INTRODUCTION TO THE CARDIAC UNIT LEVEL 6A

INTRODUCTION TO THE CARDIAC UNIT LEVEL 6A STUDENT PLACEMENT Cardiac Unit Reviewed June 2008. T Murphy. INTRODUCTION TO THE CARDIAC UNIT – LEVEL 6A Welcome to Level 6a, Cardiac Unit. This unit consists of a Cardiac Care Unit (CCU – 6 beds) and a step down ward area (13 Beds). This booklet is designed to facilitate your learning in caring for cardiac patients. As you know, it is your responsibility to organise meetings with your mentor or associate mentor at the beginning of your placement and to ensure they are aware of any skills or competency levels you need to achieve by the end. They will be available to discuss any concerns you may have regarding these. Your mentor and associate mentors are; Mentor__________________________________ Associate Mentor __________________________ We appreciate that you will come with your own learning objectives but we have also suggested some which will be appropriate whilst you are here. However, these can be tailored individually with your mentor. We hope you will enjoy your placement with us and we are sure you will gain valuable knowledge and experience whilst you are here. This should help to improve your confidence when caring for patients on general wards. Looking forward to meeting you, The Cardiac Team. Reviewed June 2008. T Murphy. ORIENTATION CHECKLIST We realise starting a new placement can be a daunting experience. To this effect we have developed a list of things to familiarise yourself with or to know the procedure regarding. You should aim to achieve these by the end of your first shift by working with your mentor. They will help you operate as part of the team. Achieved Y/N, any information Orientation to the Cardiac Unit and relevant rooms e.g. clinical, sluice, linen room Cardiac arrest procedure Location of the 2 cardiac arrest trolleys and defibrillators Fire Procedure How to fast bleep doctors How to bleep doctors How to order a porter How to perform BP, SPO2 levels and temperatures using equipment in your allocated area How to initiate cardiac monitoring and admit patients onto the monitor and setting up the telemetry system How to perform a BM Patient visiting times and restrictions CCU and ward area observation charts Nursing Documentation How to obtain blood results off the computer and when to check these Reviewed June 2008. T Murphy. ORGANISING YOUR DAY Your day will start at 0745 (or 1945hr if you are starting a night shift) when you will receive report from the previous shift. This is where you will start to organise your day by highlighting or noting important information from the handover. The person handing over should not give a long report as a bedside handover for your allocated patient’s will occur after. They should concentrate on the areas of particular concerns e.g. Diagnosis and current treatment, heart rhythm abnormalities, the patients resuscitation status, and highlighting patients which are of high to low dependency. Medications, blood results and ECG’s can be included in the individual bedside handovers. The co-ordinator of the shift will allocate the patient workload, as on CCU the patient ratio is 1 nurse to 2 patients. There are normally 3 staff members on shift except on nights where there are usually only 2. The co-ordinator will then either check the crash trolley themselves or allocate someone else to do this. As a general rule of thumb it is best to highlight which is your sickest patient and start with them so you can identify their needs and also enable you to decide how you are going to manage your time. You should then make sure that anyone going for a procedure e.g. angiogram/plasty is prepared (nil by mouth if appropriate, checklist completed, shaved, gown etc). You would then complete a full set of observations (Heart rate and rhythm, blood pressure, temperature, respiratory rate and oxygen saturation). Also observe the patients overall condition giving you a baseline of how they are when you first meet them. You should check the monitor itself to identify any changes that need to be made. For example, check the alarm histories, alarm limits and graphic trends as absolute minimum of once per shift. By the time you have carried out your first set of observations the ward round will be due to commence at 0815 on a day shift. It is a good idea to to listen to all the patients on the ward rounds as a lot can be learnt on these. When there are junior doctors on these rounds the Consultants tend to do alot of teaching which is beneficial to you also. Reviewed June 2008. T Murphy. Then complete your drug round tying in the medications with information you have already learnt about your patient. The remainder of the morning will be taken up with attending to your patients needs, making beds, discharging/admitting patient and your tea break (very important to take adequate breaks throughout the day as you are at work for long periods and must be suitably fed and watered). Keep a close eye on the white board where the co-ordinator will write up to date details of ward activities e.g. admissions, discharges, patients going for procedures. At midday we have a ‘protected meal time’ until 1300hr. Clinical contact with patients should be discouraged. We then have a two hour rest period until 1500hr. Lights should be turned off and a peaceful environment maintained. We also go for our lunch during this time. Aim to have your blood results noted down during this time as you should aim to have the bulk of your writing done by about 1600hr. Any additional events can be noted downs in your notes as they happen. All of our admissions on CCU arrive at any time 24 hours a day, as most of them are acute emergency admissions either from A&E or direct from other hospitals. If any patients come in and require to go to the cath labs for intervention you can check with the coordinator of that shift to see if you can go in and watch these procedures. Make sure the computer handover is updated with new information about your patient. The coordinator of that shift will hand over all six patients. Reviewed June 2008. T Murphy. USEFUL NAMES TO KNOW (and their roles within the trust) Cardiac Consultants SH