Cardiovascular Disorders

Introduction: We are presenting cardiovascular disorders starting with most common pathophysiological processes, subsequently we shall discuss the common diseases we come across in practice.

The symptoms caused by heart disease mainly because of four basic reasons:

1. Ischemia, which occurs because of imbalance between heart’s oxygen supply and demand

2. Pumping capacity of heart reduces leading to abnormal fluid collection causes peripheral oedema or pulmonary congestion.

3. Obstruction to blood flow as seen in valvular diseases

4. Cardiac arrhythmias develop because of disturbances in conductive system of heart.

Coronary Artery Disease: It is the most common form of the heart disease, as well as important cause of premature death.

Pathogenesis: The coronary artery disease develops almost always due to atherosclerosis and its complications like thrombosis.

Atherosclerosis is common in old age, post-menopausal women, those having family history of coronary artery disease. Hyperlipidemia, hypertension, cigarette smoking and DM enhance the process of atherosclerosis. Inflammation of blood vessels and metabolic syndrome are additional risk factors.

Pathogenesis of Atherosclerosis: It is believed that atherosclerosis denotes chronic inflammation and healing response of arterial wall to endothelial injury

When endothelial injury occurs in normal vessel wall, various inflammatory changes take place. In response to that smooth cells from media try to repair injury by forming fibrous cap and stable plaque formation occur. This stable plaque remains asymptomatic until it becomes large enough to obstruct arterial flow. When it obstructs arterial flow, mismatch between myocardial O₂ demand and supply occurs leads to symptoms of stable angina.

In an atherosclerosis plaque macrophages mediate inflammation. If inflammation predominates plaque becomes unstable. At this stage we get symptoms of unstable angina.

Unstable plaque may get complicated by ulceration or rupture. The contents of plaque get exposed to blood which trigger platelet aggregation and thrombosis formation. It causes partial or complete obstruction at the site of lesion.

If ischemic necrosis occurs in affected tissue due occlusion of either arterial supply or the venous drainage, it is called as infarction. e.g.  Myocardial infarction in heart or strokes in brain.

If thrombus gets dislodged from their site of formation, it is called as emboli e.g. thromboemboli, air embolism.

This infarction or ischemia may cause myocardial dysfunction that further leads to heart failure. Arrhythmia or altered conduction also occurs because of ischemia or infarction. Ventricular arrhythmia or massive myocardial infarction are the common causes of sudden death in cardiovascular patients.

Stable Angina: Angina pectoris or stable angina is caused by transient myocardial ischemia. It is a clinical syndrome rather than a disease. These symptoms occur as a result of imbalance between myocardial O₂ supply and demand. If myocardial O₂ demand is more in cases of HTN, left ventricular hypertrophy or tachycardia symptoms may occur. If the supply of O₂ is less because of Anemia or less oxygen saturation, then also mismatch occur.

An adult patient usually presents with diffuse chest pain, discomfort or breathlessness which is exaggerated by exertion, heavy meal or intense emotion or cold exposure. Pain may radiate to left hand, jaw etc.

When this angina pain occurs on minimal exertion or at rest in the absence of myocardial damage it is termed as unstable angina.

In cases of myocardial infarction, patient is brought to the hospital in collapse condition with severe pain associated with excessive perspiration, cold peripheries and hypotension. Patient may get vomiting, breathlessness or fever. O/E: Raised JVP, lung crepitation, Tachycardia or bradycardia.

Acute coronary syndrome is the term that includes both unstable angina and MI.

Lab investigation:

1. ECG (Resting)

Myocardial ischemia: Reversible ST segment depression or elevation with or without T wave inversion.

Acute coronary syndrome: Acute ST elevation indicates current injury to myocardium.

Development of Q wave and T wave inversion with resolution of ST elevation. These changes occur later.

2. Exercise Tolerance Test (ETT) or stress test: It is useful for assessing the severity of coronary disease and identifying high risk individual.

3. Echocardiography: useful to assess overall function of heart. It also determines the presence of many types of heart diseases. It is also useful in following progress of valvular diseases of heart.

4. Cardiac markers like:

• Trop T and CPK-MB to rule out myocardial infarction
• C reactive protein provides idea about inflammatory process

Coronary arteriography : It is indicated when non-invasive tests have failed to establish the cause of atypical chest pain. It provides detailed anatomical information about the extent and nature of coronary artery disease.

Prognosis of patient depends on number of diseased vessels and degree of left ventricular dysfunction.

