STUDY - Technical - New Dacian's Medicine
Cardiovascular
Collapse, Cardiac Arrest and Sudden Cardiac Death (3)
Translation Draft
So, as I announced, it's the turn of the treatment. The care of the collapsing patient comprises 4 stages: 1. initial intervention and basic life support; 2. advanced life support; 3. post-resuscitation care and 4. long-term care. Initial intervention and basic life support can be provided by doctors, nurses, paramedical staff and persons trained in this regard. The level of competence required increases as the patient moves to the stages of advanced life support, post-resuscitation care and long-term care.
Let's elaborate a little, addressing the initial intervention and the basic vital support! The initial intervention will confirm whether the collapse is really due to cardiac arrest. Observation of respiratory movements, skin coloration and the presence or absence of carotid or femoral pulse will immediately indicate whether life-threatening cardiac arrest has occurred.
Once a cardiac arrest is suspected or confirmed, contacting an emergency assistance system becomes a priority. Agonizing breathing may persist for a short time after the onset of cardiac arrest, but it is important to detect severe stridor with persistent pulse, a characteristic sign for foreign body aspiration or food. If suspected, the promptly executed Heimlich maneuver can remove the obstructive body.
A precordial blow or a "punch", firmly applied with the fist at the junction of the middle and lower thirds of the sternum can sometimes eliminate ventricular tachycardia (TV) or ventricular fibrillation (FV), but there is a risk of TV turning into FV. Therefore, it was recommended to use precordial blow as an advanced life support technique when monitoring and defibrillation are available.
This conservative recommendation to apply the technique remains controversial. The third manoeuvre during the initial response is the release of the airways. The head will be pushed back and the chin raised so that the oropharynx can be explored for cleaning the airways. Remove foreign bodies or false teeth, and the Heimlich maneuver can be done if there is a reason to suspect the presence of a foreign body in the oropharynx.
If cardiac arrest is suspected, a second precordial blow will be applied after the airways have been disobstructed. The basic life support, better known as cardiorespiratory resuscitation (CRC), is set up to maintain organ infusion until definitive intervention can be performed. The elements of the RCR are the establishment and maintenance of the ventilation of the lungs and compression of the chest.
Mouth-to-mouth breathing can be used if specific life-saving equipment is not immediately available (e.g. oropharyngeal artificial paths, esophageal shutter, Ambu oxygen mask). Conventional fan techniques within the RCR require instilling the lungs 10-12 times per minute, i.e. one instillation after every five chest compressions (compression is done by applying the palm of one hand to the lower sternum, with the bridge of the palm of the other hand on the dorsal face of the first; the sternum will be pressed with arms outstretched, at a rate of about 80-100 per minute , the force being sufficient to compress the heart by 3-5 cm; relaxation after pressing is sudden), when resuscitation is performed by two people and two successive instillations after 15 chest compressions, when a single person provides both ventilation and chest compression. Compression of the thorax is carried out because it is assumed that by compressing the heart it maintains its pump function by filling and sequentially emptying the atria and ventricles, with competent valves to ensure the direction of the flow.
Advanced life support is designed to ensure adequate ventilation, control of cardiac arrhythmias, stabilisation of hemodynamic status (blood pressure and cardiac flow) and restoration of adequate organ infusion. Therapeutic maneuvers used to achieve these objectives include: 1. endotracheal probe intubation, 2. defibrillation-cardioversion and/ or electrostimulation and 3. intravenous line.
Oxygen ventilation (or air in the room, if oxygen is not immediately available) can promptly eliminate hypoxemia and acidosis. The speed with which defibrillation/cardioversion is achieved is an important element for the success of resuscitation. Where possible, immediate defibrillation should prevent intubation and insertion of an intravenous line, with the RCR being performed while the defibrillator is loading. As soon as the diagnosis of TV or VF is confirmed, a shock of 200 J (joulli) should be administered. Additional shocks at higher energies, up to a maximum of 360 J, apply only if the first shock fails to convert TV or FV to sinus rhythm.
Adrenaline, 1 mg intravenously, is used after the failure of defibrillation, then a new defibrillation is attempted. The dose of adrenaline can be repeated at an interval of 3-5 minutes. If the patient is not fully conscious after conversion, or if two or three attempts fail, intubation, ventilation and rapid analysis of arterial gases will be performed. The administration of intravenous NaHCO3, which was used in large quantities in the past, is no longer considered routinely necessary and has been shown to be dangerous in large quantities.
