Diseases of Cardiovascular

system
 Chest Pain
• Chest pain” is an imprecise term

• It is often used to describe any pain,

pressure, squeezing, choking, numbness or
any other discomfort in the chest, neck, or
upper abdomen, and is often associated
with pain in the jaw, head, or arms

• It can last from less than a second to days

or weeks, can occur frequently or rarely,
and can occur sporadically or predictably.
• Chest pain is merely a symptom, not
a diagnosis

• Many medical problems can cause

chest pain, and before the chest pain
can be adequately treated, the
actual underlying cause needs to be
identified
 Differential Diagnosis of Chest
Pain
Cardiovascular Pulmonary
Typical angina pectoris
Prinzmetal’s or variant Pleuritic chest pain
angina Pneumonia
Unstable or accelerating Pulmonary embolism
angina Pulmonary
Acute myocardial infarction hypertension
Aortic dissection Spontaneous
Mitral valve prolapse pneumothorax
Pericarditis
Dressler’s syndrome
Postpericardiotomy
syndrome
 Musculoskeletal
Gastrointestinal disorders
Reflux esophagitis Costochondritis
Esophageal Tietze’s syndrome
spasm/angina Rib fracture or trauma
Cancer metastasis
Peptic ulcer Sternoclavicular arthritis
Pancreatitis Painful xiphoid syndrome
Cholecystitis Fibromyalgia
Traumatic muscle pain
Shoulder arthritis/bursitis
Miscellaneous Cervicothoracic nerve root
Herpes zoster compression
Thoracic spine arthritis
Anxiety/depressive Throracic outlet syndrome
disorder
Panic disorder
Cocaine use
Post coronary artery
bypass pain
 Differential Diagnosis of
•
Chest Pain
Myocardial ischemia

• Pain is described as dull, aching, or as a sensation of

"pressure," "tightness," "squeezing," or "gas," rather than as
sharp or spasmodic
• Ischemic symptoms usually subside within 5–20 minutes
but may last longer
• Progressive symptoms or symptoms at rest may represent
unstable angina due to coronary plaque rupture and
thrombosis
• One clue that the pain may be ischemic is other symptoms
associated with the pain, such as shortness of breath,
dizziness, a feeling of impending doom, and vagal symptoms,
such as nausea and diaphoresis
 • Myocardial infarction

• Pain is commonly accompanied by a sense of anxiety or

uneasiness
• The location is usually retrosternal or left precordial
• Because there are no appropriate sensory nerves on the
heart, the central nervous system (CNS) interpretation of
pain location often results in pressure or “heaviness”
being referred to the throat, lower jaw, shoulders, inner
arms, upper abdomen, or back
• Ischemic pain may be precipitated by exertion, cold
temperature, meals, stress, or combinations of these
factors and is usually relieved by rest, but many
episodes do not conform to these patterns
• It is not related to position or respiration and is usually
not elicited by chest palpation
• In myocardial infarction, a precipitating factor is
frequently not apparent.
• Hypertrophy of either ventricle or
stenotic aortic valvular disease may
also give rise to ischemic pain or pain
with less typical features

• Myocarditis, pulmonary hypertension,

and mitral valve prolapse are also
associated with chest pain atypical for
angina pectoris
 • Reflux oesophagitis or Oesophageal
spasm

• The most common cause of chest pain

• Heartburn

• Worse in recumbent position, but also while

straining, like angina pectoris

• No ECG changes
 • Aortic dissection

• Classically produces an abrupt onset of tearing pain

of great intensity that often radiates to the back

• Pulses may be asymmetrical

• Type A dissection sometimes obstructs the origin of a

coronary artery (usually the right) with signs of
impending inferoposterior infarction

• Sometimes broad mediastinum on chest x-ray

• New aortic valve regurgitation

 • Pericarditis
• Pericarditis may produce pain that is greater
supine than upright
• Change of posture and breathing or
swallowing influence the pain
• A friction sound may be heard
• ST-elevation but no reciprocal ST depression

• Pleuritis
• A stabbing pain when breathing
• The most common cause of stabbing pain is,
however, caused by prolonged cough
 • Pulmonary embolism
• Pain is not often marked

• Tachypnoea, hypoxaemia, hypocarbia

• No pulmonary congestion on chest x-ray

• Clinical presentation may resemble hyperventilation.

