotential, and I Ca
due to opening of the L channels produces the impulse.
 Other ion channels are also involved, and there is
evidence that local Ca2+ release from the SR (Ca2+
sparks) occurs during the prepotential.

VII. PHYSIOLOGY – Differentiate the Properties of the

Heart (Chronotropism, Inotropism, and
Dromotropism)
 Chronotropic action (autorhythmicity) – heart rate
 Dromotropic action (conductivity) – conductivity of
Figure 14: (A) Comparison of the APs in ventricular muscle and (B) the AV node; rate of electrical impulse of the heart
diagram of the membrane potential of pacemaker tissue
 Bathmotropic action (excitability) – excitability or
irritability of cardiac muscle
 Inotropic action (contractility) – contractility
 What is a response of a nerve to a stimulus? Only action
potential, electrical response. Nerves do not have the
ability to contract. It only has one physiologic property,
which is excitability. Its response is in the form of an
action potential.
 The skeletal muscles and smooth muscles also exhibit
excitability. All muscles at that! They exhibit excitability
and they exhibit it through an action potential. And this
is followed by another property, which is conductivity,
which is the ability to transmit impulses. For the
muscles, once it reaches the muscles, they contract. So
it also exhibits contractility.
Figure 15: Shape of AP in pacemaker tissue
Contraction is always preceded by action potential
• Phase 4 – K+, Ca2+, Na+ leak slowly
• Phase 0 – Ca2+ influx
• Phase 3 – K+ efflux  Cardiac muscle has another property which is
authorhytmicity. The ability of self-excitation. In the
• If – “funny” or pacemaker current
cardiac muscle, even in the absence of nerve stimulus
▪ Allows sodium to enter the cell
or mechanical stimulus, it will still create an impulse.
• ICa(T) – a membrane potential reaches -50m, T-type
(transient) Ca2+ channels open
Lecture Title: MSGD 6 – Rheumatic Heart Disease Page 8 of 18
Transcribed by: MOLINA GASE
 ▪ Increase negative intrathoracic pressure
You HAVE to know the synonyms!!!
• Factors that decrease CO:
▪ Standing
 The autorhythmic ability of the heart starts in the SA ▪ Blood is pulled downward due to
node. It is the SA node that exhibits the autorhythmicity gravity: decrease in VR 
of the heart. Once an impulse is initiated in the SA node. decreased EDV  decreased
This impulse is conducted along the specialized SV  decreased CO
conducting system (dromotropism). It is an electrical ▪ Increased intrapericardial pressure
impulse that is conducted to the atria and ventricles. ▪ Inside the pericardial sac (heart
Upon arrival of this impulse, what is the response of the will have a hard time filling up) 
cardiac muscles? Is it contractility? No, it is excitability. decreased EDV  decreased
The ability to respond to a stimulus, and the stimulus is SV  decreased CO
an electrical stimulus coming from the SA node. The ▪ Decreased ventricular compliance or
electrical response is an action potential, another action decreased elasticity of ventricles
potential. Then after this, is contractility, the actual ▪ It cannot accommodate blood
contraction of the cardiac muscle. going in  decrease in EDV 
VIII. PHYSIOLOGY – Discuss the Effects of Preload, decreased SV  decreased CO
Afterload and Inotropy on the Regulation of Afterload
Stroke Volume
• Total peripheral resistance
Factors affecting stroke volume
• Resistance to the flow of blood coming from the
ventricles during systole
𝑷𝒓𝒆𝒍𝒐𝒂𝒅
𝑺𝒕𝒓𝒐𝒌𝒆 𝒗𝒐𝒍𝒖𝒎𝒆 ∝ • Higher peripheral resistance  increased pressure to
𝒂𝒇𝒕𝒆𝒓𝒍𝒐𝒂𝒅 overcome  decrease in SV  decrease in CO

𝑺𝒕𝒓𝒐𝒌𝒆 𝒗𝒐𝒍𝒖𝒎𝒆
• 𝑪𝒂𝒓𝒅𝒊𝒂𝒄
s 𝒐𝒖𝒕𝒑𝒖𝒕 ∝
𝑻𝒐𝒕𝒂𝒍 𝒑𝒆𝒓𝒊𝒑𝒉𝒆𝒓𝒂𝒍 𝒓𝒆𝒔𝒊𝒔𝒕𝒂𝒏𝒆

Preload
• s
• = EDV
• “Directly” related to SV
• Amount of tension in the ventricles before contraction
• Ventricles contract more forcefully during systole when
it has been filled to a greater degree during diastole
(Frank-Starling Law)
• Increase in EDV (preload)  increase in SV  increase
CO Figure 17: Effects of increasing or decreasing afterload. Afterload is
• Decrease in preload  decrease in SV  decrease CO inversely related to stroke volume and thus cardiac output.

