MEDICAL FACULTY Makassar, March 15th 2017

UNIVERSITAS MUSLIM INDONESIA

PBL

1st Modul : Shortness Of Breath

Group : 14th

Tutor : dr. Wisudawan, MKes, SpJP

Members :

 St. Hediati (110 2015 0002)

 Ayu Pratiwi Hasari
 Kurnia Junita Sari R
 Zihan Ayu Pratiwi
 A. Adinda FD
 Dzulfachri K
 Fatturrachman M
 Donita Rian Utami
 Senjawati Martia U
 Nur Azizah F
(110 2015 0011)
(110 2015 0023)
(110 2015 0036)
(110 2015 0044)
(110 2015 0066)
(110 2015 0069)
(110 2015 0080)
(110 2015 0099)
(110 2015 0108)

FAKULTAS KEDOKTERAN
UNIVERSITAS MUSLIM INDONESIA
MAKASSAR
2017

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 1st Scenario

A fifty-year old woman came to hospital with shortness of breath in the

last one week. The SOB worsens with activity and relieved with rest or half-
sitting position. History of hospitalized about two months ago, and it was said as a
heart attack, but had stopped control since last two weeks. Physical examination
shown BP : 160/100 mmHg, HR : 110 beats/minute, RR : 28 times/minute, and
SO2 : 88%. Patient looks pale and had cold sweats. On auscultation there are
crackles on all lung fields, S3 and S4 gallop, no heart murmur. On ECG
examination there is presence of pathological Q waves in lead V1-V6.

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 Difficult Word

 S3 and S4 gallop:
o S3 : A third heart sound occurs early in diastole. caused by a sudden
deceleration of blood flow into the left ventricle from the left atrium.
o S4 : The fourth heart sound occurs in late diastole just prior to the first
heart sound. The fourth heart sound is produced by an increase in
stiffness of the left ventricle due to scar tissue formation.

 Heart murmur
o A heart murmur is an unusual sound heard between
heartbeats. Murmurs sometimes sound like a whooshing or swishing
noise. Murmurs may be harmless, also called innocent, or abnormal.

 SO2
o Is the amount of oxygen bound to hemoglobin in the blood, expressed
as a percentage of the maximal binding capacity.

 Heart Attack
o A heart attack is the death of, or damage to, part of the heart muscle
because the supply of blood to the heart muscle is severely reduced or
stopped.

 Shortness of Breath
o Shortness of breath is a feeling of difficult breathing. It is a
symptom of a variety of different diseases or disorders and may be
either acute or chronic.

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 Keywords

1. A fifty-year old woman

2. Had shortness of breath since 1 week ago, worsens with activity and
relieved with rest or half-sitting position
3. History of hospitalized about 2 months ago and it was said as a heart
attack
4. Had stopped control since last 2 week
5. Physical examination :
 BP : 160/100 mmHg
 HR : 110 beats/minute
 RR : 28 times/minute
 SO2 : 88%
 Crackles (+) on all lung fields
 S3 and S4 gallop
 No heart murmur
6. Patient looks pale and had cold sweats
7. ECG : pathological Q waves in lead V1-V6.

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 Questions

1. What is the pathophysiology of shortness of breath and difference between

shortness of breath that caused by cardiac and non-cardiac disease?
2. Why she feel relieved with rest and half-sitting position?
3. What’s the relation between physical examination result and symptoms on
scenario?
4. What’s the relation between pathological Q waves in lead V1-V6 and
symptoms on scenario?
5. Is there any effect when she had stopped controlling her condition with
present condition?
6. What is the differential diagnosis?
7. Explain the prevention and how to educate about cardiovascular disease!

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 Answer

1. What is the pathophysiology of shortness of breath and difference between

shortness of breath that caused by cardiac and non-cardiac disease?
Answer :
Dyspnea may be defined as an uncomfortable sensation of
breathing. Shortness of breath — known medically as dyspnea — is often
described as an intense tightening in the chest, air hunger or a feeling of
suffocation. Most cases of shortness of breath are due to heart or lung
conditions. Your heart and lungs are involved in transporting oxygen to
your tissues and removing carbon dioxide, and problems with either of
these processes affect your breathing. The mechanisms and
pathophysiology of dyspnea involve interactions between the respiratory
system (both the ventilator function and gas exchange function), the
cardiovascular system, neural responses, and oxygen carriers. For
example, common causes of dyspnea by cardiovascular system are
pulmonary edema, acute valvular disease, myocardial infarction, heart
failure, angina, constrictive pericarditis, etc. Cardiovascular disease is an
important cause of dyspnea. Many of these mechanisms overlap with those
of the respiratory system. For example, in low cardiac output states such as
systolic heart failure, the low output is unable to meet the oxygen demands
of the body causing ischemia due to inadequate tissue perfusion, resulting
in lactate generation and acidemia. Patients with cardiac insufficiency
often have pulmonary edema that impairs gas exchange as well as
increasing the work of breathing, both of which add to the feeling of
shortness of breath. Besides ischemic heart disease, other broad classes of
cardiac disease can impair oxygen delivery by decreasing cardiac output,
including arrhythmias, valvular insufficiency or stenosis, congenital
structural heart disease or remodeling from infarction. or chronic heart
failure. A commonly recognized angina equivalent in patients with acute
coronary syndromes is dyspnea, which may be the only symptom present.

