Are there any person having cured of heart arterial blocks up-to 90% by natural!
Question:
I had a mild heart problem just a few months ago and the 64 bit scanner diagnosis found one block upto 90% and other upto 60% and I am not taking any aspirin or other allopathic drugs.
Answers:
OK. time to make some clarifications. A 64-slice CT scanner is sometimes used as an alternative to more invasive coronary angiography. The fact that your CT scan showed two areas of blockage means you should probably undergo a coronary angiogram to verify these findings and to treat the disease if it is there. You should definitely start taking an aspirin, as this has been shown in studies to reduce the risk of heart attack in patients with known coronary disease. In addition, there are a handful of other drugs that have been shown in very large, well designed scientific trials to reduce your risk of heart attack, heart failure, and death. These include a beta-blocker (one kind of blood pressure medicine), an ACE-inhibitor (another blood pressure medicine), and a cholesterol-lowering drug in the "statin" class. Several alternative treatments have been tried and pushed in the past including chelation therapy, but the truth is that none of these have been shown to reverse coronary artery blockages. In fact, none of the drugs mentioned above have been shown to reliable reverse coronary blockages either. BUT you don't necessarily need these blockages to shrink for the medications to provide a benefit.
Now, I have to say that IT ISN'T TRUE THAT YOUR 90% BLOCKAGE COULD KILL YOU AT ANY MOMENT. Sure, it's POSSIBLE that you could drop dead tomorrow, but that 90% blockage probably grew gradually over the course of a few years so it is unlikely to suddenly close off at any moment. Don't panic! On the other hand, it will probably continue to progress to 95%. 97%. 99%. and eventually lead to such significant blockage that some of your heart muscle will fail to get enough blood flow, even when you are at rest. This can lead to something called a non-ST elevation MI - a heart attack. The more upstream that blockage is, the more heart muscle it supplies and the more life-threatening that heart attack can be.
With the newer technologies at our disposal, most significant blockages in the coronary arteries can be opened during the angiogram with a small, drug-eluting stent. These have a very good tendency to stay open over many years, thus avoiding the need for surgery in most patients. However, depending on the location of the blockage, some patients may still do better with surgery.
I strongly urge you to see your doctor and get the coronary angiography done. It is not something that you have to do in the next day or two, but it should definitely be taken care of in the next couple of weeks. Believe me, if there were natural medicines that are effective for treating coronary disease, your insurance company would force you to take those before it agreed to shell out $15,000 for a stent.
Other Answers:
What i know is that scanners do mistakes.For natural medicines i read about grape fruit pectin.under the name profibe.
it is best that you fully understand your illness..please read this.
Background: Complete heart block, also referred to as third-degree heart block, or third-degree atrioventricular (AV) block, is a disorder of the cardiac conduction system, where there is no conduction through the AV node. Therefore, complete disassociation of the atrial and ventricular activity exists. The ventricular escape mechanism can occur anywhere from the AV node to the bundle-branch Purkinje system. It is important to realize, however, that not all patients with AV dissociation have complete heart block. For example, patients with accelerated junctional rhythms have AV dissociation, but not complete heart block, if the escape rate is faster than the intrinsic sinus rate. Electrocardiographically, complete heart block is represented by QRS complexes being conducted at their own rate and totally independent of the P waves.
Pathophysiology: Complete heart block is caused by a conduction block at the level of the AV node, the bundle of His, or the bundle-branch Purkinje system. In most cases (approximately 61%), the block occurs below the His bundle. Block within the AV node accounts for approximately one fifth of all cases, while block within the His bundle accounts for slightly less than one fifth of all cases.
Duration of the escape QRS complex depends on the site of the block and the site of the escape rhythm pacemaker.
Pacemakers above the His bundle produce a narrow QRS complex escape rhythm, while those at or below the His bundle produce a wide QRS complex.
When the block is at the level of the AV node, the escape rhythm generally arises from a junctional pacemaker with a rate of 45-60 beats per minute. Patients with a junctional pacemaker frequently are hemodynamically stable and their heart rate increases in response to exercise and atropine.
When the block is below the AV node, the escape rhythm arises from the His bundle or the bundle-branch Purkinje system at rates less than 45 beats per minute. These patients generally are hemodynamically unstable and their heart rate is unresponsive to exercise and atropine.