• Conditions that lead to decreased afterload (increased

CO)
▪ Beri-beri: diminished ability of the tissue to
use nutrients  compensatory peripheral
vasodilation  decrease TPR  increase
CO
▪ Arteriovenous fistula (shunt): blood flow
directly from artery into vein  decreased
TPR; increased VR  increased CO
▪ Hyperthyroidism: increase metabolism 
increase O2 usage  vasodilation 
decrease TPR  increase CO
Figure 16: Effects of increasing or decreasing preload. Preload is ▪ Anemia  reduced blood viscocity 
directly related to stroke volume and thus cardiac output. diminished delivery of oxygen 
vasodilation  decrease TPR  increase
• Factors that increase CO: CO
▪ Strong atrial contraction
▪ Increase in total blood volume Contractility (also called Inotropy)
▪ Increase venous tone • Factors
▪ Increase pumping action of skeletal 1. Preload (Frank-Starling Law)
muscle (due to increase in venous return)
Lecture Title: MSGD 6 – Rheumatic Heart Disease Page 9 of 18
Transcribed by: MOLINA GASE
 2. Afterload (increase in afterload decreases pumping
power)
3. Sympathetic nerve supply
▪ Resting sympathetic tone increases
pumping power to 13-15L / min
▪ Maximal sympathetic stimulation increase
pumping power to 25L / min
4. Ventricular hypertrophy
▪ Result of prolonged strenuous activity
▪ Increase pumping power to 35L / min
5. Inotropes
▪ Positive inotropes: INCREASE
CONTRACTILITY
▪ Catecholamine
Inc. cAMP ▪ Xanthine
▪ Glucagon
▪ Glycosides
▪ Negative inotropes: DECREASE
CONTRACTILITY
Inhibit adenelyl ▪ Acetylcholine
cylase ▪ Adenosine
▪ Qunidine
▪ Barbituate
▪ Procainamide

Recall that cAMP activates PKA, which activates Ca2+ channels

leading to more Ca2+ influx from the ECF  increase
contractility
Recall that adenelyl cyclase is needed to activate cAMP 
inhibit adenelyl cyclase  inhibit cAMP  decrease
contractility

6. Others (decrease contraction)

▪ Hypercapnia
▪ Hypoxia
▪ Acidosis
▪ Myocardial infarction or heart failure 
ischemia  decrease SV

Figure 18: Effect of increase or decrease in inotropy on SV. Inotropy

is directly related to SV and CO.

Lecture Title: MSGD 6 – Rheumatic Heart Disease Page 10 of 18

Transcribed by: MOLINA GASE
Figure 19: Biological factors in rheumatic heart disease. The upper portion illustrates the initiating β-hemolytic streptococcal infection of the throat, which
introduces the streptococcal antigens into the body and may also activate cytotoxic T cells. These antigens lead to the production of antibodies against various
antigenic components of the streptococcus, which can cross-react with certain cardiac antigens, including those from the myocyte sarcolemma and glycoproteins
of the valves. This may be the mechanism for inflammation of the heart in acute rheumatic fever, which involves all cardiac layers (endocarditis, myocarditis
and pericarditis). This inflammation becomes apparent after a latent period of 2 to 3 weeks. Active inflammation of the valves may eventually lead to chronic
valvular stenosis or insufficiency. These lesions involve the mitral, aortic, and tricuspid valves, in that order of frequency.

IX. BIOCHEMISTRY - Cross-reactivity to which
component of the Group A Streptococcal bacteria
causes Rheumatic fever/Rheumatic Heart
disease?
• Rheumatic fever (RF) and rheumatic heart disease
(RHD) are complications of the immune-mediated
response to group A (beta-hemolytic) streptococcal
(GAS) throat infection.
• β-hemolytic streptococci are divided into several
serologic groups based on their cell wall
polysaccharide antigen.
• Group A is further subdivided into 130 distinct M types,
which are responsible for the vast majority of infections
• The M protein best defines the virulence of the
bacterium and has been studied most intensively with
regard to cross-reactivity with heart tissue.