However, the patient with persistent acidosis after successful defibrillation and intubation should receive 1mEq/ kg of NaHCO3 initially and another 50% of this dose repeated every 10-15 minutes. After several initially unsuccessful defibrillations or when electrical instability persists, a dose of 1mg/ kg of the lidocaine body is administered intravenously and the dose is repeated after 2 minutes in those patients who have persistent ventricular arrhythmias or remain in The VF.
This is followed by continuous infusion at a rate of 1-4 mg/ min. If lidocaine does not work, intravenous procainamide (loading dose of 100 mg/ 5 min up to the total dose of 500-800 mg, followed by continuous infusion of 2-5 mg/ min) or bretillium tosilate (loading dose of 5-10 mg/ kg in 5 minutes, the maintenance dose being 0.5-2 mg/min) may be attempted. Intravenous calcium gluconate is no longer considered safe or necessary in routine administration. It is only used in patients whose acute hypopotasemia is known to be a trigger for resistant VF in the presence of known hypocalcemia or in patients who have received toxic doses of calcium channel antagonists.
Secondary cardiac arrest of bradyarithmias or asytolia is treated differently. Once it is known that this rhythm is present, no external shock is necessary. The patient is promptly intubated, the RCR is continued and the control of hypoxemia and acidosis is attempted. Adrenaline and/ or atropine are given intravenously or intracardiacally. External electrostimulation devices are now available to try to establish regular rhythm, but the prognosis is generally unfavorable in these forms of cardiac arrest.
The only exception is bradyarrhythmic/asistolic cardiac arrest secondary to airway obstruction. This form of cardiac arrest can respond promptly to the removal of foreign bodies by the Heimlich maneuver or, to those hospitalized, by intubation and suction of secretions from the airways.
Post-resuscitation care depends on the clinical context of cardiac arrest. Primary FV in acute myocardial infarction (MI) generally responds very well to vital support techniques and is easily controlled after the initial event. Patients are kept on a lidocaine infusion at 2-4 mg/ min for 24-72 hours after the incident. In the intra-hospital environment, assisted breathing is usually only necessary for a short time, and hemodynamics stabilizes promptly after defibrillation or cardioversion.
In secondary VF in acute IM (those events where hemodynamic abnormalities predispose to potentially fatal arrhythmias), resuscitation efforts succeed less often and in those patients who are successfully resuscitated, the rate of recurrence is increased. The clinical picture is dominated by hemodynamic instability. In fact, evolution is determined more by the ability to control hemodynamic dysfunction than by electrophysiological abnormalities.
Bradiarithmia, asystolia and electromechanical dissociation are common side events in hemodynamically unstable patients and respond less to interventions. The prognosis after intrahospital cardiac arrest associated with extracardiac diseases is also unfavorable in the few patients successfully resuscitated, the post-resuscitation evolution being determined by the nature of the underlying disease.
Patients with cancer, kidney failure, acute central nervous system diseases and uncontrolled infections as a group have a 10% survival rate after an intra-hospital cardiac arrest. Some major exceptions are patients with transient airway obstruction, electrolyte imbalances, treatment with proarrhythmic drugs and severe metabolic abnormalities, many of them having excellent chances of survival if they can be promptly resuscitated and if vital functions can be maintained while transient abnormalities are corrected.
In the case of long-term maintenance treatment after survival in out-of-hospital cardiac arrest, patients who do not suffer irreversible damage to the central nervous system and achieve hemodynamic stability should benefit from extensive diagnosis and specific tests to guide long-term treatment.
This aggressive approach is based on the fact that statistics show that survival after extra-hospital cardiac arrest was followed by 30% of cardiac arrest recurrences at 1 year, 45% at 2 years and the total mortality rate was almost 60% at 2 years. Comparisons over time suggest that this rate may be significantly lower by new types of interventions, but the degree of this decrease is unknown due to the lack of simultaneous controlled studies on interventions.
For those patients in whom an acute transmural IM is the cause of cardiac arrest, the care is the same as for any other patient suffering from cardiac arrest during the acute phase of a proven IM. However, extensive diagnostic studies are done for most categories of patients to determine etiology, functional deterioration and electrophysiological instability, as guidance elements in the new treatment.