CD ADB SO’N DHS RJ Dr Dr Dr Dr Dr Dr Holmberg – lead cardiac consultant Davidson de Belder O’Nunain Hildick-Smith James Cardiac Care Centre Services Manager: Fiona Liddell Responsible for the overall management of the care centre, Fiona manages the finances and future planning of services. We are a part of ‘specialised services’ which is the biggest directorate within the trust. Fiona does not have a nursing background therefore only becomes involved with finance. Cardiac Matron: Ann Gibbins. Ann is primarily involved in setting and maintaining high standards within cardiology. Ann has a responsibility for all nursing services within the cardiac centre. Ann also has a role in cleaning, infection control and developing clinical practice and education. She would like to work with all students Cardiology Nurse Consultant: Sarah Young She has been the driving force behind ensuring the National Service Framework guidelines are met. For example, developing MI and ACS pathways and setting up Heart Failure services. Sarah has a high profile within the cardiac centre and also within the Trust ensuring the service has a voice at Trust meetings. Cardiology Co-ordinator: Tony Lee Tony is responsible for overall management of cardiac beds, both medical and surgical including organising waiting lists and operations. He also manages the waiting lists for outpatient’s angiograms, angioplasty and elective cardio versions. Ensuring Government targets within this area are met. Reviewed June 2008. T Murphy. Clinical Site Manager Team responsible for overall management of beds within the trust ensuring trolley waits are kept to a minimum. Provide clinical support. Bleep 8152. Bed Bureau Responsible for the allocation of inpatient beds on a daily basis ensuring patients are placed in the most appropriate areas. Bleep 8284. Heart Failure Nurse Specialist: Carolyn Kenny and Karen Murphy Work with both in and out patients with the diagnosis of heart failure. Providing patient education and support to manage symptoms and prevent hospital admissions. They also provide valuable support to both nursing and medical staff. Ward Pharmacist: Alison Warren Alison works Monday to Friday checking drug charts, advising, teaching and ordering. Cardiac Wards / Department Managers Gordon Pretsell – Level 6a ( Cardiac Unit) – includes CCU and Step down ward Julie Lloyd – Level 7a (Cardiac High Dependency Unit) – Includes Step down ward Sherrie Popata – Albion/Lewis Sue Yelf – Cath Labs Vicky Griffiths – Cardiac Department Reviewed June 2008. T Murphy. THE INITIAL ASSESMENT The initial assessment should be completed within the first 24 hours of admission. It gives us a baseline to the patient’s physical, emotional and social conditions on admission. The following questions are not exclusive but they do give an excellent starting point. Social Environment Does the patient live alone? If they have a partner are they fit and well? Does the patient live in a flat, house or bungalow? Do they have stairs or is a lift available? Do they have any social services or private input, if so how what and how often? Emotional Assessment Do they know the reason for their admission? Is the patient orientated, relaxed, confused, withdrawn or anxious? Have they had a previous experience of hospitals? Physical Assessment Are they over/under weight? Any recent weight lost? Do they smoke? How many and for how long? If ex smoker detail history Check the patients peripheries, are they well perfused is their oedema? Is there any sign of cyanosis, finger clubbing or breathlessness? What is the patient’s skin condition like? Is it dry, broken, clammy, oedematous? Sensory Regulation Does the patient wear glasses? If yes do they have them, do they wear them all the time or just for reading? Do they have hearing problems? Do they wear an aid? Does the patient get pain? Where, when, triggers, relievers? Temperature Regulation Is there a cannular insitu? Where and when inserted Are they pyrexial? If yes, is there an obvious source of infection? Does the patient tend to feel hot or cold? Is the patient dressed appropriately for the weather? Are they able to put on additional clothing independently? Reviewed June 2008. T Murphy. Food and Drink Do they eat three meals a day? Is it considered a healthy balanced diet containing fruit and vegetables? Any special dietary needs e.g. diabetic, low fat? How much fluid would they drink in a typical day? What do they drink? How much alcohol would they drink in a typical week? Current weight, height, body mass index to complete MUST assessment. Elimination Do they have any problems passing urine? Frequency, urgency, pain, incontinence? How often do they pass urine overnight? How often do they have their bowels open? Do they take laxatives, if yes which ones? Any recent changes in bowel habits? Rest and Relaxation Does the patient sleep well? How long do they sleep on average a night? Do they take night sedation? How many pillows do they use? What do they enjoy doing to help them relax? Any hobbies/pastimes? Activity Are they normally active? How often and what type of exercise do they get? Do they walk unaided or with a stick/zimmer? How far can they walk? Is going up hill a problem? Does the patient do their own cooking, cleaning, washing, shopping? If not who does it for them? Reviewed June 2008. T Murphy. Objectives Week 1 1. Complete the criteria for Sinus Rhythm Rate: Rhythm: P wave: PR interval: QRS complex: T wave: Achieved Y/N 2. Label the diagram of the heart (see backpage) Achieved Y/N 3. Label the diagram of the conduction system (see next page) Achieved Y/N 4. Describe the blood flow through the heart Achieved Y/N 5. Describe the normal conduction pathway through the heart and relate it to sinus rhythm P wave represents: PR interval represents: QRS complex represents: T wave represents: Achieved Y/N 6. Observe a 12 lead ECG being performed Achieved Y/N 7. Understand the basic functions of the cardiac monitors and be able to attach and admit a patient onto them correctly. Achieved Y/N Reviewed June 2008. T Murphy. Reviewed June 2008. T Murphy. Objectives Week 2 1. List the risk factors for CHD Achieved Y/N 2. List some of the descriptors