Potencial de Ação
Vetores do Coração
• Despolarização sinusal: propagação do
potencial pelo átrio – Resulta na onda P do ECG (sístole atrial).
Contração ventricular coordenada – formação do complexo QRS do ECG.
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
• Intervalo QT mede a duração do PA ventricular.
Triângulo de Einthoven
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
Fibrilação e Flutter Atrial
Fibrilação Fina e Grosseira
Síndrome de Wolff-Parkinson-White (WPW)
Torsade de Pointes
• 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+..
• 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
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.
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?
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.
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
What is the patient's underlying disorder and how is it
Hint .ECG shows a specific precordial abnormality. Also
consider the patient's family history of sudden cardiac death (SCD).
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
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.
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.
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
Hint .The ECG results suggest a chronic condition.
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).
(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).
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).
pela administração de adenosina endovenosa, com a qual houve reversão ao ritmo
sinusal e normalização do ECG (figura 2).
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
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
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
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).
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
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
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.
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
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. .
ordered (see Image). .
What is the diagnosis?
Hint .Try to
localize the abnormality.
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
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
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
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. .
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
Hint .Note the underlying atrial rhythm and the ratio of
atrial to ventricular depolarizations.
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.