Pacemaker & cabg


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Areviwe of pace maker
problem solving during CABGE acase persentation

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Pacemaker & cabg

  1. 1. Pace maker is a device that applies electricimpulses to the Rt. atrium or the Rt. Ventricle orboth to treat various electrophysiological disordersrelated to conduction and arrhythmia of the heart.
  2. 2. In 1950 the initial pacing system wasconsisted of a single lead asynchronous pace maker,which paced the heart at a fixed rate.Over the years with advanced technology,pacemakers are currently more sophisticated, withthe availability of a multi programmable devices, andAutomated Implantable Cardioverter Defibrillators(AICD) designed to treat fatal tachyarrythmias.
  3. 3. Pulse Generator: It includesEnergy source and electric circuits for pacing andsensory function. Leads:Insulated wires connecting the pulse generator. Electrode:It is an exposed metal end of the lead in contactwith:Endocardium; Endocardial PacingEpicardium; Epicardial Pacing
  4. 4. Unipolar Pacing:Cathode or active lead stimulates the heart andreturns to anode on the casing of pulse generator viathe myocardium and adjacent tissue to complete thecircuit. Bipolar Leads:Two separate electrodes located within the pacedchamber. The possibility of extraneous noise
  5. 5. R Wave Sensitivity:It is the measure of minimal voltage of intrinsicR wave, necessary to activate the sensing circuit ofthe pulse generator and thus inhibit or trigger thepacing circuit. It is about 3mV on an external pulse generator will Maintain
  6. 6. I II III IV V Pacing Sensing Response Programmability Tachycardia AICD O-None O-None O-None O-None O-None A-Atrium A-Atrium I-Inhibited C-Communicating P-PacingV-Ventricle V-Ventricle T-Triggered P-simple S-Shocks programmable D-Dual D-Dual D-Dual M-multi D-Dual (A+V) (A+V) (I+T) programmable (P+S)S-Simple S-Simple R-Rate (A or V) (A or V) modulation
  7. 7. Dual Chamber AV Sequential Pacing (DDD, DVI, DDI, and VDD)Unipolar or bipolar leads are used, for the right atrialappendage and right ventricular apex.Atrium is stimulated first to contract, then after anadjustable PR interval ventricle is stimulated to contract. Uses:Indicated in AV block, carotid sinus syncope, and sinusnode disease.
  8. 8. Advantages:- Preserve the normal AV contraction sequence.- Beneficial when atrial contraction is important for- ventricular filling (e.g. aortic stenosis.) Disadvantage: Pacemaker-mediated tachycardia (PMT) Back conduction from the ventricle to the atrium is sensed by the atrial circuit, and triggers a ventricular depolarization leading to PMT.Overcome by carful adjustment PR
  9. 9. It provides flexibility to correct abnormal device behavior. It adapts the device to patient’s specific and changing needs. Programmable Factors:- Pacing rate. - Hysteresis- Pulse duration. It is the difference between- Voltage output. intrinsic heart rate at which- R wave sensitivity. pacing begins (60 beats/min)- Refractory periods. and pacing rate (e.g.72- PR interval. beats/min).- Mode of pacing. It is useful in- Atrial tracking rate. patients with sick sinus syndrome.
  10. 10. Pacemakers, which not only sense the atrial or ventricular activity but also sense various other stimuli and thus, increase the pacemaker rate. Common sensors used in clinical practice:- Vibration. - QT interval.- Acceleration. - Preejection period.- Minute ventilation. - Rt.V. SV, & contractility.- Respiratory rate and depth. - Mixed venous oxygen- CVP. saturation.- CV pH. - Right atrial pressure.
  11. 11. A variety of clinical signs and symptoms resulting from deleterious haemodynamics induced by ventricular pacing. Intact retrograde VA conductionPathophysiology: Asynchronous with atrial rate loss of atrial systole “kicks” In Patient who can’t compensate by Reduction in COP Activation of baroreceptor reflex that Coronary blood flow increase peripheral resistance to maintain Coronary resistance systemic blood pressure
  12. 12. Incidence: Retrograde VA conduction is present in about;- 15% of patients with complete antegrade AV block.- 67% of patients with intact antegrade AV- conduction paced for sinus node disease. Onset: May be acute to chronic.
  13. 13. Clinical signs and symptoms:- Hypotension. - Syncope. - Vertigo.- Headedness. - Fatigue. - Dyspnoea.- Cough. - CHF.- Awareness of beat-to-beat variation of cardiac response from spontaneous to paced beats.- Neck pulsation or pressure sensation in the chest, neck, or head, headache.- Chest pain: loss of atrial kick, increases coronary- resistance and decreases coronary blood flow.
  14. 14. Acceleration in paced rates due to aging of the pacemaker or damage produced by leakage of the tissue fluids into the pulse generator.Treatment:- Change the pacemaker to an asynchronous mode.- Reprogram it to a lower outputs.- Changing of pulse generator if patient was hemodynamically unstable. Treatment with antiarrhythmic drugs or