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History, physical examination, and chest film are important to differentiate
the causes of dyspnea, whether it is cardiac or non-cardiac dyspnea.
In obtaining a history, the patient should be asked to describe in
his/her own words what the discomfort feels like, as well as the effect of
position, infections, and environmental stimuli on the dyspnea. Orthopnea
is a common indicator of congestive heart failure (CHF), mechanical
impairment of the diaphragm associated with obesity, or asthma triggered
by esophageal reflux. Nocturnal dyspnea suggests CHF or asthma. Acute,
intermittent episodes of dyspnea are more likely to reflect episodes of
myocardial ischemia, bronchospasm, or pulmonary e, while chronic
persistent dyspnea is typical of COPD, interstitial lung disease, and
chronic thromboembolic disease. Risk factors for occupational lung
disease and for coronary artery disease should be elicited. Left atrial
myxoma or hepatopulmonary syndrome should be considered when the
patient complains of platypnea, defined as dyspnea in the upright position
with relief in the supine position. Pulmonary edema can lead to shortness
of breath.
The physical examination should begin during the interview of the
patient. Inability of the patient to speak in full sentences before stopping to
get a deep breath suggests a condition that leads to stimulation of the
controller or an impairment of the ventilatory pump with reduced vital
capacity. Evidence for increased work of breathing (supraclavicular
retractions, use of accessory muscles of ventilation, and the tripod
position, or stiff lungs and chest wall. When measuring the vital signs, one
should accurately assess the respiratory rate and measure the pulsus
paradoxus; if it is >10 mmHg, consider the presence of COPD or acute
asthma. During the general examination, signs of anemia (pale
conjunctivae), cyanosis, and cirrhosis (spider angiomata, gynecomastia)
should be sought. Examination of the chest should focus on symmetry of
movement; percussion (dullness indicative of pleuraleffusion,
hyperresonance a sign of emphysema); and auscultation (wheezes, rales,

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rhonchi, prolonged expiratory phase, diminished breath sounds, which are
clues to disorders of the airways, and interstitial edema or fibrosis). The
cardiac examination should focus on signs of elevated right heart pressures
(jugular venous distention, edema, accentuated pulmonic component to the
second heart sound); left ventricular dysfunction (S3 and S4 gallops); and
valvular disease (murmurs). When examining the abdomen with the
patient in the supine position, it should be noted whether there is
paradoxical movement of the abdomen (inward motion during inspiration),
a sign of diaphragmatic weakness; rounding of the abdomen during
exhalation is suggestive of pulmonary edema. Clubbing of the digits may
be an indication of interstitial pulmonary fibrosis, and the presence of joint
swelling or deformation as well as changes consistent with Raynaud’s
disease may be indicative of a collagen-vascular process that can be
associated with pulmonary disease. characterized by sitting with one’s
hands braced on the knees) is indicative of increased airway resistance.
Following the history and physical examination, a chest
radiograph should be obtained. The lung volumes should be assessed
(hyperinflation indicates obstructive lung disease; low lung volumes
suggest interstitial edema or fibrosis, diaphragmatic dysfunction, or
impaired chest wall motion). The pulmonary parenchyma should be
examined for evidence of interstitial disease and emphysema. Prominent
pulmonary vasculature in the upper zones indicates pulmonary venous
hypertension, while enlarged central pulmonary arteries suggest
pulmonary artery hypertension. An enlarged cardiac silhouette suggests a
dilated cardiomyopathy or valvular disease. Bilateral pleural effusions are
typical of CHF and some forms of collagen vascular disease. Unilateral
effusions raise the specter of carcinoma and pulmonary embolism but may
also occur in heart failure. Computed tomography (CT) of the chest is
generally reserved for further evaluation of the lung parenchyma
(interstitial lung disease) and possible pulmonary embolism.

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2. Why she feel relieved with rest and half-sitting position?
Answer :
In the recumbent position, there is reduced pooling of fluid in the
lower extremities, and blood is displaced from the extra thoracic to the
thoracic compartment. A failing left ventricle cannot accommodate the
increased blood volume from the right ventricle, and pulmonary venous
and capillary pressures rise. The result is increased interstitial pulmonary
edema, reduced pulmonary compliance, increased airway resistance, and
dyspnea. This condition also known as Orthopnea. Orthopnea can be
defined as dyspnea that develops in the recumbent position and is relieved
by elevation of the head with pillows.
New York Heart Association (NYHA) Functional Classification. It
places patients in one of four categories based on how much they are
limited during physical activity :
 Class I : No limitation of physical activity. Ordinary physical
activity does not cause undue fatigue, palpitation, dyspnea
(shortness of breath).
 Class II : Slight limitation of physical activity. Comfortable at rest.
Ordinary physical activity results in fatigue, palpitation, dyspnea
(shortness of breath).
 Class III : Marked limitation of physical activity. Comfortable at
rest. Less than ordinary activity causes fatigue, palpitation, or
dyspnea.
 Class IV : Unable to carry on any physical activity without
discomfort. Symptoms of heart failure at rest. If any physical
activity is undertaken, discomfort increases.

Diseases of the myocardium resulting from coronary-artery disease

and non-ischemic cardiomyopathies resulting a greater left ventricular end
diastolic volume and an elevation of the left ventricular end diastolic, as
well as pulmonary capillary pressures. These elevated pressures lead to

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interstitial edema and stimulation of pulmonary receptors, thereby causing
dyspnea; hypoxemia due to V/Q mismatch may also contribute to
breathlessness. Diastolic dysfunction, characterized by a very stiff left
ventricle, may lead to severe dyspnea with relatively mild degrees of
physical activity, particularly if it is associated with mitral regurgitation.

