TOPIC 3 - CARDIOVASCULAR SYSTEM

NGUYEN PHAM TUONG VY - BTBTWE22137

INTRODUCTION

The cardiovascular system is sometimes called the blood-vascular, or simply the circulatory system, which serves throughout life
as a vital pipeline for transporting materials on which the cells of the body absolutely depend, showing as the figure below.

(Figure 1 - Pulmonary and systemic circulations in

relation to the heart)

The circulatory system has three components:

The heart is the pump that imparts pressure to the

blood to establish the pressure gradient needed for
blood to flow to the tissues. Like all liquids, blood
flows down a pressure gradient from an area of higher
pressure to an area oflower pressure.

The blood vessels are the passageways through which

blood is directed and distributed from the heart to all
parts of the body and subsequently returned to the
heart. The smallest of the blood vessels are designed
for rapid exchange of materials between the
surrounding tissues and the blood within the vessels.

Blood is the transport medium within which materials

being transported long distances in the body, such as
O2, CO2, nutrients, wastes, electrolytes, and hormones,
are dissolved or suspended.

Numerous control mechanisms help to regulate and

integrate the diverse functions and component parts
of the cardiovascular system in order to supply blood
to specific body areas according to need. These mechanisms ensure a constant internal environment surrounding each body cell
regardless of differing demands for nutrients or production of waste products.

The health and efficiency of the cardiovascular system are paramount for overall well-being. Unfortunately, various factors can
disrupt this delicate balance, leading to a range of cardiovascular diseases that pose a significant threat to human health.
Understanding the intricate workings of the cardiovascular system and the potential threats it faces is crucial for promoting
cardiovascular health and preventing disease.

CARDIOVASCULAR DISEASES (CDVs)

Cardiovascular diseases (CVDs) reign as the leading cause of mortality and morbidity worldwide, casting a long shadow over
global health. These encompass a spectrum of conditions affecting the heart, blood vessels, and circulation, silently weaving their
web of destruction within the human body. Despite significant advancements in medical science, CVDs continue to claim millions
of lives annually, posing a substantial healthcare burden.

A. Standard mechanism of heart diseases

Heart disease occurs due to blockage of the blood vessels supplying oxygen to the heart muscle. In any tissue where the need for
oxygen from the blood exceeds the rate at which it can be supplied, a deficiency of oxygen or ischaemia occurs. However,
ischaemia is reversible provided it is not unduly prolonged. When the ischaemia is prolonged, irreversible cell damage and cell
death can occur; this is known as infarction, and is followed by cellular breakdown and necrosis.

In the heart, ischaemia of cardiac muscle will occur if the artery supplying blood to an area of cardiac muscle becomes partially or
totally blocked. The reason that a partial blockage can also cause ischaemia is that some areas of cardiac muscle are on the
borders of the area supplied with blood by the arteries, areas called watersheds.

In a normal state they receive just enough blood to survive, but should one of the arteries become even partially blocked then
the already barely adequate supply to this muscle slips below the minimum level, thus the muscle becomes inadequately
supplied with oxygen and slides into a state of ischaemia. The ischaemia will be exacerbated if the need for oxygen increases at
the same time, for example if heavy exercise is being undertaken.

B. Symptoms

Sometimes heart disease may be "silent" and not diagnosed until a person experiences signs or symptoms of a heart attack, heart
failure, or an arrhythmia. When these events happen, symptoms may include:

- Heart attack - Chest pain or discomfort, upper back or neck pain, heartburn, nausea or vomiting, extreme fatigue,
dizziness, and shortness of breath.
- Arrhythmia - Fluttering feelings in the chest (palpitations).
- Heart failure - Shortness of breath, fatigue, or swelling of the feet, ankles, legs, abdomen, or neck veins.

C. Development of heart diseases

The first change of heart disease is the development of an atheromatous plaque in the wall of an artery. Plaques consistof
cholesterol, oxidized lipids, together with inflammatory cells such as neutrophils and macrophages, which accumulate under the
endothelial lining of the artery and extend into the arterial wall (Figure 7.6).
Heart disease begins with the development of a tear in or the erosion of the edge or the shoulder region of the plaque, which
allows blood to enter (intraplaque haemorrhage) and mix with the plaque contents. The blood clots form an intraplaque
thrombus.

