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ELETROFISIOLOGIA CARDÍACA.ECG




Daniel Damiani
Medicina e Biomedicina
2005


Potencial de Ação




ECG Normal








Vetores do Coração




ECG


• Despolarização sinusal: propagação do potencial pelo átrio – Resulta na onda P do ECG (sístole atrial).

• Contração ventricular coordenada – formação do complexo QRS do ECG.

• A onda T do ECG é resultado da repolarização ventricular.

Interpretação do ECG


• FC reflete a automaticidade do nodo sinusal.

• Duração do intervalo PR reflete o tempo de condução AV.

• Duração de QRS reflete o tempo de condução no ventrículo.

• Intervalo QT mede a duração do PA ventricular.

Triângulo de Einthoven




ECG








DII Longo


















Fármacos Antiarrítmicos




Assistolia




Bloqueio Cardíaco de I Grau


Bloqueio Cardíaco de II Grau – Tipo 1




Bloqueio Cardíaco de II Grau – Tipo 2




Bloqueio Cardíaco de III Grau – Escape Ventricular




Bradicardia Sinusal




Fibrilação e Flutter Atrial




Taquicardia




Fibrilação Fina e Grosseira




Síndrome de Wolff-Parkinson-White (WPW)




Torsade de Pointes




Case 01


• A 50-year-old woman presents to the emergency department because of recurrent syncopal episodes over the last 2 days. She has had worsening weakness and weight loss in the last 3 months. She denies having fevers, chills, dyspnea, nausea, vomiting, abdominal pain, or urinary symptoms. Her medical history is significant for a chronic pain disorder involving multiple joints and her back, with associated headaches. She is being treated with long-term risedronate, nortriptyline, carisoprodol, buspirone, and omeprazole...On physical examination, her blood pressure is 125/80 mm Hg, her temperature is 37.5°C, and her heart rate is about 90 bpm and regular, with no abnormal heart sounds. She weighed 94 lb (35 kg) 6 months ago but has lost 15 lb. She has normal sensation over her body with symmetric deep tendon reflexes and normal cranial-nerve responses, though she has diffuse weakness in all major muscle groups. Her mental status is normal. ..ECG is performed (see Figure 1). What is the diagnosis?

• Hint .What metabolic abnormality can cause the findings on this ECG?



• Hypokalemia: The ECG shows a normal sinus rhythm at a rate of 92 bpm with depression of the ST segment in the inferior and anterior leads and T-wave inversions in the lateral leads. The PR interval is normal at 126 ms, whereas the QT and QTc intervals are prolonged at 506 and 621 ms, respectively. U waves are present in all leads but are most prominent in V2 (see Figure 2). ..The results of a metabolic panel revealed a K+ level of 1.6 mmol/L. On further questioning, the patient admitted to a long history of self-induced vomiting, with a recent increase in frequency.

The patient was admitted for cardiac telemonitoring, K+ supplementation, and psychiatric evaluation. The initial ECG changes (seen in Figure 2) completely resolved when the patient's K+ level was corrected (see Figure 3). The patient was eventually discharged home for outpatient psychiatric treatment of her eating disorder. ..Hypokalemia is defined as a plasma K+ concentration of less than 3.5 mmol/L and may result from several physiologic processes: decreased net intake of K+, K+ shift into cells, or increased net loss of K+. In this patient, losses from vomiting of gastric secretions could not completely account for her severe hypokalemia. The K+ concentration of gastric fluid is too low (5-10 mmol/L) to cause the deficit of greater than 400 mmol typical of moderate-to-severe hypokalemia. In cases like this, the primary mechanism is increased renal K+ excretion due to both metabolic alkalosis and volume depletion resulting from the loss of gastric fluid. ..Clinical manifestations of mild-to-moderate hypokalemia are fatigue, myalgia, and muscular weakness of the lower extremities. Severe hypokalemia may lead to progressive weakness; hypoventilation; and, eventually, complete paralysis, rhabdomyolysis, and paralytic ileus. Characteristic ECG changes of hypokalemia are due to delayed ventricular repolarization and are not well correlated with plasma K+ concentrations. Early changes are flattening or inversion of the T wave, a prominent U wave, ST-segment depression, and a prolonged QU interval. Severe K+ depletion may result in a prolonged PR interval, decreased voltage, widening of the QRS complex, and an increased risk of ventricular arrhythmias. ..

