Introduction to Cardiovascular disease

Introduction to Cardiovascular disease dr.Faris alhialy lect. 1

Introduction
Myocardial cells constitute 75% of the heart mass but it is only about 25% of the cell number. They are designed to perform two fundamental functions: initiation and conduction of electrical impulses and contraction. Although most myocardial cells are able to perform both these functions, the vast majority are predominantly contractile cells (myocytes) and a small number are specifically designed as electrical cells. The latter, collectively known as the conducting system of the heart, The conduction system of the heart
The sinus node
The sinus node is a complex spindle-shaped structure that lies at the junction between the superior vena cava and the right atrium . Physiologically, it generates impulses automatically by spontaneous depolarization of its membrane at a rate quicker than any other cardiac cell type. It is therefore the natural pacemaker of the heart.
The atrioventricular node, His bundle and Purkinje fibres
The depolarization continues to conduct slowly through the atrioventricular (AV) node. The AV node continues as the His bundle, which penetrates the annulus fibrosus and conducts the cardiac impulse rapidly towards the ventricle. The His bundle divides into the right bundle branch and the main left bundle branch.
The coronary circulation
The left main and right coronary arteries arise from the left and right coronary sinuses of the aortic root, distal to the aortic valve . Within 2.5 cm of its origin, the left main coronary artery divides into the left anterior descending artery (LAD), and the left circumflex artery (CX)
The LAD gives branches to supply the anterior part of the septum (septal perforators) and the anterior, lateral and apical walls of the LV. The CX gives marginal branches that supply the lateral, posterior and inferior segments of the LV. The right coronary artery (RCA) runs in the right atrioventricular groove, giving branches that supply the RA, RV and inferoposterior aspects of the LV.

Nerve supply of the heart

The heart is innervated by both sympathetic and parasympathetic fibres.
Positive inotropic and chronotropic effects are mediated by β1-adrenoceptors, whereas β2-adrenoceptors predominate in vascular smooth muscle and mediate vasodilatation. Parasympathetic reach the heart through the vagus nerves.

The cardiac cycle

The first event in the cardiac cycle is atrial depolarization (a P wave on the surface ECG) followed by right atrial and then left atrial contraction. Ventricular activation (the QRS complex on the ECG) follows after a short interval (the PR interval). Left ventricular contraction starts and shortly thereafter right ventricular contraction begins. The increased ventricular pressures exceed the atrial pressures, and close first the mitral and then the tricuspid valves.
Until the aortic and pulmonary valves open, the ventricles contract with no change of volume (isovolumetric contraction). When ventricular pressures rise above the aortic and pulmonary artery pressures, the pulmonary valve and then the aortic valve open and ventricular ejection occurs. As the ventricles begin to relax, their pressures fall below the aortic and pulmonary arterial pressures, and aortic valve closure is followed by pulmonary valve closure. Isovolumetric relaxation then occurs. After the ventricular pressures have fallen below the right atrial and left atrial pressures, the tricuspid and mitral valves open. The cardiac cycle can be graphically depicted as the relationship between the pressure and volume of the ventricle.


Cardiac output
Cardiac output is the product of stroke volume and heart rate. Stroke volume is the volume of blood ejected in each cardiac cycle , and is dependent upon end-diastolic volume and pressure (preload), myocardial contractility and systolic aortic pressure (afterload). Stretch of cardiac muscle (from increased end-diastolic volume) causes an increase in the force of contraction, producing a greater stroke volume: Starling’s Law of the heart .
The contractile state of the myocardium is controlled by neuro-endocrine factors, such as adrenaline (epinephrine), and can be influenced by inotropic drugs and their antagonists. The response to a physiological change or to a drug can be predicted on the basis of its combined influence on preload, afterload and contractility .

CARDIAC INVESTIGATIONS

Cardiac biomarkers
Brain natriuretic peptide
associated with left ventricular systolic dysfunction and may aid the diagnosis and assess prognosis and response to therapy in patients with heart failure .