Management:

• Identification and control of risk factors
• Medical management
• Exercises
• Diet

Heart Failure –

Heart Failure is a clinical syndrome that develops when the heart cannot maintain an adequate cardiac output because of inherited or acquired abnormality of cardiac structure or function. Almost all forms of heart disease can lead to heart failure.

The process of heart failure starts with deranged functioning of cardiac myocytes or decreased contractility of myocardium because of underlying pathology. It leads to decreased pumping capacity of heart (Ejection fraction gets affected). This further leads to reduced cardiac output. It stimulates neurohormonal compensatory mechanism to maintain blood pressure. But same compensatory mechanism believed to contribute to end organ changes in heart and circulation and for excessive salt and water retention in advanced heart failure.

The patients of acute myocardial infarction one of the causes of heart failure, may suddenly develop progressive dyspnoea, orthopnoea and prostration. The extremities are cold, and pulse is rapid. The blood pressure usually remains high or normal in the beginning because of sympathetic nervous system activation. Then we should suspect acute heart failure precipitated by acute MI. Crepitation at lung bases is a consistent finding and may guide in suspecting heart failure.

Patients with chronic heart failure follow a relapsing and remitting course. The symptoms depend on nature of underlying cause.

Cardiomegaly, Pleural effusion, Pulmonary oedema with raised JVP indicates Left sided heart failure.

Hepatomegaly, Ascites and marked peripheral oedema indicates Right sided heart failure. These kinds of cases need further evaluation or hospitalization to find out cause of heart failure.

Valvular diseases of Heart

Valvular diseases are not common in day to day practice. These diseases are usually caused by infection of streptococci or its consequences leading to Rheumatic heart disease. Amongst all 4 valves mitral and aortic valves are frequently affected. Rheumatic heart disease presents in 2 ways:

1. Acute Rheumatic fever:

A child between 5 to 15 years presents with fever and joint pains (inflammatory arthritis), which is of migratory nature, one should suspect Acute Rheumatic Fever.

By and large it affects large joints like knee, hip and elbow.

Child may have history of prior throat infection.

O/E: Murmur on auscultation

The diagnosis is mainly clinical but raised Anti – Streptolysin O (ASO) titers supports the evidence of preceding streptococcal infection, C reactive proteins and E.S.R are good prognostic markers.

2. Chronic Rheumatic heart disease:

50% of the cases of acute rheumatic fever enter into chronic rheumatic disease.

Patient may present with exertional dyspnoea and fatigue.

When examination of patient reveals cardiac murmur patient should be sent for further investigations.

From management point of view, it is difficult in general practice, but diagnosis is important to guide the patient for further treatment.

 Arrhythmia –

It is a disturbance of electrical rhythm of the heart and may be the manifestation of structural heart disease.

Arrhythmias commonly presents with symptoms like palpitations, dyspnoea, syncope and hypertension. It often develops suddenly and may disappear suddenly.

If heart rate is more than 100/min it is called a tachycardia, and if it is less than 60/min it is called as bradycardia.

Sinus tachycardia is commonest presentation amongst all arrythmias. It is physiological response to exercise, pregnancy and emotions, etc. The common pathological causes are Anemia, thyrotoxicosis, fever and anxiety, etc.

If patient presents with tachycardia, then we need to find out underlying cause for it. We should rule out the common causes like Thyrotoxicosis or Anemia.

If heart rate is more than 120/min then it is essential to refer patient for further evaluation to rule out supraventricular and ventricular arrythmias.

E.C.G is excellent modality for diagnosis of various arrythmias.

Blood pressure: It is the hydrostatic pressure exerted by blood on the walls of blood vessels.

Pathophysiology: Blood pressure is mainly determined by 3 important factors

1) Cardiac output

2) Peripheral Resistance

3) Blood volume

The factors which influence any of these determinants will have effect on blood pressure also.

Blood pressure is not maintained by single factor but by several interrelated mechanisms, each of which performs a specific function. Thus, it is an integrated function. Each mechanism gets activated according to temporal dimension of blood pressure fluctuations. Some of the mechanisms get activated within seconds to minutes, few of them after few minutes, those are short term regulatory mechanism for blood pressure control. For persistent blood pressure rise long term regulatory mechanisms come into operation.

Short term mechanism of blood pressure control occurs through Nervous system. Sympathetic nervous system primarily affects total peripheral resistance as well as cardiac output to maintain blood pressure.