Mortality/Morbidity: Patients with complete heart block are frequently hemodynamically unstable, and as a result, the patient may experience syncope, cardiovascular collapse, or death.
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History: Complete heart block has a wide range of clinical presentations; most patients are symptomatic.
* Patients occasionally are asymptomatic or have only minimal symptoms related to hypoperfusion. In these situations, symptoms include the following:
o Fatigue
o Dizziness
o Impaired exercise tolerance
o Chest pain
* Patients with narrow complex escape rhythms (eg, those whose escape rhythm occurs above the His bundle) are more likely to have minimal symptoms. More commonly, however, the patients are profoundly symptomatic, especially if a wide-complex escape rhythm is present, indicating the origin of the pacemaker is below the His bundle. In such cases, symptoms can include the following:
o Syncope
o Confusion
o Dyspnea
o Severe chest pain
o Sudden death
* Because an acute myocardial infarction is one cause of complete heart block, patients who concurrently experience an MI can have associated symptoms from the MI, including chest pain, dyspnea, nausea or vomiting, and diaphoresis.
* Patients who have a history of cardiac disease may be on medications that affect the conduction system through the AV node, including the following:
o Beta-blockers
o Calcium channel blockers
o Digitalis cardioglycosides
Physical:
* The physical examination will be notable for bradycardia, which can be quite severe.
* Signs of congestive heart failure as a result of decreased cardiac output may be present and include the following:
o Tachypnea or respiratory distress
o Rales
o Jugular venous distention
* Patients may have signs of hypoperfusion, including the following:
o Altered mental status
o Hypotension
o Lethargy
* In patients with concomitant myocardial ischemia or infarction, corresponding signs may be evident on examination:
o Signs of anxiety such as agitation or unease
o Diaphoresis
o Pale or pasty complexion
o Tachypnea
* Regularized atrial fibrillation is the classic sign of complete heart block due to digitalis toxicity. This rhythm occurs because of the junctional escape rhythm.
Causes: Complete heart block can be either congenital or acquired.
* The congenital form usually occurs at the level of the AV node, and patients are relatively asymptomatic at rest but later develop symptoms because the fixed heart rate is not able to adjust for exertion. In the absence of major structural abnormalities, congenital heart block is often associated with maternal antibodies to SS-A (Ro) and SS-B (La).
* Causes of acquired complete heart block include the following:
o Complete heart block can develop from isolated, single-agent overdose, or often from combined or iatrogenic coadministration of AV-nodal, beta-adrenergic, and calcium channel blocking agents. Drugs or toxins associated with heart block include the following:
+ Class Ia antiarrhythmics (eg, quinidine, procainamide, disopyramide)
+ Class Ic antiarrhythmics (eg, flecainide, encainide, propafenone)
+ Class II antiarrhythmics (beta-blockers)
+ Class III antiarrhythmics (eg, amiodarone, sotalol, dofetilide, ibutilide)
+ Class IV antiarrhythmics (calcium channel blockers)
+ Digoxin or other cardiac glycosides
o Infectious causes include the following:
+ Profound hypervagotonicity
+ MI - Anterior wall MI can be associated with an infranodal AV block. Complete heart block develops in slightly less than 10% of cases of acute inferior MI and often resolves within hours to a few days.
+ Cardiomyopathy, eg, Lyme carditis and acute rheumatic fever
+ Metabolic disturbances, eg, severe hyperkalemia
DIFFERENTIALS Section 4 of 11 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic
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Heart Block, Second Degree
Myocardial Infarction
Myocarditis
Sinus Bradycardia
Other Problems to be Considered:
Bradycardia with a ventricular escape
Bradycardia with a junctional escape
Accelerated junctional escape rhythm
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Lab Studies:
* Serum electrolytes levels, including potassium and magnesium, to look for metabolic imbalance, indications of renal insufficiency or failure, and particularly for severe hyperkalemia.
* A digoxin level should be obtained for patients on digoxin or in whom ingestion of digoxinlike compounds (eg, Lily of the Valley, Oleander, Foxgrove, Bufonidae toads) is suspected.