Cardiac troponins

are cardiac muscle proteins that are released during myocyte damage and necrosis, and represent the cornerstone of the diagnosis of acute myocardial infarction.
Electrocardiogram (ECG)
The ECG is used to assess cardiac rhythm and conduction.
It provides information about chamber size and is the main test used to assess for myocardial ischaemia and infarction.
Chest X-ray
Ideally, this is taken in the postero-anterior (PA) direction at maximum inspiration , Heart size can be reliably assessed only from the PA chest film. The maximum transverse diameter of the heart is compared with the maximum transverse diameter of the thorax measured from the inside of the ribs (the cardiothoracicratio). The cardiothoracic ratio (CTR) is usually <50% . if may mean Cardiomegaly.

SYMPTOMS OF HEART DISEASE
The following symptoms occur with heart disease:
 Chest pain
 Breathlessness
 Palpitations
 Syncope
 Fatigue
 Peripheral oedema.


Chest pain
Chest pain is a common presentation of cardiac disease but can also be a manifestation of anxiety or disease of the lungs or musculoskeletal or gastrointestinal systems .
Central chest pain
This is the most common symptom associated with heart disease. The pain of angina pectoris and myocardial infarction is due to myocardial hypoxia. Types of pain include:
 Retrosternal heavy or gripping sensation with radiation to the left arm or neck that is provoked by exertion and eased with rest or nitrates this is (angina pectoris)
 Similar pain at rest (acute coronary syndrome)
 Severe tearing chest pain radiating through to the back (aortic dissection)
 Sharp central chest pain that is worse with movement or respiration but relieved with sitting forward (pericarditis pain)

Dyspnoea

Left ventricular failure causes dyspnoea due to oedema of the pulmonary interstitium and alveoli. This makes the lungs stiff (less compliant), thus increasing the respiratory effort required to ventilate the lungs. Tachypnoea (increased respiratory rate) is often present owing to stimulation of pulmonary stretch receptors.
Orthopnoea refers to breathlessness on lying flat. Blood is redistributed from the legs to the torso, leading to an increase in central and pulmonary blood volume. The patient uses an increasing number of pillows to sleep.
Paroxysmal nocturnal dyspnoea (PND) is when a patient is woken from sleep fighting for breath. It is due to the same mechanisms as orthopnoea. However, as sensory awareness is reduced whilst asleep, the pulmonary oedema can become quite severe before the patient is awoken.
Palpitations
These represent an increased awareness of the normal heart beat or the sensation of slow, rapid or irregular heart rhythms.
The most common arrhythmias felt as palpitations are premature ectopic beats and paroxysmal tachycardias.

Syncope

Syncope is a transient loss of consciousness due to inadequate cerebral blood flow. The cardiovascular causes are

Vascular:

A vasovagal attack is a simple faint and is the most common cause of syncope.
Postural (orthostatic) hypotension is a drop in systolic blood pressure of 20 mmHg or more on standing from a sitting or lying position.
Carotid sinus syncope occurs when there is an exaggerated vagal response to carotid sinus stimulation provoked by wearing a tight collar, looking upwards or turning the head.
Obstructive.
The obstructive cardiac causes lead to syncope due to restriction of blood flow from the heart into the rest of the circulation, or between the different chambers of the heart.
Arrhythmias.
Stokes–Adams attacks are a sudden loss of consciousness unrelated to posture and due to intermittent high-grade AV block, profound bradycardia or ventricular standstill.
Fatigue
Fatigue may be a symptom of inadequate systemic perfusion in heart failure. It is due to poor sleep, a direct side-effect of medication, particularly beta-blockers, electrolyte imbalance due to diuretic therapy and as a systemic manifestation of infection such as endocarditis.
Peripheral oedema
Heart failure results in salt and water retention due to renal underperfusion and consequent activation of the reninangiotensin-aldosterone system . This leads to dependent pitting oedema.