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Slide 1 :
Disorders of Cardiovascular System
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Learning Outcomes At the end of the lecture, the student is able to: Define the specified terms Review anatomy of the cardiovascular system 3 a. Identify the common cardiovascular disorders b. Identify and discuss the risk factors of cardiovascular disorders c. List the signs and symptoms of the common disorders d. Discuss the pathophysiology of the common disorders e. Discuss the pharmacological treatment of the common disorders
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Learning Outcome 4 a. Define arrhythmia b. Discuss the different types of arrhythmia c. Discuss the pharmacological treatment of different arrhythmias. 5 a. Identify the different diagnostic tests/procedures to assess cardiac patients b. Identify the normal ECG c. Describe the conduction system of the heart. d. Identify the ECG changes in the common disorders e. Discuss the purpose and significance of different diagnostic tests/procedures.
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Learning Outcomes 6. Discuss cardiac surgeries, its indication, risk factors and complications. 7 a. Identify the vascular problems b. Discuss the risk factors of the common vascular problems c. Discuss the pathophysiological changes associated with the vascular problems 8 a. Identify different types of anemia b. Discuss the pathological changes associated with the disorders of the blood.
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The normal heart is cone shaped and is located in the mediastinum,one third to the right of the sternum and the remaining two thirds to the left. The size of the heart is about the size of a person’s fist. The heart wall has three(3) layers. They are endocardium,myocardium and pericardium Heart has four chambers. The walls of the four chambers of the heart are made up of cardiac muscle (myocardium) and are lined with endocardium which is smooth epithelial tissue that prevents abnormal clotting.
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The pathway of the blood through the heart Blood flows into the right atrium through the right ventricle and is then pumped out of the heart. Right and left atria-receive blood Right and left ventricle-pump blood out of the heart. Pulmonary circulation and Systemic circulation???? The conduction Pathway The cardiac conduction pathway is the pathway of electrical impulses that generate a heartbeat. The SA node or the natural pacemaker of the heart initiates each cardiac cycle. It is a specialized mass of the cardiac muscle that depolarizes rhythmically and most rapidly, 60-80 times per minute and this initiates each heartbeat.
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From the SA node, the electrical impulses travel to the AV node, to the bundle of His, to the right and left bundle branches, and to the purkinje fibers. When SA node does not function,AV node can initiate heart beat, but at the slower rate of 40-60 beats per minute. The bundle of His is also capable of generating heart beat of the ventricles, but at a much slower rate of 15-40 beats per minute.
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Electrocardiogram Components Of an ECG A normal ECG will have a P wave, PR interval,QRS complex, T wave, U wave, and ST segment. Steps for interpreting ECG Regularity of the rhythm Heart rate P waves PR interval QRS complex A normal sinus rhythm is a normal cardiac rhythm
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Electrocardiogram Atrial Depolarization- is shown by a P wave in the ECG.Atrial depolarisation(excitation) causes the atria to contract wave is usually small as the atria is small. Ventricular Depolarization- is shown by QRS complex in the ECG.This causes the ventricles to contract. QRS complex is larger than P wave because the ventricles are larger. Ventricular Repolarization- is shown by T wave in the ECG.This occurs when the ventricles relax.
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Cardiac Cycle Divided into three phases Ventricular Filling – When AV valves open, blood returning to the heart flows into the atria and through the ventricles. The P wave on the ECG occurs, that is atria are excited and then they contract, so the pressure in the atria becomes greater than the pressure in the ventricles, pushing some more blood to the ventricles. Now the ventricles are filled with the blood.
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Ventricular Systole- The QRS complex occurs in the ECG, that is the ventricles are electrically excited and then they contract, so increasing the pressure in the ventricles. When the pressure in the ventricles are greater than the atria, the AV valves close (causing the first heart sound). Now the AV, aortic and pulmonary valves are closed, so the pressure in the ventricles rises until it is greater than the aorta and the pulmonic trunk and the aortic and the pulmonic valves open. Then the blood is rushed from the ventricles into the aorta and the pulmonary trunk.