• Both arterial oxygen pressure (PaO2) and partial

arterial pressure of carbon dioxide (PaCO2) decreased.

• D-dimer assay positive

 • Musculoskeletal Chest Pain
• Pain on palpation

• Cholecystitis
• Character of pain; RUQ tenderness with +
Murphy’s sign; age; gender; obesity;
relationship to eating fatty foods
•
• Psychogenic
• Unexplained chest pain and
hyperventilation;
 DIAGNOSTIC STUDIES
• An immediate diagnostic study would
include a 12 lead electrocardiogram (ECG)
• Examine the ECG for Q waves and ST
segment elevation greater than 1 mm in two
contiguous leads which would indicate injury
and/or myocardial infarction
• ST segment depression greater than 0.5 mm
is suggestive of myocardial ischemia
• Further evaluation would include cardiac
enzymes including CK-MB and a chest x-ray
 Palpitations
• Awareness of the heartbeat

• It may be a normal phenomenon

• It may reflect increased cardiac or stroke

output in patients with many noncardiac
conditions (eg, exercise, thyrotoxicosis,
anemia, anxiety

• It may also be due to cardiac

abnormalities that increase stroke volume
(regurgitant valvular disease, bradycardia)
• It may be a manifestation of cardiac
dysrhythmia

• Ventricular premature beats may be

sensed as extra or "skipped" beats

• Supraventricular or ventricular
tachycardia may be felt as rapid, regular
or irregular palpitations or "fluttering”
• If the abnormal rhythm is associated with
a sufficient decline in arterial pressure or
cardiac output, it may—especially in the
upright position—impair cerebral blood
flow, causing lightheadedness, blurring of
vision, loss of consciousness (syncope),
or other symptoms

• Dizziness in particular is nonspecific and

is an uncommon symptom of cardiac
disease or dysrhythmia
 Cardiogenic syncope
Most commonly results from:

• Bradyarrhythmias (sinus node arrest or exit block,

atrioventricular [AV] conduction block)

• Very rapid supraventricular rhythms

• Ventricular tachycardia or fibrillation

• The absence of premonitory symptoms helps

distinguish cardiogenic syncope from vasovagal
faints, postural hypotension, or seizure but is not a
reliable screening tool

• Although recovery is often immediate, some patients

may exhibit seizure-like movements
• Aortic stenosis and hypertrophic obstructive
cardiomyopathy may also cause syncope, which
is usually exertional or postexertional

Neurocardiogenic syncope
• Commonly known as vasovagal syncope

• There is an inappropriate increase in vagal

efferent activity, often resulting from a precedent
increase in sympathetic cardiac stimulation

• Syncope may follow presyncopal symptoms and

may accompany a brief period of nausea and/or
diaphoresis, or it may be abrupt in onset,
mimicking arrhythmia-induced syncope
• Autonomic dysfunction due to venous
insufficiency or peripheral neuropathy can
result in a positional fall in blood pressure
(BP), and supine and upright BPs should be
checked in all patients with syncope

• Carotid sinus hypersensitivity may also result

in syncope that is related to stimulation of the
baroreceptors in the carotid sinus

• Gentle carotid massage while monitoring the

BP and cardiac rhythm usually can elicit the
response
 Edema
General Concepts

• Edema is defined as soft tissue

swelling due to expansion of the
interstitial volume

• Edema can be localized or

generalized. 
• Generalized edema involves an
increase in extracellular fluid only

• Generalized edema is due to

increases in both total body water
and sodium

• Generalized edema can occur with

low, normal, or high serum sodium
concentration. 
Mechanisms maintaining interstitial fluid
volume

• The volume of interstitial fluid is determined

by Starling's Law:
• Hydrostatic Pressure (capillary - tissue)
- Oncotic pressure (capillary - tissue) =
net fluid movement out of capillary into
interstitium.

