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Adenosine; Digoxin; Magnesium sulfate; Work by other or unknown mechanisms Contraindicated in ventricular arrhythmias; Adenosine is used to treat supraventricular tachycardias, especially in heart failure and atrial fibrillation [9] Magnesium sulfate is used to treat torsades de pointes, a type of arrhythmia
Cardiogenic shock is most commonly precipitated by a heart attack. [4] Treatment of cardiogenic shock depends on the cause with the initial goals to improve blood flow to the body. If cardiogenic shock is due to a heart attack, attempts to open the heart's arteries may help. Certain medications, such as dobutamine and milrinone, improve the ...
Both doctors say that signs and symptoms of valve damage can vary, but the main ones to be aware of are shortness of breath (particularly during exercise or any form of exertion) and chest pain or ...
Vagal maneuvers, such as the Valsalva maneuver, are often used as the initial treatment. [4] If not effective and the person has a normal blood pressure the medication adenosine may be tried. [4] If adenosine is not effective a calcium channel blocker or beta blocker may be used. [4] Otherwise synchronized cardioversion is the treatment. [4]
All these ECG-based technologies also enable the distinction between AVNRT and other abnormal fast heart rhythms such as atrial fibrillation, atrial flutter, sinus tachycardia, ventricular tachycardia and tachyarrhythmias related to Wolff-Parkinson-White syndrome, all of which may have symptoms that are similar to AVNRT. [citation needed]
A normal resting heart rate is 60 to 100 beats per minute. A resting heart rate of more than 100 beats per minute is defined as a tachycardia. During an episode of SVT, the heart beats about 150 to 220 times per minute. [9] Specific treatment depends on the type of SVT [5] and can include medications, medical procedures, or surgery. [5]
Calcium channel blocker toxicity is the taking of too much of the medications known as calcium channel blockers (CCBs), either by accident or on purpose. [3] This often causes a slow heart rate and low blood pressure. [1] This can progress to the heart stopping altogether. [2]
The mechanisms of sympathomimetic drugs can be direct-acting (direct interaction between drug and receptor), such as α-adrenergic agonists, β-adrenergic agonists, and dopaminergic agonists; or indirect-acting (interaction not between drug and receptor), such as MAOIs, COMT inhibitors, release stimulants, and reuptake inhibitors that increase the levels of endogenous catecholamines.
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