The next stage is the formation of a white thrombus, as platelets amass and aggregate over the tear in the plaque in an attempt to
repair the damage. Platelet aggregation eventually reaches a stage where clumps break off into the blood and are swept
downstream where they can lodge in and block small blood vessels, a process called downstream embolization. This pathological
sequence is not inevitable and plaques may repair themselves even after they reach the stage of platelet aggregation.

D. Myocardial infarction (MI)

1. Definition (Table 27.1)
 2. Pathology

The underlying pathology in MI is atherosclerosis, an inflammatory process located within the arterial wall in the form of
atheromatous plaques (Figure 27.1). These cause narrowing of the arterial lumen, resulting in reduced coronary perfusion, the
clinical manifestation of which is chest pain (angina pectoris). If an unstable plaque ruptures, the released contents precipitate
the formation of a clot. This process, known as thrombosis, may result in sudden complete occlusion of the affected artery and
infarction of the area of myocardium it supplies.

MONITORING AND EVALUATION OF CARDIOVASCULAR DISEASES

A. Electrocardiogram (ECG)

The crucial test that is always carried out before a blood test
is an electrocardiogram (ECG) recording on the patient.

ECG is a recording of that part of the electrical activity

present in body fluids from the cardiac impulse that reaches
the body surface.

Because electrical activity triggers mechanical activity,

abnormal electrical patterns are usually accompanied by
abnormal contractile activity of the heart. Thus, evaluation
of ECG patterns can provide useful information about the
heart’s status.
 The main deviations (Figure 9-15) from normal that can be
found through an ECG are:

● Abnormalities in rate - Heart rate can be determined from

the distance between two consecutive. A rapid heart rate of
more than 100 beats per minute is called tachycardia,
whereas a slow heart rate of fewer than 60 beats per minute
is called bradycardia.
● Abnormalities in rhythm - Rhythm refers to the regularity
or spacing of the ECG waves. Any variation from the normal
rhythm and sequence of excitation of the heart is termed an
arrhythmia. It may result from ectopic foci, alterations in SA
node pacemaker activity, or interference with conduction.
Heart rate is also often altered.
● Cardiac myopathies - Abnormal QRS waveforms appear
when part of the heart muscle becomes necrotic.

B. Cardiac Biomarker

When myocardial cells die, they break up and release their contents. This is the basis for the role of cardiac biomarkers in MI
diagnosis. Historically, various cardiac enzymes have been used (Figure 27.3). However, at present, cardiac troponins are used in
the diagnosis of MI.

Troponin is a complex contractile protein comprising of three subunits: C, T and I. Troponin T and I are cardiospecific, therefore
used in MI diagnosis. (Tables 27.2, 27.3 and Figure 7.7), whereas C is also present in skeletal muscle.
 Advantages of troponin T and I in diagnosis

First, measurements of cTnT and cTnI are specific: cardiac

damage is the only cause of any increase in cardiac troponin in
the blood. Therefore, immunoassays for troponin have none of
the drawbacks associated with measurements of CK
activitiesand myoglobin concentrations.

Second, cardiac troponin measurements are highly sensitive.

The background level (reference value) of cardiac troponin in the
circulation is extremely low.

Third, assaying for cardiac troponin detects patients with an MI

who are not detectable by measurements of CK and CKMB.

Troponins rise within a few hours on onset of symptoms and remain elevated for 1–2 weeks. This property enables early as well as
late diagnosis. The diagnostic sensitivity of troponin reaches 100% 12 hours after onset of symptoms, i.e. MI can be excluded with
confidence with a negative (undetectable) troponin if the blood sample is collected 12 hours or more after the onset of chest pain.

Crucially, any elevation of troponin (i.e. detectable levels in the blood), especially with the newer ultra-sensitive assays, implies a
greater risk of morbidity and mortality from a cardiac event over the next 30–60 days. Therefore its application has extended from
just the diagnosis of MI to risk stratification and therapy modification in ACS.
REFERENCES

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Colour Text.
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4. About heart disease. (2024, May 15). Heart Disease. https://www.cdc.gov/heart-disease/about/index.html
5. Introduction to the cardiovascular system. SEER training. (n.d.). https://training.seer.cancer.gov/anatomy/cardiovascular/