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• Pathogenesis of RF still remains unclear
• It is thought that antibodies directed against the M
protein of certain strains of streptococci cross-react with
glycoprotein antigens in the heart, joints, and other
tissues to produce an autoimmune response through a
phenomenon called molecular mimicry.
Ang molecular mimicry kasi parang ganito. May pathogen
ka (in this case GAS) that has a similar genetic sequence
as your antigens in your body.
So in essence, when your B or T cells are activated because
of infection from your GAS, akala nila yung normal cells mo
GAS din dahil nga molecularly similar sila. Kaya
nagkakaroon ka ng case of autoimmunity.
Think of it as a case of mistaken identity… akala mo siya
kambal lang pala niya.
X. The Case!
A 14 year old female came in your emergency
department presenting with a 5-day history of difficulty
of breathing relieved by leaning forward. Upon history
taking, the patient noted chest pain when coughing, 2-
pillow orthopnea, easy fatigability, and persistent
productive cough green to yellow in color in moderate
amounts. Further history revealed upper respiratory
tract infection 3 weeks ago and no consult was done
The past medical history is unremarkable. Family
medical history revealed bronchial asthma, heart
disease, lung cancer and tuberculosis. Review of
systems were unremarkable.
On physical examination, the patient was alert,
cooperative, in moderate cardiorespiratory distress.
Vital signs were as follows: BP= 110/60, HR= 116,
RR= 56cpm, T= 36.6, O2 sat= 97%. No cyanosis
noted. On auscultation of the heart, you noted a
dynamic precordium, S2>S1 at the apex, with heaves,
and a loud systolic murmur with a blowing quality at
the apex radiating to the axilla.
XII. CASE – Discuss the Pathogenesis of RHD
• Molecular mimicry
• There are structural similarities in Streptococci proteins
and proteins lining the valves of the heart
• Antibodies are created in response to Streptococci
infection (M antigen)
• Recurrent episode of Streptococci infection result in the
exaggerated T-cell mediated immune response
• Antibodies cross-react with cardiac myosin and other
alpha-helical proteins such as laminin, tropomyosin,
keratin and vimentin
• In other words, antibodies attack the valves of the heart
XIII. CASE – What is the significance of elevated Anti-
Streptolysin O Titer?
• An elevated ASO titer means that a Px has had a recent
strep infection.
• ASO titer
• Looks for antibodies that your body made while fighting
off group A Streptococcus bacteria. These are
antibodies against a substance called streptolysin O
made by bacteria.
• Normal results are negative, meaning you have no
antibodies to the strep bacteria in your blood. Because
it takes time for the number of antibodies to increase in
your blood after you are infected, you may need to
repeat the ASO titer 2 weeks after the first blood
sample.
• A positive result means that antibodies have been found
and that you may have had a recent strep infection. But
in 1 in 5 cases, this test won’t show an increase in
antibodies when you have an illness such as rheumatic
fever.
XIV. CASE – Identify the Murmur being described in
the patient
Table 1: Mitral valve stenosis and regurgitation

Chest x-ray revealed hazy infiltrates in both lungs, Mitral Valve Quality Timing Location
noting an enlarged heart with a water bottle
Stenosis Low Diastole 5th ICS and
configuration. 2D-echocardiography was also
frequency, the apex (left
performed revealing these results: Left atrial and
weak mid-
ventricular enlargement, no thickening, no
rumbling clavicular
vegetations, (+) pansystolic murmur, and (+) friction
sound w/ line)
rub. Elevated WBC, Neutrophils, and decreased
radiation
Hemoglobin levels. ESR, CRP, and ASO titers are
elevated. Decreased sodium and potassium levels. Regurgitation High Systole
The patient was started on Penicillin G, prednisone, frequency,
furosemide, captopril, and with potassium which swishing
improved the patient’s condition after a few days’ time. sound

XI. CASE – Discuss the etiology and risk factors of

RHD. Factors present in the patient.
• Children between ages 5 and 15
• Frequent cases of strep throat infections
• Poor access to medical care

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Table 2: Aortic valve stenosis and regurgitation • The chest pain of pericarditis is usually sharp and
stabbing. It can radiate to the back, neck, or arm.
Aortic Valve Quality Timing Location ▪ Caused by rubbing of irritated layers of the
Stenosis Harsh, Systole 2nd ICS, right pericardium
LOUD parasternal • The pain may worsen when taking a deep breath or
sound upper chest lying flat and lessen when leaning forward.
▪ Sitting up and leaning forward tend to
Regurgitation Blowing Diastole reduce pressure on the parietal
sound, pericardium, particularly with inspiration
relatively and may allow for splinting of the
high pitched
diaphragm thereby decreasing the
intensity of pericarditis pain.
▪ When you cough, there is a sudden
increase in pressure on the parietal
pericardium due to forceful expiration

