Diabetic Ketoacidosis

Caused by an absence or markedly inadequate amount of insulin in the body. Diabetic ketoacidosis occurs most often in patients with type 1 diabetes the amount of glucose entering in the cell for energy consumption is inadequate, thus our body begins to burn fats as alternative source of energy. Free fatty acids and glycerol (product of lipolysis) are converted into ketones in the liver, this ketones are acidic. Ketones are acids that build up in the blood and appears in the urine when the body have inadequate insulin. Increase level of ketones in blood is a warning manifestation that you diabetes is worsening. Stress also triggers production of glucose, interfering the utilization of glucose in the muscle and fat tissue, thus increasing the level of ketones through lipolysis.

Pathophysiology Decrease in amount of insulin in the body may affect the amount of glucose level that enters in our cell, this may trigger our liver through gluconeogenesis to release glucose and may lead to hyperglycemia. In attempt to get rid of the excess glucose in our system, our kidney attempt to excrete excess glucose together with urine and other electrolyte such as potassium. This osmotic diuresis is characterized by excessive urination and may lead to dehydration and electrolyte loss, which will manifested with body weakness and headache. Because of excessive urination, our body will attempt to replace the fluid loss by activating the thirst mechanism that will result to polydipsia. Insufficient amount of insulin in our system, will result to decrease consumption of glucose as our primary source of energy, thus our body will look for another source of energy and that is fats, this fats will be converted to free fatty acids through lipolysis and there will be an increase in fatty acids in our body, this fatty acids will be then converted in our liver into ketone bodies, this ketones are acidic, thus accumulation of ketones in our circulation may cause acidosis due to lack of insulin, leading to metabolic acidosis. Too much ketone will manifest fruity breath odor. Nausea, vomiting and abdominal pain are the major indication of G.I tract problem that are commonly seen in patient with DKA. Due to acidosis, our body will try to compensate by excreting carbon dioxide through respiratory system as manifested by Kussmaul respiration.

Lack of Insulin

*Decreased utilization of glucose by muscles, fats and liver. *Increased production of glucose by liver

Increase breakdown of fats

Hyperglycemia

Increased Fatty Acids

Blurred Vision

Polyuria

Increase Ketone Bodies

Dehydration

*Acetone Breath *Poor Appetite *Nausea

Acidosis

Weakness Headache

Increase thirst (POLYDIPSIA)

*Nausea *Vomiting *Abdominal Pain

Increasingly rapid respirations

Clinical Manifestation

Excessive thirst- due to excessive urination, to replace fluid loss cause by activated thirst mechanism Frequent urination- the kidney trying to neutralized the glucose level in the blood through urination. General weakness- because of the electrolytes that are excreted and insufficient glucose for energy consumption Vomiting- gastrointestinal symptoms of ketosis and acidosis Abdominal pain- manifestation of severe condition that they resemble an acute abdominal disorder that requires surgery. Hyperventilation- represents the bodys attempt to decrease the acidosis, counteracting the effect of the ketone build up. Dry skin and mouth Increased heart rate- due to depletion of blood volume. Orthostatic hypotension due to depleted intravascular volume Distinctive fruity odor on the breath- because of high level of ketones in the blood.

Diagnostic Procedure and Findings Blood Glucose Level -to determine if the body have enough insulin to allow sugar to enter your cells, your blood sugar level will rise (hyperglycemia). As your body breaks down fat and protein for energy, your blood sugar level will continue to rise. 300-800 mg/dL Ketone level. When your body breaks down fat and protein for energy, toxic acids known as ketones enter your bloodstream. Small: < 20 mg/dL Moderate: 30 - 40 mg/dL Large: > 80 mg/dL Blood acidity. If you have excess ketones in your blood, your blood will become acidic (acidosis) with a pH of 6.8-7.3 and low partial pressure of carbon dioxide (10-30mmHg). Normal pH value 7.35- 7.45 Urinalysis- to determine the presence of ketones. Normal Result- Negative Creatinine and Blood Urea Nitrogen and Hematocrit may increase as a result of dehydration.

Diagnostic Criteria of Diabetic Ketonacidosis Diagnostic criteria Plasma glucose Arterial pH Serum bicarbonate Urine ketone Serum ketone Mild DKA >250 mg/dl 7.25-7.30 15-18 Positive Positive Moderate DKA >250 mg/dl 7.00-<7.24 10- <15 Positive Positive Severe DKA >250 mg/dl <7.00 <10 Positive Positive

Medical Management

Fluid replacement. -important for rehydration for tissue perfusion - enhance the secretion of glucose by the kidneys.

-about 6-10 liters of IV (isotonic solution) fluid to replace fluid loses cause by polyuria, hyperventilation, vomiting and nausea. -0.9% NaCl is administered at a rapid rate for 2-3 hours. -for patients who have hypertension and hypernatremia and those who are at risk for heart failure half-strength normal saline may be given. -half-strength normal saline solution is the fluid of choice for continued rehydration, provided that the blood pressure is stable and the sodium level is not low. -for glucose level that reaches 300mg/dL, the IV solution may be changed to dextrose 5%in water to avoid precipitous decline in the blood glucose.

Electrolyte replacement - excessive loss of potassium is the major electrolytes that needs intervene in DKA. -depletion potassium is caused by shifting of potassium from intracellular to extracellular. -Rehydration also leads to increase urinary secretion of potassium. -the entire course of treatment of DKA may also affects the serum level of potassium, such as insulin therapy. Insulin therapy decreases potassium levels in the blood by redistributing it into cells.

Insulin therapy. -Insulin reverses the processes that cause diabetic ketoacidosis, by inhibiting the fat breakdown thereby stopping acid buildup. -Insulin is infused intravenously at a slow rate, hourly blood glucose measurement should be done. - IV fluid solutions with higher concentration of glucose is to be used (D5NS, D5.45NS) when blood glucose level reaches 250-300mg/dL to avoid too rapid drop of blood glucose during treatment. -Insulin must be infused continuously until subcutaneous administration of insulin can be resumed.

Nursing Management Assessment: -the nurse monitors the ECG for possible dysrhtymias indication abnormal potassium level, in Hypokalemia prominent U waves can be seen, while in Hypekalemia tall tented T waves can be seen. -Monitor vital signs especially the blood pressure and pulse should be closely monitored. -Arterial Blood Gases analysis -assess for breath odor, fruity breath odor is an indicative sign of increasing level of ketones in the body. -Mental status should be assessed hourly and should be properly recorded on a flow sheet. Diagnosis: Risk for fluid volume deficit related to polyuria and dehydration. Fluid and electrolyte imbalance related to fluid loss or shift. Deficient knowledge about diabetes self-care skills. Anxiety related to fear of inability to manage diabetes, misinformation related to diabetes, fear of diabetes complications. Planning and Goals: The major goal of management for the patient with diabetic ketoacidosis includes: maintenance of fluid and electrolyte balance and restoring electrolytes. Optimal control of blood glucose level Rehydration to replace fluid that was excreted. and Reversing the Acidosis Nursing Interventions: Maintaining Fluid and Electrolyte Balance Measure intake and output. IV fluid and electrolytes as prescribe by the physician.