The treatment of hypokalemia is K+ repletion and correction of the cause to minimize ongoing loss. Patients with severe hypokalemia or those unable to take anything by mouth require intravenous replacement therapy with KCl. The concentration of intravenous K+ should not exceed 40 mmol/L for administration via a peripheral vein or 60 mmol/L for a central vein. The rate of infusion should not exceed 20 mmol/h unless muscular paralysis or malignant ventricular arrhythmias are present. Ideally, KCl should be mixed in normal saline because dextrose solutions may initially exacerbate hypokalemia as a result of insulin-mediated intracellular movement of K+..





Case 02


• A 53-year-old African American woman presents to the emergency department with a feeling that her "heart is racing in her chest." This feeling began a few hours earlier, after she had multiple episodes of diarrhea throughout the day. She denies having any abdominal pain, nausea, or vomiting and says that this has never happened before. She has had occasional periods of shortness of breath since the diarrhea started and reports feeling "pins and needles" in her chest. The patient has no significant medical history and takes no medications. She smokes a pack of cigarettes per day and denies recreational drug use. ..Her vitals sign are as follows: blood pressure = 175/88 mm Hg, pulse = 120 beats per minute, respiratory rate = 20 breaths per minute, and oral temperature = 98.1°F. Her physical findings are remarkable only for tachycardia. Findings on chest and abdominal examination are normal. Laboratory tests are ordered, and ECG is performed. ..What is the diagnosis?

• Hint .Look closely at the flutter waves.



Tachycardia with U waves resulting from hypokalemia and dehydration secondary to diarrhea: The initial interpretation of the ECG in lead II (see bottom of Image 1) was atrial flutter with a 4:1 block. On the basis of this interpretation, the patient was given diltiazem 5 mg to chemically cardiovert the rhythm to a sinus rhythm or to slow the ventricular response. However, this treatment had little effect. On reexamination of the complete 12-lead ECG, the flutter waves were determined to be T, U, and P waves of approximate height occurring in close succession. This pattern created the characteristic sawtooth appearance normally observed in atrial flutter. Beyond lead II, the waves clearly had different morphologies. For example, the aVL lead clearly shows 3 waves on the baseline with notable differences in morphology.

Soon after this reinterpretation of the ECG, the patient's laboratory results returned and showed a potassium level of 3.0 mEq/L. This ECG demonstrates a characteristic finding in hypokalemia: that is, the presence of U waves (see Image 1). U waves may be found on normal ECGs (in the high lateral precordial leads), but they are usually small in amplitude (< 0.2 mV). Prominent and positive U waves, as seen in this case, are most commonly associated with hypokalemia, though they may also occur in other conditions, such as thyrotoxicosis, hypercalcemia, and treatment with certain pharmacologic agents (eg, digoxin, quinidine, epinephrine). Other characteristic ECG findings of hypokalemia are flattening of the T wave and ST-segment depression, which are also present on this ECG. Inverted U waves are almost uniformly pathologic and represent myocardial ischemia or left ventricular strain. The etiology of U waves is thought to represent repolarization of the His-Purkinje system or the papillary muscles.

The patient was given intravenous fluid (for dehydration) containing potassium chloride 40 mEq and additional oral potassium 20 mEq. Her repeat ECG (see Image 2) showed improvement in the tachycardia and U waves. (The U waves are still visible, but their height is reduced.) .

Findings from the remainder of the patient's workup were unremarkable. The patient was thought to have an acute decrease in serum levels due to diarrhea, rather than a total-body depletion of potassium. She was discharged home with potassium supplements and instructions to see her primary care physician within the week for a check-up and repeat testing of her serum potassium level. A follow-up call approximately 1 month after her initial presentation revealed that the diarrhea resolved spontaneously and that her potassium level had returned to the normal range.





Case 03


A 65-year-old man with altered mental status and a known history of lung cancer is brought to the emergency department (ED) by ambulance. On arrival, he is vomiting. He developed a gradual onset of lethargy and depression after a recent episode of abdominal pain due to constipation and poor oral intake.