used and the sites given for possible cardiac pain Achieved Y/N 3. Performs a technically correct 12 lead ECG Achieved Y/N 4. States the normal paper speed and ECG measurements Achieved Y/N 5. Discusses the anatomical landmarks when performing a 12 lead ECG Achieved Y/N 6. Is able to recognise normal sinus rhythm on a monitor and state why it is sinus Achieved Y/N 7. Is able to demonstrate how to calculate heart rate from a 6 second rhythm strip Achieved Y/N Objectives Week 3&4 Work through objectives not yet met and spend time with other specialities pertinent to CCU to understand their role within this speciality. I.e. Cardiac rehabilitation, heart failure nurses, cardiac department to observe exercise tolerance tests and echos, follow a patient through cardiac surgery, follow a patient through angiography +/- plasty and to observe a TOE and cardioversion. Reviewed June 2008. T Murphy. Objectives Week 5 1. Discuss how a typical AMI/ACS patient may present Achieved Y/N 2. Describe appropriate pain relief for each condition Achieved Y/N 3. Describe the use of thrombolytic agents Achieved Y/N 4. Discuss the psychological impact an AMI/Heart failure diagnosis may have on a patient and their family Achieved Y/N 5 Have an understanding of the following drugs and are able to discuss some of them, to include the indications for their use, some of the common side effects and nursing care and observations to be taken: Aspirin Sterptokianase/rTPA Heparin Clexane Atenolol/Metoprolol Ramipril Diltiazem Isosorbide mononitrate / GTN Nicorandil Amiodarone Digoxin Frusemide Achieved Y/N Reviewed June 2008. T Murphy. Objectives Week 6 1. Be able to recognise Atrial Fibrillation (AF) on a monitor Achieved Y/N 2. Be able to discuss how an acute MI may present on the ECG Achieved Y/N 3. Be able to discuss how unstable angina may present on the ECG Achieved Y/N 4. Explain how an infarct would evolve over a 24 hour period in relation to an ECG Achieved Y/N 5. Accurately interprets four 12-lead ECGs Achieved Y/N Reviewed June 2008. T Murphy. Your Role in a Cardiac Arrest Understandably, this causes concern for many of you. Firstly, let us reassure you that cardiac arrests do not usually occur as often as you may think on CCU. The multidisciplinary team tries to prevent a cardiac arrest from occurring, however, this is not always possible. In the event of a cardiac arrest, your role will be to act as runner, observer, and to reassure the other patients on the unit, who are likely to be more anxious than you! We do not expect any more from you. If you feel you would like to be more involved, and it is appropriate to do so, we will aim to support you as much as possible throughout this stressful time. However, please remember it is a stressful time for all involved, therefore explanations may not always be offered immediately, but we will aim to debrief at the end of the arrest, at an appropriate opportunity. Reviewed June 2008. T Murphy. The Conduction System  The cardiac impulse originates in the SA node and is located in the upper wall of the right atrium. It has an elongated oval shape and is larger than the AV node. It is known as the pacemaker of the heart and beats at between 60-100 bpm. The cardiac impulse spreads through both atria by way of the internodal pathways. This causes both atria to depolarise and then to contract, which is represented on the ECG as the P wave. The internodal pathways are able to initiate beats of greater than 100bpm. The depolarisation wave then arrives at the AV node, which is located on the right side of the intraatrial septum. The wave is delayed here for approximately 0.1 seconds, before arriving at the Bundle of His. The Bundle of His connects the AV node to the bundle branches, and is located just above the ventricles, to the right side of the intraatrial septum. The Right Bundle Branch is a slender fascicle and runs along the right side of the interventricular septum. It supplies the electrical impulses to the right ventricle. The Left Bundle Branch supplies impulses to the left ventricle. It runs along the left side of the interventricular septum, and divides almost immediately into an anterior and posterior fascicle. These supply the anterior and posterior surfaces of the left ventricle. The cardiac impulses then travel into the Purkinje Fibres, which are located in both the left and right ventricular walls. The Bundle of His, Bundle Branches and Purkinje Fibres cause ventricular depolarisation and then ventricular contraction, which is represented by the QRS complex on the ECG. The ventricular conduction system is able to initiate beats of less than 40 beats per minute.       Reviewed June 2008. T Murphy. The Cardiac Cycle  The duration of the cardiac cycle is 0.8 seconds and produces an average heart rate of 75bpm. It is normally initiated by the spontaneous generation of an action potential at the SA node. The impulse travels through the atrial muscle to produce systole (contraction), this lasts approximately 0.18 seconds and is graphically recorded on the ECG as a P wave. There is a delay of electrical transmission at the AV node for approximately 0.1 seconds. Atrial repolarisation is not represented on the ECG as it is lost within the QRS complex. The impulse then travels through the ventricular conduction system causing ventricular systole and lasts approximately 0.12 seconds. This is represented on the ECG as the QRS complex. Ventricular diastole (relaxation or depolarisation) makes up the rest of the cardiac cycle, and is represented on the ECG as the T wave.      Reviewed June 2008. T Murphy. Atrial Function   Venous blood drains into the atria which acts as a reservoir storing blood. AV ring moves up at the end of ventricular systole and causes an increase in atrial pressure. This causes the AV valves to open and ventricles to fill. Atria then contract. Blood is forced through the AV valves into the ventricles. This increases ventricular filling by 25-30% and primes the ventricles for contraction. Delay of electrical transmission at AV node allows atria to empty completely before ventricular systole begins.    