Vital signs needs to be closely monitored and watch out for possible sign of hypotension and tachycardia Encourage the client to increase fluid intake. Increasing Knowledge About Diabetes Management

Carefully assess the patients understanding of and adherence to the diabetes management plan. - If the patient had eaten yet , do NOT stop your insulin completely. Our body needs insulin even if we are not eating. If the patient has not previously diagnosed with diabetes, the opportunity is to teach the patient about the need for maintaining blood glucose at a normal level and learning about diabetes management. Include the family member in the health teaching for management of diabetes. Monitoring and Managing Potential Complications

Fluid Overload -may occurs due to administration of a large volume of fluids at a rapid rate which is often required to treat patient with DKA. To avoid fluid overload, the nurse must closely monitor the patient during the treatment, by measuring the intake and output and obtaining vital signs. -Central Venous Pressure should be also monitored to provide additional measure of fluid status. -Normal Values of Central Venous Pressure is 2-6mmHg Hypokalemia -is a potential complication during the treatment of DKA as potassium is lost from the body stores cause by rehydration, increase urinary excretion of potassium and movement of potassium from the extracellular fluid into the cell with insulin administration. Teaching Patient Self-Care

The patient is taught survival skills which includes diets, insulin administration, monitoring blood glucose and monitoring of urine ketones. - monitoring of blood sugars as instructed by your health care practitioner. - Be alert for signs of infection and be hydrated by drinking sugar free fluids throughout the day. - Checking the blood glucose level at least every three to four hours. Evaluation

1. Achieves fluid and electrolyte balance. A. Demonstrate intake and output balance B. Exhibits electrolyte values within normal limits C. Exhibits vital signs that remain stable 2. Demonstrate knowledge about DKA A. Identifies factors leading to DKA B. Describe the signs and symptoms of DKA C. Identifies different strategies to prevent the development of DKA 3. Absence of complications A. Exhibits normal cardiac rate and rhythm and normal breath sound B. Exhibits no jugular venous distention C. Exhibits blood glucose and urine ketone level within target range D. Exhibits no manifestation of hypoglycemia and hyperglycemia.

References: Brunner and Suddarths Textbook of Medical- Surgical Nursing 12th Edition pages nos. 276-277 1225-1227, 1229-1230 http://www.barbaradaviscenter.org. British Society of Paediatric Endocrinology and Diabetes (BSPED) guidelines for management of DKA in young people under the age of 18 years can be found at: http://www.bsped.org.uk/professional/guidelines/docs/DKAGuideline.pdf Abbas E. Kitabchi, Ph.D., M.D. Maston K. Callison Professor of Medicine The University of Tennessee Health Science Center Memphis, Tennessee

DYSRHYTHMIAS
Dysrhythmias are disorders of the formation or conduction of the electrical impulse within the heart. These disorders can cause disturbances of heart rate, the heart rhythm or both. Disorders of the formation or conduction or both of the electrical impulse within the heart. Disorders can cause disturbances of the heart rate, the heart rhythm or both. Dysrrhythmias may initially be evidenced by the hemodynamic effect they cause (e.g. a change in conduction may change the pumping action of the heart and cause decreased blood pressure. Dysrrhythmias are diagnosed by analyzing the electrocardiographic waveform.

Pathophysiology Normal electrical activity Each heart beat originates as an electrical impulse from a small area of tissue in the right atrium of the heart called the sinus node or Sino-atrial node or SA node. The impulse initially causes both atria to contract, then activates the atrioventricular (or AV) node which is normally the only electrical connection between the atria and the ventricles (main pumping chambers). The impulse then spreads through both ventricles via the Bundle of His and the Purkinje fibres causing a synchronised contraction of the heart muscle and, thus, the pulse. Bradycardias A slow rhythm (less than 60 beats/min), is labelled bradycardia. This may be caused by a slowed signal from the sinus node (sinus bradycardia), a pause in the normal activity of the sinus node (sinus arrest), or by blocking of the electrical impulse on its way from the atria to the ventricles (AV block or heart block). Heart block comes in varying degrees and severity. It may be caused by reversible poisoning of the AV node (with drugs that impair conduction) or by irreversible damage to the node. Bradycardias may also be present in the normally functioning heart of endurance athletes or other well-conditioned persons. Tachycardias In adults and children over 15, resting heart rate faster than 100 beats/minute is labelled tachycardia. Tachycardia may result in palpitation; however, tachycardia is not necessarily an arrhythmia. Increased heart rate is a normal response to physical exercise or emotional stress. This is mediated by the sympathetic nervous system on the

sinus node and called sinus tachycardia. Other things that increase sympathetic nervous system activity in the heart include ingested or injected substances, such as caffeine or amphetamines, and an overactive thyroid gland (hyperthyroidism). Tachycardia that is not sinus tachycardia usually results from the addition of abnormal impulses to the normal cardiac cycle. Abnormal impulses can begin by one of three mechanisms: automaticity, re-entry or triggered activity. A specialised form of re-entry problem is termed fibrillation Heart defects causing tachycardia

Congenital heart defects are structural or electrical pathway problems in the heart that are present at birth. Anyone can be affected with this because overall health does not play a role in the problem. Problems with the electrical pathway of the heart can cause very fast or even deadly arrhythmias. Wolf-Parkinson-White syndrome is due to an extra pathway in the heart that is made up of electrical muscle tissue. This tissue allows the electrical impulse, which stimulates the heartbeat, to happen very rapidly. Right Ventricular Outflow Tract Tachycardia is the most common type of ventricular tachycardia in otherwise healthy individuals. This defect is due to an electrical node in the right ventricle just before the pulmonary artery. When the node is stimulated, the patient will go into ventricular tachycardia, which does not allow the heart to fill with blood before beating again. Long QT Syndrome is another complex problem in the heart and has been labeled as an independent factor in mortality. There are multiple methods of treatment for these including cardiac ablations, medication treatment, or altering your lifestyle to have less stress and exercise. It is possible to live a full and happy life with these conditions. Automaticity

Automaticity refers to a cardiac muscle cell firing off an impulse on its own. All of the cells in the heart have the ability to initiate an action potential; however, only some of these cells are designed to routinely trigger heart beats. These cells are found in the conduction system of the heart and include the SA node, AV node, Bundle of His and Purkinje fibers. The sinoatrial node is a single specialized location in the atrium which has a higher automaticity (a faster pacemaker) than the rest of the heart and, therefore, is usually responsible for setting the heart rate and initiating each heart beat. Any part of the heart that initiates an impulse without waiting for the sinoatrial node is called an ectopic focus and is, by definition, a pathological phenomenon. This may cause a single premature beat now and then, or, if the ectopic focus fires more often than the sinoatrial node, it can produce a sustained abnormal rhythm. Rhythms produced by an ectopic focus in the atria, or by the atrioventricular node, are the least dangerous dysrhythmias; but they can

still produce a decrease in the heart's pumping efficiency, because the signal reaches the various parts of the heart muscle with different timing than usual and can be responsible for poorly coordinated contraction. Conditions that increase automaticity include sympathetic nervous system stimulation and hypoxia. The resulting heart rhythm depends on where the first signal begins: If it is the sinoatrial node, the rhythm remains normal but rapid; if it is an ectopic focus, many types of dysrhythmia may ensue. Re-entry

Re-entrant arrhythmias occur when an electrical impulse recurrently travels in a tight circle within the heart, rather than moving from one end of the heart to the other and then stopping. Every cardiac cell is able to transmit impulses of excitation in every direction but will only do so once within a short time. Normally, the action potential impulse will spread through the heart quickly enough that each cell will only respond once. However, if there is some essential heterogeneity of refractory period or if conduction is abnormally slow in some areas (for example in heart damage) so the myocardial cells are unable to activate the fast sodium channel, part of the impulse will arrive late and potentially be treated as a new impulse. Depending on the timing, this can produce a sustained abnormal circuit rhythm. As a sort of re-entry, the vortices of excitation in the myocardium (autowave vortices) is considered to be the main mechanism of life-threatening cardiac arrhythmias. In particular, the autowave reverberator is a typical in thin walls of the atria, with the atrial flutter producing. Re-entry is also responsible for most paroxysmal supraventricular tachycardia, and dangerous ventricular tachycardia. These types of re-entry circuits are different from WPW syndromes in which the real pathways existed. Fibrillation

When an entire chamber of the heart is involved in a multiple micro-reentry circuits and, therefore, quivering with chaotic electrical impulses, it is said to be in fibrillation. Fibrillation can affect the atrium (atrial fibrillation) or the ventricle (ventricular fibrillation); ventricular fibrillation is imminently life-threatening. Atrial fibrillation affects the upper chambers of the heart, known as the atria. Atrial fibrillation may be due to serious underlying medical conditions and should be evaluated by a physician. It is not typically a medical emergency.