On physical examination, the patient has a blood pressure of 123/87 mm Hg and a heart rate of 114 beats per minute. His temperature is 99.2°F, and the pulse oximetry reading is 97% on room air. The patient opens his eyes and is arousable to command. He can follow simple commands; however, he is generally disoriented and slow to respond. His mucous membranes are dry, and he has poor skin turgor. His neurologic examination shows nonfocal findings. A finger-stick blood glucose measurement is 114 mg/dL, and ECG is performed (see Image). ..

What is the diagnosis?



Hypercalcemia in malignancy: This patient's presentation of altered mental status with severe dehydration, vomiting, and abdominal pain in the setting of malignancy suggests paraneoplastic syndrome of hypercalcemia. Electrolyte tests confirmed the diagnosis, revealing the following levels: Ca, 14.8 mg/dL; K, 5.8 mmol/L; BUN, 90 mg/dL; and creatinine, 2.4 mg/dL. Hypercalcemia is relatively common. More than 90% of cases are associated with hyperparathyroidism leading to increased Ca absorption mediated by parathyroid hormone (PTH) or to malignancy due to increased osteoclastic activity or a paraneoplastic process secondary to the production of a PTH-related peptide; the latter is the most common in the ED.

The classic ECG finding is shortening of the QT interval, the opposite of that seen in hypocalcemia. This finding occurs because the refractory period after the action potential is shortened. In general, life-threatening dysrhythmias are rare with isolated hypercalcemia, unless they are coupled with concomitant hyperkalemia. Hyperkalemia may be due to the loss of renal concentrating ability secondary to the elevated Ca levels and resultant dehydration with prerenal failure or the renal insult from the deposited Ca in the tubules that leads to direct renal injury and, ultimately, renal failure. Cardiac conduction abnormalities may also occur, with bradydysrhythmias being the most common.

Patients with hypercalcemia (total Ca levels generally 14-16 mg/dL) typically present with weakness, lethargy, and confusion. Significant hypercalcemia (usually with Ca level >15 mg/dL) may present with stupor and coma. A mnemonic often used to characterize the signs and symptoms of hypercalcemia is "stones, bones, moans, and groans," indicating renal calculi, osteolysis and resultant bone pain, psychiatric disorders (eg, depression), and abdominal pain (due to peptic ulcer disease, pancreatitis, and constipation). Hypercalcemia should be suspected in any patient with metastatic bone disease, especially if the primary cancer involves the lungs, breast, or kidneys, as well as in patients with a combination of medical problems, such as kidney stones, pancreatitis, and peptic ulcer disease.

Treatment of hypercalcemia is generally based on the clinical signs and not on a specific absolute serum level, though empiric therapy is often initiated for Ca levels greater than 14 mg/dL. The mainstay of treatment is intravenous volume repletion with normal saline 200-500 mL/h and intravenous bisphosphonate therapy (inhibition of osteoclastic bone resorption). A diuretic may be added as an adjunct to promote calciuresis and volume overload if the patient is euvolemic or if he or she has been adequately rehydrated. Because of their Ca-sparing effect, thiazide diuretics should be avoided. Loop diuretics, such as furosemide, can be used.

Calcitonin, a naturally occurring hormone that prevents bone resorption and increases Ca excretion, can be added, though its effect is often short lived. Other slower-acting agents should also be used. Plicamycin (Mithracin), another osteoclast inhibitor, was the mainstay of therapy for hypercalcemia of malignancy; however, bisphosphonates have largely replaced it because of their favorable adverse-effect profile. Gallium nitrate is approved in the United States for treatment of hypercalcemia of malignancy, but the need for continuous intravenous administration over 5 days limits its use. Hydrocortisone and other steroids do not directly treat hypercalcemia, but they have been used in some cases related to vitamin D toxicity and in specific malignancies (sarcoid, multiple myeloma, and some lymphomas); results have been mixed.

Hemodialysis may be required in refractory cases, especially in patients with renal failure, hyperkalemia, or congestive heart failure (when large volumes of saline are contraindicated). Attention must be paid to the treatment of the specific cancer and to end-of-life issues, as the prognosis of a patient with hypercalcemia in malignancy can be dismal.



Case 04


A 30-year-old man of Japanese descent presents to the emergency department (ED) after he had a syncopal event, which his wife witnessed. Apparently, he had several such episodes in the past, though he never sought medical evaluation for them. His wife states that they had been talking in the kitchen when her husband complained of feeling dizzy and nauseous. He then slumped over and fell out of his chair, hitting his head on the floor. Within a few seconds, he was awake and conversant. No tongue biting or jerky body movements were observed.

