Arrest rhythms

Cardiac arrest is a medical emergency. Prompt intervention can save lives. There are four principle arrest rhythms  

Of the four only VF and VT are rhythms that can be treated by deflbrillation (passing an electrical current through the heart to reinitialise it M). Deflbrillation should only be attempted by a trained professional. The survival outcomes of Cardiac arrest tend to be more favourable if the rhythm is VT or VF as oppose to PEA or asystole. 

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Keywords Arrhythmias Hutter Fibrillation Arrest rhythms Reentry Ectopic s... 

Lethal Arrhythmias. Arrhythmias are a second significant source of cardiovascular problems. An arrhythmia is an abnormal or irregular heart rhythm. Bradyarrhythmias result in heart rates that are too slow tachyarrhythmias cause abnormally fast rates. A bradyarrhythmia can be debiUtating, causing a person to be short of breath, unable to climb stairs, black out, or even to go into cardiac arrest. Tachyarrhythmias can be un settling and painful at best, life-threatening at worst. 

Rapid diagnosis of cardiopulmonary arrest is vital to the success of CPR. Patients must receive early intervention to prevent cardiac rhythms from degenerating into less treatable arrhythmias. 

Cardiopulmonary arrest is diagnosed initially by observation of clinical manifestations consistent with cardiac arrest. The diagnosis is confirmed by evaluating vital signs, especially heart rate and respirations. Electrocardiography (ECG) is useful for determining the cardiac rhythm, which in turn determines drug therapy. 

Hypothermia should be implemented in unconscious adult patients with ROSC after out-of-hospital cardiac arrest when the initial rhythm was VF. These patients should be cooled to 32°C (89.6°F) to 34°C (93.2°F) for 12-24 hours. 

Hypothermia can protect from cerebral injury by suppressing chemical reactions that occur after restoration of blood flow following cardiac arrest. Based on the results of two clinical trials, unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32°C (89.6°F) to 34°C (93.2°F) for 12 to 24 hours when the initial rhythm is VF. Cooling may also benefit other rhythms or in-hospital cardiac arrest in adults there is insufficient evidence to recommend therapeutic hypothermia in children. 

The Petco2 falls rapidly over the course of a few breaths. With hyperventilation, the fall would be slower. Any condition that acutely reduces cardiac output may be the cause, including cardiac arrest, pulmonary embolism or acute rhythm disturbances. If the Pco2 falls instantly to zero, then the cause is disconnection, auto-calibration or equipment error. 

Injection - To relieve respiratory distress in bronchial asthma or during acute asthma attacks and for reversible bronchospasm in patients with chronic bronchitis, emphysema, and other obstructive pulmonary diseases severe acute anaphylactic reactions, including anaphylactic shock and cardiac arrest to restore cardiac rhythm. 

Epinephrine (adrenaline) should be given every 3-5 min whilst the patient remains in cardiac arrest, immediately if the patient has an initially non-shockable rhythm (asystole or pulseless electrical activity) but delayed until before the third shock for shockable rhythms. Continued administration of epinephrine (adrenaline), cardiac massage, and DC shock may be required for several cycles. 

Unlabeled Uses Control of hemodynamicallystableventriculartachycardia, control of rapid ventricular rate due to accessory pathway conduction in preexcited atrial arrhythmias, conversion of atrial fibrillation to normal sinus rhythm, in cardiac arrest with persistent ventricular tachycardia or ventricular fibrillation, paroxysmal supraventricular tachycardia, polymorphic ventricular tachycardia or wide complex tachycardia of uncertain origin, prevention of postoperative atrial fibrillation... 

Following the acute phase, most infected people enter into a chronic phase. The chronic phase of the infection is considered as an intermediate phase by some authors because the infection may remain silent for decades or even for life. The chronic phase is characterized by the presence of T. cruzi in the patient s organs like the heart and intestine. The symptoms of the chronic phase are cardiac complications (e.g., cardiomyopathy, heart failure, altered heart rate or rhythm, and cardiac arrest) and digestive complications, especially megaesophagus and megacolon. 

Amyl nitrite, as with other inhalants, have the potential to cause sudden sniffing death (SSD) syndrome. The condition is brought on by unexpected disturbances in the heart s rhythm, causing heart failure and death. SSD syndrome can result when a user deeply inhales a chemical for its intoxicating effect. This causes a decrease in available oxygen to the body. If the user becomes startled or engages in sudden physical activity, the flow of adrenaline increases from the brain to the heart, inducing cardiac arrest. Death occurs within minutes. 

Inhalants make the heart extra sensitive to adrenaline, a hormone secreted in reaction to stresses. Adrenaline can trigger an irregular heartbeat, which disrupts the body s ability to ship oxygen-rich blood to the brain. Lastly, if an abuser is startled or sent into a fight-or-flight reaction, the body will release extra adrenaline. The extra-sensitivity can disturb the heart rhythm to the point of fatal cardiac arrest. 

Because digitoxin has a very low therapeutic index, toxicity occurs rather routinely and can be fatal patients must be monitored closely. Moderate overdoses can be picked up by GI or CNS complaints however, more serious toxicity on cardiac rhythm is more difficult to distinguish from the effects of heart disease. Digitalis antibody fragments are available for serious toxicity, i.e., when cardiac arrest is imminent. The fragments bind the drug and are excreted by the kidneys. 

Cardiac ischaemia may trigger abnormal electrical activity, causing fibrillation. Defibrillators deliver a large DC shock across the heart (cardioversion), to arrest abnormal activity and allow re-establishment of sinus rhythm. 

Two reviews of the cardiac effects of psychotropic drugs briefly mentioned lithium and dysrhythmias, with a focus on sinus node dysfunction (122,123), reports of which, as manifested by bradycardia, sinoatrial block, and sinus arrest, continue to accumulate in association with both toxic (124) and therapeutic (125,126) serum lithium concentrations. The rhythm disturbance normalized in some cases when lithium was stopped (124,126), persisted despite discontinuation... 

A 25-year-old man had a cardiac arrest after taking one knot or sealed bag of crack cocaine (2.5 g) and was resuscitated. His arterial blood pH was 6.92 and an electrocardiogram showed sinus rhythm, QRS axis 300°, and terminal 40 msec of the QRS axis 285°. After an infusion of sodium bicarbonate, his blood pH was 7.30, his QRS axis 15°, and the terminal 40 msec QRS axis 30°. He passed the bag of cocaine rectally within 12 hours of admission. 

In 72 patients with paroxysmal atrial fibrillation randomized to either amiodarone 30 mg/kg or placebo, those who received amiodarone converted to sinus rhythm more often than those given placebo (22). The respective conversion rates were about 50 and 20% at 8 hours, and 87 and 35% after 24 hours. The time to conversion in patients who converted did not differ. One patient developed slow atrial fibrillation (35/minute) with a blood pressure of 75/ 55 mmHg. Three other patients who received amiodarone had diarrhea and one had nausea. In the control group two patients had headache, one had diarrhea, one had nausea, and two had episodes of sinus arrest associated with syncope during conversion to sinus rhythm the last of these was thought to have sick sinus syndrome. 

Figure 8.34 Patient of 68 years of age who suffered sudden death 10 days after an acute infarction. A progressive depression of the automatism (with the appearance of a slow escape rhythm) is shown in the Holter ECG recording, until cardiac arrest occurs, due to an electromechanical dissociation caused by cardiac rupture.

The progressive depression of sinus node automatism and the occurrence of a progressively slower escape rhythm that leads to cardiac arrest (Figure 8.34) are usually detected in patients with... 

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