  15. 15. I - Evaluation of the Patient.II- Evaluation of the pace maker.
  16. 16.  Evaluation of severity cardiac disease, & its current functional status responsible for the insertion of pacemaker. Associated medical problems: “CAD, DM, HTN, & CHF” Concurrent medical treatments. Preimplantation symptoms: Light headedness Dizziness even after pace maker Fainting. insertion ……. Why?
  17. 17.  Type of pacemaker “fixed or demand rate.” Time since it was implanted. Rate pacemaker at the time of implantation. Half life of the pacemaker battery. 10% decrease in the rate from the time of implantation indicates power source depletion. These information can be taken from the manufacture’s book kept with the patient
  18. 18. It is important, to consider the location of an operative procedure in relation to:• The site of the plus generator.• When a sensor for rate modulation is in use. In our case plus generator is
  19. 19. Inappropriatel y inhibit or trigger stimulation
  20. 20. Direct interference Indirect interference- MRI. - Orthopedic saw.- Surgical electrocautery. - Telemetric devices.- Dental pulp vitality tester. - Mechanical ventilators. - Lithotriptors. - Cellular telephones.,
  21. 21. Defibrillation Stimulation loss of threshold capture
  22. 22. - Positive pressure ventilation.- Nitrous oxide entrapment in the pacemaker pocket.- Insertion of pulmonary artery or central venous catheter. Only multipurpose PA catheter with pacing facilities can also be used when highly indicated
  23. 23. The minimum amount of energy required to consistently cause depolarization and contraction of the heart. It is measured in terms of:- Amplitude: programmed in volts or in milliampers.- Duration: measured in milliseconds.
  24. 24. - 1-4 weeks after implantation.- Myocardial ischemia / infection.- Hypothermia, Hypoxia, & Hypothyroidism.- Hyperkalaemia.- Acidosis/Alkalosis.- Antiarrythmics (class Ic,3, IA/B,2).- Severe hypoxia.- Hypoglycemia.- Local Anesthetic drugs.- The use of Defibrillator.
  25. 25. - Increased catecholamines.- Stress, & anxiety.- Sympathomimetics drugs.- Anticholinergics.- Glucocorticoides.- Hyperthyroidism.- Hyper metabolic status.
  26. 26. MR: 1002067625Name: Samel Mahal SayerDate of birth: 9/5/1948Date of admission: 13/12/12CCU: bed 5
  27. 27. A known diabetic, HTN. Pt. presented to ER on13/12/12 Pt complaining of un relieved chest painfor the last 24 hr.His ECG showed Q waves in leads II, & AVFPatient was diagnosed as acute inferior MI.Pt. received Aspirin, Plavix and was admitted to theCCU, during which he suffered complete heart blocknecessitated insertion of trans femoral pace makerwith the following setting: Rate: 70/min., mV: 2, IVV. Blood pressure was 110/68
  28. 28. Na K Urea Creat. Glucose 136 3.9 5.2 63 10 Hb HCT Plat 15 43.3 157 Other investigations regarding liverfunction, coagulation profile were within normal.
  29. 29. - Shortness of breath, & orthopnic- Recent non inflammatory productive cough- on top of restricted lung disease.- Auscultation: revealed rhonchi and wheezy chest. As Pt was booked for emergency CABG, and AVR pulmonary function tests were not available
  30. 30. - Myoclonic movements of Etomidate andketamine should be avoided in vibration rate responsive PM.- Even though, inhibition of myoclonic movementsby priming dose of NDMR, and Dormicum cansolve this problem in such PM.
  31. 31. Owing to close proximity of the pericardium to themyocardium non pacing electric signals of theunipolar surgical cautery coming from all directionsinhibited the pacemaker pacing signals of the plusgenerator.In addition, electric signals of the cautery resulted infatal arrhythmias in absent of internal AV conductionor external pacing of the ventricle.
  32. 32. coronary Resistance coronary Perfusion,Un favor &blood flow AorticStenosis
  33. 33. A clinical prove that retrograde VA conduction was going on
  34. 34. Under the effective management of adrenaline BPwas raised to 130/70.At this good per fusing BP ischemia of Av node andconducting system was decreased, resulted in a goodintrinsic conduction with an R wave > 2 mV thuspacing was inhibited. This was a considerable prognostic singeUnfortunately such BP could not be maintained for
  35. 35. It happened during prepartion for great vesselscannulation and elevation of the LL for dressingvenous grafting site. Dislodgment of electrodes form its site of insertion A gentle tap on the Rt. Ventricle was able to retune pacing to the heart.
  36. 36. Placing temporarytranscutaneouselectrodes in the leftshoulder area anteriorlyconnected to a temporarypacemaker generator.
  37. 37. Two additional pacemakerelectrodes are placedcutaneously on theposterior wall of the chest andconnected to a secondtemporary pacemakergenerator.
  38. 38. Increasing the rate of the temporary extra cardiactissue pacemaker above that of the permanentcardiac pacemaker, results in; Inhibition of permanent demand activity.