Ventricular Function      During atrial diastole pressure of blood decreases whilst pressure of blood in ventricles begins to increase. Cusps of AV valves snap shut (causes 1st heart sound S1 lub). After closure of AV valves BP increases (due to isometric contraction of ventricular muscle). During this phase the ventricles become shorter and fatter although not altering their volume, this is isovolumetric contraction. When the increased ventricular pressure is greater than the pressure in the aorta and pulmonary artery, the semilunar and aortic and pulmonary valves open. Isotonic phase of contraction begins and ventricular contents ejected. As ventricular muscle relaxes and pressure decreases below that in the aorta and pulmonary artery the semilunar valves close. (2nd heart sound dub) The aortic valves close slightly before the pulmonary valve. Simultaneously the blood enters the atria and intra-atrial pressure gradually increases so when AV valves open blood flows rapidly from the atria to the ventricles. Whole cycle continues on.........................      Reviewed June 2008. T Murphy. The Cardiac Cells The Cells Each myocardial cell is polarised through positive and negative ions. The resting state of a myocardial cell has a negative charge. When an impulse reaches the cells, each one will have a sudden influx of sodium (positive) ions, causing the cell to become positive and therefore the cell and the myocardium as a mass will contract. This is called depolarisation. Following this, other positive ions (potassium, calcium, magnesium) will then exchange within the cell more slowly, until the exchange will cease and the cell will return to its negative charge (resting state). This process is called repolarisation. The cell is now ready to recieve the next impulse. Action Potential 5 phases involved, 0-4. Each phase is represented by a different part of the ECG. All drugs have an effect on the different stages of action potential and can therefore have an effect on the ECG. In Brief!  Sodium ions move into the cell and start depolarisation  Calcium ions extend that depolarisation  When calcium ions stop entering the cell potassium ions move in and repolarisation of the cell begins  E.g Sodium starts cell stimulation Calcium extends that stimulation to allow the entire muscle to contract before potassium comes along and tells it to relax for a moment and get ready for the next wave.  NB An impulse during the 'resting' period can cause premature contractions leading to compromised filling and poor ejection of blood from the heart. This may in turn lead to life-threatening arrhythmias. Some drugs (i.e amiodarone) can effect the length of time the heart is in its resting phase and therefore put it more at risk of these lifethreatening arrhythmias. Reviewed June 2008. T Murphy. Basic Electrocardiography An ECG is a recording of the electrical activity occurring in the heart each time it contracts. The impulse, when filtered through a specially designed machine, produces characteristic waveforms that we can compare to established normal waveforms and determine a few things about the current state of the heart. By noting the shape, consistency and time between these waveforms we can learn more about the conduction system, damaged areas and areas that aren't receiving enough oxygen to meet their needs. In order to standardise measurements specific speeds are used and the waveforms are printed out on a grid at a speed of 25mm a second, the boxes are formed by the lines and represent 0.04 seconds for the small boxes and 0.2 seconds for the large boxes. A way of obtaining heart rate from a rhythm strip is to measure out a 6 second strip and then count the number of R waves in that strip then multiply by 10. Electrodes are placed on designated areas of the patients body and by the use of various combinations of these electrodes, 12 different views of the same electrical activity are demonstrated on the ECG graph paper. Each separate view of the heart is called an ECG lead. In routine testing we use a 12 lead ECG consisting of 3 standard leads and 3 augmented leads that view the heart in the frontal plane and 6 precordial or chest leads that view the heart in the horizontal plane. Electrodes are placed on both the wrists and on the left ankle of the patient to obtain the standard and augmented leads but the electrodes actually may be placed anywhere on the respective limbs or upper and lower torso and the same view of the heart is recorded. A fourth electrode is placed on the right ankle to stabalise the ECG but this electrode takes no part in lead formation. The 3 electrodes placed on the left arm, right arm and left leg are used in different combinations to produce 6 leads. Reviewed June 2008. T Murphy. The standard leads (also known as bipolar) are leads I, II, and III. The augmented leads (unipolar) are leads AVR, AVL and AVF. The standard leads form a triangle over the body and have a mathematical relationship to one another as described by Einthoven. The height or depth of the recordings in lead I plus Lead III equals the height or depth of the recordings in lead II. Precordial leads The 6 precordial leads are unipolar leads and view the electrical activity of the heart in the horizontal plane. The following positions are used for electrode placement on the chest to obtain the correct precordial lead placement: V1: 4th intercostal space immediately to the right of the sternum. V2: 4th intercostal space immediately to the left of the sternum. V3: Directly between V2 and V4. V4: 5th intercostal space - left midclavicular line. V5: 5th intercostal space - left anterior axillary line. V6: 5th intercostal space - left midaxillary line. Reviewed June 2008. T Murphy. Which parts of the heart do the various leads look at? V1-V2 show indirectly the true posterior surface. V1-V2 (sometimes V3) look at the septum of the heart. V1-V4 look at the anterior surface. Often at angiography the Left Anterior Descending Artery is found to be narrowed/blocked if there are changes in these leads. I, AVL, V5-V6 overly the lateral left ventricle. Often at angiography the circumflex artery is found to be narrowed/blocked if there are changes in these leads. Leads II, III and AVF view the inferior