• Oncotic pressure = osmotic pressure

created by plasma protein molecules that
are impermeable across the capillary
membrane.
 Causes of generalized
edema
I. Decreased oncotic pressure
•             Nephrotic syndrome
•             Cirrhosis
•             Malnutrition

II. Increased vascular permeability to proteins

•             Angioneurotic edema (usually allergic)

III. Increased hydrostatic pressure

•             Congestive heart failure
•             Cirrhosis

IV. Obstruction of lymph flow

•             Congestive heart failure

V. Inappropriate renal sodium and water

retention
•             Renal failure
•             Nephrotic syndrome
Edema formation in congestive
heart failure (CHF)
• CHF implies a primary failure of the pumping ability of
the heart
• When the heart begins to fail, blood backs up in the
venous system, while arterial volume is initially reduced
• This reduction in arterial filling is detected by arterial
volume receptors, triggering sympathetic nerve-
mediated vasoconstriction in an attempt to restore the
ratio of cardiac output to vascular capacitance
• The net result of this vasoconstriction is that the brain,
heart and lungs continue to receive as much blood flow
as possible
• In contrast, blood flow to the kidney and other organs is
reduced, having been shunted to the organs necessary
for immediate survival. 
• Thus, blood flow to the kidney is reduced and the kidney
begins to retain sodium and water.
• In more severe degrees of CHF, the patients can
become hyponatremic

• This occurs because more water is retained by

the kidney than is sodium

• In this setting, serum ADH levels are markedly

elevated, resulting in a very concentrated urine

• Additionally, proximal tubule sodium and water

reabsorption are very high, permitting relatively
little water to reach the urine

• Finally, ADH stimulates thirst, resulting in

increased water intake. 
 Edema formation in
•
cirrhosis
Cirrhosis of the liver is defined as increased
fibrous tissue in the liver associated with
regeneration of focal areas of damaged liver
parenchyma
• If severe, scarring and distortion of normal
liver architecture can lead to marked hepatic
dysfunction.
• This can cause sodium retention and edema
formation by the following mechanisms:

1. Decreased total peripheral resistance:

Damaged liver fails to degrade or
overproduces vasodilating factors
2. Increased portal pressure (portal
hypertension)
3. Decreased hepatic albumin synthesis
 Edema formation in
nephrotic syndrome
• The nephrotic syndrome is defined as a glomerular disease
which results in proteinuria (urinary protein losses of ≥ 3.5
gm/day), hypoproteinemia, edema, and hyperlipidemia

• Most patients with nephrotic syndrome have an expanded

plasma volume due to an intrinsic, as yet unidentified,
defect in renal sodium and water excretion

• Hypoalbuminemia due to urinary protein losses favors fluid

movement from the intravascular to the interstitial
compartment and exacerbates edema formation in the
nephrotic syndrome

• In some patients, urinary protein loss and

hypoalbuminemia can be so severe that plasma volume
becomes reduced, leading to renal hypoperfusion and
further stimulating sodium and water retention
 Rationale for treatment
• Edema of the skin, particularly in the lower
extremities can be painful, interferes with normal
blood circulation, impairs wound healing, increases
the likelihood of infection, and is unattractive

• Ascites can impair normal respiration, decrease

venous blood return to the heart, and promotes
intraperitoneal infection

• Pulmonary edema interferes with respiratory gas

exchange and is a major cause of morbidity and
mortality

• Most importantly, edema is a sign of an

underlying disease process which needs to
be treated.
 Treatment of edema
• The basic approaches to treatment are as follows.
 
• 1. First, treat the underlying disease.
• 2. Decrease sodium and water intake, either
dietary or intravenous. 
• 3. Increase excretion of sodium and water
            a. Diuretics - remember, these are palliative,
not curative.
            b. Bed rest, local pressure
• 4. Do not make the disease worse.  Other than
treatment of severe pulmonary edema, treatment of
edema is not usually an emergency.  The use of all
diuretics entails one major risk: excessive diuresis

• Overdiuresis causes volume depletion,

hypotension, inadequate organ perfusion and a
host of complications