In general, patients who have suffered an extra-hospital cardiac arrest due to chronic ischemic heart disease without acute IM are evaluated to determine whether transient ischemia or chronic electrophysiological instability were the most likely causes of cardiac arrest. If there is any reason to suspect an ischemic mechanism, coronary revascularization or drugs, most often beta-blockers, are used to reduce ischemia. Electrophysiological instability is most correctly detected using programmed electrical stimulation to determine whether sustained TV or FV can be induced.
If sustained TV or FV can be induced, this information is a reference line for assessing the effectiveness of medicines in preventing this inductibility, or it can determine whether map-guided antiarrhythmic surgery is more appropriate, or whether the best solution is an implantable defibrillator/cardioconverter (DCI). Using this technique in patients with ejection fraction of 30% or more, the rate of cardiac arrest recurrence decreases to less than 10% in the first year, when the rate of inductibility is suppressed by medication.
The prognosis is not as good for patients with ejection fraction below 30%, but may be better than the apparentnatural history of survival after cardiac arrest. For patients in whom appropriate drug therapy cannot be identified by this technique, empirical treatment with amiodarone, insertion of an implantable cardioconverter/defibrillator or antiarrhythmic surgery (such as coronary bypass, aneurysmectomy, cryolation) may be chosen.
The initial success of the operation, defined by survival after intervention and a non-inducible condition without drug therapy, is greater than 90% when selecting patients who can be mapping (mapping) in the operating room. However, only a small number of patients meet this criterion. In addition, TV/FV cannot be induced in a large number of cardiac arrest survivors (30-50%), and inducible arrhythmias can be suppressed by drugs in less than 20-30% of those in which arrhythmia could be induced.
Due to these limitations of drug therapy and surgical methods, DCI treatment has become the most widely used strategy for cardiac arrest survivors. DCI have a very good success rate in detecting and converting life-threatening arrhythmias, but the improvement in long-term evolution is not yet well documented. The ESVEM study suggested that ambulatory suppression of monitoring arrhythmias is equivalent to electrophysiological guided, predictive testing for long-term evolution. This conclusion has generated a controversy that remains to be resolved.
I'll see you on June 10th when I start gastrointestinal disorders...
So, as I announced, it's the turn of the treatment. The care of the collapsing patient comprises 4 stages: 1. initial intervention and basic life support; 2. advanced life support; 3. post-resuscitation care and 4. long-term care. Initial intervention and basic life support can be provided by doctors, nurses, paramedical staff and persons trained in this regard. The level of competence required increases as the patient moves to the stages of advanced life support, post-resuscitation care and long-term care.
Let's elaborate a little, addressing the initial intervention and the basic vital support! The initial intervention will confirm whether the collapse is really due to cardiac arrest. Observation of respiratory movements, skin coloration and the presence or absence of carotid or femoral pulse will immediately indicate whether life-threatening cardiac arrest has occurred.
Once a cardiac arrest is suspected or confirmed, contacting an emergency assistance system becomes a priority. Agonizing breathing may persist for a short time after the onset of cardiac arrest, but it is important to detect severe stridor with persistent pulse, a characteristic sign for foreign body aspiration or food. If suspected, the promptly executed Heimlich maneuver can remove the obstructive body.
A precordial blow or a "punch", firmly applied with the fist at the junction of the middle and lower thirds of the sternum can sometimes eliminate ventricular tachycardia (TV) or ventricular fibrillation (FV), but there is a risk of TV turning into FV. Therefore, it was recommended to use precordial blow as an advanced life support technique when monitoring and defibrillation are available.
This conservative recommendation to apply the technique remains controversial. The third manoeuvre during the initial response is the release of the airways. The head will be pushed back and the chin raised so that the oropharynx can be explored for cleaning the airways. Remove foreign bodies or false teeth, and the Heimlich maneuver can be done if there is a reason to suspect the presence of a foreign body in the oropharynx.
If cardiac arrest is suspected, a second precordial blow will be applied after the airways have been disobstructed. The basic life support, better known as cardiorespiratory resuscitation (CRC), is set up to maintain organ infusion until definitive intervention can be performed. The elements of the RCR are the establishment and maintenance of the ventilation of the lungs and compression of the chest.
Mouth-to-mouth breathing can be used if specific life-saving equipment is not immediately available (e.g. oropharyngeal artificial paths, esophageal shutter, Ambu oxygen mask). Conventional fan techniques within the RCR require instilling the lungs 10-12 times per minute, i.e. one instillation after every five chest compressions (compression is done by applying the palm of one hand to the lower sternum, with the bridge of the palm of the other hand on the dorsal face of the first; the sternum will be pressed with arms outstretched, at a rate of about 80-100 per minute , the force being sufficient to compress the heart by 3-5 cm; relaxation after pressing is sudden), when resuscitation is performed by two people and two successive instillations after 15 chest compressions, when a single person provides both ventilation and chest compression. Compression of the thorax is carried out because it is assumed that by compressing the heart it maintains its pump function by filling and sequentially emptying the atria and ventricles, with competent valves to ensure the direction of the flow.
Advanced life support is designed to ensure adequate ventilation, control of cardiac arrhythmias, stabilisation of hemodynamic status (blood pressure and cardiac flow) and restoration of adequate organ infusion. Therapeutic maneuvers used to achieve these objectives include: 1. endotracheal probe intubation, 2. defibrillation-cardioversion and/ or electrostimulation and 3. intravenous line.
Oxygen ventilation (or air in the room, if oxygen is not immediately available) can promptly eliminate hypoxemia and acidosis. The speed with which defibrillation/cardioversion is achieved is an important element for the success of resuscitation. Where possible, immediate defibrillation should prevent intubation and insertion of an intravenous line, with the RCR being performed while the defibrillator is loading. As soon as the diagnosis of TV or VF is confirmed, a shock of 200 J (joulli) should be administered. Additional shocks at higher energies, up to a maximum of 360 J, apply only if the first shock fails to convert TV or FV to sinus rhythm.
Adrenaline, 1 mg intravenously, is used after the failure of defibrillation, then a new defibrillation is attempted. The dose of adrenaline can be repeated at an interval of 3-5 minutes. If the patient is not fully conscious after conversion, or if two or three attempts fail, intubation, ventilation and rapid analysis of arterial gases will be performed. The administration of intravenous NaHCO3, which was used in large quantities in the past, is no longer considered routinely necessary and has been shown to be dangerous in large quantities.
However, the patient with persistent acidosis after successful defibrillation and intubation should receive 1mEq/ kg of NaHCO3 initially and another 50% of this dose repeated every 10-15 minutes. After several initially unsuccessful defibrillations or when electrical instability persists, a dose of 1mg/ kg of the lidocaine body is administered intravenously and the dose is repeated after 2 minutes in those patients who have persistent ventricular arrhythmias or remain in The VF.
This is followed by continuous infusion at a rate of 1-4 mg/ min. If lidocaine does not work, intravenous procainamide (loading dose of 100 mg/ 5 min up to the total dose of 500-800 mg, followed by continuous infusion of 2-5 mg/ min) or bretillium tosilate (loading dose of 5-10 mg/ kg in 5 minutes, the maintenance dose being 0.5-2 mg/min) may be attempted. Intravenous calcium gluconate is no longer considered safe or necessary in routine administration. It is only used in patients whose acute hypopotasemia is known to be a trigger for resistant VF in the presence of known hypocalcemia or in patients who have received toxic doses of calcium channel antagonists.
Secondary cardiac arrest of bradyarithmias or asytolia is treated differently. Once it is known that this rhythm is present, no external shock is necessary. The patient is promptly intubated, the RCR is continued and the control of hypoxemia and acidosis is attempted. Adrenaline and/ or atropine are given intravenously or intracardiacally. External electrostimulation devices are now available to try to establish regular rhythm, but the prognosis is generally unfavorable in these forms of cardiac arrest.
The only exception is bradyarrhythmic/asistolic cardiac arrest secondary to airway obstruction. This form of cardiac arrest can respond promptly to the removal of foreign bodies by the Heimlich maneuver or, to those hospitalized, by intubation and suction of secretions from the airways.
Post-resuscitation care depends on the clinical context of cardiac arrest. Primary FV in acute myocardial infarction (MI) generally responds very well to vital support techniques and is easily controlled after the initial event. Patients are kept on a lidocaine infusion at 2-4 mg/ min for 24-72 hours after the incident. In the intra-hospital environment, assisted breathing is usually only necessary for a short time, and hemodynamics stabilizes promptly after defibrillation or cardioversion.
