Case Study in CVS

Semester 2 - IMU

Professor P L Ariyananda
Department of Internal Medicine
Learning objective: To correlate what is
learned in cardiovascular physiology
& pathology to a common clinical scenario.

Learning outcome: To sensitize to students to

the process of application of basic sciences
in learning clinical sciences (vertical integration).
Mr C, a 55 year old diabetic & hypertensive
Chinese man was rushed to hospital
with severe crushing, central chest pain of
30-minutes duration, whilst at work.
Mr C did not give a past history
of any other major illness.
What is most likely diagnosis?
Myocardial infarction.

Give a differential diagnosis.

Dissection of the aorta.
What would have predisposed him
to myocardial infarction?
Hypertension, diabetes, dyslipidaemia,
smoking, obesity, sedentary life style,
male gender, age, family history of IHD.
What are these called?
Risk factors.
They are either, modifiable or non-modifiable.
What are the non-modifiable risk factors?
Gender, age & family history.
How would you confirm a diagnosis
of myocardial infarction?

Look for ECG changes &

a rise in levels of cardiac markers.
Normal ECG
 Mr C’s ECG

What are the changes seen in this ECG?

How would you interpret those changes?
Changes in cardiac risk markers
after acute myocardial infarction
Normal coronary angiogram Coronary angiogram in AMI
Pathology of acute MI
Mr C was given oxygen, morphine, streptokinase
and aspirin, in the Emergency Department
and was relieved of his pain. He was transferred
to the Acute Medical Ward, 2 hours later.
The following day around 2am the
Houseman (HO) was called see him as he had
developed acute shortness of breath.

What is the most likely cause of his breathlessness?

Left ventricular/heart failure
(pulmonary oedema)
When the HO rushed to the ward,
he found Mr C to be restless, agitated, extremely
breathless with his clothes drenched in sweat;
and was seated up in bed.
His vital signs were: pulse 125/min;
BP 180/90 mmHg; respiratory rate 28/min;
temperature 370C. He had central cyanosis
and auscultation of his chest revealed
fine bi-basal crepitations.
He had no other positive physical signs.
Explain his clinical features on a
pathophysiological basis.
 Pathophysiology
Excessive catecholamines Hypoxia
• Sweating • Breathlessness
• Tachycardia • Agitation
• Hypertension • Restlessness
• Tachycardia
• Tachypnoea
• Cyanosis
What are the mechanisms for
development of hypoxia?

• Interstitial pulmonary oedema

• Alveolar pulmonary oedema
• Increased cardiac work
• Overworking of skeletal muscles
 Chest radiograph
On admission 2-days, later
Alveolar-capillary membrane
Besides hypoxia, what are the other factors
that contribute to breathlessness?

• Pulmonary congestion
• Chest pain
• Anxiety
What is ventricular remodelling?
Mr C’s BNP level was reported as 175pg/ml (Normal <100).
How would you interpret this result?

BNP (brain natriuretic peptide) is raised in heart

failure. In heart failure, BNP granules in ventricular
myocytes are released in response to the
ventricular dilatation. Its estimation is useful
for diagnosis, in determining response to
treatment and in prognostication of heart failure.
Pathophysiology of
heart failure
What is Frank-Starling mechanism?
Mechanisms of chronic heart failure
Mechanisms of chronic heart failure
Renin-angiotensin-aldosterone-system
(RAAS)
 Summary
• Diagnosis of myocardial infarction (MI)
• Correlation of changes seen in the ECG & the
coronary angiogram and the rise of cardiac
markers to pathological changes in MI
• Acute Heart failure (left ventricular failure) - as
a complication of MI: Presentation & diagnosis
• Pathophysiology of chronic heart failure