Ventricular fibrillation occurs in the ventricles (lower chambers) of the heart; it is always a medical emergency. If left untreated, ventricular fibrillation (VF, or V-fib) can lead to death within minutes. When a heart goes into V-fib, effective pumping of the blood stops. V-fib is considered a form of cardiac arrest. An individual suffering from it will not survive unless cardiopulmonary resuscitation (CPR) and defibrillation are provided immediately. CPR can prolong the survival of the brain in the lack of a normal pulse, but defibrillation is the only intervention that can restore a healthy heart rhythm. Defibrillation is performed by applying an electric shock to the heart, which resets the cells, permitting a normal beat to reestablish itself. Triggered beats

Triggered beats occur when problems at the level of the ion channels in individual heart cells result in abnormal propagation of electrical activity and can lead to sustained abnormal rhythm. They are relatively rare and can result from the action of anti-arrhythmic drugs. See early and delayed after depolarizations. Normal Sinus Rhythm

In a normal heart rhythm, the sinus node generates an electrical impulse which travels through the right and left atrial muscles producing electrical changes which is represented on the electrocardiogram (ECG) by the p-wave. The electrical impulse then continues to travel through specialized tissue known as the atrioventricular node, which conducts electricity at a slower pace. This will create a pause (PR interval) before the ventricles are stimulated. This pause is helpful since it allows blood to be emptied into the ventricles from the atria prior to ventricular contraction to propel blood out into the body.

The ventricular contraction is represented electrically on the ECG by the QRS complex of waves. This is followed by the T-wave which represents the electrical changes in the ventricles as they are relaxing. Therefore, on an ECG in normal sinus rhythm p-waves are followed after a brief pause by a QRS complex, then a T-wave.

Types of Sinus Node Sinus Tachycardia

Sinus tachycardia occurs when heart rate increases, usually due to some stimulus that has affected the heart muscle. Causes of sinus tachycardia include severe fright, distress, exercise, fever, and use of recreational, over-the-counter, or prescription drugs. In many cases, sinus tachycardia is considered normal, and the heart rate often lowers itself without treatment. If sinus tachycardia is more persistent, however, it may be the result of an underlying condition. When drugs of any type are implicated in increased heart rate, drug use habits may need to be reconsidered. The increase in heart rate known as sinus tachycardia typically occurs when the nerve bundle known as the sinoatrial (SA) node stimulates the heart to beat more rapidly. The SA node can be found in the upper portion of the right atrium of the heart. It normally produces the electrical impulses that regulate heartbeat. Most people have a normal resting heart beat of 60 to 70 beats per minute, but sinus tachycardia can cause the heart to beat much faster.

ECG criteria for sinus tachycardia Ventricular & atrial rate: greater then 100 in the adult Ventricular & atrial rhythm: regular QRS shape & duration usually normal, but may be regularly abnormal P wave: normal & consistent shape: always in front of the QRS, but may be buried in the preceding T wave PR interval Consistent interval between 0.12 & 0.20 seconds P: QRS ratio: 1:1 Sinus Bradycardia

People who have a very slow heartbeat may find that they actually have a condition known as sinus bradycardia. Patients with this condition may still have normal, regular heart beats, however, they are much slower than average heartbeats, at only 60 beats per minute or less while at rest. Some common causes of sinus bradycardia include rigorous physical exercise, irregular sleep patterns, hypothermia, and the use of some medications. Aside from a rather slow heartbeat, some patients also experience additional symptoms such as light headedness, chest pain, and shortness of breath.

Cause: Lower metabolic needs (sleep, athletic training, hypothermia, hypothyroidism) Vagal Stimulation (vomiting, suctioning, severe pain, extreme emotions) Medications (calcium channel blockers, amiodarone, beta-blockers Incensed intracranial pressure and myocardial infarction (MI), especially of the inferior wall.

Characteristics of Sinus bradycardia: Ventricular & atrial rate : less than 60 in the adult Ventricular & atrial rhythm : regular QRS shape & duration: Usually normal, but may be regularly abnormal P: QRS ration: 1:1 Sinus Arrhythmia

Sinus arrhythmia is a disruption in the heartbeat that originates in the sinus node of the heart, where the heart's natural pacemaker is located. A number of problems involving the heart's natural pacing can cause the heartbeat to be irregular. Sinus arrhythmia is usually benign, but it can be a cause for concern in certain cases. Other arrhythmias located in this node such as sinus bradycardia, where the heart beats too slowly, or sinus tachycardia, where the heart beats too quickly, can be serious medical issues. Another common form of sinus arrhythmia is a respiratory sinus arrhythmia, characterized by small variations in the heartbeat associated with breathing in. In patients with this type of arrhythmia, the heartbeat changes slightly with each breath, but the patient is not in danger. Sinus arrhythmia can also occur in response to medications, stress, environmental factors, and recreational drugs. Some of these arrhythmias can become dangerous if they are not corrected. Patients who repeatedly expose themselves to common causes of cardiac arrhythmias over the long term can damage their hearts. This can lead to the development of a more serious arrhythmia that may put the patient at risk of a heart attack or other medical complications.

Causes: Nonrespiratory causes include heart disease & valvular disease, but these are rarely seen

ECG criteria for sinus arrhythmia Ventricular & atrial rate: 60 to 100 in the adult Ventricular and atrial rhythm: irregular QRS shape & duration: usually normal, but may be regularly abnormal P wave: normal & consistent shape: always in front of the QRS PR interval: consistent interval between 0.12 and 0.20 seconds P: QRS ratio: 1:1 Premature atrial contractions (PACs)

This type of arrhythmia occurs when the atria, the two upper chambers of the heart, beat before they are supposed to. Many people never even notice that a premature atrial contraction is occurring, although some people feel the contraction as a faint flutter or palpitation, as though the heart has skipped a beat. With the use of an electrocardiogram (ECG) or the wearing of a heart rate monitor, a doctor can track the contractions, determining how often and when they occur. Causes: Caffeine, alcohol, nicotine, stretched atrial myocardium (as in hypervolemia), anxiety, hypokalemia (low potassium level), hypermetabolic states, or atrial ischemia, injury or infarction

Characteristics of PACs Ventricular and atrial rate: depends on the underlying rhythm (e.g. sinus tachycardia) Ventricular and atrial rhythm: Irregular due to early P waves, creating a PP invertal that is shorter than the others. This is sometimes followed by a longer than normal PP interval, but one that is less than twice the normal PP interval. This type of interval is called a noncompensatory pause. QRS shape and duration: the QRS that follows the early P wave is usually normal, but it may be abnormal (aberrantly conducted PAC). It may even be absent (blocked PAC) P wave: an early and different P wave may be seen or may be hidden in the T wave: other P waves in the strip are consistent. PR interval: The early P wave has a shorter than normal PR interval but still between 0.12 & 0.20 seconds P: QRS ratio: usually 1:1 Atrial Flutter atrial flutter occurs in the atrium and creates impulses at an atrial rate between 250 & 400 times per minute. Because the atria rate is faster than the AV node can conduct, not all trial impulses are conducted into the ventricles, causing a therapeutic block at the AV node. Atrial tachycardia

The problem stems from an abnormal cardiac rhythm which occurs when the electrical impulses which regulate the heartbeat originate in the wrong area of the heart. Within the heart is a small node of tissue known as the sinoatrial node, located in the right atrium, the upper right corner, of the organ. It is this node which originates the electrical impulses that cause the heart to beat, and which is responsible for setting the pace of the heartbeat. In a person with atrial tachycardia, these electrical impulses come from the upper chambers of the heart, called the atria, instead of from the sinoatrial node.

Signs and Symptoms: heart palpitations, pain or pressure in the chest, difficulty breathing, fainting, and dizziness. A feeling of fatigue which may be persistent despite periods of resting is another common symptom of atrial tachycardia. Children who are experiencing abnormal heart rhythm or other symptoms may find it difficult to articulate these sensations, but may simply express a need to rest or may have problems keeping up with other children at play. An episode of paroxysmal atrial tachycardia can occur in the complete absence of any heart disease or defect, and this condition is not usually dangerous. Atrial fibrillation

Atrial fibrillation, also known as afib, is a term used to describe a disorder of the heart. Atrial fibrillation is a form of cardiac arrhythmia, which means that the hearts normal beating rhythm is interrupted. The condition may be permanent, may come and go without treatment, or may be stopped only with treatment. Atrial fibrillation can cause heart palpitations, chest pain, dizziness, shortness of breath, weakness, and fatigue, although many people experience no symptoms at all. Heart disease and high blood pressure are the two main known causes of atrial fibrillation. Both of these conditions can cause damage to the heart, making it more susceptible to cardiac arrhythmia. After the body has depleted the oxygen in the blood, it enters the heart through the right atria. From the right atria the blood is pumped to the right ventricle, where it is pumped to the lungs, which replenishes the blood with oxygen. Once replenished with oxygen, the blood is transported from the lungs to the left atria, where it is pumped into the left ventricle. From the left ventricle, the oxygen-rich blood flows into the aorta, which is the largest artery in the body. From the aorta, blood re-enters the bloodstream and is distributed throughout the body.

Characteristics of Atrial Fibrillation Ventricular and atrial rate: Atrial rate is 300 to 600. Ventricular rate usually 120 to 200 in untreated atrial fibrillation Ventricular and atrial rhythm: Highly Irregular QRS shape & duration: usually normal, but may be abnormal P wave: no discernible P waves: Irregular undulating waves are seen and are referred to as fibrillatory or F waves PR interval: cannot be measured P: QRS ratio: many:1 Atrial flutter

An atrial flutter is arrhythmia, or abnormal rhythm, of the atria of the heart. Atrial flutter is characterized by palpitations, or an abnormal awareness of the heart's beating, along with tachycardia, or an abnormally fast heartbeat. In extreme cases, atrial flutter can lead to chronic breathlessness and even heart failure. It can also cause blood to pool in the atria and eventually form a blood clot in the heart. If the blood clot travels to the brain, stroke can result. A re-entrant rhythm in the right or left atrium causes atrial flutter. When the heart is functioning normally, a heartbeat will involve electrical impulses passing through each cell of the atrium only once. During atrial flutter, some cells are slow to respond to the impulse. This causes the initial impulse to be misinterpreted, when the slow cells finally respond, resulting in a continued loop of electrical activity. The resulting heartbeat will not be as fast as the impulses in the atria, since heartbeat is measured by the contractions of the ventricles, the lower two chambers of the heart; however, it will be faster than normal. The atria transmit an electrical impulse to the ventricles via the atrio-ventricular node, which is able to slow down excessively fast

impulses coming from the atria. When the atrio-ventricular node slows the impulse in this manner, heart block occurs, resulting in the symptoms that characterize atrial flutter. Cardioversion, the application of a low current electrical energy to the heart, can also help return the heartbeat to normal in the case of atrial flutter. Ablation, in which a scar is surgically created to destroy the circuit in the heart causing atrial flutter, is another option.

Characteristics of Atrial Fibrillation Ventricular and atrial rate: Atrial rate is 300 to 600. Ventricular rate usually 120 to 200 in untreated atrial fibrillation Ventricular and atrial rhythm: Highly Irregular QRS shape & duration: usually normal, but may be abnormal P wave: no discernible P waves: Irregular undulating waves are seen and are referred to as fibrillatory or F waves PR interval: cannot be measured P: QRS ratio: many:1

Types of Ventricular Arrhythmias A ventricular arrhythmia begins in the hearts ventricles. Types of ventricular arrhythmias include: Premature ventricular contractions (PVCs)

Premature ventricular beats are heartbeats that originate in the ventricles, rather than the sinoatrial node of the heart, occurring shortly before a regular heartbeat would have happened.

In a premature ventricular beat, an electrical impulse triggers a contraction of the ventricles before they receive a signal from the sinoatrial node. This causes the heart to beat too early. Also known as premature ventricular contractions (PVCs), they are often the result of stress or environmental factors. An electrocardiograph will show premature ventricular beats. They show up on the readout as a distinctive spike. The doctor can determine how frequently they occur and collect other information to determine if a patient needs treatment. Patients with heart failure, valvedisorders, and coronary artery disease are more prone to premature ventricular beats, and a doctor may try to control the heart rhythm with treatment for the underlying medical condition. They can also be a response to stress or too much caffeine, in which case a doctor may recommend that a patient make some lifestyle changes to prevent complications. Adjusting caffeine intake and using techniques to limit stress can help eliminate the problem. Age is also a factor, with older adults being more likely to experience this abnormal heart rhythm. Causes: Cardiac ischemia or infarction, increased workload on the heart (e.g. exercise, fever, hyperrolemia, heart failure, tachycardia), digitalis toxicity, hypoxia, acidosis or electrolyte imbalances,especially hypokalemia ECG characteristics of PVC

Ventricular & atrial rate: Depends on the underlying rhythm (e.g. sinus rhythm) Ventricular & atrial rhtythm: Irregular due to early QRS, eveating one RR interval that is shorter than the others. PP interval may be regular, indicating that the PVC did not depolarize the sinus node QRS shape and Duration: Duration is 0.12 seconds or longer shape is bizarre and Abnormal P wave visibility of P wave depends on the timing of the PVC: may be absent (hidden in the QRS or T wave) or in front of the QRS If the P wave follows the QRS, the shape of the P wave may be different

PR interval: If the P wave is in front of the QRS, the PR interval is less than 0.12 seconds P: QRS ratio: 0:1, 1:1

Ventricular tachycardia (V-tach)

Ventricular tachycardia or V-tach is an abnormally rapid heartbeat. Three or more heartbeats at a rate of 100 beats per minute or above fit the diagnostic criteria for ventricular tachycardia. In some patients, the rapid heartbeat resolves on its own within 30 seconds, while in others, it may be sustained, lasting more than 30 seconds. As the name suggests, ventricular tachycardia originates in the ventricles of the heart. The part of the heart muscle responsible for regulating contractions of the ventricles fires prematurely, causing the ventricles to contract too soon. A distinctive heart rhythm can be seen on an electrocardiograph (ECG), allowing a doctor to diagnose ventricular tachycardia. Since the condition can be intermittent, patients at risk may be asked to wear a mobile monitor to record heart rhythms, allowing a doctor to identify periods of rapid heart rate as they occur over the course of the day.

Characteristics for VT: Ventricular and atrial rate: ventricular rate is 100 to 200 beats per minute: atrial rate depends on the underlying rhythm (e.g. sinus rhythm) Ventricular and atrial rhythm: usually regular; atrial rhythm may also be regular QRS shape and duration: Duration is 0.12 seconds or more bizarre; abnormal shape P wave: very difficult to detect, so atrial rate and rhythm may be indeterminable PR interval: very irregular, if P waves seen P: QRS ratio: Difficult to determine, but if P waves are apparent, there are usually more QRS complexes than P waves

Treatment: Immediate defibrillation for the patient who is unconscious and without a pulse

Ventricular fibrillation (V-fib)

Ventricular fibrillation refers to an abnormal heart rhythm that changes the way the ventricles contract. It is usually sudden and always life threatening. It thus constitutes a medical emergency, requiring treatment right away, since the heart can easily stop and not restart. It is absolutely necessary that CPR (cardio-pulmonary resuscitation) begin immediately, with someone else contacting emergency services, if a person appears to have had an episode. Better yet, and with a greater survival rate is the use of a portable defibrillator, which may able to shock the heart back to a regular rhythm state.

Causes: Same as for Ventricular Tachycardias Electrical shock & brugada syndrome

Characteristics of ventricular Fibrillation Ventricular rate: Greater than 300 per minute Ventricular rhythm: Extremely irregular, without specific pattern QRS shape and duration: Irregular, undulating waves without recognizable QRS complexes Treatment: immediate defibrillation and activation of emergency services

Atrioventricular Blocks An atrioventricular block (or AV block) involves the impairment of the conduction between the atria and ventricles of the heart. Under normal conditions, SA node in the atria sets the pace for the heart, and these impulses travel down to the ventricles. In an AV block, this message does not reach the ventricles or is impaired along the way. The ventricles of the heart have their own pacing mechanisms, which can maintain a lowered heart rate in the absence of SA stimulation. The causes of pathological AV block are varied and include ischaemia, infarction, fibrosis or drugs, and the blocks may be complete or may only impair the signaling between the SA and AV nodes. Certain AV blocks can also be found as normal variants, such as in athletes or children, and are benign. Strong vagal stimulation may also produce AV block. The cholinergic receptor types affected are the muscarinic receptors.

First degree Atrioventricular Block First degree heart block occurs when all the atrial impulses are conducted through the AV node into the ventricles at a rate slower than normal Causes: hemodynamic effect causing a decrease in perfusion to vital organ, such as the brain, heart, kidneys, lungs, & skin Characteristics of First degree: Ventricular and atrial rate: Depends on the underlying rhythm Ventricular and atrial rhythm: Depends on the underlying rhythm QRS shape and duration: usually normal, but maay be abnormal P wave: In front of the QRS complex: shows sinus rhythm, regular shape PR interval: Greater than 0.20 seconds: PR interval measurement is constant P: QRS ratio 1:1

Second degree atrioventricular Block, type I Second degree, type I heart block occurs when all but one of the atrial impulses are conducted through the AV node into the ventricles. Each atrial impulse takes a longer time for conduction than the one before, until one impulse is fully blocked. Atrial impulse, the AV node has time to fully repolarize, so that the next atrial impulse can be conducted within the shortest amount of time. Characteristics of 2nd degree:

Ventricular and atrial rate: Depends on the underlying rhythm Ventricular and atrial rhythm: The Pp interval is regular if the patient has an underlying normal sinus rhythm: the RR interval characteristically reflects a pattern of change. Starting from the RR that is the longer, the RR interval gradually shortens until there is another long RR interval again QRS shape & duration usually normal, but may be abnormal P wave: In front of the QRS complex, shape depends in underlying rhythm PR interval: PR interval becomes longer with each succeeding ECG complex until there is a P wave not followed by a QRS. The changes in the PR interval are repeated between each dropped QRS, creating a pattern in the irregular PR interval measurements. P: QRS ratio: 3:2, 4:3, 5:4 and so forth

Second Degree Alrioventicular Block, Type II Second degree, type II heart block occurs when only some of the atrial impulses are conducted through the AV node into the ventricles. Characteristics of 2nd degree Av block, type II: Ventricular & atrial rate: Depends on the underlying rhythm Ventricular & atrial rhythm: The PP interval is regular if the patient has an underlying normal sinus rhythm. The RR interval is usually regular but may be irregular, depending on the P: QRS ratio QRS shape & duration: usually abnormal, but may be normal P wave: In front of the constant for those P waves just before QRS complexes P: QRS ratio: 2:1, 3:1, 4:1, 5:1, and so forth

Third Degree Atrioventicular Block Third degree heart block occurs when no atrial impulse is conducted through the AV node into the ventricles. In third degree heart block, two impulses stimulate the heart: one stimulates the ventricles, represented by the QRS complex, & one stimulates the atria, represented by the P wave. P waves may be seen, but the atrial electrical activity is not conducted down into the ventricles to cause the QRS complex, the ventricular electrical activity this is called AV dissociation Characteristics of 3rd degree AV block: Ventricular & atrial rate: Depends on the escape and underlying Rhythm Ventricular and atrial rhythm: The PP interval is regular & the RR interval is regular: however, the PP interval is not equal to the RR interval

QRS shape & duration: Depends on the escape rhythm; in junctional escape, QRS shape & duration are usually normal, and inventricular escape, QRS shape & duration are usually abnormal P wave: Depends on underlying rhythm PR interval: Very irregular P: QRS ratio: more P waves than QRS complexes

It is directed toward increasing the heart rate to maintain a normal cardiac ouput. If the patient is stable and has no symptoms, treatment is indicated other than decreasing or evadicating cause. If the patient does not respond to atrophine or has an acute m1, transcutaneous pacing should be stared Diagnostic Procedures and Findings Electrocardiogram (ECG or EKG): A picture of the electrical impulses traveling through the heart muscle. An ECG is recorded on graph paper, through the use of electrodes (small, sticky patches) that are attached to your skin on the chest, arms and legs. Ambulatory monitors, such as: Holter monitor: A small portable recorder that is attached to electrodes on your chest. It continuously records your hearts rhythm for 24 hours. Transtelephonic monitor: A small monitor is attached to electrode leads, usually on your finger or wrist. With the help of this device, your hearts rhythm is transmitted over the phone line to your doctors office. Transtelephonic monitor with a memory loop: A small, portable recorder that is worn continuously for an extended period of time to record and save information about your hearts rhythm around the time you experience an arrhythmia. The recording is triggered by pushing a button (event button). The rhythm is recorded, saved and transmitted over the phone line. Stress test: A test used to record arrhythmias that start or are worsened with exercise. This test also may be helpful in determining if there is underlying heart disease or coronary artery disease associated with an arrhythmia. Echocardiogram: A type of ultrasound used to provide a view of the heart to determine if there is heart muscle or valve disease that may be causing an arrhythmia. This test may be performed at rest or with activity. Cardiac catheterization: Using a local anesthetic, a catheter (small, hollow, flexible tube) is inserted into a blood vessel and guided to the heart with the help of an X-ray machine. A contrast dye is injected through the catheter so X-ray movies of your coronary arteries, heart chambers and valves may be taken. This test helps your doctor

determine if the cause of an arrhythmia is coronary artery disease. This test also provides information about how well your heart muscle and valves are working. Electrophysiology study (EPS): A special heart catheterization that evaluates your hearts electrical system. Catheters are inserted into your heart to record the electrical activity. The EPS is used to find the cause of the abnormal rhythm and determine the best treatment for you. During the test, the arrhythmia can be safely reproduced and terminated. Tilt table test (also called a passive head-up tilt test or head upright tilt test): Records your blood pressure and heart rate on a minute-by-minute basis while the table is tilted in a head-up position at different levels. The test results may be used to evaluate heart rhythm, blood pressure and sometimes other measurements as you change position.

Medical Management of Patient with Dysrhythmias A. Vagal Maneuvers Vagal stimulation to terminate supraventricular tachydysrhythmias Carotid Sinus Massage Valvasa Maneuver

B. Cardioversion Synchronized counter shock to convert an undesirable rhythm to stable rhythm.

C. Defribillation Asynchronous counter shocks use to terminate pulses VT or VF Three rapid consecutive shocks: 200 joules, 300 joules and 360 joules

D. Automatic external Defibrillator (AED) is a portable electronic device that automatically diagnoses the potentially life threatening cardiac arrhythmias of ventricular fibrillation and ventricular tachycardia in a patient, and is able to treat them through defibrillation, the application of electrical therapy which stops the arrhythmia, allowing the heart to re-establish an effective rhythm.

E. Implanted Cardioverter Defibrillator is a small battery-powered electrical impulse generator that is implanted in patients who are at risk of sudden cardiac death due to ventricular fibrillation and ventricular tachycardia. The device is programmed to detectcardiac arrhythmia and correct it by delivering a jolt of electricity. In current variants, the ability to revert ventricular fibrillation has been extended to include both atrial and ventricular arrhythmias. There

also exists the ability to perform biventricular pacing in patients withcongestive heart failure or bradycardia. F. Anti-arrhythmic Class I : Na + channel blocker ( Quinidine, Procanamide, Disopyridamole, Lidocaine, Flocainaide, Profapenone) Class II : Beta - blockers ( propanolol, metopolol, aenolol, esmolo) Class III : K + channel blockers ( Amiodarone) Class IV : Calcium channel blockers ( Verapamil, Diltiazem)

G. Pacemakers Implanted on the anterior chest and connected to the heart devices that provide electrical stimulation to the heart to maintain the heart rate when the clients pacemakers fails.

Types: Temporary Pacemakers - an electronic pacemaker used as an interim treatment when the heart rate is excessively low. It consists of either a pulse generator and battery attached outside the patient's body and connected to a transvenous electrode in the right ventricle or conductive pads placed on the chest and connected to an external pulse generator by cables. Permanent Pacemaker - any electric pacemaker implanted inside a patient's body for permanent use.

Sinus Node Dysrhythmias: Sinus bradycardia Administration of Atropine Sulfate (Symptomatic Bradycardia: Initially 0.5 - 1.0 mg rapid IV/IO push (minimum dose 0.3 mg), followed by incremental doses of 0.5 - 1.0 mg every 3 - 5 minutes, not to exceed a total dosage of 3.0 mg.) Oxygen administration, since heart beats at less than 60 per minute .Perfusion is lessened as also the oxygen supply. Increasing O2 increase perfusion and oxygen that the body demands. Insertion of pacemaker. Pacemaker is placed under or over the clients skin and put wirings into the heart as a resultant of restored normal rhythm.

Sinus Tachycardia Beta blockers such as; atenolol, metoprolol,

Calcium channel blockers like; Amlodipine Besylate (Norvasc)

Sinus Arrhythmia Sinus arrhythmia does not cause any significant hemodynamic effect and usually is not treated

Atrial dysrhythmias Premature Atrial Complex If PAC are infrequent, no treatment is necessary. If PAC are frequent more than 6 per minute, this is a signal of worsening condition, treatment directed at the cause. May be caused by atrial fibrillation. Treatment of atrial fibrillation.

Atrial Flutter Treatment includes administration of Diltiazem (Cardizem), BetaBlockers(Metoprolol,Atenolol), Digitalis(Digoxin) to slow the conduction to the AV node Cardioversion, o Synchronized electrical cardioversion uses a therapeutic dose of electric current to the heart, at a specific moment in the cardiac cycle. o Pharmacologic cardioversion, also called chemical cardioversion, uses antiarrhythmia medication instead of an electrical shock.

Atrial Fibrillation Quinidine(Quinidex), Amiodarone(Cordarone), Digoxin(Digitalis), Verapamil(Calan) , Verapamil is used to achieve conversion to sinus rhythm

Ventricular Dysrhythmias Premature Ventricular Contractions Lidocaine is used to relax the premature ventricular contractions. It should be prepared accordingly to 1-1.5mg/kg. A 75 mg to 100mg bolus of lidocaine will maintain adequate blood levels for only 20 minutes. It is important to distinguish patterns of PVC's that are likely to lead to serious arrhythmias

Ventricular Tachycardia

For stable ventricular tachycardia IV procainenamide(Procan) 17 mg/kg discontinued when dysrhythmia is suppressed if hypotension ensues, the QRS complex widens by 50% or more, or the maximum dose is achieved. Patients suffering from pulseless VT or unstable VT are hemodynamically compromised and require immediate cardioversion. Synchronized electrical cardioversion, done to an unconscious or sedated pt. If the patient still has a pulse, it is usually possible to terminate a VT episode with a direct current shock across the heart, that is delivered from one side of the chest to the other, front to back. Ideally synchronized to the patient's heartbeat Catheter ablation is an invasive procedure used to remove or terminate a faulty electrical pathway from sections of the hearts of those who are prone to developing cardiac arrhythmias such as atrial fibrillation, atrial flutter, supraventricular tachycardias (SVT) and Wolff-Parkinson-White syndrome.

Nursing Management ASSESSMENT A health history is obtained to identify any precious occurrences of decreased cardiac output, such as syncope (fainting), light headedness, dizziness, fatigue, chest discomfort and palpitations. Coexisting conditions that could be a possible cause of the dysrhythmia (e.g. heart disease, COPD) may also be identified. A; medications prescribed and OTC (e.g. herbs and nutritional supplements), as well as route of administration, are reviewed. Some medications (e.g. Digoxin) can cause dysrhythmias. Laboratory results are reviewed to assess levels of medications as well as factors that could contribute to the dysrhythmia (e.g. anemia). A thorough psychosocial assessment is performed to identify the possible effects of the dysrhythmia, the patients perception of the dysrhythmia and whether anxiety is a contributing factor. The nurse conducts a physical assessment to confirm the data obtained from the history and to observe for signs of diminished cardiac output during the dysrhythmic event, especially changes in the level of consciousness. The nurse assesses the patients skin which may be pale and cool. Signs of fluid retention such as neck vein distention and crackles and wheezes auscultated in the lungs, may be detected. The rate and rhythm of the apical and peripheral pulses are also assessed, and any pulse deficit is noted. The nurse also auscultates for extra heart sounds (especially s3 and s4) and for heart murmurs, measures blood pressure, and determines pulse pressure.

A declining pulse pressure indicates reduced cardiac output. Just one assessment may not disclose significant changes in cardiac output; therefore, the nurse compares multiple assessment findings over time, especially those that occur with and without dysrhythmia.

DIAGNOSIS Nursing Diagnoses Decreased cardiac output Anxiety r/t fear of the unknown Deficient knowledge about the dysrhythmia and its treatment

PLANNING ANG GOALS Major goals include eliminating or decreasing the occurrence of the dysrhythmia (by decreasing contributory factors) to maintain cardiac output, minimizing anxiety, and acquiring knowledge about dysrhythmia and its treatment.

NURSING INTERVENTION Monitoring and Managing the Dysrhythmia Nurse evaluates blood pressure, pulse rate and rhythm, rate and depth of respirations, and breath sounds to determine dysrhythmias hemodynamic effect. Ask about episodes of light headedness, dizziness, or fainting as part of ongoing assessment If patient is hospitalized, a 12 lead ECG may be obtained to continuously monitor the patient and the nurse may analyze rhythm strips to track the dysrhythmia. Antiarrhythmic medications used to control the occurrence or the effect of the dysrhythmia, or both. The nurse assesses and observes for beneficial and averse effects of each medication. The nurse also manages medication administration carefully so that a constant serum blood level of the medication is maintained. Administration of a 6 minute walk test to identify patients ventricular rate in response to exercise. Assessment for factors that contribute to the dysrhythmia (caffeine, stress and non adherence to the medication) and assistance in developing a plan to make lifestyle changes.

Minimizing anxiety When the patient experiences episodes of dysrhythmia, the nurse must maintain a calm and reassuring attitude. This assists in reducing anxiety (reducing the sympathetic response) and fosters trusting relationship with the patient.

The nurses goal is to maximize the patients control and make the episode less threatening.

Promoting Home and Community-Based Care Teaching patients self-care When teaching patients, nurse must present information in terms that are understandable and in a manner that is not frightening or threatening. The nurse must explain importance of maintaining therapeutic serum levels of antiarrythmic medications so that patient understands why medications should be taken regularly. If the patient has a potentially lethal dysrhythmia it is important to establish with the patient and family a plan of action to take in case of emergency. Health teaching regarding potential effects of the dysrhythmia and their signs and symptoms.

Continuity of care A referral for home care usually is not necessary for the patient with a dysrhythmia unless the patient is hemo-dynamically unstable and has significant symptoms of decreased cardiac output.

Source: Textbook of Medical Surgical Nursing by Brunner & Suddarth pp. 840-842; www.slideshare.net/thinkm/dysrhythmias-nursing-lecture

Hyperosmolar Hyperglycemic Nonketotic Syndrome

Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS), is a serious condition most frequently seen in older persons. This can happen to people either type 1 or type 2, diabetes is not being controlled properly, but it occurs more often in people with type 2. HHNS is usually brought on by something else, such as an illness or infection and characterised by severe hyperglycaemia, a marked increase in serum osmolality, and clinical evidence of dehydration without significant accumulation of ketoacids. HHNS is typically observed in elderly patients with non-insulin-dependent diabetes mellitus, although it may rarely be a complication in younger patients with insulin-dependent diabetes, or those without diabetes following severe burns, parenteral hyperalimentation, peritoneal dialysis, or haemodialysis. Patients receiving certain drugs including diuretics, corticosteroids, betablockers, phenytoin, and diazoxide are at increased risk of developing this syndrome. Patients usually present with a prolonged phase of osmotic diuresis leading to severe depletion of both the intracellular andextracellular fluid volumes. Losses of water exceed those of sodium, resulting in hypertonic dehydration. In HHNS blood sugar levels rise and your body tries to get rid of the excess sugar by passing it into your urine. You make lots of urine at first, andyou have to go to the bathroom more often. Later you may not have to go to the bathroom as often, and your urine becomes very dark. Also, you may be very thirsty. Even if you are not thirsty, you need to drink liquids. If you don't drink enough liquids at this point, you can get dehydrated. If HHNS continues, the severe dehydration will lead to seizures, coma and eventually death. HHNS may take days or even weeks to develop. Know the warning signs of HHNS.

What are the Warning Signs?

Blood sugar level over 600 mg/dl Dry, parched mouth Extreme thirst (although this may gradually disappear) Warm, dry skin that does not sweat High fever (over 101 degrees Fahrenheit, for example) Sleepiness or confusion Loss of vision Hallucinations (seeing or hearing things that are not there) Weakness on one side of the body

If you have any of these symptoms, call someone on your health care team.

How Can I Avoid It? HHNS only occurs when diabetes is uncontrolled. The best way to avoid HHNS is to check your blood sugar regularly. Many people check their blood sugar several times a day, such as before or after meals. Talk with your health care team about when to check and what the numbers mean. You should also talk with your health care team about your target blood sugar range and when to call if your blood sugars are too high, or too low and not in your target range. When you are sick, you will check your blood sugar more often, and drink a glass of liquid (alcohol-free and caffeine-free) every hour. Work with your team to develop your own sick day plan.

Related Information Another condition to watch signs for is ketoacidosis, which means dangerously high levels of ketones, or acids, that build up in the blood. Ketones appear in the urine when your body doesn't have enough insulin, and can poison the body.

Hyperglycemic hyperosmolar nonketotic coma (HHNKC) is an extremely serious complication of type 2 diabetes, most often occurring in those who are non-insulin dependent. HHNKC is caused by severely elevated blood glucose levels, usually over 600 mg/dl. Symptoms can include weakness, increased thirst, nausea, lethargy, confusion and ultimately, convulsions, and coma. Onset of these symptoms can be slow and insidious, building over a period of days or weeks. Clinical manifestations The clinical picture of HHNS is one of hypotension, profound dehydration, dry mucous membranes, poor skin turgor, tachycardia, and variable neurologic signs, alteration of sensorium, seizures, hemiparesis. The mortality rate ranges from 10 to 40% usually related to an underlying illness, the vulnerability of the elderly patient, and the severity of HHNS. Assessment and Diagnostic Findings Diagnostic assessment includes a range of laboratory tests, including blood glucose, electrolytes, BUN, CBC, serum osmolality, and ABG analysis. The blood glucose level is usually 600 to 1200 mg/dl, and the osmolality exceeds 350 m0sm/kg. Electrolytes and BUN

levels are consistent with the clinical picture of severe dehydration. Mental status changes, focal neurologic deficits, and hallucinations are common secondary to the cerebral dehydration that results from extreme hyper osmolality. Postural hypotension accompanies the dehydration.

Medical Management The correction of the syndrome will ultimately require administration of hypotonic fluids. Patients presenting with HHNS also have significant depletion of potassium and other electrolytes that will need to be replaced. The principal goal at the outset of therapy must be restoration of the intravascular volume to assure adequate perfusion of vital organs. It remains controversial whether 0.9% or 0.45% NaCl should be the initial fluid infused intravenously. We prefer to administer 0.9% NaCl until the vital signs have stabilised and then substitute 0.45% NaCl. 10 to 15 units of regular human insulin should be injected as a bolus, followed by a continuous infusion of approximately 0.1 U/kg/h. Once the blood glucose approaches 13.9 to 16.7 mmol/L (250 to 300) mg/dl, 5% dextrose should be added to the intravenous fluids and the rate of insulin infusion reduced. Following recovery many patients presenting with HHNS will not require long term insulin therapy and can be managed effectively with diet or oral agents. Precipitating causes of HHNS must be identified and treated simultaneously with correction of the metabolic abnormalities.

Nursing Management Pathophysiology The initiating event in hyperosmolar hyperglycemic state is glucosuric diuresis. Glucosuria impairs the concentrating capacity of the kidney, further exacerbating water loss. Under normal conditions, the kidneys act as a safety valve to eliminate glucose above a certain threshold and prevent further accumulation. However, decreased intravascular volume or underlying renal disease decreases the glomerular filtration rate, causing the glucose level to increase. The loss of more water than sodium leads to hyperosmolarity. Insulin is present, but it is not adequate to reduce blood glucose levels, particularly in the presence of significant insulin resistancepakilagay po sa diagram Precipitating Factors

Precipitating factors may be divided into six categories: infections, medications, noncompliance, undiagnosed diabetes, substance abuse, and coexisting diseases Infections are the leading cause of hyperosmolar hyperglycemic Nonketotic Syndrome. The most common infection is pneumonia, often gram negative, followed by urinary tract infection and sepsis. Poor compliance with diabetic medications also is thought to be a frequent cause. Undiagnosed diabetes often is associated with hyperosmolar hyperglycemic non ketotic syndrome because of failure to recognize early symptoms of the disease. Myocardial infarction, cerebro vascular accident, pulmonary embolus, and mesenteric thrombosis have been identified as causes of hyperosmolar hyperglycemic state. In one study of an urban population presenting with hyperosmolar hyperglycemic state, the three leading causes were poor compliance with medication, ethanol ingestion, and cocaine use. Long-term steroid use and gastroenteritis are common causes of hyperosmolar hyperglycemic state in children.

Clinical Evaluation Patients presenting with hyperosmolar hyperglycemic Nonketotic Syndrome are older and haveundiagnosed diabetes or type 2 diabetes managed by diet and/or oral diabetic medication. They often take medications that aggravate the problem, such as a diuretic that causes mild dehydration. These patients often live alone or may be in a nursing home environment in which they are unable to communicate their needs secondary to restraints, sedation, or coma. In addition to one or more of the precipitating factors patients with hyperosmolar hyperglycemic Nonketotic Syndrome typically present with weakness, visual disturbance, or leg cramps. Nausea and vomiting may occur, but are much less frequent than in patients with diabetic ketoacidosis. Eventually, patients develop neurologic symptoms of lethargy, confusion, hemiparesis (often misdiagnosed as cerebrovascular accident), seizures, or coma that eventually lead to medical care. Physical findings reveal profound dehydration that is manifested by poor tissue turgor (which may be difficult to evaluate in older patients) dry buccal mucosa membranes; soft, sunken eyeballs; cool extremities; and a rapid, thready pulse.A low-grade fever often is present. Abdominal distention may occur because of gastroparesis induced by hypertonicity, but resolves quickly following adequate rehydration. Abdominal distention that persists after rehydration may be related to other underlying causes. Various changes in mental status may manifest, ranging from complete lucidity to disorientation to lethargy to coma. The degree of neurologic impairment is related directly to the effective serum osmolarity,with coma often occurring once the serum osmolarity is greater than 350 mOsm per kg (350 mmol per kg). Seizures are present in up to 25 percent of patients and may be generalized, focal, myoclonic jerking, or movement induced.Hemiparesis may occur but it is reversible with correction of the fluid deficit.

Treatment The treatment of hyperosmolar hyperglycemic Nonketotic Syndrome involves a five-pronged approach: (1) Vigorous intravenous rehydration, (2) Electrolyte replacement, (3) Administration ofintravenous insulin (4) Diagnosis and management of precipitating and coexisting problems, and (5) Prevention FLUID REPLACEMENT The first and most important step in the treatment of hyperosmolar hyperglycemic Non Ketotic Syndrome is aggressive fluid replacement, which should begin with an estimate of the fluid deficit (usually 100 to 200 mL per kg. The use of isotonic fluids may cause fluid overload andhypotonic fluids may correct deficits too rapidly with a potential for diffuse myelinolysis and death.Therefore, 1 L of normal saline should be given per hour to start. If the patient is in hypervolemic shock, plasma expanders also needed. If the patient is in cardiogenic shock, hemodynamic monitoring is required. Details about the addition of potassium to the intravenous fluids are provided in the next section. Once there is only mild hypotension, the corrected serum sodium level should be calculated. If the corrected serum sodium level is high (greater than 145 mEq per L) Then 0.45 percent sodium chloride may be administered at a rate of4 to 14 mL per kg per hour depending on the state of dehydration. If the corrected serum sodium level is low (less than 135 mEq perL), 0.9 percent sodium chloride is infused at the same rate. When the serum glucose level is less than 300 mg per dL (16.7 mmol per L), the fluid may be changed to 5 percent dextrose solution with 0.45 percent sodium chloride. One half of the calculated deficit should be given in the first 18 to 24 hours and the remainder over the next 24 hours. In adults, the risk of cerebral edema is low and the consequences of under treatment include vascular occlusion and increased rate of mortality. Good clinical judgment should be employed, especially when the patient has comorbid conditions such as acute myocardial infarction, a history of congestive heart failure, or renal failure. In such cases, close hemodynamic monitoring is indicated. Early in the course of treatment, the plasma glucose level will decrease, even before insulin is started, and this may serve as an index for the adequacy of fluid replacement. If the plasma glucose level fails to decline by 75 to 100 mg per dL (4.2 to 5.6 mmol per L) per hour, this usually implies inadequate fluid volume or renal impairment. Children are at greater risk of developing potentially fatal cerebral edema during treatment. For this reason, the rate at which serum tonicity is returned to normal should be somewhat slower than in adults.

ELECTROLYTE MANAGEMENT

Electrolyte replacement is critical. Total body potassium depletion often is unrecognized because the level of potassium in the blood may be normal or high. The serum potassium level may plummet when insulin is replaced because this forces potassium into the cell. Once urine output is established, potassium replacement should be initiated. Electrolytes should be followed closely (every one to two hours initially) and the patients cardiac rhythm should be monitored continuously. If the patients serum potassium level is less than 3.3 mEq per L (3.3 mmol per L) initially, insulin should be held and potassium given as two thirds potassium chloride and one third potassium phosphate until the potassium level reaches at least 3.3 mEq per L. If the potassium level is greater than 5.0 mEq per L (5.0 mmol per L), potassium should be held until the level is less than 5.0 mEq per L, but the potassium level should be monitored every two hours. If the initial serum potassium level is between 3.3 and 5.0 mEq per L, 20 to 30 mEq of potassium should be given in each liter of intravenous fluid (two thirds as potassium chloride, one third as potassium phosphate) to maintain the serum potassium level between 4.0 mEq per L (4.0 mmol per L) and 5.0 mEq per L.25.Despite a lack of evidence that treatment with phosphate, calcium, or magnesium alters outcomes,these electrolytes must be considered. Most studies that have examined the need for phosphate replacemen involved patients with diabetic ketoacidosis that developed over hours to days. However, because hyperosmolar hyperglycemic occurs slowly (over days to weeks), the patient is much more likely to be phosphate depleted. Although phosphate replacement makes physiologic sense, no controlled data have demonstrated improved outcomes. Phosphate replacement may be considered when the patients serum phosphate level is below 1.0 mEq per L (1.0 mmol per L) and muscle weakness is a concern, as in patients with respiratory impairment. Because phosphate replacement can cause severe hypocalcemia in this setting, serum calcium levels should be monitored closely.Hypomagnesemia may manifest as arrhythmias, muscle weakness, convulsions, stupor, and agitation. Hypomagnesemia may be present in up to 90 percent of patients withuncontrolled diabetes.Unless the patient is in renal failure, administration of magnesium is safe and physiologic. INSULIN THERAPY The critical point regarding insulin management is to remember that adequate fluids must be given first. If insulin is administered before fluids, the water will move intracellular, causing potential worsening of hypotension, vascular collapse, or death. Insulin should be given as an initial bolus of 0.15 U per kg intravenously, followed by a drip of 0.1 U per kg per hour until the blood glucose level falls to between 250 mg per dL (13.9 mmol per L) and 300 mg per dL. If the glucose level does not decrease by 50 to 70 mg per dL per hour, this rate of administration may be doubled. Once the serum glucose concentration is below 300 mg per dL, dextrose should be added to the intravenous fluid and insulinshould be titrated by a low-dose

sliding scale until the mental obtundation and hyperosmolarityare resolved. When the patient is able to eat,subcutaneous insulin or the previoustreatment regimen may be initiated.

IDENTIFY AND TREAT THE CAUSE Although routine administration of antibiotics for all patients with suspected infection is not recommended, antibiotic therapy is warranted while awaiting culture results in older patients or in those with hypotension. According to a recent study, elevated Creactive protein and interleukin-6 levels are early indicators of sepsis in patients with hyperosmolar hyperglycemic state. It also is important to review any medicationthat may have precipitated or aggravated the event, and discontinue or reduce the dosage of any suspected agent.

Complications of Treatment Complications from inadequate treatment include vascular occlusions and rhabdomyolysis. Over hydration may lead to adult respiratory distress syndrome and induced cerebral edema, which is rare but often fatal in children and young adults. Cerebral edema should be treated with intravenous mannitol (Osmitrol) in a dose of 1 to 2 g per kg over 30 minutes and intravenous dexamethasone (Decadron). Slowing the correction of hyperosmolarity in children may prevent cerebral edema.

Prevention The patient and another responsible party should be engaged in a significant educational effort that encourages adherence to blood glucose monitoring and compliance with prescribed medications. It is especially important that the patient have access to an adequate water supply. If the patient lives alone, a family member or friend should check in on the patient daily to watch for any changes in mental status and to notify the physician if this occurs. In the nursing home setting, the above recommendations should be followed and the nursing home staff should be educated regarding the signs and symptoms of hyperosmolar hyperglycemic non ketotic Syndrome and the importance of adequate fluid intake and monitoring. Nursing diagnosis -Deficient fluid volume loss related to absolute loss. - Decreased cardiac output related to alteration in preload.

-Anxiety related to threat to biologic, psychologic, and/or social integrity. -Disturbed body image related to functional dependence on life sustaining technology. Nursing Interventions Restoring Fluid Balance Assess patient for increasing signs and symptoms of dehydration, hyperglycemia, or electrolyte imbalance. Institute fluid replacement therapy as ordered (usually normal or half-strength saline initially), maintaining patent I.V. line. Assess patient for signs and symptoms of fluid overload and cerebral edema as I.V. therapy progresses. Administer regular insulin I.V. as ordered, and add dextrose to I.V. infusion as blood glucose falls below 300 mg/dL, to prevent hypoglycemia. Monitor hydration status by monitoring hourly intake and output and urine specific gravity. Preventing Aspiration Assess patient's LOC and ability to handle oral secretions. Cough and gag reflex Ability to swallow Properly position patient to reduce possibility of aspiration. Elevate head of bed unless contraindicated. If nausea is present, use side-lying position. Suction as frequently as needed to maintain patent airway. Withhold oral intake until patient is no longer in danger of aspiration. Insert NG tube as indicated for gastric decompression. Monitor respiratory rate and breath sounds for signs of aspiration pneumonia. Provide mouth care to maintain adequate mucosal hydration. Patient Education and Health Maintenance Advise the patient and family that it may take 3 to 5 days for symptoms to resolve. Instruct the patient and family in signs and symptoms of hyperglycemia and use of sick-day guidelines Explain possible causes of HHNS. Review changes in medication, activity, meal plan, or glucose monitoring for home care. It may not be necessary to continue insulin therapy following HHNS; many patients can be treated with diet and oral agents.