* Lyme titers should be obtained from patients who might have been exposed to Lyme disease. Remember that cardiac manifestations of Lyme disease are delayed, so Lyme-induced heart block can occur during any season.
* Myocarditis-related laboratory studies should be performed in patients suspected of having myocarditis. Such studies include Lyme titers, HIV serologies, enterovirus polymerase chain reaction (PCR), adenovirus PCR, and Chagas titers, as clinically appropriate.
* For most patients with illness serious enough to cause third-degree AV block, a complete blood count is indicated to screen for coincident problems (eg, anemia, infection) that may require ED intervention.
Imaging Studies:
* A chest radiograph should be obtained.
* If myocarditis or a pericardial effusion is a concern, an echocardiogram should be performed.
Other Tests:
* Cardiac enzymes are indicated for any patient with suspected myocardial ischemia.
* All patients must have at least one 12-lead electrocardiogram. Ideally, serial electrocardiograms should be performed.
Procedures:
* Cardiac pacing may be initially indicated or may be indicated if a patient deteriorates. Because the situation may be urgent, all patients should have transcutaneous pacing pads applied.
o For patients who are symptomatic (dyspnea, chest pain, myocardial ischemia or MI, CHF, altered mental status), the transcutaneous pacer should be activated immediately. If the external pacer fails to capture, a transvenous pacer should be inserted emergently.
o For patients who are asymptomatic, the transcutaneous pacer should be tested. If the external pacer fails to capture, urgent placement of a transvenous pacer should be considered. Indications for placement would include bradycardia that is ineligible or unresponsive to treatment with medications.
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Prehospital Care:
* All patients should be rapidly transported to the nearest available facility, applying advanced life support (ACLS) with continuous cardiac monitoring, as per local protocols.
* For any symptomatic patient, transcutaneous pacing is the treatment of choice.
* In all patients, oxygen should be administered and intravenous access should be established.
* Maneuvers that are likely to increase vagal tone (eg, Valsalva maneuvers, painful stimuli) should be avoided.
* Atropine can be administered but should be given cautiously, because it is likely to be ineffective in a wide complex QRS rhythm and can be dangerous if the patient is having a concurrent MI.
Emergency Department Care:
* Treatment in the ED should continue that already established in the prehospital setting, which includes administering oxygen, maintenance of an intravenous line, frequent monitoring of blood pressures, and continuous cardiac monitoring.
* AV nodal agents should be withheld, and anti-ischemic therapy should be started, when appropriate.
* Transcutaneous pacing pads should be applied and tested, if not already done so.
* As stated above, patients in whom capture cannot be obtained with a transcutaneous pacemaker need urgent placement of a transvenous pacemaker, even if the patient is asymptomatic.
* Hemodynamically stable patients in whom transcutaneous pacing can be successfully performed can go to a telemetry or intensive care unit at the discretion of the treating cardiologist.
* Hemodynamically unstable patients may be treated with atropine. However, if the rhythm is a wide complex escape rhythm, atropine is likely to be unsuccessful. In addition, caution should be taken when administering atropine to a patient with a suspected acute MI, as the resulting vagolysis leads to unopposed sympathetic stimulation, which can cause increased ventricular irritability and potentially dangerous ventricular arrhythmias. Similarly, isoproterenol may be attempted to accelerate a ventricular escape rhythm with a low probability for efficacy.
* Hemodynamically unstable patients for whom timely cardiologic consultation is unavailable should undergo temporary transvenous pacemaker insertion in the ED by the ED physician.
Consultations:
* Cardiologic consultation is indicated for all patients with third-degree AV block. The consultation is urgent in patients with concomitant acute MI, active myocardial ischemia, CHF, wide complex escape rhythm, or symptoms of hypoperfusion because patients in this group may require early placement of a permanent pacemaker or assistance may be needed if difficulty is encountered obtaining capture from an external or transvenous pacer.
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MEDICATION Section 7 of 11 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic
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The goal of therapy is to improve conduction through the AV node by reducing vagal tone via atropine-induced receptor blockade. However, this method is unlikely to be successful in wide-complex bradyarrhythmias, where the level of the block is below the level of the AV node, and this method should be given with caution in patients suspected of experiencing an MI. In addition, atropine is ineffective in patients with a deinnervated heart (eg, those patients who are post cardiac transplant).