surface. Often at angiography the Right Coronary Artery is found to be narrowed/blocked if there are changes in these leads. Reviewed June 2008. T Murphy. Waves and Complexes A wave of depolarisation begins in the SA node and spreads to both atria by way of the internodal pathways and both atria depolarise. Atrial depolarisation is represented by the P wave. P waves are usually upright and slightly rounded. Atrial repolarisation coincides with the QRS complex and is impossible to recognise. The wave of depolarisation then spreads to the AV node, the bundle of His, the bundle branches, the Purkinje fibres and the ventricular myocardium. Ventricular depolarisation occurs and is represented by the QRS complex. Ventricular repolarisation is represented by the T wave. is normally upright and slightly rounded. The T wave A U wave is sometimes seen after the T wave. It is thought to relate to the events of late repolarisation of the ventricles. The U wave should be in the same direction as the T wave. Reviewed June 2008. T Murphy. Intervals and segments A point that helps in remembering the measurements we are going to discuss is that intervals contain waves and segments are the lines between the waves. PR interval: the time from the beginning of the P wave to the beginning of the QRS complex is called the PR interval. This time interval represents depolarisation of the atria and spread of the depolarisation wave up to and including the AV node. Normal measurements are 0.12 seconds to 0.2 seconds. QRS Interval: measured from the beginning of the 1st wave in the QRS to the last wave in the QRS returns to the baseline. Normal measurements are 0.04 seconds to 0.12 seconds QT Interval: measured from the beginning of QRS waves to end of the T wave. Normal measurements are based on heart rate and generally should be less than 0.4 seconds. ST segment: The distance between the QRS complex and the T wave from the point where the QRS complex ends to the onset of the ascending limb of the T wave is called the ST segment. On the ECG the ST segment is a sensitive indicator of myocardial ischaemia or injury. Our reference point on the ECG is the isoelectric line. This is the flat line before the P wave or right after the T or U wave. Any stylus movement above this line is considered positive and any stylus movement below this line is considered negative. Reviewed June 2008. T Murphy. Heart rhythms There are many different types of heart rhythms that can occur in the patients on CCU. However, it is not essential that you recognise all of these! The most important ones you should know are the normal ones and the very abnormal ones which can occur in an arrest situation. These are described and illustrated below. Of course throughout your placement as you are exposed to more you may wish to discuss these with your preceptor. Sinus rhythm is the name given to a rhythm reflecting normal electrical activity – that is, the rhythm originated in the SA node and followed the normal pathway of conduction, resulting in atrial and ventricular depolarisation. Criteria for Sinus Rhythm: Is Regular The rate is 60-100 beats per minute. There is a P wave before every QRS. The QRS is 0.04 - 0.12 seconds. The PR interval is 0.12 - 0.2 seconds. Sinus bradycardia is below 60 beats per minute and has all the other criteria for sinus rhythm. Sinus tachycardia is above 100 beats per minute but less than 150 and has all the other criteria for sinus rhythm. Atrial Fibrillation The atria are beating very irregularly (appear to quiver) and has no noticeable/distinguishable P waves. Reviewed June 2008. T Murphy. Is irregular. Can allow blood to clot in atria as blood is not flowing smoothly therefore there is a risk of clots travelling to other parts of the body and causing strokes/PEs etc. Arrest rhythms Ventricular tachycardia is a rhythm originating in the ventricles which can occur without a pulse. QRS complexes are essentially regular but wide and bizarre , the T wave is frequently in the opposite direction of the QRS complex. The rate is 100-250 beats per minute. P waves may be present but they have no set relationship to the QRS complex. Treatment of VT without a pulse is defibrillation. Ventricular fibrillation is a chaotic rhythm that originates in the ventricles. In VF there is no organised depolarisation of the ventricles. The ventricular myocardium quivers and, as a result, there is no effective myocardial contraction and no pulse. There are no normal looking waveforms visible. Treatment of VF is defibrillation. Asystole implies there is no spontaneous electrical activity, and thus the ECG is simply a flat line. This requires CPR. Pulseless electrical activity occurs when the heart continues to work electrically (the ECG continues to show QRS complexes), but fails to provide a circulation. This requires CPR. Reviewed June 2008. T Murphy. Ischaemia and Infarction The ST segment lies between the end of the S wave and the start of the T wave. Normally the ST segment is isoelectric, meaning that it lies at the same level as the ECG’s baseline, the horizontal line between the end of the T wave and the start of the P wave. ST segments can be abnormal in one of two ways, so the questions you need to ask about the ST segments when you review them are: Are the ST segments elevated?  