In secondary VF in acute IM (those events where hemodynamic abnormalities predispose to potentially fatal arrhythmias), resuscitation efforts succeed less often and in those patients who are successfully resuscitated, the rate of recurrence is increased. The clinical picture is dominated by hemodynamic instability. In fact, evolution is determined more by the ability to control hemodynamic dysfunction than by electrophysiological abnormalities.
Bradiarithmia, asystolia and electromechanical dissociation are common side events in hemodynamically unstable patients and respond less to interventions. The prognosis after intrahospital cardiac arrest associated with extracardiac diseases is also unfavorable in the few patients successfully resuscitated, the post-resuscitation evolution being determined by the nature of the underlying disease.
Patients with cancer, kidney failure, acute central nervous system diseases and uncontrolled infections as a group have a 10% survival rate after an intra-hospital cardiac arrest. Some major exceptions are patients with transient airway obstruction, electrolyte imbalances, treatment with proarrhythmic drugs and severe metabolic abnormalities, many of them having excellent chances of survival if they can be promptly resuscitated and if vital functions can be maintained while transient abnormalities are corrected.
In the case of long-term maintenance treatment after survival in out-of-hospital cardiac arrest, patients who do not suffer irreversible damage to the central nervous system and achieve hemodynamic stability should benefit from extensive diagnosis and specific tests to guide long-term treatment.
This aggressive approach is based on the fact that statistics show that survival after extra-hospital cardiac arrest was followed by 30% of cardiac arrest recurrences at 1 year, 45% at 2 years and the total mortality rate was almost 60% at 2 years. Comparisons over time suggest that this rate may be significantly lower by new types of interventions, but the degree of this decrease is unknown due to the lack of simultaneous controlled studies on interventions.
For those patients in whom an acute transmural IM is the cause of cardiac arrest, the care is the same as for any other patient suffering from cardiac arrest during the acute phase of a proven IM. However, extensive diagnostic studies are done for most categories of patients to determine etiology, functional deterioration and electrophysiological instability, as guidance elements in the new treatment.
In general, patients who have suffered an extra-hospital cardiac arrest due to chronic ischemic heart disease without acute IM are evaluated to determine whether transient ischemia or chronic electrophysiological instability were the most likely causes of cardiac arrest. If there is any reason to suspect an ischemic mechanism, coronary revascularization or drugs, most often beta-blockers, are used to reduce ischemia. Electrophysiological instability is most correctly detected using programmed electrical stimulation to determine whether sustained TV or FV can be induced.
If sustained TV or FV can be induced, this information is a reference line for assessing the effectiveness of medicines in preventing this inductibility, or it can determine whether map-guided antiarrhythmic surgery is more appropriate, or whether the best solution is an implantable defibrillator/cardioconverter (DCI). Using this technique in patients with ejection fraction of 30% or more, the rate of cardiac arrest recurrence decreases to less than 10% in the first year, when the rate of inductibility is suppressed by medication.
The prognosis is not as good for patients with ejection fraction below 30%, but may be better than the apparentnatural history of survival after cardiac arrest. For patients in whom appropriate drug therapy cannot be identified by this technique, empirical treatment with amiodarone, insertion of an implantable cardioconverter/defibrillator or antiarrhythmic surgery (such as coronary bypass, aneurysmectomy, cryolation) may be chosen.
The initial success of the operation, defined by survival after intervention and a non-inducible condition without drug therapy, is greater than 90% when selecting patients who can be mapping (mapping) in the operating room. However, only a small number of patients meet this criterion. In addition, TV/FV cannot be induced in a large number of cardiac arrest survivors (30-50%), and inducible arrhythmias can be suppressed by drugs in less than 20-30% of those in which arrhythmia could be induced.
Due to these limitations of drug therapy and surgical methods, DCI treatment has become the most widely used strategy for cardiac arrest survivors. DCI have a very good success rate in detecting and converting life-threatening arrhythmias, but the improvement in long-term evolution is not yet well documented. The ESVEM study suggested that ambulatory suppression of monitoring arrhythmias is equivalent to electrophysiological guided, predictive testing for long-term evolution. This conclusion has generated a controversy that remains to be resolved.
I'll see you on June 10th when I start gastrointestinal disorders...
Let's hear it for good!
Dorin, Merticaru