Cases where complete heart block results from calcium channel blocker should be managed in the standard fashion for other etiologies of third-degree block (eg, pacemaker) but should also receive appropriate treatment for calcium channel blockers. This therapy includes the administration of IV fluids, calcium, glucagons, vasopressors, and high-dose insulin (hyperinsulinemic euglycemia [HIE] therapy). Further explanations of calcium channel blocker overdose can be found in the article on Toxicity, Calcium Channel Blocker. Overdoses on beta-blockers are managed a similar fashion as calcium channel blockers (see Toxicity, Beta-blocker, although HIE therapy for beta-blocker overdoses is less well established.
Drug Category: Anticholinergic agents -- These agents improve conduction through the AV node by reducing vagal tone via muscarinic receptor blockade.
Drug Name
Atropine (Atropair) -- Enhances sinus node automaticity. In addition, blocks effects of acetylcholine at AV node, thereby decreasing the refractory time and speeding conduction through AV node. At inefficient doses, atropine can have paradoxical effects, further slowing heart rate.
Adult Dose0.5 mg rapid IV push; for patients in PEA arrest, 1 mg can be administered; maximal IV dose is 0.04 mg/kg; atropine can also be administered via endotracheal tube, in which dose should be increased by 2-3 fold; when administered via endotracheal tube, absorption is less predictable when compared with IV administration
Pediatric Dose0.02 mg/kg IV push, with minimum of 0.1 mg; single dose should not exceed 0.5 mg in children, or 1 mg in adolescents; maximal total IV dose is 0.04 mg/kg; as stated in adult dosing, atropine can be administered via endotracheal tube
ContraindicationsDocumented hypersensitivity to atropine; documented hypersensitivity to belladonna alkaloids or related products; concomitant acute myocardial infarction/ischemia; thyrotoxicosis; narrow-angle glaucoma; congestive heart failure; tachycardia
Interactions Coadministration with other anticholinergics have additive effects; pharmacologic effects of atenolol and digoxin may increase with atropine; antipsychotic effects of phenothiazines may decrease with this medication; tricyclic antidepressants with anticholinergic activity may increase effects of atropine
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsCaution in Down syndrome and/or children with brain damage to prevent hyperreactive response; caution also in coronary heart disease, tachycardia, congestive heart failure, cardiac arrhythmias, hypertension, peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in prostatic hypertrophy, prostatism can have dysuria and may require catheterization
Drug Category: Catecholamines -- These agents improve hemodynamics by acting on the beta-adrenergic receptors to increase the heart rate and contractility, and by acting on the alpha-adrenergic receptors to increase the systemic vascular resistance.
Drug Name
Dopamine (Intropin) -- Naturally occurring endogenous catecholamine that stimulates beta1-and alpha1-adrenergic and dopaminergic receptors in a dose-dependent fashion; stimulates release of norepinephrine.
In low doses (2-5 mcg/kg/min), acts on dopaminergic receptors in renal and splanchnic vascular beds, causing vasodilatation in these beds. In midrange doses (5-15 mcg/kg/min), acts on beta-adrenergic receptors to increase heart rate and contractility. In high doses (15-20 mcg/kg/min), acts on alpha-adrenergic receptors to increase systemic vascular resistance and raise BP.