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3. What’s the relation between physical examination result and symptoms
based on scenario?
Answer :
Physical Examination Result Sign and Symptoms
BP : 160/100 mmHg HR : 110 bpm SOB
RR : 28 tpm SO2 : 88% Orthopnea
Crackles (+) S3 and S4 Pale & Cold Sweat
gallop
No heart murmur DOE

A. Blood Pressure

(JNC 7. Blood Pressure Classification. https://www.nhlbi.nih.gov/files/docs/guidelines/express.pdf)

Hypertension is defined as a systolic blood pressure (SBP) of 140

mm Hg or more, or a diastolic blood pressure (DBP) of 90 mm Hg or
more, or taking antihypertensive medication. Hypertension is the most
important modifiable risk factor for coronary heart, stroke, congestive
heart failure, end-stage renal disease, and peripheral vascular disease.
The pathogenesis of essential hypertension is multifactorial and
complex. Multiple factors modulate the blood pressure (BP) including
humoral mediators, vascular reactivity, circulating blood volume,

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 vascular caliber, blood viscosity, cardiac output, blood vessel
elasticity, and neural stimulation. Blood pressure also increases
steadily with age as arteries become stiffer and narrower due to plaque
build-up. Vascular and heart disease also contribute to rising blood
pressure in older adults, and a high systolic reading is a major risk
factor for cardiovascular disease in adults over 50 years old.

B. Heart Rate
Normal : 60-100 bpm
Bradicardia : <60 bpm
Tachycardia : >100 bpm
Tachycardia. Tachycardia refers to a fast resting heart rate -
usually at least 100 beats per minute. Heart rates are controlled by
electrical signals that are sent across the tissues of the heart. When the
heart produces rapid electrical signals, tachycardia occurs. When the
heart beats too rapidly, it pumps less efficiently and blood flow to the
rest of the body, including the heart itself, is reduced. Because the
heart is beating quicker, the muscles of the heart (myocardium) need
more oxygen - if this persists, oxygen-starved myocardial cells can die
off, leading to a heart attack (myocardial infarction). The sign and
symptoms are shortness of breath. Tachycardia can be caused by high
blood pressure.

C. Respiration Rate
Normal : 16-24 tpm
Bradypnea : <16 tpm
Tachypnea : >24 tpm
Tachypnea is a rapid, shallow breathing, occurs when a person
take more breaths than normal in a given minute. When a person
breathes rapidly, it’s sometimes known as hyperventilation. Either

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 term applies to this condition. Rapid, shallow breathing can be the
result of anything from a lung infection to heart failure.

D. Oxygen Saturation
Normal : 95% - 100%
Hypoxemia : <90%
Hypoxemia is a below-normal level of oxygen in your blood,
specifically in the arteries. Hypoxemia is a sign of a problem related to
breathing or circulation, and may result in various symptoms, such as
shortness of breath. Normal pulse oximeter readings usually range
from 95 to 100 percent. Values under 90 percent are considered low.
Several factors are needed to continuously supply the cells and tissues
in body with oxygen:
 There must be enough oxygen in the air
 Lungs must be able to inhale the oxygen-containing air — and
exhale carbon dioxide
 Bloodstream must be able to circulate blood to lungs, take up
the oxygen and carry it throughout your body
A problem with any of these factors — for example, high altitude,
asthma or heart disease — might result in hypoxemia, particularly
under more extreme conditions, such as exercise or illness. When
blood oxygen falls below a certain level, body might experience
shortness of breath, headache, and confusion or restlessness.

E. Crackles Sound
Crackles are the sounds that heard in a lung field that has fluid in
the small airways. As stated before, crackles and rales are the same
thing, and this can often lead to confusion. Crackles come in two
flavours: fine and coarse. Fine crackles sound like salt heated on a
frying pan or the sound of rolling your hair between your fingers next
to your ear. Coarse crackles sound like pouring water out of a bottle or

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 like ripping open Velcro. This lung sound is often a sign of adult
respiratory distress syndrome, early congestive heart failure, asthma,
and pulmonary oedema. Crackles occur with other symptoms, such as
shortness of breath, fatigue, chest pain, etc. Pulmonary edema may
cause crackling sounds in your lungs. People with congestive heart
failure (CHF) often have pulmonary edema. CHF occurs when the
heart cannot pump blood effectively. This results in a backup of blood,
which increases blood pressure and causes fluid to collect in the air
sacs in the lungs.

F. S3 dan S4 Gallop
The third heart sound (S3) occurs during the rapid filling phase of
ventricular diastole. The third heart sound (S3), also known as the
“ventricular gallop,” occurs just after S2 when the mitral valve opens.
It can be a normal finding in children, adolescents, and young adults;
how-ever, in older patients it signifies heart failure. A left-sided S3 is a
low-pitched sound best heard over the left ventricular (LV) apex. A
right-sided S3 is usually better heard over the lower left sternal border
and becomes louder with inspiration. A left-sided S3 in patients with
chronic heart failure is predictive of cardiovascular morbidity and
mortality. Interestingly, an S3 is equally prevalent among heart failure
patients with and without LV systolic dysfunction. A S3 heart sound
is often a sign of systolic heart failure, however it may sometimes be a
normal finding.
The fourth heart sound (S4) occurs during the atrial filling phase of
ventricular diastole and indicates left ventricular presystolic expansion.
The fourth heart sound (S4), also known as the “atrial gallop,” occurs
just before S1 when the atria contract to force blood into the left
ventricle. An S4 is more common among patients who derive
significant benefit from the atrial contribution to ventricular filling,
such as those with chronic left ventricular hypertrophy or active

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 myocardial ischemia. An S4 is not present with atrial fibrillation. A S4
heart sound is often a sign of diastolic heart failure, and it is rarely a
normal finding.
S3 and S4 gallop can be found on left ventricular dysfunction. Both
the third and fourth heart sounds (S3 and S4) are low frequency. S4 is
lower than S3. This is a pattern that occurs with improvement of heart
failure.

G. Heart Murmur
Heart murmurs result from audible vibrations that are caused by
increased turbulence and are defined by their timing within the cardiac
cycle. Not all murmurs are indicative of structural heart disease, and
the accurate identification of a benign or functional systolic murmur
often can obviate the need for additional testing in healthy subjects.
The duration, frequency, configuration, and intensity of a heart
murmur are dictated by the magnitude, variability, and duration of the
responsible pressure difference between two cardiac chambers, the two
ventricles, or the ventricles and their respective great arteries. The
intensity of a heart murmur is graded on a scale of 1 to 6; a thrill is
present with murmurs of grade 4 or greater intensity. Other attributes
of the murmur that aid in its accurate identification include its location,
radiation, and response to bedside maneuvers. Although clinicians can
detect and correctly identify heart murmurs with only fair reliability, a
careful and complete bedside examination usually can identify
individuals with valvular heart disease for whom transthoracic
echocardiography and clinical follow-up are indicated and exclude
subjects for whom no further evaluation is necessary.

H. DOE (Dyspnea on Exertion)

Shortness of breath with exertion is referred to as dyspnea on
exertion. Dyspnea on exertion occurs because the lungs cannot supply

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enough oxygen and the heart cannot adequately pump oxygen-rich
blood to the body. Initially, the shortness of breath may occur when
walking long distances or up flights of stairs, but as the heart failure
progresses, less activity may produce more symptoms. An
exacerbation of heart failure may be described as a sensation of
shortness of breath with exertion. Dyspnea on Exertion (DOE) is a
condition where a person finds it difficult to breathe or becomes
breathless upon any type of exertion. By exertion, it does not only
mean exercise, but also simple physical activities of daily living such
as going to the mailbox or walking up the stairs. Congestive heart
failure is one of the commonest causes of dyspnea on exertion. Low
body oxygenation is an important causative factor and this is always
seen in patients who present with dyspnea on exertion. Congestive
heart failure (CHF) where the patient has dyspnea on exertion or
shortness of breath on exertion initially, then also feels dyspnea on
rest. Other accompanying symptoms include chest pain and
palpitations.

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4. What’s the relation between pathological Q waves in lead V1-V6 and
symptoms on scenario?
Answer :
An 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
then are amplifi ed and recorded by the electrocardiograph. ECG leads
actually display the instantaneous differences in potential between the
electrodes. The ECG, however, records only the depolarization
(stimulation) and repolarization (recovery) potentials generated by the
atrial and ventricular myocardium.

(Images shown a normal ECG)

The QRS complex represents ventricular depolarization, and the
ST-T-U complex (ST segment, T wave, and U wave) represents
ventricular repolarization. The J point is the junction between the end of
the QRS complex and the beginning of the ST segment. The QRS interval
(normally 100–110 ms or less) reflects the duration of ventricular
depolarization. The QT interval includes both ventricular.depolarization
and repolarization times and varies inversely with the heart rate

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 A Q wave is any negative deflection that precedes an R wave. The
Q wave represents the normal left-to-right depolarisation of the
interventricular septum. Small ‘septal’ Q waves are typically seen in the
left-sided leads (I, aVL, V5 and V6).

Small Q waves are normal in most leads. Deeper Q waves (>2 mm)
may be seen in leads III and aVR as a normal variant. Under normal
circumstances, Q waves are not seen in the right-sided leads (V1-3). Q
waves are considered pathological if :
 40 ms (1 mm) wide
 > 2 mm deep.
 > 25% of depth of QRS complex
 Any Q wave in leads V1- V3 with a duration of >0.02seconds
is likely to be pathological.
 Seen in leads V1-3. A pathological Q wave may also be broad,
in appearance, but again, must be seen in two contiguous leads.
A pathological Q wave is a result of absence of electrical activity,
following myocardial damage. They generally take several hours to
develop after an MI, and usually persist indefinitely. The exception to this
is if seen during an acute MI, but the myocardial tissue is reperfused early
by Primary PCI (Percutaneous Coronary Intervention). The myocardial
tissue can then recover, and the pathological Q waves disappear. Necrosis
of sufficient myocardial tissue may lead to decreased R-wave amplitude or
abnormal Q waves. Previously, abnormal Q waves were considered
markers of transmural myocardial infarction, whereas subendocardial
infarcts were thought not to produce Q waves. However, careful ECG-
pathology correlative studies have indicated that transmural infarcts may

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occur without Q waves and that subendocardial (nontransmural) infarcts
sometimes may be associated with Q waves. Therefore, infarcts are more
appropriately classified as “Q-wave” or “non-Q-wave.” The differential
diagnosis of Q waves includes physiologic or positional variants,
ventricular hypertrophy, acute or chronic noncoronary myocardial injury,
hypertrophic cardiomyopathy, and ventricular conduction disorders.
Myocardial infarction, Cardiomyopathies — Hypertrophic (HOCM),
infiltrative myocardial disease, Rotation of the heart — Extreme clockwise
or counter-clockwise rotation, and Lead placement errors — e.g. upper
limb leads placed on lower limbs also can give Q wave pathologic result.

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5. Is there any effect when she had stopped controlling her condition with
present condition?
Answer :
Patients with heart failure have complex medication regimens and
dietary restrictions requiring frequent medication adjustments and
monitoring. They also often have difficulty in adhering to complex
treatment, which may lead to a more rapid progression of their disease and
problems that require emergency care or hospitalization. Cardiac
rehabilitation (rehab) is a supervised program that uses exercise,
education, and support to help people recover from a heart attack, heart
surgery, or other heart problems. Cardiac rehab programs are medically
supervised and individually designed based on a person's needs and overall
health. The heart failure clinic staff follow up periodically to ensure he’s
on track. Most people with heart failure are treated with medication. Often
you'll need to take two or three different medicines. Medicines can,
Relieve or control symptoms, treat other health problems you have, such
as coronary artery disease, Improve your daily quality of life, Slow the rate
at which your heart failure gets worse, Reduce the chance of other
problems from heart failure, such as stroke, Reduce hospital stays, and
Help you live as long as possible. The medicines you take will depend on
the type of heart failure you have. The most commonly used medicines
medicines for pumping problems (heart failure with reduced ejection
fraction, or systolic heart failure), medicines for filling problems (heart
failure with preserved ejection fraction, or diastolic heart failure), etc.

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6. What is the differential diagnosis?
Answer:
A. Coronary artery disease (CAD)

Coronary artery disease (CAD) is the most common type of heart

disease. CAD happens when the arteries that supply blood to heart
muscle become hardened and narrowed. This is due to the buildup of
cholesterol and other material, called plaque, on their inner walls. This
buildup is called atherosclerosis. As it grows, less blood can flow
through the arteries. As a result, the heart muscle can't get the blood or
oxygen it needs. This can lead to chest pain (angina) or a heart attack.
Most heart attacks happen when a blood clot suddenly cuts off the
hearts' blood supply, causing permanent heart damage. Over time,
CAD can also weaken the heart muscle and contribute to heart failure
and arrhythmias. Heart failure means the heart can't pump blood well
to the rest of the body. Arrhythmias are changes in the normal beating
rhythm of the heart. Coronary heart disease is a common term for the
buildup of plaque in the heart’s arteries that could lead to heart attack.
Over time, plaque can harden or rupture (break open). Hardened
plaque narrows the coronary arteries and reduces the flow of oxygen-
rich blood to the heart. If the plaque ruptures, a blood clot can form on

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its surface. A large blood clot can mostly or completely block blood
flow through a coronary artery. Over time, ruptured plaque also
hardens and narrows the coronary arteries.
Pathophysiology. CAD is a chronic process that begins during
adolescence and slowly progresses throughout life. Independent risk
factors include a family history of premature CAD, cigarette smoking,
diabetes mellitus, hypertension, hyperlipidemia, sedentary lifestyle,
and obesity. These risk factors accelerate or modify a complex and
chronic inflammatory vascular process that ultimately manifests as
fibrous atherosclerotic plaque. The most widely accepted theory of
atherosclerosis states that the process represents the body's attempt to
heal in response to an endothelial injury. The first step in the
atherosclerotic process is the development of fatty streaks, which
contain atherogenic lipoproteins and macrophage foam cells. These
streaks form between the endothelium and internal elastic lamina. Over
time, an intermediate lesion composed of an extracellular lipid core
and layers of smooth muscle and connective tissue matrix eventually
forms a fibrous cap. The edge of the fibrous cap (the shoulder region)
plays a critical role in the development of acute coronary syndromes.
The shoulder region is the site where most plaques lose their integrity
or rupture. Plaque rupture exposes the underlying thrombogenic core
of lipid and necrotic material to circulating blood and its thrombogenic
particulates. This exposure results in platelet adherence, aggregation,
and progressive luminal narrowing, which can rapidly progress and—
often in the absence of coronary artery collateral development—are
associated with acute coronary syndromes.

21
22
 Vascular inflammation has emerged as a critical and
established component of atherosclerosis genesis, activity, and
potential plaque instability. Patients with established CAD who

23
possess a confluence of risk factors known as the metabolic syndrome
remain at particularly high risk for a future vascular event, such as an
acute MI or cerebrovascular accident. Biochemical markers such as
elevated levels of high sensitivity or ultra-sensitive C-reactive protein
in the absence of systemic inflammation are thought to signal an
increased likelihood of vascular inflammation and to portend a higher
risk of vascular events. This marker may also signal more rapidly
advancing CAD and the need for aggressive preventive measures.

Risk factor. Coronary artery disease (CAD) is more frequently

associated with dysfunction of the coronary microcirculation in women
than in men. Other risk factors for heart disease include:
 Age
 Family history
 High blood pressure
 High cholesterol
 Smoking
 Poor diet
 Overweight or obesity
 Inactivity (sedentary lifestyle)
 Other health problems (such as diabetes)
Symptoms. Coronary artery disease may take years to develop.
You may not notice any symptoms of coronary artery disease until the
disease progresses. As your arteries become blocked you may
experience, angina (a squeezing pain or pressing feeling in your chest),
shortness of breath and heart attack.
Examination :
 A review of your medical history and a physical exam.
 Blood tests.
 Electrocardiogram (EKG, ECG) :

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 An EKG is a simple, painless test that detects and
records the heart's electrical activity. The test shows how
fast the heart is beating and its rhythm (steady or irregular).
An EKG also records the strength and timing of electrical
signals as they pass through the heart. An EKG can show
signs of heart damage due to CHD and signs of a previous
or current heart attack. Early diagnosis of coronary
atherosclerosis is mainly based on some risk stratification
approaches, including medical history, physical
examination, an electrocardiogram and serum cardiac
marker measurements and therefore the diagnosis requires a
careful review of cardiac ischemia manifestations. The
recognition and management of patients with CAD has
relied to a large extent on the ECG for assessing ST-
segment changes, T inversion and Q wave appearance
associated with ischemia. Q wave had the highest
sensitivity for detection of involvement in both RCA and
LCX arteries.

 Chest X-ray.
 Echocardiogram (echo).
 Brain natriuretic peptide (BNP).
 Magnetic resonance imaging (MRI).

25
  Cardiac blood pool scan.
An echocardiogram may be used to diagnose heart failure.
It also can help guide treatment. Tests also may be done to find
areas of the heart that are not getting enough blood. These tests
include:
 Cardiac perfusion scan. This test can show poor blood flow
to the heart.
 Cardiac catheterization. This test can be used to check for
blocked or narrowed heart arteries and to measure pressures
inside the heart.
Treatments. Most people who have CAD take medicine to
help control their condition. Medicines called beta-blockers,
calcium channel blockers and nitrates can help relieve angina.
Taking low-dose aspirin every day can reduce the chance of a
second heart attack in people who have already had one. Medicines
for pumping problems (heart failure with reduced ejection fraction,
or systolic heart failure) :
 ACE inhibitors (angiotensin-converting enzyme inhibitors) relax
and widen blood vessels. This makes it easier for blood to flow.
 Aldosterone receptor antagonists, a type of diuretic, make the
kidneys get rid of extra fluid.
 ARBs (angiotensin II receptor blockers) make it easier for blood
to flow through the vessels. You might take an ARB that is
combined with another medicine in one pill.
 Beta-blockers slow the heart rate. They also may help the heart
fill with blood more completely.
 Digoxin helps the heart pump more blood with each beat.
 Diuretics help relieve symptoms like swelling in the legs.
 Hydralazine taken with a nitrate widens blood vessels. This
medicine can lower blood pressure and reduce the workload on
the heart.

26
  Ivabradine slows the heart rate. This medicine may help prevent
some people from being hospitalized for heart failure.
Medicines for filling problems (heart failure with preserved
ejection fraction, or diastolic heart failure) such as ACE inhibitors,
ARBs, Beta-blockers, and diuretics. Other medicines for health
problems that can cause heart failure or for problems caused by heart
failure are Antiarrhythmics prevent very fast and sometimes irregular
heart rhythms and Blood thinners, also known as anticoagulants,
prevent dangerous blood clots.
Angioplasty is a surgical treatment for CAD. Angioplasty uses
a tiny balloon to push open blocked arteries around the heart. The
balloon is inserted in an artery in the arm or leg. A small metal rod
called a stent might be put into the artery where the blockage was to
hold the artery open. Another surgical treatment for CAD is bypass
surgery. Pieces of veins or arteries are taken from the legs and sewn
into the arteries of the heart to bring blood past a blockage and
increase the blood flow to the heart. Bypass surgery is usually done
when angioplasty isn't possible or when doctor feels it's a better
choice.

B. Left-sided Heart-Failure
Heart failure is characterized by the heart’s inability to pump an
adequate supply of blood. Without sufficient blood flow, all major
body functions are disrupted. Heart failure is a condition or a
collection of symptoms that weaken your heart. In some people with
heart failure, the heart has difficulty pumping enough blood to support
other organs in the body. Other people may have a hardening and
stiffening of the heart muscle itself, which blocks or reduces blood
flow to the heart. Heart failure can affect the right or left side of your
heart, or both at the same time. It can be either an acute (short-term) or
chronic (ongoing) condition. In acute heart failure, the symptoms

27
appear suddenly but go away fairly quickly. This condition often
occurs after a heart attack. It may also be a result of a problem with the
heart valves that control the flow of blood in the heart. In chronic heart
failure, however, symptoms are continuous and don’t improve over
time. The vast majority of heart failure cases are chronic.

Left-sided heart failure is the most common type of heart failure.

The left heart ventricle is located in the bottom left side of your heart.
This area pumps oxygen-rich blood to the rest of your body. Left-sided
heart failure occurs when the left ventricle doesn’t pump efficiently.
This prevents your body from getting enough oxygen-rich blood. The
blood backs up into your lungs instead, which causes shortness of
breath and a buildup of fluid.
There are two types of left-sided heart failure:
1. Preserved ejection fraction (HFpEF), also called diastolic heart
failure—the heart muscle contracts normally but the ventricles
do not relax as they should during ventricular filling (or when
the ventricles relax).

2. Reduced ejection fraction (HFrEF), also called systolic heart

failure —the heart muscle does not contract effectively and less
oxygen-rich blood is pumped out to the body.