The patient is awake and alert, and his vital signs are stable. He does not have a specific complaint other than the bruise on his forehead and mild embarrassment. Electrocardiography is ordered (see Image). When you ask the patient if he has any family members who suddenly died at a young age, he mentions that his uncle died in his 30s without apparent cause.

What is the patient's underlying disorder and how is it treated?

Hint .ECG shows a specific precordial abnormality. Also consider the patient's family history of sudden cardiac death (SCD).



Brugada syndrome: The patient presents with syncope in the context of a family history of SCD. The vast majority of SCDs are due to ventricular fibrillation (VF) associated with structural heart disease, and SCD in the normal heart is uncommon, accounting for up to 5% of all cases. In patients with normal hearts, causes of SCD include Brugada syndrome, long-QT syndrome, preexcitation syndrome, and commotio cordis.

Brugada syndrome was originally described in 1992. It consists of the Brugada pattern on ECG and 1 or more of the following associated clinical features: syncopal episodes, documented VF, self-terminating polymorphic ventricular tachycardia (VT), family history of SCD in a relative younger than 45 years, and evidence of ST-segment elevation in family members.

The syndrome is characteristically caused by an autosomal dominant genetic defect resulting in the loss of function or dysfunction of the sodium channel. Brugada syndrome most commonly affects middle-age men (average presentation at 30 y) and can be recognized by its characteristic ECG pattern, ie, downsloping ST-segment elevation in leads V1-V3 and QRS morphology resembling that of a right bundle branch block. Brugada syndrome can be distinguished from benign early repolarization (BER) in that the former has downsloping precordial ST-segment elevation, which is typically followed by a negative T wave, whereas the latter usually has a positive T wave. This patient has the characteristic ECG changes consistent with Brugada syndrome (see Image). v In the United States, the prevalence of Brugada syndrome is unknown. In some countries in Southeast Asia, the syndrome accounts for 40-50% of all cases of idiopathic VF.

A high index of suspicion should be maintained, especially when patients present with syncope in the setting of a family history of sudden death, even if their initial ECG is normal. Intermittent or concealed forms of Brugada syndrome can often be diagnosed by using the provocative administration of a class Ia antiarrhythmic, such as procainamide, in the electrophysiology laboratory. If the patient's history or ECG findings suggest Brugada syndrome, a cardiologist specializing in electrophysiology should be consulted. Not all patients presenting with syncope require admission. Patients who have had a syncopal episode in the setting of electrocardiographic abnormalities or family history of SCD (as in this case study) should be admitted to the hospital. An episode of VT/VF should prompt admission to a monitored setting, and early placement of a cardioverter-defibrillator should be considered. In addition, the treating cardiologist should arrange for an evaluation of the patient's family members, given the genetic pattern of autosomal dominance.



Case 05


A 65-year-old man presents to the emergency department complaining of difficulty breathing. He describes worsening dyspnea on exertion, which is often associated with chest tightness, wheezing, and coughing. The patient's dyspnea has worsened so that he can hardly walk from his couch to the bathroom without becoming extremely short of breath. He had been getting over a cold, with several days of nasal congestion, clear rhinorrhea, and nonproductive cough. He reports having been healthy his whole life and has not been to see a physician in at least 2 decades. However, on the review of symptoms, the patient mentions that he has gradually curtailed his activities, such as gardening, shoveling snow, and even walking in the mall, because he is increasingly "getting winded." He smokes 2 packs of cigarettes daily, a habit he has be been trying to break for at least 30 years.

On examination, the patient is alert but appears to be in respiratory distress, with mild retractions and pursed-lipped breathing. He is afebrile. His blood pressure is 140/85 mm Hg, and his pulse rate is 103 beats per minute and mostly regular. His respiratory rate is 22 breaths per minute, and pulse oximetry shows a reading of 91% on room air. His breath sounds are diminished throughout, with a markedly prolonged expiratory phase and faint expiratory wheezes in the upper lung fields. Cardiac examination reveals distant heart sounds with a somewhat prominent P2. He has no murmur, gallop, or pericardial rub. His skin is cool and dry. He has trace edema at his ankles but no cyanosis or clubbing. Electrocardiography (ECG) is performed (see Image).

What is the diagnosis?

Hint .The ECG results suggest a chronic condition.



Chronic obstructive pulmonary disease (COPD): This ECG demonstrates a constellation of findings that suggests COPD, namely, sinus tachycardia, a vertical or rightward axis, P pulmonale, low QRS voltage (particularly in the limb leads), and an incomplete right bundle branch block (RBBB).

COPD is generally not diagnosed on the basis of ECG findings. However, the signs and symptoms of cardiac and pulmonary disease overlap substantially (Marantz, 1990). It is not unusual for ECG to be the first diagnostic test performed in patients with long-standing COPD. Knowledge of the usual ECG manifestations of COPD enables the clinician to recognize uncharacteristic abnormalities, which often represent the effects of superimposed illnesses or drug toxicity (Rodman, 1990).

Tachycardia is common in individuals with exacerbations of COPD, occurring as a compensatory mechanism for low oxygen delivery (in the setting of hypoxia) or poor right ventricular function (in the setting of cor pulmonale). Sinus tachycardia is most common, but other supraventricular arrhythmias, such as atrial tachycardia (unifocal or multifocal), atrial fibrillation, and atrial flutter, can also be seen (McCord, 1998; Gorecka, 1997).

P pulmonale (ie, a P wave amplitude of >2.5 mm) is a frequently reported but relatively insensitive predictor of right atrial enlargement (Kaplan, 1994). In patients with COPD, the amplitude of the P wave is in fact dynamic and tends to be more prominent during an acute exacerbation than at other times (Asad, 2003).

A vertical or rightward axis is another manifestation of pulmonary hypertension (Bossone, 2003). Similarly, complete or incomplete RBBB and/or right ventricular hypertrophy are common in patients with cor pulmonale.

Low voltage, particularly in the limb leads, is another ECG characteristic of patients with COPD. This finding is classically attributed to increased impedance through a hyperinflated chest. However, low voltage is not directly correlated with hyperinflation, and it is neither sensitive nor specific for COPD (Sorbello, 1982).



Caso 06


MJOS, 70 anos, sexo feminino, em tratamento ambulatorial de hipertensão arterial sistêmica, encaminhada ao Serviço de Eletrocardiografia do HCFMUSP apresentava taquicardia supraventricular com freqüência cardíaca de 130 bpm (figura 1).



Decidiu-se pela administração de adenosina endovenosa, com a qual houve reversão ao ritmo sinusal e normalização do ECG (figura 2).



A paciente permaneceu em observação durante alguns minutos e, curiosamente, estando ela assintomática e estável, o ECG de controle tardio mostrou expressiva alteração da repolarização ventricular (figura 3).



A revisão do prontuário revelou que tal alteração eletrocardiográfica era preexistente, como pode ser observado em ECG registrado anteriormente (figura 4). .Assim aventou-se a possibilidade de que no ECG aparentemente normal logo após a reversão da taquicardia houve uma pseudonormalização da onda T por mecanismo de memória elétrica.



Caso 7


A 49-year-old man presents to the emergency department with fatigue and palpitations over the last 24 hours. His family states that he has also been drowsy and fatigued for the past 2-3 days. They state that, when he is awake, he appears to be somewhat confused. The patient denies having a fever or chills, shortness of breath, chest pain, or abdominal pain. He does not have a headache and has not vomited or had diarrhea. His medical history includes chronic hepatitis C, cirrhosis, chronic renal failure, and hypertension. His current medications are lamivudine, nadolol, lactulose, and spironolactone.

On physical examination, the patient is awake but somnolent. His temperature is 98.2°F, his heart rate is 96 bpm, and his blood pressure is 114/72 mm Hg. His oxygen saturation is 94% on room air. Findings on pulmonary and cardiac examination are unremarkable, but his abdomen is slightly distended. Trace peripheral edema is observed. Findings on neurologic examination are nonfocal. The patient does not know the date, though he can state his name and knows that he is in an emergency department.

The patient is attached to a cardiac monitor and given oxygen. A full set of laboratory investigations and 12-lead ECG are ordered (see Image 1). Soon after the initial ECG is obtained, the nurse calls you into the room to examine the patient, who has become diaphoretic. His heart rate is now about 40 bpm. He appears ashen and uncomfortable. Repeat ECG is performed (see Image 2).

