Medication
The clinician is often faced with the dilemma of finding PVCs in a patient and deciding whether the PVCs should be treated. Management of PVCs includes discernment of associated heart disease and other predisposing conditions prior to the decision to specifically treat the PVCs. Prevalence
Procedures
No treatment is indicated in patients with asymptomatic PVCs in absence of cardiac disease. Symptomatic patients without cardiac disease may be managed by identifying and correcting reversible causes.
What should the clinician do if the patient has PVCs?
DKA treatment generally consists of two phases: first, we must manage the ketoacidosis. Later, we must prepare the patient to transition back to their home insulin regimen. During both phases, success depends on balancing insulin dose and insulin requirement.
What are the treatment options for asymptomatic PVCs in absence of cardiac disease?
Other antiarrhythmic drugs should be considered if those initial drugs fail and ablation has been declined, has been unsuccessful, or has been deemed inappropriate. Catheter ablation is the most efficacious approach to eradicate PVCs but may confer increased upfront risks.
What is the treatment for diabetic ketoacidosis (DKA)?
When are other antiarrhythmic drugs indicated in the treatment of PVCs?
What is the drug of choice for the treatment of PVCs?
Patients with frequent symptomatic PVCs with underlying heart failure benefit from beta blockade regardless of the etiology of the cardiomyopathy. Carvedilol, extended release metoprolol succinate, and bisoprolol have all been shown to decrease all-cause mortality in clinical trials of heart failure.
What is the treatment for excessive PVCs?
Eliminating common PVC triggers — such as caffeine or tobacco — may reduce the number of extra beats and lessen symptoms. Medications. Blood pressure medications may be prescribed to reduce the premature contractions. Those used for PVCs may include beta blockers and calcium channel blockers.
What beta blockers are used for PVCs?
Carvedilol is one of the most effective beta-blockers in reducing ventricular tachyarrhythmias and mortality in patients with heart failure. One of the possible antiarrhythmic mechanisms of carvedilol is the suppression of store overload-induced Ca2+ release, especially for the triggered activity.
Why in DKA there is arrhythmia?
The autonomic dysfunction resulting from the high levels of glucose was believed to be the root cause of the arrhythmias (11, 12). The potassium deficit is one of the most important electrolyte abnormalities found in the DKA, which could lead to severe arrhythmias.
Do beta blockers stop PVCs?
While they may reduce the PVCs themselves, beta blockers work better at reducing the symptoms PVCs cause. The more powerful antiarrhythmic drugs are often reasonably effective at suppressing PVCs.
How does lidocaine treat PVCs?
A drug serum concentration which is in the therapeutic range is initially achieved and maintained by an open-loop infusion regimen. The lidocaine infusion rate is then adjusted using closed-loop control to regulate the rate of premature ventricular contractions (PVC rate) at a setpoint.
Can amlodipine help PVCs?
Losartan, enalapril and amlodipine reduced the number of premature ventricular contractions (PVCs) in patients with essential hypertension as well as blood pressure.
Does amiodarone stop PVCs?
Conclusions: Amiodarone can significantly suppress PVCs and subsequently improve LV function predominantly in non-ischemic CM. The rate of PVC-CM in CHF-STAT study was 40% in all patients with CM and up to 66% with non-ischemic CM.
How much metoprolol can I take for PVCs?
Adults—At first, 25 milligrams (mg) once a day for 2 weeks. In patients with severe heart failure, the starting dose is 12.5 mg once a day. Your doctor may adjust your dose as needed.
Can ketoacidosis cause heart palpitations?
Several cardiovascular complications are associated with ketoacidosis as a result of electrolyte imbalances, including arrhythmias, ECG changes, ventricular tachycardia, and cardiac arrest, which can be prevented with appropriate initial treatment.
How does DKA affect heart rate?
Hyperglycemia, acidosis, and electrolyte imbalances can directly affect the heart by inducing toxicity, impairing myocardial blood flow, autonomic dysfunction, and altering activation and conduction of electrical impulses throughout the heart, increasing the risk of arrhythmias and ischemia.
What is a Somogyi effect?
If the blood sugar level drops too low in the early morning hours, hormones (such as growth hormone, cortisol, and catecholamines) are released. These help reverse the low blood sugar level but may lead to blood sugar levels that are higher than normal in the morning.
What is the best treatment for PVCs?
In the presence cardiac disease such as cardiac ischemia, infarction, or heart failure and symptoms from PVCs, optimal medical therapy including beta-blockers and ACE inhibitors may improve symptoms. Amiodarone and ablation may be considered for refractory symptoms in all patients.
What is the dilemma of finding PVCs in a patient?
The clinician is often faced with the dilemma of finding PVCs in a patient and deciding whether the PVCs should be treated. Management of PVCs includes discernment of associated heart disease and other predisposing conditions prior to the decision to specifically treat the PVCs. Prevalence.
How common are PVCs?
The prevalence of PVCs in the general population may be as high as 80% in healthy young adults1,2and increases with age. 3PVCs are more common in men, in African-Americans, and in individuals with underlying heart disease, hypertension, hypokalemia or hypomagnesaemia .3Mechanisms for ectopic electrical activity include reentry from a previous scar or underlying heart disease, triggered activity from afterdepolarizations from a previous action potential precipitated by drugs such as digoxin or QT interval prolonging medications, and enhanced automaticity provoked by catecholamines, electrolyte abnormalities, or ischemia. It is important to investigate these underlying causes because initial management, if needed, is focused on identifying and treating these causes. See Table 1.
How to treat ectopy without structural heart disease?
Treatment includes correcting electrolyte abnormalities (hypokalemia, hypomagnesemia, hypercalcemia), improving respiratory status (hypercapnea, hypoxia), treating hyperthyroidism, and avoiding medications that may precipitate ectopy such as digoxin, sympathomimetics, and tricyclic antidepressants. Avoidance of alcohol, amphetamines, caffeine, cocaine, and tobacco is also recommended. As anxiety can result in an increase in catecholamines resulting in increased ectopy, reassurance and treatment of underlying anxiety disorder may help. Daily magnesium supplementation with potassium supplementation has also been shown in a randomized clinical trial to decrease the occurrence of PVCs.13While this trial did not demonstrate any improvement in symptoms, daily magnesium and potassium supplementation may be beneficial by promoting electrical stability and may be considered given the few side effects of additional electrolytes.
What is amiodarone used for?
Amiodarone, a class III antiarrhythmic agent, can also be used if beta blockade is unsuccessful in suppressing the symptomatic PVCs. During treatment with amiodarone, thyroid, hepatic, and pulmonary function needs to be closely monitored given the side effects of long term amiodarone use.
Why is it important to examine a patient for signs of structural heart disease such as cardiac murmurs, heart failure?
Most important is examination of the patient for signs of structural heart disease such as cardiac murmurs, heart failure, or hypertension because these conditions are associated with an increased incidence of PVCs.
Do PVCs increase mortality?
In young healthy patients, isolated PVCs have not been shown to be associated with any increase in mortality compared to the general population. In some studies, frequent and complex PVCs in the absence of coronary heart disease were found to be associated with an increase in sudden cardiac death in an older population.8,9Other studies have not demonstrated such an association.10Frequent PVCs during exercise in the absence of known cardiovascular disease is predictive of a higher rate of cardiovascular mortality.11In patients with suspected or known coronary disease, development of frequent ventricular ectopy during the recovery phase after exercise stress testing was found to be associated with increased cardiovascular mortality.12
What is DKA in diabetes?
DKA causes an acute metabolic disorder, which is primarily characterized by an increased presence of circulating ketone bodies, and the development of severe ketoacidosis in the presence of prolonged uncontrolled hyperglycemia, usually due to insulin deficiency[3]. It is more commonly seen in patients with insulin-dependent diabetes mellitus (IDDM), especially among children and young adults. Occasionally, patients with insulin resistant DM can present this complication; especially those that are noncompliant with insulin therapy or who present severe infection[3]. DKA has arbitrarily been classified by some as mild, moderate and severe, according to the initial diagnostic criteria (which includes plasma glucose, arterial pH, serum bicarbonate, urine and serum ketones, serum osmolality and anion gap; and the alteration in the mental status)[4].
What is a diabetic ketoacidosis?
Diabetic ketoacidosis (DKA) is defined as an acute metabolic disorder, which is characterized by an increased presence of circulating ketones, and the development of ketoacidosis in the presence of hyperglycemia. This syndrome occurs as a result of insulin deficiency. Patients can be dramatically ill, however, with aggressive treatment, most patients recover rapidly. Despite being a low-risk condition, the development of acidosis, is one of the admission criteria to the intensive care unit (ICU) for these patients, in order to provide close monitoring, and recognize complications that could result from the use of aggressive therapy, such as continuous infusions if insulin. In some institutions, DKA is treated in the emergency department and general medical/surgical wards to avoid ICU overcrowding.
How many patients per group for hypoglycemic event?
Hypoglycemic event presented in each group in only 1 patient per group. No complications, no recurrence of ketoacidosis and no mortality
Can DKA be treated in the ICU?
In many institutions, and for decades, DKA has been routinely treated in ICU environments, including recommendations by the American Diabetes Association guidelines for DKA treatment[3,4,7-9]. The primary reason for these level of care requirements, has been the presence of severe metabolic acidosis, even if patients are grouped as mild or moderate in severity[10]. Frequent blood glucose monitoring, the need for intravenous insulin infusions, and the requirement of frequent vital signs is cited as the hospital structural requirements for this ICU level of care[11]. However, several studies have shown that DKA can be safely treated in the ED or even in medical wards (Table (Table11)[12-17]. By taking this lower level of care approach, we can potentially avoid ICU hospitalization rate and higher costs, bed overcrowding and reserving the beds for patients who present complications such as hypotension, coma, acute myocardial ischemia, or those with several comorbidities (i.e., end-stage renal disease, congestive heart failure) and anyone categorized as suffering severe DKA[12,18,19]. In some observational studies DKA patients admitted to the ICU have a shorter length of stay when compared to non-diabetic mellitus ICU patients[20,21]. A recent retrospective cohort study of 156, 842 hospitalizations among 94 acute-care hospitals, analyzed the adjusted cost of hospitalizations in lower and higher ICU utilizations groups, and concluded that the overuse of ICU only increases the cost and the utilization of invasive procedures but with no improvement in hospital mortality[22].
How can clinicians help patients in the ED?
By establishing a rapid diagnosis and starting treatment in the ED, clinicians can help patients to decrease their costs and hospital stay.
Is ketoacidosis a complication?
Core tip:Diabetic ketoacidosis is a complication for some patients with insulin-dependent diabetes mellitus as well as for non-insulin dependent. It is treated commonly in the intensive care unit (ICU), even though clinical data from many studies support management in regular (medical/surgical) wards, avoiding expensive critical care unit costs and preventing bed crisis in these higher level of care units for sicker patients. Once the patient is treated, adequate follow up and education is mandatory. Noncompliance remains the primary concern for repeated admissions.
Do you need to switch to IV insulin?
No need to switch to IV regular insulin, no hypoglycemic events, no complications, no recurrence of ketoacidosis and no mortality
How to diagnose PVC?
PVCs can be diagnosed only by ECG. The 12-lead ECG is useful to provide the initial evidence of PVC frequency and remains the best noninvasive tool to determine the PVC location. When a PVC is suspected from either the history or physical examination, it is useful to continue to run a rhythm strip over 30 to 50 seconds in the hopes of determining a better sense of PVC frequency and to catch the PVC during recording of all 12 contemporaneous leads to allow for the most accurate morphology assessment. Attention to the remainder of the ECG may also reveal clues to the underlying substrate: careful measurement of the QT interval is mandatory, precordial T-wave inversion beyond lead V 2 or right ventricular conduction delay may be indicative of arrhythmogenic right ventricular dysplasia, 30 pathological Q waves can reflect discrete areas of scar, an early precordial transition accompanied by a prominent S wave in V 6 may signal a basolateral scar observed in nonischemic cardiomyopathy, 31 and conduction disease may be a manifestation of cardiac sarcoidosis. 32 It is also important to emphasize that PVCs arising from common sites, such as the right ventricular outflow tract, may commonly trigger ventricular fibrillation in patients with the Brugada syndrome 33 and torsade de pointes in patients with the long-QT syndrome. 33, 34
What are the causes of PVCs?
Premature ventricular complexes (PVCs) are extremely common, found in the majority of individuals undergoing long-term ambulatory monitoring. Increasing age, a taller height, a higher blood pressure, a history of heart disease, performance of less physical activity, and smoking each predict a greater PVC frequency. Although the fundamental causes of PVCs remain largely unknown, potential mechanisms for any given PVC include triggered activity, automaticity, and reentry. PVCs are commonly asymptomatic but can also result in palpitations, dyspnea, presyncope, and fatigue. The history, physical examination, and 12-lead ECG are each critical to the diagnosis and evaluation of a PVC. An echocardiogram is indicated in the presence of symptoms or particularly frequent PVCs, and cardiac magnetic resonance imaging is helpful when the evaluation suggests the presence of associated structural heart disease. Ambulatory monitoring is required to assess PVC frequency. The prognosis of those with PVCs is variable, with ongoing uncertainty regarding the most informative predictors of adverse outcomes. An increased PVC frequency may be a risk factor for heart failure and death, and the resolution of systolic dysfunction after successful catheter ablation of PVCs demonstrates that a causal relationship can be present. Patients with no or mild symptoms, a low PVC burden, and normal ventricular function may be best served with simple reassurance. Either medical treatment or catheter ablation are considered first-line therapies in most patients with PVCs associated with symptoms or a reduced left ventricular ejection fraction, and patient preference plays a role in determining which to try first. If medical treatment is selected, either β-blockers or nondihydropyridine calcium channel blockers are reasonable drugs in patients with normal ventricular systolic function. Other antiarrhythmic drugs should be considered if those initial drugs fail and ablation has been declined, has been unsuccessful, or has been deemed inappropriate. Catheter ablation is the most efficacious approach to eradicate PVCs but may confer increased upfront risks. Original research remains necessary to identify individuals at risk for PVC-induced cardiomyopathy and to identify preventative and therapeutic approaches targeting the root causes of PVCs to maximize effectiveness while minimizing risk.
Why does absence of PVC occur intermittently?
It is important to note that the absence of a PVC may occur intermittently because of ventricular refractoriness related to the separate underlying rhythm, and therefore multiples of the parasystolic PVC interval should be considered before excluding automaticity.
Where is the most common PVC?
PVCs from the outflow tract appear to be the most common. 1, 16 Outflow tract PVCs characteristically exhibit negative QRS complexes in both aVL and aVR, consistent with a vector that is predominately arising from the top of the heart, and, by the same token, the inferior leads will all be positive. Right ventricular outflow tract PVCs will have a left bundle-branch morphology, meaning a predominately negative QRS in V 1. If the precordial transition (the precordial lead that first exhibits a QRS that is more positive than it is negative) occurs at V 4 or later and the other limb-lead criteria just described are present, the PVC is almost certainly arising from the right ventricular outflow tract. 16, 36 If an otherwise similar PVC has a precordial transition that occurs in V 1 or V 2, it is almost certainly left-sided, most likely arising from the right or left coronary cusp (or just in-between the 2). If an otherwise similar PVC precordial transition occurs at V 3, it may be either right or left sided. 16, 36 The distinction is relevant to both the effectiveness and the risks of potential catheter ablation, which, as will be described in more detail later in this article, are both more favorable for right-sided PVCs. Understanding these morphological characteristics is also relevant because right ventricular PVCs that are not arising from the right ventricular outflow tract may be a sign of underlying pathology, such as arrhythmogenic right ventricular dysplasia, sarcoidosis, or other infiltrative diseases. For example, although idiopathic PVCs may arise from various locations within the right ventricle in the absence of structural heart disease, a frequent left bundle-branch, late-precordial transition (more positive than negative starting in V 4) PVC that is not negative in both aVR and aVL and that is negative in the inferior leads should prompt further evaluation with cardiac magnetic resonance imaging (MRI). Commonly observed PVC morphologies from the left ventricle include the papillary muscles, 37–39 which may often exhibit variable morphologies within the same patient, the left anterior or left posterior fascicles (which may occur because of either reentry or automaticity), 40 and along the mitral annulus. 41–43 PVCs also arise relatively frequently in proximity to venous structures, such as the great cardiac vein and anterior intraventricular vein 44–46 and from the crux of the heart, where all 4 chambers meet. 47
What is reentry in PVC?
Although reentry is usually considered most pertinent to sustained arrhythmias , it can play a role in single PVCs. Reentry requires 2 distinct electric pathways and either transient or permanent unidirectional block in 1 limb. Those pathways may be anatomically quite distinct, such as a right ventricular PVC blocking in the retrograde limb of the right bundle (commonly attributable to phase 3 block), crossing the ventricular septum through cardiomyocytes, conducting in a retrograde fashion up the left bundle, and then continuing on down the right bundle, producing a bundle-branch reentry complex (recognized as having a typical, usually left, bundle-branch block appearance). A similar phenomenon may occur involving the left anterior and left posterior fascicles, resulting in a fascicular PVC (recognized as having the appearance of a right bundle-branch block with left anterior hemiblock if exiting the left posterior fascicle or left posterior hemiblock if exiting the left anterior fascicle). Instead, in the absence of anatomically well-defined pathways, different tissue properties, such as 2 adjacent regions with different conduction velocities and refractory periods, may suffice to host reentry. In general, an area of scar, or a series of electrically connected cardiomyocytes meandering through an area of fibrosis, may provide a pathway that conducts much more slowly than surrounding healthier tissue during a sinus beat, such that the resultant exiting depolarizing wave front would meet myocardium that was no longer refractory, producing a PVC.
What is the first indication of PVC frequency?
Similarly, that physical examination may be the first indication of PVC frequency, which ultimately may prove to be clinically relevant.
Is a PVC asymptomatic?
PVCs are commonly asymptomatic but can also result in palpitations, dyspnea, presyncope, and fatigue. The history, physical examination, and 12-lead ECG are each critical to the diagnosis and evaluation of a PVC. An echocardiogram is indicated in the presence of symptoms or particularly frequent PVCs, and cardiac magnetic resonance imaging is ...
How can pharmacists help with DKA?
In the community and ambulatory care settings, pharmacists can also be valuable assets to educate patients on prevention of DKA and AKA. These pharmacists often see patients on a more frequent basis and can play a pivotal role in educating patients on the signs and symptoms of acidosis, and when to seek urgent medical care. Furthermore, these pharmacists have access to important information about patient medication compliance , and when an intervention may be necessary to prevent the development of ketoacidosis. Patients with diabetes should be educated to not stop their insulin abruptly without consulting their physician and to monitor for signs and symptoms of ketoacidosis in times of acute illness. Alcoholics should be educated on their risk of complications such as ketoacidosis and referred for alcohol abuse counseling.
What can a pharmacist do for patients with ketoacidosis?
Hospital pharmacists can help ensure standardization and improve the safety of pharmacotherapy for ketoacidosis. In the outpatient setting, pharmacists can educate patients on prevention of ketoacidosis and when to seek medical attention.
How does catecholamine release affect the cardiovascular system?
Catecholamine release during ketoacidosis has direct effects on the cardiovascular system. 11 Reduction in serum pH normally results in increased ventilation and Kussmaul respiration. Although cardiac contractility can be depressed, catecholamine release results in normal inotropic function. 1 During mild acidosis (pH 7.2-7.35), catecholamine release is increased and countered by increased cardiac output via increased chronotropic and inotropic function. Once the pH level drops below 7.2, there is direct cardiac depression due to the hydrogen ions. This ultimately leads to reduced cardiac output and potentially severe shock. 11 Extremely elevated blood glucose levels result in osmotic diuresis, and this may lead to volume contraction. This state is associated with elevated cortisol levels and catecholamine secretion, which further stimulates free fatty-acid production and ketogenesis. 2
How does ketoacidosis occur?
Alcoholics can also develop ketoacidosis during abrupt alcohol cessation in the presence of poor nutrition, in which the body does not have enough glucose to serve as a source of energy. During this state the body increases fatty-acid metabolism, which is enhanced by a decrease in insulin secretion and an increase in glucagon. AKA usually presents with an elevated anion gap acidosis and elevated serum lactate concentration. Some patients may have a normal blood pH due to mixed acid-base disorders owing to vomiting and respiratory alkalosis. 10 Patient symptoms include nausea, vomiting, and abdominal pain. 6
What are the two types of ketoacidosis?
Types of Ketoacidosis. Two common types of ketoacidosis are diabetic ketoacidosis (DKA) and alcoholic ketoacidosis (AKA). The mortality rate of DKA is between 1% and 10%, with the most common cause of death being infection or cardiovascular-related events such as circulatory collapse and hypokalemia.
What is metabolic acidosis?
Metabolic acidosis occurs as a result of increased endogenous acid production, a decrease in bicarbonate, or a buildup of endogenous acids. 1 Ketoacidosis is a metabolic disorder in which regulation of ketones is disrupted, leading to excess secretion, accumulation, and ultimately a decrease in the blood pH. 2 Acidosis is defined by a serum pH <7.35, while a pH <6.8 is considered incompatible with life. 1,3 Ketone formation occurs by breakdown of fatty acids. Insulin inhibits beta-oxidation of fatty acids; thus, low levels of insulin accelerate ketone formation, which can be seen in patients with diabetes. Extremely elevated blood glucose levels lead to osmotic diuresis, which results in excess secretion of cortisol and catecholamines, further promoting fatty-acid oxidation and ketone formation. Increased levels of glucagon, which is stimulated by hypoglycemia and insulin deficiency, leads to lipolysis, resulting in additional free fatty-acid production and ketogenesis. 2
What hormones are released during ketoacidosis?
2,8 Insulin depletion increases counterregulatory hormone release such as glucagon, catecholamines, cortisol, and growth hormone.
How does DKA work?
DKA treatment generally consists of two phases: first, we must manage the ketoacidosis. Later, we must prepare the patient to transition back to their home insulin regimen. During both phases, success depends on balancing insulin dose and insulin requirement.
What happens during DKA resuscitation?
During a DKA resuscitation, patients may display different types of metabolic acidosis. Understanding the physiologic problem will facilitate logical and effective treatment.
What is the titration of insulin in DKA?
Insulin titration in DKA may be driven by either ketoacidosis or glucose (above). For example, the American guidelines recommend titrating the insulin based on the glucose level ( Kitabchi 2009 ). Alternatively, the Canadian guidelines recommend insulin titration based on the degree of ketoacidosis. British guidelines use a hybrid strategy, with monitoring of both ketones and glucose (4).
Why does ketoacidosis occur?
Ketoacidosis occurs due to an imbalance between insulin dose and insulin requirement: Individuals differ in their baseline insulin resistance and insulin requirements. Physiologic stress (e.g. hypovolemia, inflammation) increases the level of catecholamines and cortisol, which increases insulin resistance.
Why is it important to reverse acidosis?
The patient is depending on respiratory compensation to maintain their pH. If they should fatigue and lose the ability to hyperventilate, their pH would drop. It is important to reverse the acidosis before the patient may fatigue or develop respiratory failure (e.g., due to aspiration or pulmonary edema) (2).
How to measure ketoacidosis?
Ketoacidosis can be measured either directly (using a point-of-care ketone meter or perhaps measuring the beta-hydroxybutyrate level) or indirectly (by measuring the anion gap). The British seem to use point-of-care ketone testing, whereas this may be less common in the United States.
Is there any evidence for acidosis in DKA?
Management of acidosis in DKA is an ongoing source of confusion. There isn’t much high-quality evidence, nor will there ever be (1). However, a clear understanding of the physiology of DKA may help us treat this rationally and effectively.
What happens when you start DKA with normal saline?
A common phenomenon observed when starting a DKA resuscitation with normal saline (NS) is worsening of the patient’s acidosis with decreasing bicarbonate levels (example below). This occurs despite an improvement in the anion gap, and is explained by a hyperchloremic metabolic acidosis caused by bolusing with NS. This could be a real problem for a patient whose initial bicarbonate level is extremely low. 1 A while ago I made the switch from NS to lactated ringers (LR) for resuscitation of DKA patients, and have not observed this phenomenon when using LR.
How long to hold insulin for DKA?
The traditional approach to managing DKA has been to hold the long-acting insulin until the patient has recovered and subsequently to overlap this with the insulin infusion for a few hours. Recent British guidelines suggest continuing the patient’s long-acting insulin throughout treatment of DKA.
Why should we care about hyperchloremic acidosis?
Why should we care? Some evidence suggests that hyperchloremic acidosis may cause renal vasoconstriction and worsen renal function. Many DKA protocols suggest delaying initiation of subcutaneous insulin until the bicarbonate is above 18 mEq/L, so a hyperchloremic acidosis may delay transition off the insulin infusion. My bias is that patients feel better and breathe easier when their bicarbonate is normalized so they don’t need to maintain a compensatory respiratory alkalosis.
What is the debate about bicarbonate?
The usual debate about bicarbonate is regarding the initial treatment of the patient when the pH is extremely low. This has already been debated extensively and I’m not going to go there.
Is LR or Normosol better for DKA?
LR, Plasmalyte, or Normosol are better choices. 2. 0.
When approaching a critically ill patient, securing the airway is often an initial consideration.?
When approaching a critically ill patient, securing the airway is often an initial consideration. However, in DKA this is fraught with hazard and often destabilizes the patient. With the exception of a patient who has truly developed respiratory muscle fatigue (and lost the ability to generate a compensatory respiratory alkalosis), intubation will typically worsen the patient.
Can insulin drip be titrated?
Occasionally this increase in glucose may cause the insulin drip to be titrated up, which can be beneficial in terms of speeding the resolution of ketoacidosis. However, care should be taken to avoid hypoglycemia if the insulin drip remains at a high rate.
Can diabetic ketoacidosis cause brain damage?
I have no way of telling whether severe brain damage occurred. Hope this helps, Dr T. Follow-up Answer: Diabetic ketoacidosis (DKA) is a potentially life-threatening complication in patients with diabetes mellitus. In some circumstances it may cause a diabetic coma and severe dehydration.
Can dehydration cause a diabetic coma?
In some circumstances it may cause a diabetic coma and severe dehydration. If dehydration is so severe, shock (severely decreased blood pressure with insufficient blood supply to the body’s organs) may be the result. If not treated quickly, it may be fatal.
When is DKA resolved?
DKA is considered resolved when metabolic parameters are met: Sugars <200, absence of ketonemia, atleast two of the closure of anion gap or Bicarb>15 or PH>7.3, . However, don't get caught up strictly with the absolute numbers. Follow patient clinically.
What is the key element in the pathogenesis of DKA?
Insulin: The key element in the pathogenesis of DKA is insulin deficiency and hence, replacing insulin is the cornerstone of DKA therapy, with or without iv fluids. Insulin will quickly shift the potassium into the cells resulting in hypokalemia, sometime very severe to the point of rsking life.
How long does it take to get potassium in IV fluid?
Most commonly, physicians add 20meg kcl to the iv fluid bag and run it at 100cc/hr, to keep potassium above 4. please be aware that at 100cc/hr, it would take 10 hours for the patient to get 20meq of kcl. Some times, even with severe hypokalemia, we may fail to correct potassium soon enough thinking that they are already getting potassium as drip in the iv fluids. This may lead to adverse events. My personal preference is to correct potassium separately with extra doses of iv or oral Kcl.
Is acetoacetate low in DKA?
Ketonemia or ketonuria ( In early DKA, acetoacetate concentration is low and could be falsely negative. Conversely, β-OHB is an early and abundant ketoacid, which may first signal the development of DKA )
Does insulin help with ketoacid anions?
The loss of these ketoacid anion salts into the urine represent "potential" bicarbonate loss from the body. Insulin therapy will have no further effect on the acidosis when this stage evolves. This doesn't mean an ongoing DKA and hence, there is no need to continue insulin drip once the gap is closed. The hyperchloremic acidosis will slowly resolve as the kidneys excrete ammonium chloride (NH4Cl) and regenerate bicarbonate.
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