XVI. CASE – What are the other manifestations of

Rheumatic Fever
• Jones Criteria for Rheumatic Fever (see above)
• May also show signs of
▪ Joint pain and swelling
▪ Rash
▪ Small, hard, round bumps under the skin
(nodules)
▪ Irregular or jerky movements
▪ Belly (abdominal) pain
▪ Bloody nose
▪ Fever

XVII. CASE – What could have been done to lessen the

Figure 20: Heart murmurs. Note that mitral stenosis has
decrescendo sound beginning at the first third – the rapid filling
phase – of the diastole after the opening snap or end of
isovolumetric relaxation.
XV. CASE – Explain why the Patient’s Chest Pain is
worse with coughing and is relieved by leaning
forward
• Pericarditis is an inflammation of the tissue layers
surrounding the heart.
risk of developing RHD in the patient
• Avoid contact with persons who have strep throat
• Wash your hands
• Replace your toothbrush regularly
• Steps that you need to do in order to prevent sore throat
(kasi ‘di ba ang Strep throat naman is a type of sore
throat)

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Itong following section talagang pa-extra ko siya always sa
dulo ng bawat MSGD… kasi important na alam ang
immediate management and then treatment. You can also
insert yung mga recent researches, pero mas necessary na
alam mo yung management and treatment.

XVIII. EXTRA – What is the immediate management

needed for patients with RHD?
• It is important that streptococcal infections be promptly
diagnosed and treated to prevent RHD.
• Immediate management of RHD is designed to control
the acute inflammatory response and prevent cardiac
complications and recurrence of disease.
• During the acute phase, anti-biotics, anti-inflamatory
drugs, and selective restriction of activities are
prescribed.

XIX. EXTRA – What is the treatment (pharmacology,

surgery or otherwise) for RHD
• Penicillin G – antibiotics
• Prednisone – corticosteroid drug (anti-inflammatory or
anti immune suppressant drug)
• Furosemide – used to treat fluid retention (edema) in
patients with congestive heart failure, liver disease, or
kidney diseases
• Captopril – an ACE inhibitor, used to treat
hypertension, congestive heart failure, kidney problems
due to diabetes and to improve the survival after a heart
attack
• Potassium – potassium lowers the heart rate

Lecture Title: MSGD 6 – Rheumatic Heart Disease Page 14 of 18

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 PHYSIOLOGY MSGD6
TOPIC
LECTURER

XX. Appendix

Lecture Title: MSGD6 – Rheumatic Heart Disease

Transcribed by: MOLINA GASE
 Figure 21: Autoimmune Response of RHD

Lecture Title: MSGD 6 – Rheumatic Heart Disease Page 16 of 18

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 Summary of Heart Valve Disease
Heart Valve Location Disease/Abnormality Timing Murmur / Quality
Harsh, loud, systolic
Stenosis Systole
2nd ICS right ejection murmur
Aortic
parasternal Blowing, high pitch,
Regurgitation Diastole
early diastolic murmur

Semilunar Systolic ejection

Stenosis Systole
murmur

Pulmonary 2nd – 3rd ICS left Can be high-pithed or

low-pitched, often
Regurgitation Diastole
faint, blowing
decrescendo
5th ICS and apex (mid Low frequency, weak
Stenosis Diastole
clavicular line) rumbling
Mitral High frequency,
Regurgitation Systole swishing (“a
Atrioventricular whispered letter r”)
Rumbling murmur,
3rd to 6th ICS (lower
Stenosis Diastole increases with
Tricuspid left sternal edge)
inspiration
Regurgitation Systole Pansystolic murmur

Factors in evaluating heart murmurs

1) Intensity – depends on the volume of blood flow across the valve and the pressure gradient across which the blood flow
occurs
2) Timing – when they are best heard in the cardiac cycle
3) Location

4) Quality / Character – different murmurs have different qualities (i.e., harsh blowing, rumbling, musical or cooing)
5) Pitch – can be high or low pitched depending on the frequency of the murmur

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 6) Radiation – murmurs tend to radiate to certain specific areas (i.e., MR radiates to the axilla or base of the heart; AS
radiates to the carotids; AR radiates along the left sternal border)
7) Configuration – shape of murmur intensity over time (i.e., plateau, decrescendo, crescendo-decrescendo or crescendo)

Lecture Title: MSGD 6 – Rheumatic Heart Disease Page 18 of 18

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