The long-term control of arterial pressure is closely related to homoeostasis of body fluid volume. Body fluid volume is determined by balance between fluid intake and output. This task is performed by multiple nervous and hormonal controls and by local control systems within the kidneys that regulate their excretion of salt and H₂O.

A. Short term pressure control mechanism

1) Baroreceptor Reflex: Baroreceptors are situated in arch of aorta and carotid sinus in our body. They get stimulated in response to blood pressure changes and sends message to cardiovascular centre (CVC) in medulla oblongata. Then CVC sends impulse to Heart and Adrenal gland via sympathetic or parasympathetic nerve and maintain blood pressure by making appropriate changes in heart rate, strength of contraction and blood vessels.

2) Chemoreceptor reflex: These are situated in carotid and aortic bodies close to baroreceptors. These gets stimulated in response to hypoxia (lowered O₂ availability), acidosis (increase in H⁺ concentration) or hypercapnia (excess CO₂), and impulse reaches CVC. In response CVC sends impulse similar to baroreceptor reflex to maintain blood pressure.

3) Ischemic Control Nervous System Response: When blood flow to vasomotor centre in brain stem decreases, vasoconstrictor and cardioaccelerator neuron in CVC strongly gets excited leads to immediate increase in blood pressure.

 B. Intermediate Pressure Control Mechanism

1) Renin-Angiotensin vasoconstriction mechanism (Ref Lesson 6 from section II)

2) Stress relaxation of vasculature: If blood pressure increases, blood vessels get stretched to certain extent but after a few minutes or hours rebound relaxation occurs which leads to drop in blood pressure.

3) Capillary Fluid Shift Mechanism: Whenever capillary pressure falls too low fluid is absorbed from tissues and comes into circulation and increases the pressure. When capillary pressure rises too high, fluid is lost out of circulation which causes reduction in pressure.

C. Long term pressure control mechanism:

Renal Body Fluid Mechanism: When excess Na is present in blood, Extracellular volume increases which further leads to increase in cardiac output. Finally, blood pressure rise occurs. When blood pressure increases flow to the organs (kidney) also increases. You are aware that, there is auto regulatory mechanism in our body to maintain the blood flow. In kidney same mechanism gets activated to avoid excess flow of blood. Therefore, increased intrarenal vascular resistance increases the blood pressure. In response to blood pressure rise 1) atria secrete Atrial Natriuretic peptic hormone and excrete salt and water.  2) Hypothalamus release less ADH and reduce absorption of water and sodium. 3) Reflex dilation of afferent arteriole causes decreased secretion of Renin. All these mechanism tries to bring blood pressure back to almost normal at the expense of increased GFR and by reducing absorbing capacity of renal tubules. The chronic rise of blood pressure damages major blood vessels in brain, increases workload of heart and damages kidney further. The resulting vicious cycle continues.

Therefore, we have to take into account all these multiple mechanisms while thinking of management of blood pressure. In homoeopathy we may have to choose different drug for short term as well as long term on the basis of concomitant systems affected and peculiar symptoms of that particular patient.

Hypertension -When arterial blood pressure remains chronically elevated it is called as hypertension.

Multiple factors like high salt intake, heavy consumption of alcohol, obesity, lack of exercise and family history etc. contribute to hypertension. In more than 95% of cases, specific cause cannot be found. It is termed as Essential hypertension. In about 5% cases HTN is a consequence of specific underlying disease like chronic kidney disease.

When systolic pressure is < 120 mm Hg, diastolic < 80 mm Hg then we term it as normal.

In prehypertensive stage systolic pressure is 120-139 and diastolic is 80-89.

If systolic pressure is 140- 159 and diastolic is 90-99 it is stage I hypertension.

 If systolic pressure is > 160 and diastolic is > 100 it is stage II hypertension.

If systolic pressure is > 140 and diastolic is less than 90 then it is termed as isolated systolic hypertension. This type of isolated systolic hypertension is common at old age because of atherosclerosis.

Generally, blood pressure tends to be higher in early morning hours soon after waking. Headache occurs mostly with severe hypertension especially in the morning and in occipital region. Sometimes patients may get symptoms like dizziness, palpitation, fatigue, impotency etc. Many times, patients are asymptomatic, and they are diagnosed during routine checkup.

The diagnosis is made by measurement of B.P. in sitting position.

Whenever we find hypertensive patient, usually we start with treatment. It is necessary to advice healthy diet and salt restriction. If blood pressure still remains high, then there is a need to investigate the patient to rule out secondary hypertension.