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Early Diastole – The ventricles relax.(T waves occurs in the ECG) and the ventricular pressure decreases. When it is less then the pressure in the aortic and pulmonic trunk, the aortic and pulmonary valves close again causing the 2nd heart sound and thus preventing the blood flowing back into the ventricles. After this the ventricles can fill again with blood from the atria and start the whole process again.
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Cardiac Cycle Is a sequence of mechanical events during one heart beat. When two atria contracts simultaneously, this is followed by a simultaneous contraction of two ventricles. When contraction or systole occurs to each chambers (atria and ventricles), relaxation or diastole also occurs to the same set of chambers. When the atria relaxes or is in diastole, it receives blood from the veins.
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When there is an increased pressure in the atria, the AV valves are forced to open and this causes most blood to flow to the ventricles. Then atria systole occurs i.e. when atria contracts, the remaining blood is pumped into the ventricles and then the atria relaxes. Then ventricular systole occurs. the pressure in the venticles causes the AV valve to close and forces the semilunar valves to open. Blood is then pumped to the semilunar valves and the artery.
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When the blood leaves the ventricle, it must be pumped. Towards the end of ventricular contractions (systole), the pressure drops and blood starts to backflow. This backflow of the blood closes the semilunar valves. The ventricles and the atria relaxes. The atria continues to fill until pressure opens the AV valve and the cycle starts again. These events creates the normal heart sounds. The first sounds are caused by the closure of the AV valves during ventricular systole (contraction) and the second sound is caused by the closure of the aortic and pulmonary semilunar valves.
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Cardiac output- amount of blood ejected by each ventricles in a minute. Can be calculated as follows: Heart Rate x stroke volume = cardiac output Stroke volume is the amount of blood pumped by a ventricle in one beat and averages to 60-80 mls. Ejection fraction- is a measure of the ventricular efficiency. stroke volume / total blood in the ventricle. usually it is 120-130 mls. Low values indicate that the ventricles are not pumping well and more blood remains in the ventricle.
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Preload- Pressure generated at the end of the diastole Afterload- resistance to ejection during systole. An increase in afterload means increase in the work of the heart.
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Blood Vessels and Circulation Arteries- carry blood away from the heart and distribute it appropriately Veins- bring blood back to the heart - also act as blood reservoirs Capillaries- are only blood vessels that allow exchange of materials between blood and tissue cells Circulation of Blood Pulmonary Circulation Systemic Circulation
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Blood Pressure (BP) Blood Pressure is the force exerted by blood against the inner walls of the blood vessels. Systolic Pressure- maximum pressure during ventricular contraction, arterial walls expand due to surge of blood Diastolic Pressure- lowest pressure during ventricular relaxation. Pulse Pressure- Systolic pressure – Diastolic pressure. Mean Arterial Pressure (MAP) - offers the average pressure in the arterial system during one complete cycle of systole and diastole.
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Tests and Procedures to assess cardiac functioning Blood Tests Urea & electrolytes (U&E’s). - Sodium and potassium is very important to note Full Blood Count Aptt- activated partial thromboplastin time Lipid Profile –HDL - LDL - triglyceride - Total cholesterol/ HDL ratio
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Electrolyte Imbalances Potassium During Depolarization and Repolarization of nerve and muscle fibres, potassium and sodium exchange occurs intracellularly and extracellularly The potassium gradient across the cell membrane determines the conduction velocity and helps confine pacing activity to the sinus node.
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Hyperkalemia This elicits significant changes in the cardiac Electrocardiogram (ECG) because it decreases the rate of ventricular depolarization, shortens repolarizations and also depresses AV conduction. Tall, Peaked T waves are usually indicative of early hyperkalemia and are followed by widening of the QRS complex and prolongation of p wave and PR interval. With severe Hyperkalemia, depressed AV conduction leads to ventricular fibrillation. This life threatening condition can be treated with glucose/insulin infusion.
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Hypokalemia Also reflected by ECG The earliest ECG change is often Premature Ventricular Contractions (PVC’s) which can detoriate into ventricular tachycardia or ventricular fibrillation without appropriate potassium relacement. Hypokalemia impairs myocardial conduction and prolongs ventricular repolarization. This can be seen by a prominent u wave in an ECG.