28
Risk Factor. Risk factor of having left-sided heart failure are :
 Drinking too much alcohol
 Heart attack history
 Heart muscle infections
 High blood pressure
 Hypothyroidism
 Leaking or narrow heart valves
 Any other disease that damages the heart muscle
 Poor left-side heart function due to prior heart attacks
Pathogenesis.
A. Myocyte loss and/or dysfunction In addition to global
mechanical dysfunction in heart failure, another key player in
this process may be dysfunction at a cellular level.
 Myocyte loss
o Necrosis – resulting from insults such as MI or exposure
to cardiotoxic drugs
o Apoptosis (programmed cell death) from elevated
catecholamines, angiotensin II, inflammatory cytokines,
and mechanical strain from increased wall stress
 Changes activated in expression of contractile proteins, ion
channels, enzymes, receptors and secondary messengers
o Reduced cellular ability to maintain calcium homeostasis
o Changes in handling of high-energy phosphates
B. Compensatory mechanisms. These mechanisms attempt to
maintain sufficient blood pressure to perfuse vital organs by
compensating for the decrease in cardiac output that occurs in
heart failure.
 Frank-Starling mechanism. Frank-Starling relationship:
Ventricular output increases in relation to preload, i.e. with a

29
 greater stretch of myocardial fibers (larger diastolic volume),
there will be a greater force of contraction generated. In heart
failure, a decreased stroke volume results in reduced chamber
emptying, with higher than normal diastolic volume. This
induces a greater stroke volume for the subsequent
contraction to help empty the ventricle and preserve forward
cardiac output. However this mechanisms has limits, and at
markedly elevated diastolic volumes, the stretch of myofibers
becomes too great and suboptimal for generating a strong
contraction
 Myocardial hypertrophy. Wall stress is often increased in
heart failure due to either ventricular dilatation or the need to
generate high systolic pressures to overcome excessive
afterload. In response to a sustained increase in pressure and
chamber radius, hypertrophy of the ventricular myocytes is
stimulated. The increased mass of muscle fibers serves to
maintain contractile force and counteract the elevated
ventricular wall stress. Eventually, the chamber may dilate
out of proportion to wall thickness, resulting in excessive
hemodynamic burden on the contractile units, rapid
deterioration of ventricular function and worsening of
symptomatology. Lowering wall stress as a way to slow the
remodelling process is a common therapeutic targe.
 Neuro-hormonal mechanisms. In the early stages of heart
failure, these mechanisms help maintain a near normal
perfusion to vital organs by increasing systemic vascular
resistance as a way to balance the fall in cardiac output
(blood pressure (BP) = cardiac output (CO) × total peripheral
resistance (TPR)). In addition, activation of neuro-hormonal
mechanisms leads to salt and water retention with a
consequent increase in intravascular volume and preload,

30
 which maximizes stroke volume via the Frank-Starling
mechanism.
o Renin-angiotensin-aldosterone system (RAAS): The
pathway leads to the activation of angiotensin II.
o Angiotensin II. Vasoconstriction: Increases TPR to
maintain BP. Increased intravascular volume to increase
preload to raise the SV via Frank-Starling mechanism.
Angiotensin II does this by (i) stimulating thirst at
hypothalamus and (ii) increasing aldosterone secretion at
adrenal cortex.
o Aldosterone. Increased water retention via increased
sodium resorption. This increases preload, in turn
increasing the SV
o Antidiuretic hormone (ADH, aka vasopressin).
Increased secretion thought to be induced by arterial
baroreceptors (detecting decreased CO) and increased
angiotensin II levels. Promotes water retention in the
distal collecting tubule, in order to increase preload
 Adrenergic nervous system. Decreased CO results in
decreased perfusion pressure sensed by baroreceptors in
carotid sinus and the aortic arch. Central and peripheral
chemoreflex activation induces epinephrine, norepinephrine,
and vasopressin release. This results in an increased
sympathetic outflow to heart and peripheral circulation, and
decreased parasympathetic tone. Increased HR and
contractility directly increase cardiac output (CO = HR ×
SV). Peripheral vasoconstriction. Venous: Increases preload
(venous return). Arteriolar: Raises peripheral vascular
resistance, to maintain BP. Unfortunately, despite these
compensatory mechanisms, there is progressive decline in the
heart’s ability to contract and relax in the face of persistent

31
 hemodynamic challenges. Furthermore, chronic activation of
the above mechanisms ultimately becomes maladaptive and
induces further worsening of cardiac performance.
 Deleterious consequences of compensatory mechanisms.
Continuous sympathetic activation results in downregulation
of β-adrenergic receptors with decreased sensitivity to
circulating catecholamines and less inotropic response.
Increased heart rate augments metabolic demands and can
further reduce performance by increasing myocardial cell
death. Increased circulating volume and preload ultimately
overwhelm Frank-Starling mechanism and heart’s ability to
maintain forward flow, resulting in worsening of lung
vasculature congestion. Increased total peripheral resistance
results in higher afterload, impeding the left ventricle’s stroke
volume and reducing cardiac output. Chronically elevated
angiotensin II and aldosterone trigger production of
cytokines, which activate macrophages an stimulate
fibroblasts resulting in adverse heart remodelling.
Symptoms :
 Cough (produces frothy or blood-tinged mucus)
 Decreased urine production
 Difficulty lying down; need to sleep with the head elevated
to avoid
 shortness of breath
 Fatigue, weakness, faintness
 Irregular or rapid pulse
 Sensation of feeling the heartbeat (palpitations)
 Shortness of breath
 Waking up due to shortness of breath (paroxysmal
nocturnal dyspnea)

32
  Weight gain from fluid retention

Examination. An echocardiogram is the most effective way to

diagnose heart failure. It uses sound waves to create detailed pictures
of your heart, which help to evaluate the damage of heart and
determine the underlying causes. The use of echocardiogram may be
done along with other tests, including the following:
 Chest X-rays can provide images of the heart and the
surrounding organs.
 An electrocardiogram (EKG) measures the electrical
activity of the heart.