Are the ST segments depressed? ST segment elevation can represent anything from a potentially lifethreatening condition to a normal variant, making it particularly important to identify the cause. Possible diagnoses of ST elevation are: Acute MI  Pericarditis  High take-off  Left ventricular aneurysm  Prinzmetal’s (vasospastic) angina If ST depression is present, think of the following possible causes:     Myocardial ischaemia Acute posterior MI Drugs (eg. Digoxin, Quinidine) Ventricular hypertrophy with strain Reviewed June 2008. T Murphy. Unlike with MI, ischaemia is reversible and so the associated ECG abnormalities are seen only while the patient is experiencing an episode of pain. Other changes seen in ischaemia include T-wave inversion and T-wave flattening, although the latter is a non-specific finding. Reviewed June 2008. T Murphy. Strategy for ECG Interpretation 1. Look at rhythm strip 2. Calculate rate 3. Is it regular/irregular 4. Calculate PR interval if abnormal state that it is 5. Calculate QRS width if abnormal state that it is 6. Check for ischaemia territory by territory 7. Check for infarction territory by territory 8. Report findings to preceptor Reviewed June 2008. T Murphy. ATHEROSCLEROSIS This is a complex disease that is characterised by the proliferation of smooth muscle cells and accumulation of lipid within the intima of large and medium arteries. An important feature is the focal distribution of the lesion as plaques. Atherosclerotic lesions are not evenly distributed around the arteries but are more often found at the bifurcation of arteries. Therefore when endothelial injury occurs such as from toxins, vasospasm and other haemodynamic stresses, these lesions are at increased risk of rupture due to their location. Atherosclerotic plaques are divided into 3 types: Fatty streaks These are flat lipid rich lesions that begin in early childhood, they cause little or no obstruction of the artery but are thought to be precursors to advanced atheromatous lesions  Fibrous plaques These are white lesions that become elevated and protrude into the lumen of the artery. During the development of the plaque there is a proliferation of smooth muscle cells to form a fibrous cap, containing a lipid rich pool. Reviewed June 2008. T Murphy.  Advanced lesions These are composed of fibrous tissue, fibrin, intracellular and extracellular lipid and often extravasated blood. The necrotic lipid rich core increases in size and often becomes calcified. The atheromatous plaque causes narrowing of the lumen and may become fissured. The fissures allow blood to dissect inwards forming a platelet rich thrombus within the intima. If the fissure heals a large plaque containing thrombus remains, which partially or ccompletely occludes the lumen. Alternatively fresh thrombus may extend into the lumen and may cause complete obstruction. The symptoms of myocardial ischaemia results from an imbalance between myocardial oxygen demand and supply. Critical restriction to ordinary flow occurs when the diameter of the lumen is reduced by more than 50%, usually resulting in angina. An abrupt diminution or total loss of coronary blood supply will result in acute MI Reviewed June 2008. T Murphy. RISK FACTORS FOR IHD Epidemiological studies have sought associations between the occurrence of CHD and physical, biochemical and environmental characteristics of populations and individuals. As a result predictive variables, termed risk factors, have been defined. Unavoidable risk factors have been identified as : Being male, although after menopause women are of similar risk  Increasing age  Positive family history for heart disease  Diabetes Other treatable risk factors are: Hypercholestraemia, and hyperlipidemia, Low density lipoproteins (LDLs) and High density lipoproteins (HDLs) being the 2 of main concern.  Smoking  Hypertension  Obesity  Lack of exercise  Stress Reviewed June 2008. T Murphy. On admission to CCU it is important to obtain from the patient what risk factors they may have for CHD and what treatment they are receiving for any of them. During their stay in hospital an introduction into the ways of reducing the patients and their families risk factors is very beneficial, this will often be followed up by cardiac rehabilitation after the patient has been discharged. Reviewed June 2008. T Murphy. MYOCARDIAL INFARCTION Pathophysiology Myocardial Infarction (MI) refers to necrosis of myocardial cells caused by cessation of or reduction in their blood supply. It is usually associated with an occlusive thrombus in one or more of the coronary arteries, superimposed on a discrete and fissured atherosclerotic plaque. If more than two-thirds of the ventricular wall is involved, then the infarction is termed transmural. If it involves less than this, it is termed subendocardial. When discussing MI’s we are generally referring to the left ventricle, although on occasions the right ventricle can become involved. Coronary occlusion quickly leads to transmural myocardial ischaemia. Pain is experienced within 1 minute, and the ECG changes within 30 seconds. After about 20-30 minutes necrosis begins and progresses from endocardium to epicardium. If reperfusion occurs early then there is potential for full recovery. This is why the National Service Framework (NSF) has set standards for patients to receive thrombolysis within 20 minutes of arriving in A&E, this is referred to as door to needle times Reviewed June 2008. T Murphy. (DTNT). After an MI the infarcted area of the heart is replaced by fibrous scar tissue over the course of 1 week to 3 months. Patient presentation An MI will often present as severe crushing central chest pain radiating to the arm and jaw, unrelieved by GTN and accompanied by sweating, faintness, nausea and vomiting. However it is important to note that although these are the classic symptoms, not all have to be present to constitute an MI, and the description of chest pain may also vary. The ECG will also show ST elevation in one or more of the territories. Management of an MI An MI is a medical emergency and requires swift and effective management including admission to a cardiac care unit. The initial management should be aimed at, limiting myocardial work load and oxygen consumption by:- -relieving chest pain and associated symptoms -limiting infarct size -prompt recognition and treatment of any ensuing complications Reviewed June 2008. T Murphy. Relieving chest pain and associated symptoms Chest pain is often best relieved by IV diamorphine, however whilst this is being obtained a GTN tablet should be administered sublingually if BP tolerates it. IV anti-emetics may be given and Oxygen therapy should also be administered. For continuing chest pain an infusion of IV GTN may be required, this may also be administered if the patient is hyper-tensive pre thrombolysis. Post thrombolysis, IV Beta-blockade may be administered to reduce pain, ischaemia and mortality, provided there is no bradycardia, hypotension or heart failure. Angiotensin converting enzyme (ACE) inhibitors may also be added within 48 hours of infarct, particularly in presence of LVF. Limiting infarct size Re-establishing coronary perfusion is the principal way of improving oxygenation to the injured myocardium and is first attempted by: 300mg of soluble aspirin should be given at the earliest opportunity as it enhances the effects of thrombolysis and has been shown to reduce morbidity. Reviewed June 2008. T Murphy. Thrombolysis should be administered within 20 minutes of admission to A&E after the risk of any contraindications have been determined. The drugs used at this trust for thrombolysis are Streptokinase and rTPA, in this trust the former is the drug of choice. Contraindications to thrombolysis include:  High risk of bleeding (i.e. Recent surgery, trauma, stroke or active peptic ulcer)   If Uncontrolled hypertension (>200/120) Diabetic Retinopathy these measures are unsuccessful at re-establishing coronary perfusion, then angioplasty and stenting may be necessary, or if this is not viable, cardiac bypass surgery may be considered. prompt recognition and treatment of any ensuing complications General observation and assessment of patient to determine any changes in condition, including regular assessment of chest pain. Performing regular blood tests to observe cardiac enzyme levels to determine infarct size, urea and electrolyte imbalance to ensure Reviewed June 2008. T Murphy. reduction of risk of cardiac arrhythmias, and full blood counts to observe risk of bleeding post thrombolysis. Chest X-rays and regular observation of Oxygen saturations and respiratory rate to determine if patient has any signs of heart failure. Observation of patient by means of cardiac monitoring for episodes of arrhythmia or ST segment change and 12 lead ECGs daily or during episodes of chest pain. Reviewed June 2008. T Murphy. UNSTABLE ANGINA Pathophysiology: several mechanisms may be involved. These include rupture of an atheromatous plaque, with or without superimposed thrombosis and coronary artery spasm. In contrast to myocardial infarction, the thrombus is sub-occlusive and platelet rich. Patient presentation Unstable angina presents with recurrent and usually prolonged episodes of angina occurring on minimal exertion or at rest and may be the first manifestation of coronary artery disease or may occur as an abrupt change in an established pattern of chronic stable angina. Clinical signs during episodes of pain may include transient T-wave/ST-segment changes on the ECG. The pain is not relieved with nitroglycerine. Unstable angina is a medical emergency requiring admission to a cardiac unit. The general principle of management of the patient is to minimise the imbalance between myocardial oxygen demand and supply. Goals are:- - reduction in frequency of ischaemic episodes improvement in ventricular function prevention of progression to infarction or death Patients are usually managed medically until their symptoms have settled. They are then investigated by coronary angiography with a view to possible angioplasty or surgery. Patients who do not settle on medical treatment require urgent angiography. Initial Management - Bed rest Pain relief and oxygen as required. IV Diamorphine is necessary for pain unresponsive to GTN. Reviewed June 2008. T Murphy. - Nitrates. IV is necessary for patients with ongoing pain. Heparin. Either low molecular weight heparins eg. Clexane s/c bd or unfractionated IV Heparin. Soluble Aspirin daily. Beta-blockade unless there are contra-indications. Platelet IIb/IIIa antagonists eg. Integrilin are now frequently used in high risk patients. These are used in conjunction with IV Heparin. Other measures include observation of cardiac monitoring for episodes of arrhythmia or ST segment change, 12-Lead ECGs daily or during episodes of pain and daily bloods to monitor cardiac enzymes and urea and electrolytes. Reviewed June 2008. T Murphy. CARDIAC FAILURE This is a clinical syndrome which results from an inability of the heart to provide an adequate cardiac output for the body’s metabolic requirements. Heart failure may be left or right sided and be an acute or chronic condition. The majority of heart failure patients seen in CCU are suffering from acute left ventricular failure (LVF). Causes of cardiac failure can be sub-divided into:- ● Disorders of myocardial function. Eg. Due to MI or severe ischaemia where damage to myocardial tissue causes diminished contractility. ● Inappropriate heart rates. Severe bradycardias and tachycardias. ● Excessive pressure or volume loading on the ventricle. Eg. Aortic stenosis, hypertension, thyrotoxicosis, anaemia, aortic regurgitation, mitral regurgitation, VSD. ● Restriction of ventricular filling. restrictive cardiomyopathy. Eg. Tamponade, hypertrophic and Physiological Response Several compensatory mechanisms are activated to maintain cardiac output and tissue perfusion. The decrease in blood pressure caused by the decrease in cardiac output stimulates the baroreceptors and sympathetic nervous system. This causes vasoconstriction of arteries and veins with an increase in blood pressure, heart rate and myocardial contractility. An adverse effect of this is that myocardial oxygen demand is exacerbated. Reviewed June 2008. T Murphy. - Blood flow to the gut and liver is decreased so that supply to the heart and skeletal system is increased. Decreased blood flow to the kidneys activates the renin-angiotensinaldosterone response. The rise in levels of angiotension II causes vasoconstriction and indirectly sodium retention and expansion of blood volume through aldosterone secretion. This maintains preload but causes oedema. If heart failure is long-standing the left ventricle hypertrophies to maintain pump action. - - Acute LVF Describes a sudden deterioration of left ventricular function associated with pulmonary oedema and severe dyspnoea. NB: Pulmonary oedema means there is excessive fluid either in the alveoli or the interstitial spaces of the lungs. This causes decreased gaseous exchange and subsequent arterial hypoxaemia. Signs Exhausted, ill-looking patient Dyspnoea at rest or on minor effort Tachypnoea Cold peripheries Agitation and anxiety Cough and wheeze Blood tinged sputum (caused by small haemorrhages in congested broncial mucosa). Management The underlying cause should always be treated where possible. The main aims are to:Decrease pressure and volume overload in the heart. Increase sodium and water excretion. Increase myocardial contractility Reviewed June 2008. T Murphy. This is achieved by:Bed rest in upright position Oxygen administration Reassurance IV Diamorphine to relieve dyspnoea by a combination of vasodilator, respiratory depression and relief of anxiety IV diuretic therapy. Eg. Frusemide. This decreases intravascular volume by providing a diuresis, promotes sodium excretion and causes vasodilation. IV vasodilator therapy. Eg. GTN. This acts predominantly as a venodilator by decreasing venous return to the heart. Also dilates peripheral arterioles and, therefore, decreases blood pressure. Should be titrated against blood pressure and infused at high rates if tolerated to optimise haemodynamic status. Fluid restriction. - - In severe refractory LVF positive inotropic agents such as Dobutamine and Dopamine may be used aswell as intra-aortic balloon pump therapy. Reviewed June 2008. T Murphy. ABBREVIATIONS ACE ACS AF ARF AS AV AV node AVR CABG CCF CHB CK CRF CT CVA CXR CX DCCV DVT DW Dx ECG ETT HOCM Hx ICD IHD INR IV K+ KUB Angiotensin Converting Enzyme Acute Coronary Syndrome Atrial Fibrillation (P proximal, F fast) or Flutter Acute Renal Failure Aortic Stenosis Aortic Valve Atrio-ventricular Node Aortic Valve Replacement Coronary Artery Bypass Graft Congestive Cardiac Failure Complete Heart Block Creatinine Kinase Chronic Renal Failure Computed Tomography Cerebrovascular Accident Chest X-ray Circumflex Direct Current Cardio Version Deep Vein Thrombosis Daily Weigth Diagnosis Electrocardiogram Exercise Tolerance Test Hypertropic Obstructive Cardiomyopathy History Internal Cardiac Defibrillator Ischaemic Heart Disease International Normalisation Ratio Intra-Venous Potassium Kidney Ureter Bladder Reviewed June 2008. T Murphy. LAD LBBB LVH LMS LVF Mg MI MR MRI MV Na+ NSTEMI PE PND PPM PTCA PVD RAD RAH RBBB RCA RVF SA node SBE SR SK SVT TOE tPA TTE TWOC U&E USA USS Left Anterior Descending Left Bundle Branch Block Left Ventricular Hypertrophy Left Main Stem Left Ventricular Failure Magnesium Myocardial Infarction Mitral Regurgitation Magnectic Resonance Imaging Mitral Valve Sodium Non ST Elevation Myocardial Infarction Pulmonary Embolus Paroxysmal Nocturnal Dyspnoea Permanent Pacemaker Percutaneous Transluminal Coronary Angioplasty Peripheral Vascular Disease Right Axis Deviation Right Atrial Hypertrophy Right Bundle Branch Block Right Coronary Artery Right Ventricular Failure Sino Atrial node Subacute Bacterial Endocarditis Sinus Rhythm Streptokinase Supra Ventricular Tachycardia Transoesephageal Echocardiogram Tissue Plasminogen Activator Transthoracic Echocardiogram Trial With Out Catheter Urea and Electrolytes Unstable Angina Ultra Sound Scan Reviewed June 2008. T Murphy. VE VF VQ VT WCC WPW Ventricular Ectopic Ventricular Fibrillation Variant Quota Ventricular Tachycardia White Cell Count Wolfe Parkinson White Reviewed June 2008. T Murphy. BLOOD RESULTS Blood results are extremely important within cardiac nursing, often leading to changes in the patient’s treatment. Obtaining and then interpreting the blood results therefore forms a very important part of the nurse’s role. Please state the normal values for the following. CK – creatine phosphokinase Troponin T Urea Creatinine Sodium Potassium Haemoglobin White Cell Count Platelets International Normalisation Ration INR How may blood results change in certain conditions? Comment on how results may change in the following conditions.      Myocardial Infarction Acute Coronary Syndrome Acute Renal Failure Heart Failure Anaemia Reviewed June 2008. T Murphy. PHARMACOLOGY Look up the following medications commonly used within cardiology. Your knowledge and understanding of medications is improved if you make notes on the various medications used. Find out why these drugs are used in patients with cardiac conditions. What are the common side effects and interactions of each drug? Beta Blockers Atentolol, Bisoprolol Metoprolol, Carvedolol, ACE Inhibitors Diuretics Ramipril, Lisinopril, Perindopril Frusemide, Spirolactone, Metolazone, Bumetanide Amiodarone, Digoxin, Sotolol Amoldipine, Diltizam, Verapamil Nicorandil Glyceryl Trinitrate, Mononitrate Heparin, Warfarin, Enoxaparin Aspirin, Clopidogrel Simvastatin, Atorvastatin, Pravastatin Isosorbide Anti-Arrythmics Calcium Channel Blockers Potassium Channel Blocker Nitrates Anti-Coagulatants Anti-Platelets Statins Reviewed June 2008. T Murphy. It is important to understand different cardiac conditions and why drugs are used. Consider the following questions. 1. What are thrombolytics and why are they used? 2. What dugs are used for patients following a myocardial infarction? Name two and explain why. 3. What drugs are used in a cardiac arrest? How are they given and what effects do they have? 4. A patient is admitted to the ward with an Acute Coronary Syndrome develops chest pain. What medication would you use? What would you monitor and why? 5. What drugs would be used for patients with atrial fibrillation? How would you monitor their effectiveness? 6. A patient develops increased shortness of breath, becomes hypotensive and has diminished urine output. Over the last two days the patient has been in a positive balance of two litres. What is happening to the patient? List the medication you would give and how they aid the individual’s recovery. 7. What medication would you suspect a patient to be on following admission with unstable angina? How would these benefit the patient haemodynamically? 8. A patient is on twice daily intravenous frusemide. How would this be administered and what would you monitor? 9. A patient is being treated with IV glyceryl Trinitrate (GTN) for chest pain. How does this benefit the patient? What nursing observations would you perform? 10. A patient is taking warfarin and has an INR of 5.5. Why is warfarin prescribed? This person is also taking erythromycin. Why would this affect the INR? What other drugs affect the INR? Reviewed June 2008. T Murphy.