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CALCIUM - Is an important mediater of many cardiovascular functions because of its effect on the vascular tone, myocardial contractility, and cardiac excitability. Hypercalcemia - This condition has a cardiovascular effect of strengthening contractility and shortening ventricular repolarization.The ECG demonstrates the shortened repolarization with a shortened QT interval. Rhythemdisturbances may include bradycardia,1st, 2nd, and 3rd degree heart block.
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Hypocalcemia Cardiovascular effects of hypocalcemia include myocardial contractility,reduced cardiac output, decreased cardiac responsiveness to digitalis and hypotension. Rhythm disturbances are variable ranging bradycardia to venricular tachycardia and asystole Usually ECG demonstrates a prolonged QT interval.
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Cardiac Enzymes AST – 10-37 Creatinine Kinease- 39-308 Lactic dehydrogenase - 135-225 Troponin- are proteins in the cardiac muscle. - highly sensitive indicators of myocardial damage, which is helpful in diagnosing myocardial infarction. TNT- < 0.03
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Electrocardiogram- primary purpose of ECG is to detect ischemia or acute coronary injury. ECG depicts the electrical activity of the heart. By placing electrodes at various sites on the surface of the body, the depolarization and repolarisation of the myocardial cells can be can be detected. ECG is recorded using 12 leads: six standard limb leads and six precordial leads.
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Electrocardiogram The precordial leads are V1-V6 and are positioned around the chest wall. The limb leads are I,II.III,aVR,aVL,and aVF By using the six standard limb leads and six precordial leads, the electrical activity at various surface of the heart can be interpretated.This is used in diagnosing the area where a myocardial infarction has taken place. The areas are summarized as follows:
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Leads V1-V2 - Right Ventricle Leads V3 – V4 - anterior wall of the left ventricle Leads V5-V6 – anterior and lateral walls of the left ventricle Leads II, III, aVF- inferior surface of the heart. Leads I, aVL,V5-V6 - lateral surface of the heart. Lead aVR- atria
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The 12 lead ECG is used to classify patients into one of three groups: those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with thrombolytics. those with ST segment depression or T wave inversion (suspicious for ischemia), and those with a so-called non-diagnostic or normal ECG
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Coronary Angiogram - allows visualization of narrowing and obstructions of the heart vessels. Chest XRAY- shows the size,position,contour and structures of the heart. It shows the heart enlargement and the fluid around the heart. Echocardiogram- is an ultrasound test that records the motion of the heart structures, including the valves, as well as the heart size, shape and position.
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Cardiac Catheterization – allows the study of hearts anatomy and physiology - it measures the pressures in the heart chambers, blood vessels and coronary arteries and provides information on cardiac output and oxygen saturation. Right sided catheterization Left sided catheterization.
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Central Venous Pressure- measures the fluid volume in the body. Exercise Stress Test- measures the cardiac function during an exercise protocol.
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Cardiovascular Disorders Arthrosclerosis – is a term used to describe the conditions that affects arteries and may lead to occlusive cardiovascular disease. The lining of the artery becomes thick and hard and may lose elasticity. Is the formation of plague in the arterial wall. Pathophysiology - affects the inner lining of the art. In the beginning there is an injury to the epithelial cells that line up in the arterial wall. This injury causes inflammation and immune reactions. Lipids, platelets and other clotting factors accumulate The build up of fatty deposits is known as plague.
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This build up in the vessel becomes calcified and hardened. As the vessel becomes narrow, there is a partial or total occlusion of artery thus there would be reduced blood flow. Causes Genetic related Diabetes mallitus Hypertension Smoking Obesity Lifestyle
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Signs and Symptoms - usually asymptomatic - Chest pain and dizziness causes by decreased blood supply and oxygen to the heart. Diagnostic Tests - Lipid Profile- LDL, HDL,Triglyceride,Total Cholestrol Treatment - Statins
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Coronary Artery Disease Is caused by obstructed blood flow through the coronary arteries to the heart muscle. Primary cause is arthrosclerosis. Can cause myocardial infarction-due to reduced blood flow. Pathophysiology - blood flow to the myocardium is reduced. If myocardial oxygen demands are not met, ischemia results and can lead to chest pain. - This pain is due to lack of oxygen to the myocardium.
