1 The cardiovascular system

1Anatomy at a glance

Physiology you need to know

Angina pectoris

Myocardial infarction

Hypertension

Heart failure

Peripheral vascular disease

Deep vein thrombosis

Ten top tips

ANATOMY AT A GLANCE

The basic structure of the heart together with the electrical conducting system is shown in Figure 1.1.

Figure 1.1 The electrical conduction system.

Note that the left atrium drains blood into the left ventricle with the left atrioventricular valve preventing reflux back into the atrium. The right atrioventricular valve prevents blood from regurgitating back into the right atrium from the right ventricle.

PHYSIOLOGY YOU NEED TO KNOW

The cardiac cycle is the term used to describe the activity associated with one heart beat and involves the two phases of diastole and systole.

Diastole is the resting period during which the two ventricles fill with blood draining under gravity from the atria. During diastole, the right atrium is filled with venous blood from the systemic circulation and the left atrium is filled with oxygenated blood returning from the lungs.

Systole corresponds to the powerful contraction of the ventricular muscle which simultaneously sends blood from the right ventricle via the pulmonary arteries to the lungs and from the left ventricle via the aorta around the systemic circulation. The term ‘atrial systole’ is used to describe contraction of the atria at the end of diastole. This ensures that the ventricles are filled to maximum capacity before systole.

The cardiac cycle is controlled by the conducting mechanism of the heart. Cardiac muscle possesses autorhythmicity, i.e. it initiates its own contractions as a result of a wave of depolarization spreading from the sinoatrial (SA) node through the atria. The rate at which the SA node fires (and hence the heart beats) is governed by many factors of which the activity of the sympathetic and parasympathetic divisions of the autonomic nervous system are the most important, together with the release of the hormones epinephrine and norepinephrine from the medulla of the adrenal glands.

The wave of depolarization initiated by the SA node is picked up by the atrioventricular (AV) node, conducted via the bundle of His, the left and right bundle branches and the spreading network of Purkinje fibres into the ventricular muscle where it initiates ventricular contraction. This electrical activity is recorded as the electrocardiogram (ECG) whose components are as follows:

P wave	SA node discharge and atrial depolarization
PQ interval	Delay while electrical impulse is conducted through conducting fibres
QRS waves	Ventricular contraction
T wave	Repolarization for next heart beat (diastole).

The left and right coronary arteries leave the aorta immediately after the aortic valve and conduct blood to the cardiac muscle. The aorta is the main arterial trunk carrying oxygenated blood via a succession of other arteries to the rest of the body. Venous drainage eventually reaches the heart via the superior and inferior vena cava.

Blood pressure is determined by the strength of the heart beat, volume of blood in the circulation, the elasticity of vessels and the resistance offered to blood passing through blood vessels. Both systolic and diastolic blood pressures are important in assessing hypertension.

ANGINA PECTORIS (P280)

PATHOLOGY: Key facts

Inadequate blood supply to cardiac muscle means there is insufficient oxygen to meet the metabolic needs of muscle during increased activity leading to central chest pain. The cause is usually atheroma, the development of plaques composed of lipids, collagen fibres and smooth muscle cells which narrow the lumen of the coronary artery. Approximately 2 million people in the UK have angina.

WHAT TO LOOK OUT FOR

Central chest pain upon exertion or during periods of stress which is relieved by rest.

The pain may radiate to the shoulders, arms, neck or jaw and may not even be felt in the chest at all.

As the arterial disease process advances, anginal pain becomes more frequent and occurs with less exertion or even at rest; this is unstable angina.

MEDICAL MANAGEMENT

The aim is to balance oxygenated blood supply to the myocardium with demand in order that painful episodes may be avoided. The presence of angina indicates advanced arterial disease which could lead to a more serious and possibly fatal event such as a myocardial infarction (MI) or cerebrovascular accident (CVA). The patient will therefore be investigated and key indicators such as blood pressure and blood lipids monitored regularly. Direct interventions to relieve the symptoms include percutaneous transluminal coronary angioplasty (PTCA) which involves passing a catheter to within the atherosclerotic lesion and then inflating a balloon to stretch the artery, widening the lumen of the artery and increasing blood flow (p282).

PHARMACOLOGY FOCUS

Glyceryl trinitrate (GTN) is the main drug used, this dilates blood vessels reducing the volume of blood returning to the heart (preload) and the diastolic blood pressure against which the heart has to work to pump blood around the body (afterload). As a result the amount of work that the ventricular muscle has to perform is reduced, thereby reducing oxygen demand. It also dilates the coronary arteries, improving blood supply to the myocardium.

PRIORITIES FOR NURSING CARE

Health education to focus on

• Patient understanding of the cause and meaning of pain.

• Ensure that patient fully understands use of GTN and coping with acute episodes.

• Preventive strategies to avoid episodes of angina.

• Discuss anxieties and fears associated with angina.

Lifestyle modification

• If needed, weight loss, smoking cessation and alteration to healthier diet.

• Moderate exercise that will not bring on pain such as walking should be encouraged and built into a supervised programme of increased activity.

Primary care

• Assess home/family circumstances.

• Discuss health education and lifestyle modification with carers/family.

• Ensure that district nurse is involved if necessary.

MYOCARDIAL INFARCTION (P284)

PATHOLOGY: Key facts

Arteriosclerosis of a coronary artery advances to the stage where blood supply to a portion of myocardium is so reduced that the myocardium suffers necrosis through lack of oxygen. This may be associated with the formation of thrombus in advanced complex atherosclerotic lesions which completely occludes the artery at the site of the lesion. Part of the thrombus may break off as an embolism and occlude the arterial lumen further down the artery. The area of necrosed tissue may be small or large and may extend through the full thickness of the ventricular wall. Death can be immediate or within a few hours while survival depends upon the volume of tissue destroyed and its location within the myocardium.

WHAT TO LOOK OUT FOR

Severe central chest pain, often crushing in nature, unrelieved by GTN.

Shortness of breath, nausea and possibly vomiting.

Fatigue and anxiety.

Pale skin due to reduced cardiac output.

Low blood pressure.

There is a potential for cardiac arrhythmias some of which may prove rapidly fatal (ventricular tachycardia or fibrillation).

Up to 25% of patients may not experience pain and this is known as the ‘silent MI’. This is particularly common in older persons.

MEDICAL MANAGEMENT

Early diagnosis is crucial as most deaths occur within the first hour and prompt treatment to dissolve away the clot in the coronary artery greatly improves the prognosis amongst survivors. A 12-lead ECG should be performed at the earliest opportunity as an elevated ST section is diagnostic of acute MI. Bloods are taken for the presence of certain chemicals known to be in myocardial cells. Their presence in the blood indicates that they have leaked from damaged myocardium and this confirms the diagnosis of MI. Troponin T or I levels rise within a few hours of MI. Myoglobin is another marker for damaged myocardial cells and together with troponin can be measured with a bedside test. The cardiac enzyme creatine phosphokinase (CPK) peaks between 12 and 24 hours while lactic dehydrogenase (LDH) peaks between 3 and 6 days and is useful for a late presentation.

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