Many cardiac conditions present suddenly, requiring a rapid response from healthcare practitioners. ‘Rapid Cardiac Care' provides a concise text to guide the assessment and management of patients experiencing a variety of cardiac conditions. A systematic approach has been used to structure your assessment of the patient data and to prioritise management interventions. An overview of cardiac anatomy and physiology precedes sections on cardiac assessment, investigations, history taking, physical examination, symptom review and cardiac rhythm evaluation. The 12-lead ECG is a pivotal investigation in the evaluation of many cardiac conditions and therefore a tool to guide rapid interpretation is also provided. The care of patients with a range of cardiac conditions is presented in an A–Z format, which will direct the reader straight to the relevant sections.

We would like to thank the team at Wiley for their assistance throughout the production of this book.

Sincere thanks are extended to our families, for their constant support, patience and encouragement. We would especially like to acknowledge our fathers who influenced our lives immensely.

The heart is a cone-shaped, muscular organ with four chambers that propel blood through the circulatory system (Figure 1.1). The two upper chambers, the atria, and the ventricles below are separated by the annulus fibrosus (AV ring), a layer of connective tissue that forms the cardiac skeleton, seen on the external surface of the heart as the atrio-ventricular (AV) groove. The mitral and tricuspid (AV) valves and aortic and pulmonary (semilunar) valves form part of the AV ring. Each valve consists of two or three cusps arising from an annulus. Healthy valves maintain forward blood flow through the heart, opening and closing in response to changes in pressure between the chambers. The interatrial septum separates the two atria; the ventricles are separated by the interventricular septum, which is visible on the outside of the heart as anterior-posterior interventricular groove.

The heart wall is formed from three layers of tissue that provide different functions. The external layer is the pericardium, which surrounds the heart and the roots of the aorta and pulmonary arterial trunk. It consists of two distinct layers: the outermost fibrous layer and serous layer beneath. The serous pericardium has a visceral layer, known as the epicardium, which surrounds the myocardium and doubles back on itself to form the parietal pericardium, which lines the tough, outer fibrous layer. The space between the two layers contains a small volume of fluid to reduce friction during myocardial contraction. The central, thickest layer of the heart wall is the myocardium. It contains clusters of cardiac muscle cells known as myocytes, each surrounded by connective tissue and a network of capillaries. The internal surface of the heart is lined with a single, continuous layer of endothelial cells known as the endocardium. This facilitates smooth blood flow through the chambers and across the valves and provides some protection from the formation of thrombi.

Cardiac output is the volume of blood ejected from the left ventricle (LV) in one minute, i.e. heart rate × stroke volume. It is approximately 4–7 L/min. The cardiac conduction system controls heart rate variability and co-ordinated systolic (contraction) and diastolic (relaxation and filling) activity of the cardiac chambers to maximise cardiac output.

The superior and inferior vena cava empty into the right atrium, enabling the return of deoxygenated blood to the heart. The coronary sinus, a large cardiac vein, also drains deoxygenated blood from the myocardium into the right atrium. The tricuspid valve opens to permit blood to enter the right ventricle (RV); atrial contraction provides extra force to expel blood from the chamber, known as the ‘atrial kick’, to optimise the end diastolic volume (EDV) of the ventricles.

During systole, the three papillary muscles in the RV contract, tightening the chordae tendineae, attached to the cusps of the tricuspid valve to ensure the valve leaflets remain closed, preventing regurgitation of blood into the right atrium. Pressure within the RV will rise until it exceeds the pressure within the pulmonary circulation beyond, forcing the pulmonary valve to open and blood to flow into the pulmonary arterial trunk. During ventricular diastole, the pulmonary arteries will rapidly recoil to enable blood to fall back towards the RV, closing the pulmonary valve.

Having completed gaseous exchange within the alveoli and pulmonary capillaries, oxygenated blood returns to the left atrium via four pulmonary veins. The increase in pressure within the atrial chamber forces the mitral valve to open and ventricular filling to begin. During diastole, the ventricular myocytes will stretch to accommodate the volume of blood, which directly correlates with the force of contraction that occurs during systolic contraction (Frank Starling’s Law). The two papillary muscles contract first, once systole begins, tightening the chordae tendineae attached to the two cusps of the mitral valve to prevent regurgitation. The LV and septum then contract to increase the pressure (preload) within the LV. Once the preload pressure exceeds the pressure in the aorta beyond the aortic valve (afterload), blood will leave the LV, referred to as the stroke volume, crossing the aortic valve into the aorta to supply the arterial circulation. The term ‘ejection fraction’ refers to the stroke volume as a percentage of the left ventricular EDV (LVEDV), usually approximately 60–70% at rest. As systole ends, diastole begins again and a small volume of blood in the aorta will return towards the LV, closing the aortic valve cusps and simultaneously perfusing the coronary arteries originating at the aortic root.