What finding on the repeat ECG indicates the need for immediate therapy?

Hint .Changes are most pronounced in leads V2 and V3. Note the patient's medications.





Hyperkalemia: This patient's repeat ECG shows peaked T waves, which are most pronounced in leads V2 and V3. .A presumptive diagnosis of hyperkalemia was made, and the patient was immediately given 2 ampules of calcium chloride 10 mL of 10% solution. The ECG was repeated (see Image 3). The calcium was followed by insulin 10 U with 1 ampule of dextrose, 1 ampule of sodium bicarbonate 44 mEq, intravenous Lasix 60 mg, and oral sodium polystyrene sulfonate (Kayexalate) 30 g. A final ECG was performed before the patient is admitted (Image 4). As suspected, initial laboratory tests reveal a potassium level of 6.8 mmol/L, and the patient's creatinine level had worsened to 6.2 mg/dL from 3.6 mg/dL 2 weeks earlier.

Hyperkalemia is uncommon in healthy individuals, as potassium secretion normally increases to compensate for the increased plasma potassium concentration. Mechanisms involve an increase in the serum aldosterone levels and an increase in the delivery of water to the distal nephron. However, patients who have increased serum potassium levels due to increased efflux of intracellular potassium or decreased renal excretion of potassium can have increased serum potassium levels. This change results in the characteristic ECG changes and clinical deterioration. Peaking of the T waves, usually across the entire 12-lead ECG, is the earliest and most common finding. Other characteristic ECG changes (not seen in this case) are prolongation of the PR interval and progressive widening of the QRS complex until it merges with the T wave to form a sine-wave pattern (see eMedicine Hyperkalemia).

Several common medical conditions can increase the efflux of intracellular potassium. Any medical condition resulting in a metabolic acidosis can cause hyperkalemia. To reduce the serum acidemia, potassium is exchanged for hydrogen ions at the cellular membrane. Tissue breakdown due to burns, trauma, or cytotoxic or radiation therapy may also disrupt the integrity of the cell, causing the release of excess potassium into the extracellular fluid. In addition, uncontrolled diabetes mellitus with concomitant hyperglycemia leads to osmotic water movement out of cells, creating a gradient for potassium to passively exit from them. The relative insulin deficiency in diabetes compounds this phenomenon because insulin normally promotes the entry of potassium into the cell by increasing activity of the Na-K adenosine triphosphatase (ATPase) pump. Last, activation of beta-2 receptors on cell membranes also increases Na-K ATPase activity; therefore, nonselective beta-blockers can also contribute to hyperkalemia.

The kidneys normally excrete excess potassium from the body. Therefore, disorders that reduce their ability to excrete potassium result in hyperkalemia. Insufficient renal function may result from disorders such as acute or chronic renal failure, lupus nephritis, rejection of a renal transplant, obstructive uropathy, and glomerulonephritis. Aldosterone normally causes reabsorption of sodium in exchange for potassium in the distal tubule of the kidney, and its deficiency can result in total body hyperkalemia. Furthermore, inhibitors of the renin-angiotensin-aldosterone axis, including angiotensin-converting enzyme (ACE) inhibitors (eg, lisinopril, enalapril), angiotensin II receptor blockers (ARBs, eg, losartan, valsartan), and aldosterone antagonists (eg, spironolactone) can lead to hyperkalemia, especially in the setting of renal insufficiency. Decreased urinary excretion of potassium can also result from conditions such as heart failure or cirrhosis due to decreased water delivery to the distal nephron.

A phenomenon of pseudohyperkalemia (falsely elevated potassium levels) also exists. The chief cause is hemolysis of RBCs during placement of an intravenous line. If hyperkalemia is incidentally noted in an otherwise asymptomatic patient without risk factors for hyperkalemia, the blood sample should always be redrawn and the potassium level rechecked.

Treatment for asymptomatic hyperkalemic patients is conservative. Any medications that may be contributing to the electrolytic disorder should be discontinued, and correction of underlying factors, such as acute renal insufficiency, should be considered. An exchange resin, such as sodium polystyrene sulfonate (Kayexalate), binds potassium in the gut and may be administered.

Rapid increases in serum potassium levels or absolute levels above approximately 7.0 mmol/L usually lead to symptoms, with muscle weakness and characteristic ECG changes. If these occur, immediate treatment is necessary. The first-line medication that should be administered to an unstable patient is calcium chloride, which stabilizes cell membranes in minutes without changing the serum potassium concentration. Calcium can be repeated every 5 minutes to treat persistent ECG changes, but it has a brief duration of action of 15-20 minutes and should be followed with other measures. Insulin is the second agent that should be administered. A glucose solution may be needed to prevent hypoglycemia, though the rapid infusion of a hypertonic glucose solution may transiently exacerbate hyperkalemia by means of osmotic effects. The effect of insulin does not begin for 30 minutes, but it lasts several hours.

Sodium bicarbonate reduces potassium levels by stimulating the cellular exchange of hydrogen for potassium. This effect begins in about 30-60 minutes and lasts several hours. Beta-2 agonists, such as albuterol, can also help lower potassium values, with the intravenous form acting more rapidly than the inhaled form. In addition, loop and thiazide diuretics can help with potassium excretion, though patients with renal insufficiency may not effectively respond to such therapy. Sodium polystyrene sulfonate (Kayexalate) is also indicated to reduce the potassium level for a prolonged period. If all measures fail, hemodialysis may be used.

In most cases, hyperkalemia results from a combination of factors. In this patient, the salient factors are cirrhosis, renal insufficiency, and use of a potassium-sparing diuretic (ie, spironolactone). At-risk patients should be identified early and regularly monitored to prevent hyperkalemia. This patient was successfully treated in the acute setting. He was discharged home 3 days later. .





Caso 8


An 81-year-old woman presents to the emergency department with altered mentation. The patient was in her usual state of health until today, when she vomited on several occasions. The vomiting was attributed to her family's discontinuation of her metoclopramide (Reglan) therapy because they were concerned that this medication was aggravating her facial dyskinesia. Today, the patient was noted to have difficulty communicating (both understanding and verbalizing), and she was unable to move her left upper extremity. She has a medical history of end-stage renal disease requiring hemodialysis, insulin-dependent diabetes mellitus, and coronary artery disease with hypertension. She takes insulin, sevelamer hydrochloride (Renagel), simvastatin, labetalol, and enalapril..On physical examination, the patient appears ill, with temperature of 98.4°F, blood pressure of 180/89 mm Hg, heart rate of 72 bpm, and respiratory rate of 14 breaths per minute. Her oxygenation is 96% on room air. Findings on pulmonary, cardiac, and abdominal examination are benign, but she is aphasic and has left hemiparesis on the neurologic examination. Her finger-stick blood glucose level is 112 mg/dL. .

ECG is ordered (see Image). .

What is the diagnosis?

Hint .Try to localize the abnormality.



Cerebrovascular disease–induced T-wave inversion: The ECG demonstrates a sinus rhythm of 60 bpm with a prolonged QT interval of 680 msec and deep, symmetric T-wave inversion in leads I-III, AVF, and V2-V6. Head CT demonstrated bilateral, frontal subdural hemorrhages (see Image 2). The patient was admitted to the intensive care unit for medical treatment.

Acute myocardial infarction often occurs in the setting of acute stroke. However, the diagnosis of myocardial infarction is complicated by the fact that clinical symptoms such as chest pain may not accompany myocardial damage in acute stroke. In addition, the stress of acute stroke may cause nonspecific elevations of the biochemical markers of myocardial damage, as well as various ECG abnormalities consistent with early repolarization and ischemic-like changes.

Repolarization, ischemic-like ECG changes, and/or QT prolongation are found in approximately 75% of patients with subarachnoid hemorrhage, irrespective of a history of heart disease. Similar changes are present in more than 90% of unselected patients with ischemic stroke or intracerebral hemorrhage, but the prevalence decreases if patients with preexisting heart disease are excluded. Other methods for diagnosing acute myocardial injury are necessary for a definitive diagnosis. Examples of such methods are echocardiography to detect cardiac-wall motion, laboratory tests to detect elevated levels of biochemical markers of myocardial injury, autopsy, and thallium scintigraphy.

Acute cerebrovascular disease can produce ECG changes, including ST-segment and T-wave changes similar to those associated with cardiac ischemia. A prolonged QRS complex, an increased QT interval, and prominent peaked or deeply inverted and symmetric T waves are commonly seen. The changes can occur soon after the neurologic event, or they can evolve over a few days. In patients with intracranial hemorrhage, T-wave inversion is not an isolated ECG anomaly; it might also be associated with ventricular contraction abnormalities demonstrable on follow-up echocardiograms or cardiac perfusion studies. Several mechanisms have been suggested to explain the acute reversible cardiac injury, including microvascular spasm and increased levels of circulating catecholamines. .



Caso 9


An 82-year-old man is brought in to the emergency department by rescue ambulance because of a sudden loss of consciousness, which occurred at home while he was walking to the bathroom. The patient's wife heard a thump from the other room and came to find her husband lying on the floor. She reported that his upper extremities twitched a couple of times, and his eyes rolled back, but within a minute he was awake and alert and asking what had happened. He remained stable during transport, and the main finding that the ambulance personnel mentioned was that his pulse seemed irregular and sometimes slow.

On arrival the patient was alert and awake with his baseline normal mental status; he was not groggy or confused. Given the lack of premonitory symptoms and the abnormal pulse rhythm, you are concerned that the patient has had cardiac syncope. The monitor shows an irregularly irregular rhythm and a heart rate of 62 bpm. The patient's blood pressure is 150/82 mm Hg, and his oxygen saturation is 99% on room air. You ask for a 12-lead ECG.

Hint .Note the underlying atrial rhythm and the ratio of atrial to ventricular depolarizations.



Atrial flutter with variable block: Note the sawtooth f waves in the inferior leads (II, III, aVF) and in V1. These leads are usually where flutter waves are most easily recognized. Also note the variability in the timing of the QRS complexes that follow. The atrial rate in flutter is generally 250-350 bpm; in this case, the atrial rate is 300 bpm. Patients with atrial flutter typically present with a regular ventricular response of about 150 bpm as a result of 2:1 arteriovenous (AV) conduction. Slower rates may occur with a diseased conduction system, as in this case, or with the use of rate-slowing agents, such as beta-blockers, calcium channel blockers, or digoxin. The structurally normal heart that is not given rate-slowing medications typically produces ventricular rates of 100-180 bpm in atrial flutter.

Remember that patients with digoxin toxicity classically present with atrial tachycardia or atrial flutter with block. Moreover, the main differential diagnoses for the patient with an irregular rhythm on the ECG (aside from respiratory variation and premature atrial or ventricular beats) are atrial fibrillation, atrial flutter, and multifocal atrial tachycardia. The first of these is the most common; however, the latter 2 are often not diagnosed because they are not considered in the differential.

Atrial flutter is a rhythm that has increasing incidence with the elderly population of about 50-90 cases per 1000 people aged 65-90 years. Patients may present with variable block (as in this case); especially prone are the elderly, who may have a diseased conduction system and underlying sick sinus syndrome (SSS). In fact, one of the common presenting rhythms in SSS is atrial fibrillation or flutter, which may be associated with a slow ventricular rate depending on the degree of block. Patients with SSS may present with syncope as a result of the tachycardia-bradycardia ("tachy-brady") syndrome. This syndrome occurs when a combination of fast and slow supraventricular rhythms occur in the presence of SSS. Either bradycardia or tachycardia (often atrial fibrillation or flutter) may cause syncope. A concomitant lack of a sufficient junctional or ventricular escape rhythm is necessary for SSS-related symptomatic bradycardia to cause syncope.

Because patients with SSS nearly always have AV nodal disease, the treatment for the atrial fibrillation or flutter has important differences from the standard rate control or cardioversion therapy. Rate-slowing agents or cardioversion in such patients may produce disastrous consequences, including worsening of the heart block and progression to clinically significant bradycardia and hypotension. In this patient (whose syncope was likely due to the high degree of block and resultant bradycardia), rate-slowing agents and cardioversion are contraindicated. Patients such as this one generally require a pacemaker to manage recurrent syncope or symptomatic bradycardia. The need for cardiac medications to treat tachydysrhythmias (which may be intermittent) is a separate indication for pacemaker placement, as these medications alone may worsen the existing heart block. Therefore, pacing to treat bradycardia and drug therapy to treat the tachycardia are required for those with tachycardia-bradycardia syndrome.