33
  An MRI produces images of the heart without the use of
radiation.
 During a nuclear scan, a very small dose of radioactive
material is injected into your body to create images of the
chambers of your heart.
 A catheterization or coronary angiogram is a type of X-ray
exam in which inserts a thin tube called a catheter into
blood vessel, usually in the groin or arm. Then it guides
into the heart. This test can show how much blood is
currently flowing through the heart.
 During a stress exam, an electrocardiogram machine
monitors heart function while running on a treadmill or
perform another type of exercise.
 Electrode patches can be placed on chest and attached to a
small machine called a Holter monitor. This machine
records the electrical activity of heart for at least 24 to 48
hours.
Pharmacologic Therapy. The 2013 American College of
Cardiology/American Heart Association (ACC/AHA) updated
guidelines, 2010 Heart Failure Society of America (HFSA) guidelines,
and the 2008 European Society of Cardiology (ESC) guidelines, with
varying levels of evidence, recommend the following:
 Diuretics (to reduce edema by reduction of blood volume
and venous pressures) and salt restriction (to reduce fluid
retention) in patients with current or previous heart failure
symptoms and reduced left ventricular ejection fraction
(LVEF) for symptomatic relief
 Angiotensin-converting enzyme inhibitors (ACEIs) for
neurohormonal modification, vasodilatation, improvement
in LVEF, and survival benefit

34
  Angiotensin receptor blockers (ARBs) for neurohormonal
modification, vasodilatation, improvement in LVEF, and
survival benefit
 Hydralazine and nitrates to improve symptoms,
ventricular function, exercise capacity, and survival in
patients who cannot tolerate an ACEI/ARB or as an add-on
therapy to ACEI/ARB and beta-blockers in the black
population for survival benefit
 Beta-adrenergic blockers for neurohormonal
modification, improvement in symptoms and LVEF,
survival benefit, arrhythmia prevention, and control of
ventricular rate
 Aldosterone antagonists, as an adjunct to other drugs for
additive diuresis, heart failure symptom control, improved
heart rate variability, decreased ventricular arrhythmias,
reduction in cardiac workload, improved LVEF, and
increase in survival
 Digoxin, which can lead to a small increase in cardiac
output, improvement in heart failure symptoms, and
decreased rate of heart failure hospitalizations
 Anticoagulants to decrease the risk of thromboembolism
 Inotropic agents to restore organ perfusion and reduce
congestion
Invasive therapies. Invasive therapies for heart failure include
electrophysiologic intervention such as cardiac resynchronization
therapy (CRT), pacemakers, and implantable cardioverter-
defibrillators (ICDs); revascularization procedures such as coronary
artery bypass grafting (CABG) and percutaneous coronary intervention
(PCI); valve replacement or repair; and ventricular restoration.

35
 Complication are Pulmonary edema, Total failure of the heart to
function (circulatory collapse), Abnormal heart rhythm, Side effects of
medications, and death.
Prognosis. Heart failure is a serious condition that can result in
early death. How well a person does depends on the cause of the heart
failure, as well as the person's age and ability to tolerate exercise. In
many cases, there is little chance that the heart will fully recover.
However, many forms of heart failure are well controlled with
medication and the condition can remain stable for many years with
only occasional flare ups of symptoms

36
7. Explain the prevention and how to educate about cardiovascular disease!
Answer :
Some things that can be done to prevent congestive artery disease are :
o Don't smoke. Nicotine raises blood pressure because it causes
body to release adrenaline, which makes blood vessels constrict
and heart beat faster.
o Control your blood pressure. If you have high blood pressure,
your doctor can suggest ways to lower it. If you're taking medicine
for high blood pressure, be sure to take it just the way your doctor
tells you to.
o Exercise. Regular exercise can make your heart stronger and
reduce your risk of heart disease. Exercise can also help if you
have high blood pressure. Before you start any new exercise
program, talk to your doctor about the right kind of exercise for
you.
o Ask doctor about taking a low dose of aspirin each day. Aspirin
helps prevent CAD, but taking it also has some risks.
o Ask doctor about taking vitamin supplements. While foods that
are rich in vitamin E and beta-carotene are very healthy and help
reduce cardiovascular risk, the U.S. Preventive Services Task
Force and the American Academy of Family Physicians
recommend against taking vitamin E or beta-carotene supplements
for the prevention of cardiovascular disease. Even though a diet
rich in healthy foods reduces cardiovascular risk, there is no clear
evidence that taking multivitamins does the same thing.
o Eat a healthy diet. Choose fruits, vegetables, meats, fish, and
whole grains. Try to avoid processed foods, white flour, sugars,
and high fructose corn syrup. The Mediterranean Diet is also very
good for heart health. If you have questions, talk to your doctor
about how to make heart-healthy changes to your diet.

37
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