Adult Dose5-20 mcg/kg/min; at doses of 2-5 mcg/kg/min, dopamine acts on dopaminergic receptors in renal and splanchnic vascular beds, thereby causing vasodilation in these areas; in mid range doses (5-15 mcg/kg/min), dopamine acts preferentially on beta-adrenergic receptors to increase heart rate and contractility; at high doses (15-20 mcg/kg/min), dopamine acts on alpha-adrenergic receptors to increase systemic vascular resistance and raise the blood pressure; medication should be given via continuous IV infusion; ideally, should be administered via a central venous line
Pediatric DoseAdminister as in adults
ContraindicationsDocumented sensitivity to dopamine related products; pheochromocytoma; ventricular fibrillation
InteractionsMAO inhibitors may prolong effects of dopamine; beta-adrenergic blockers may antagonize peripheral vasoconstriction caused by high doses of dopamine; butyrophenones (eg, haloperidol) and phenothiazines can suppress dopaminergic renal and mesenteric vasodilation induced with low-dose dopamine infusion; concurrent administration of diuretic agents with low-dose dopamine may produce additive effects on urine flow; hypotension and bradycardia may occur with phenytoin; dopamine may decrease effects of phenytoin
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsClosely monitor urine flow, cardiac output, pulmonary wedge pressure, and blood pressure during the infusion; prior to infusion, correct hypovolemia with either whole blood or plasma, as indicated; monitoring central venous pressure or left ventricular filling pressure may be helpful in detecting and treating hypovolemia; patients that have received MAO inhibitors within 2-3 wk prior to administration of dopamine, should receive initial doses no greater than 1/10 initial dose; ventricular arrhythmias and hypertension may occur when administering dopamine to patients receiving cyclopropane or halogenated hydrocarbon anesthetics
Drug Name
Norepinephrine (Levophed) -- Naturally occurring catecholamine with potent alpha-receptor and mild beta-receptor activity. Stimulates beta1- and alpha-adrenergic receptors, resulting in increased cardiac muscle contractility, heart rate, and vasoconstriction. Increases blood pressure and afterload. Increased afterload may result in decreased cardiac output, increased myocardial oxygen demand, and cardiac ischemia. Generally reserved for use in patients with severe hypotension (eg, systolic blood pressure <70 mm Hg) or hypotension unresponsive to other medication.
Adult Dose2-12 mcg/min IV infusion; start 0.5-1 mcg/min and titrate upwards; refractory shock may require up to 30 mcg/min; drug should ideally be administered via central venous line
Pediatric Dose0.1-2 mcg/kg/min IV; start 0.05-0.1 mcg/kg/min; 2 mcg/kg/min maximum dose; should ideally be administered via central venous line
ContraindicationsDocumented hypersensitivity; peripheral or mesenteric vascular thrombosis because ischemia may be increased and the area of the infarct extended; hypercapnia, volume depletion, caution if sulfite allergy
InteractionsEffects increase when administered concurrently with tricyclic antidepressants, MAO inhibitors, antihistamines, guanethidine, methyldopa, ergot alkaloids; atropine may block reflex tachycardia caused by norepinephrine and enhances pressor response
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsCorrect blood-volume depletion, if possible, before giving norepinephrine therapy; extravasation may cause severe tissue necrosis and, thus, should be administered into a large vein; caution in occlusive vascular disease
Drug Category: Antidotes -- These agents are used in select cases for patients with third-degree block secondary to digoxin toxicity. They should receive digoxin-specific antidote.
Drug Name
Digoxin immune Fab (Digibind) -- Immunoglobulin fragment with a specific and high affinity for both digoxin and digitoxin molecules. Removes digoxin or digitoxin molecules from tissue-binding sites.
Each vial of Digibind contains 40 mg of purified digoxin-specific antibody fragments, which will bind approximately 0.6 mg of digoxin or digitoxin.
The dose of antibody depends on total body load (TBL) of digoxin; estimates of TBL can be made in 3 ways:
(1) Estimate the quantity of digoxin ingested in the acute ingestion and assume 80% bioavailability (x mg ingested X 0.8 = TBL)
(2) Obtain a serum digoxin concentration and, using a pharmacokinetics formula, incorporate the Vd of digoxin and the patient's body weight in kg (TBL = digoxin serum level [ng/mL] X 6 L/kg X body weight in kg)
(3) Use an empiric dose based on average requirements for an acute or chronic overdose in an adult or child
If the quantity of ingestion cannot be estimated reliably, it may be administered empirically (safest to use the largest calculated estimate); alternatively, be prepared to increase dosing if resolution is incomplete.