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Risk Factors Hereditary - Diabetes . Lifestyle - Obesity Gender/ age - Stress Hypercholesterolemia - Smoking Hypertension Medications Aspirin Cholestrol lowering drugs
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Surgical management Coronary Artery Bypass Graft Coronary Stents Acute Coronary Syndromes Group of conditions that are caused by lack of oxygen to the heart muscle. They include unstable Angina ,non-Q wave myocardial infarction, ST elevation myocardial infarction
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Angina Pectoris ( chest Pain) When there is increased workload on the heart, there is increased demand for oxygen. Normally, when heart needs more oxygen, the coronary arteries have to dilate and supply the heart with extra blood. Incase of coronary artery disease the narrowed blood vessels are unable to dilate and supply the heart with extra blood and oxygen thus results in myocardial ischemia. Chest pain results from the ischemia but usually lasts for few minutes.
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Signs and symptoms - pain is heavy,tight,squeezing and crushing - Pain can radiate to both the arms, neck, shoulders, jaw and back During pain patient may be diaphoretic, dyspneic and pale Pain is brought on by exertion and subsides at rest. Can be relieved with vasodilator.
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Stable Angina - occurs when the atherosclerotic arteries cannot dilate to increase the blood supply to the myocardium. When there is an increased physical activity, there is a demand for more blood and oxygen by the heart so patient develops mid-sternal chest pain. The pain subsides when the activity stops or when a vasodilator is used.
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Unstable angina Occurs in patients with worsening coronary artery disease. Rest does not decrease/subside the chest pain Pain may even occur when patient is at rest Pain increases in frequency and severity, placing the patient at risk for myocardial damage or even death. Prinzmetal’s Angina or Variant Angina Pain is same as in stable angina but it has longer duration and can occur at rest. Has a pattern of occurrence i.e. occurs at the same time each day. Usually caused by coronary artery spasms and does not cause damage to the myocardium.
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Diagnostic Tests ECG – may have inverted T waves and a ST segment elevation indicating a myocardial injury. Exercise Stress Test Angiogram Treatment Vasodilators- GTN,Isosobide Dinitrate Calcium Channel Blockers- Diltazem Betablockers- Atenolol
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Cardiovascular Disorders Myocardial Infarction - commonly known as heart attack. - is the interruption of the blood supply to the part of the heart causing heart cells to die. - this is commonly due to occlusion (blockage) of a coronary artery by lipids and white blood cells esp. macrophages. Pathophysiology Myocardial Infarction reflects the death of the cardiac muscle cells caused by prolonged ischemia, platelet aggregation, transient thrombosis and vasoconstriction. This produces reductions in blood flow. If blood flow to the myocardium is severely impaired for more than 20minutes.Usually the whole part is not affected unless blood flow is impaired for more than 2 hours.
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Non – ST elevation Myocardial infarction - presents with the symptoms of myocardial ischemia, but without ST elevation on the presenting ECG.The ECG usually changes but it may be normal and there is sufficient myocardial damage as the cardiac enzymes and troponin would be elevated. ST elevation Myocardial infarction - presents with the symptoms of the condition and definite ST elevation on the ECG.
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This subsequently evolves to Q waves and also includes some new bundle branch block and posterior ECG changes. Symptoms Sudden onset of chest pain- typically radiating to left arm, left side of the neck, and shoulder. May also experience locking of the jaw. Shortness of breath Nausea and vomiting Palpitations Profuse sweating Anxiety.
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Risk Factors Family history of ischemic heart disease Age Hypercholesterolemia Smoking Obesity Diabetes Hypertension
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Diagnosed through family history, physical examination, and ECG Diagnostic Tests - ECG - Chest X-Ray - Blood Tests- cardiac enzymes,troponin and aptt, U&E’s, FBC. - ECHO
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Treatment - Statins- atrovastatin - Aspirin - Thrombolytic Therapy- streptokinase - Sublingual glyceryl trinitrate - Morphine with maxalon - Beta-blockers-Atenolol -Ace- Inhibitors- Enalapril - Anticoagulant- Heparin Infusion
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Anterior Infarction- Q wave, ST elevation, T inversion in leads I, aVL, V1 & V2 in reciprocal changes in leads II,III,aVF,V3 & V4 Anterolateral Myocardial Infarction- Q wave and inverted T wave in leads I,II,V5 &V6 Anteroseptal Myocardial Infarction- Q wave,ST elevation inversion in any one of the following.V1-V4. Inferior Myocardial Infarction- Q wave, ST elevation and T inversion in leads II,III,aVF, with reciprocal changes in leads I,aVL & V1-V6. Posterior Myocardial Infarction- only reciprocal changes in leads V1-V4,tall R & T waves in leads V1-V2.
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Lateral Myocardial Infarction- Q wave,ST elevation & T inversion in leads I & aVL. Inferolateral Myocardial Infarction- Q wave, ST elevation & T inversion in leads II,III,aVF,V5-V6 with reciprocal changes in I,& aVF. Right ventricular infarct- ST elevation in V3R and V4R.
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Heart Failure Is a syndrome that occurs as a result of the progressive inability of the heart to pump enough blood to meet the body’s needs. Pathophysiology Normally the heart is divided into two separate pumping systems. Conditions that cause heart failure may affect both the pumping systems or on of them. It is the ventricles of the heart that fails. Left ventricle is the one to weaken because of greater workload. Right and left heart failure
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Causes Myocardial infarction Ischemic heart disease Hypertension Valvular heart disease Cardiomyopathy Symptoms Shortness of breath – gets worse when lying flat which is called orthopnea Caughing , ankle swelling
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Diagnostic Tests Chest X-ray Arterial blood gases ECG Treatment Morphine – low dose Diuretics- Lasix Vasodilators- GTN
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Acute Pulmonary Oedema Acute heart failure Is severe fluid accumulation/congesion in the alveoli of the lungs Leads to impaired gas exchange and may cause respiratory failure. Severe pulmonary edema causes the left ventricle to fail. Pathophysiology Pressure rises in the lungs venous blood vessel's and blood builds up. As pressure continues to rise, fluid moves into the interstitial spaces. Then, with continued increase in pressure fluid containing red blood cells moves into the alveoli.Finally, the alveoli and airways are filled with fluid thus reducing gas exchange and oxygen levels
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Signs and symptoms Difficulty in breathing Pink frothy sputum-due to increased lung congestion and pressures that allow leakage of fluid into the alveoli Excessive sweating Anxiety Pale skin Death due to hypoxia Nocturia- frequent urination at night Pedal edema Orthopnea Paroxysmal noctural dyspnea- episodes of severe sudden breathlessness at night.
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Diagnosis history of previous cardiovascular diseases Physical examination Crackles on auscultation Blood tests for electrolytes- Na & K+,renal function-Cr, Ur Full blood count ApTT Chest X-ray- will show the evidence of increased fluid in the alveoli walls. - increased blood flow to the higher parts of the lungs 8. Abnormal ABG’s- will show decrease in PaO2 and continues as the edema worsens and an increase in PaCO2, causing respiratory acidosis
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ECG changes -Sinus tachycardia - Minimal ST and T wave changes with prolongation of the QT intervals. Treatment Morphine- to reduce anxiety, relax airways. Diuretics- Lasix- reduce fluid congestion. Vasodilators- GTN
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Common Cardiac Arrythmia’s Sinus Bradycardia Occurs when the SA node takes longer to depolarize than usual. Caused by fewer impulses originating from the SA node. Causes Myocardial infarction affecting the blood supply to the SA node. Use of beta blockers Hyperkalemia Heart Block Electrolyte imbalance
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Signs and Symptoms - Syncope attacks ( fainting episodes) Treatment If symptomatic then use atropine to a maximum dose of 3mg If there is a risk for systole then pacemaker may be required - If complete heart block may need isoprenaline infusion. Salbutamol tablets or nebulizers are also used to maintain the heart rate. Sinus Tachycardia - Due to more impulses generating from the SA NODE Results in a normal sinus beat but at a rate greater then 100bpm. May cause decrease cardiac output together with a reduced myocardial blood supply. Also increases myocardial work and may extend the size of myocardial infarction Following a MI, sinus tachycardia may indicate poor left ventricular function.
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Usually asymptomatic Treat the underlying cause. May experience angina or dyspnea Causes Pain, anxiety, stress. Medications- salbutamol, isoprenaline adminitration
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Atrial Fibrillation One of the most common arrythmia Atrial rate is extremely rapid and chaotic AV node blocks most of the impulses so the ventricular rate is much lower then the atrial rate. Causes ischemia/ hypoxia Hypertension Cardiomyopathy Heart failure Coronary artery disease Decreased cardiac output
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ECG changes Irregular heart rate with indefinite P wave Wide QRS complex Because atrial rate is irregular and only few atrial impulses are allowed to pass through the AV node, the R waves are irregular Treatment Digoxin,betablockers or calcium channel blockers cardioversion
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Atrial Flutter The atria may depolarize at a rate of 250-350 bpm but are blocked by AV node. Only some impulses get through the AV node and reach the ventricles resulting in a QRS complex. Rapid and irregular P wave. More than one P wave appear before a QRS complex Signs and symptoms - symptoms depend on the ventricular rate Ventricular rate – normal – no symptoms - abnormal – palpitations, angina and dyspnea
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Treatment medications- beta blockers and calcium channel blockers can control the rate and digoxin can control the rhythm. May require cardioversion. Causes Coronary artery disease Heart failure Chronic pulmonary disease.
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Bigeminy- PVC that occurs after every normal beat. Trigeminy- PVC that occurs after 2(two) normal beats Quadrigeminy- PVC that occur after 3 (three) normal beats. Signs and symptoms PVC’s may be felt by the patient Palpitations Cardiac output can be decreased leading to fatigue,dizziness.
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Premature Ventricular Contractions Originate in the ventricles but not from the SA node. The ventricles get irritated and they fire prematurely before the SA node. When the ventricles fire first, the impulses are not conducted normally through the electrical pathway as a result there is a wide QRS PVC’s can be unifocal, multifocal. There can be several repetitive cycles of PVC’S
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Treatment Depends on the number and type of PVC’s Lignocaine and amiodarone is used. Causes- use of caffeine,anxiety,hypokalemia,cardiomyopathy,ischemia, and myocardial infarction Ventricular Tachycardia Occurrence of three of more PVC’s in a row. There is a continuous firing of ventricular impulses. ventricles become the pacemaker Pathway of ventricular impulses is different from the normal conduction producing a wide QRS complex
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Causes Myocardial infarction Cardiomyopathy Respiratory acidosis,hypokalemia. Signs and symptoms - dyspnea,palpitation,light headedness, angina If left ventricles fail the complete cardiac arrest occurs. Treatment – if patient is not breathing and pulseless-CPR. Immediate defib is required. Antiarrythmic drugs If patient is stable- medications can be tried first and if does not subside – cardioversion.
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Ventricular Fibrillation - occurs when many ventricular impulses fire at the same time. Ventricular activity is chaotic. No cardiac output Causes Hyperkalemia Coronary artery disease, myocardial infarction Signs and symptoms Patients lose consciousness immediately No heart sounds, peripheral pulses or blood pressure
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Heart Block First degree AV block Second degree AV block – Mobitz Type I Wenchbach Second degree – Type II Third degree – complete heart block Causes Coronary heart disease Myocardial infarction Valvular heart disease Acute rheumatic fever Cardiomyopathy
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Treatment - if symptomatic – isoprenaline- urgent pacemaker - salbutamol Bundle branch block There is a conduction disturbances in the bundles- right or left. If the bundles are blocked,conduction through the ventricles are delayed and thus gives a wide QRS. Precordial leads-V1-V6
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Causes of BBB - Pulmonary embolism Coronary disease Ischemia Cardiomyopathy.
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