Adult DoseNumber of vials = Amount ingested (in mg) X 0.8/0.5
For example, for a patient who ingests 10 mg of digoxin, 16 vials should be administered
For a patient who ingests digitoxin instead of digoxin, substitute "1" for "0.8" in above formula, as digitoxin has higher bioavailability than digoxin
If digoxin concentration is known, the number of vials to administer can be calculated by the following formula:
Number of vials = Concentration (ng/mL) X weight (in kg)/100
For example, for a 100-kg male with digoxin concentration of 10 ng/mL, administer 10 vials of Digibind
If amount ingested is not known, then 10 vials can be empirically administered
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity
InteractionsNone reported
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsCaution in cardiac and renal failure; hypokalemia may occur following reversal of digoxin intoxication
Drug Category: Sympathomimetic agents -- These agents act on beta-adrenergic receptors and increase heart rate and contractility.
Drug Name
Isoproterenol (Isuprel) -- Synthetic sympathomimetic acting directly on beta-receptors. Should only be used as a temporary measure until more definitive and less risky treatments (eg, transvenous pacing) can be arranged. Cardiac ischemia or high cardiac risk profile suggesting possible coronary artery disease is contraindication for use. Telemetry monitoring should always accompany use of this agent because of risks of proarrhythmia.
Adult Dose0.5-2 mcg/min IV infusion, titrate prn to desired effect (emergent use range 2-10 mcg/min)
Pediatric Dose0.5 mcg/min IV infusion, titrate prn to desired effect
ContraindicationsDocumented hypersensitivity; tachyarrhythmias, tachycardia or heart block caused by digitalis intoxication, ventricular arrhythmias which require inotropic therapy, and angina pectoris
InteractionsBretylium increases action of vasopressors on adrenergic receptors, which may in turn result in arrhythmias; guanethidine may increase effect of direct-acting vasopressors, possibly resulting in severe hypertension; tricyclic antidepressants may potentiate pressor response of direct-acting vasopressors
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsBy increasing myocardial oxygen requirements while decreasing effective coronary perfusion, isoproterenol may have a deleterious effect on the injured or failing heart; in some patients, presumably with organic disease of the AV node and its branches, isoproterenol may paradoxically worsen heart blocks or precipitate Adams-Stokes attacks; caution in coronary artery disease, coronary insufficiency, diabetes or hyperthyroidism, and sensitivity to sympathomimetic amines; if heart rate exceeds 110 beats/min, may be advisable to decrease infusion rate or temporarily discontinue infusion
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Further Inpatient Care:
* The admitting cardiologist will determine the need for and timing of permanent pacemaker implantation.
* All patients with third-degree heart block need to be admitted to either a telemetry floor (if hemodynamically stable and transcutaneous pacing achieves capture) or an intensive care unit. The decision on telemetry versus intensive care should be made in conjunction with the cardiologist.
* Any patient who is hemodynamically unstable, has persistent complete heart block, has electrolyte abnormalities, or who is in complete heart block as a result of an overdose or myocardial infarction should be admitted to the intensive care unit.
Transfer:
* Patients may be transferred to a higher level of care if the hospital does not have intensive care capabilities or if appropriate consultation services (eg, cardiology) are not available.
Deterrence/Prevention:
* Patients with renal insufficiency or failure, dehydration, and certain electrolyte disturbances are predisposed to develop digoxin toxicity. Careful monitoring of electrolytes, drug levels, and renal function is essential in patients on chronic digoxin therapy.
* Patients on multiple nodal agents (eg, beta-blockers and calcium channel blockers) are at an increased risk to develop complete heart block; the more nodal blockade that occurs, the higher the chance of developing complete heart block.
Complications:
* Complications from complete heart block include cardiovascular collapse and death.
* Ventricular arrhythmias from atropine or catecholamines may occur.
* Common complications include those related to line and/or transvenous pacemaker placement. These complications include arterial injury, hemothorax, pneumothorax, or cardiac tamponade.
Patient Education:
* Patients should be educated about possible drug interactions when starting any new medication.
* Patients who are on digoxin should be educated about possible early symptoms of digoxin toxicity.
MISCELLANEOUS Section 9 of 11 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic
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Medical/Legal Pitfalls:
* Failure to initiate temporary transcutaneous or transvenous pacing in a timely fashion
* Failure to interpret cardiac dysrhythmia correctly
* Failure to diagnose and treat underlying etiology of the third-degree block
* Failure to ensure the patient is admitted to an appropriate level of care
* Failure to seek, identify, or treat reversible causes of third-degree AV block, such as hyperkalemia or digoxin toxicity
Answers: