02 Cardiology

SECTION 2

Cardiology 12.

Ethics and Protocols in Management of Cardiac Illness Asif Hasan, Muhammad Uwais Ashraf

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13.

ECG in Non-cardiac Conditions M Chenniappan, Kader Sahib

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14.

Practical Approach to the Patient with Palpitations MS Aditya, K Sarat Chandra

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15.

Transcatheter Aortic Valve Implantation (TAVI or TAVR) G Sengottuvelu

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16.

Practical Approach to a Person with Chest Pain Suresh V Sagarad, Swetha A Biradar, NS Javali, AB Patil

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17.

Practical Approach to a Patient with ECG Changes Shirish MS Hiremath

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C H A P T E R

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Ethics and Protocols in Management of Cardiac Illness

Hippocratic Oath is taken in the beginning of medical career so as to create a permanent impression on the minds of young and budding doctors that throughout their professional lives they will abide by ethics and they will maintain morality and discipline while treating their patients. Young medical graduates go on to choose a specialty to practice, and they are made to cling on to certain guidelines, in order to rectify their practices and they are expected not to deviate too much from these guidelines.

We now follow evidence based medicine and that is resting completely on a scientific approach. Hence it is not proper to base our practice on our fantasies and to prescribe at our free will. Even then, guidelines are not sacrosanct like God- sent orders and there definitely is some flexibility according to practical situation and presentation of the patient. But this flexibility does not mean that we can mould the guidelines or manipulate them as per our convenience or to justify our vested interests.

Cardiology especially requires updated knowledge while managing patients, more so if some intervention is required. This balance is to be maintained and the crucial intersect of knowledge and update if culminates in a fine error, due to lack of updated knowledge can be disastrous to the patient and his family, putting financial burden without any benefit. Maximum commercialization of medical practice and intervention guidelines is seen in the practice of cardiology. Vested financial gains meeting the targets of corporate hospitals, and corruption conveniently force the cardiologists to look the other way round while prescribing irrational treatment.

CORONARY REVASCULARIZATION

Proper revised guidelines are available and there is no acceptable excuse if a cardiologist is unaware of them and it is unethical, rather criminal, to practice beyond these guidelines and to ascribe it to unawareness.

Reversibility of ischemia is the mainstay of management of CAD.1 This should be documented clinically on the basis of investigations like stress echocardiography and Nuclear imaging etc and then the burden of ischemic myocardium should be quantified, so as to justify the intervention and its type. The routine corrupt practice of stenting arteries supplying necrotic myocardium is not unheard of. Such procedures bring bad name and loss of faith to cardiologists in particular and to medical personnel in general. Even in the scenario of multi-vessel stenting, selecting the culprit and significant vessel is

Asif Hasan, Muhammad Uwais Ashraf

ethical over performing carpentry in each and every distal and small lesion not looking good in angiograms!

Use of biovascular scaffold in controversial grey zones is unacceptable and should not be encouraged.

CONSENT

The issue of consent while explaining multi-vessel stenting vs. CABG has been seen to be dictated by the fact that who is explaining- the cardiologist or the cardiothoracic surgeon and not by guidelines. It has been witnessed by all of us, how the horrified attendants of a critical patient of CAD are explained while the patient being on table, and the attendants ultimately nod their heads over what the cardiologist wants to do.

Consent should be clear and simple, in the language that the patient understands well and should be based on guidelines. We should not temper the protocols and play with the fear and anxiety of the patient.

RHEUMATIC HEART DISEASE (RHD)

In case of interventions for valvular heart disease secondary to RHD, clear cut guidelines are mentioned regarding valvular repair, replacement or balloon valvotomy. The deicisions are to be taken based on the clinical situation and the practicality of the problem, based on ACC guidelines and after a detailed discussion with the CTVS team. It is seen so many times, that a procedure which is fit for a particular patient is omitted due to lack of expertise and the patient is not informed regarding referral to a centre where this procedure can be done. In such situations, procedures, uncalled for as per guidelines, are carried out and the patient gets a suboptimal benefit.

CARDIOMYOPATHIES

Protocol based practices in cardiology extend very much into cardiomyopathies as well. In case of dilated cardiomyopathies (DCMP), no cardiologist seems interested in ascertaining the etiology. Treatment is prescribed on free will rather than according to guidelines. The importance of an angiography in an adult before a cardiac resynchronization therapy (CRT) is so often ignored.2 Endomyocardial biopsy is almost never performed in patients labeled to be having DCMP. So many patients have died on table while undergoing CRT for DCMP, just because a prior angiography was not performed.

In case of resctrictive cardiomyopathy also, etiology is hardly a concern of the cardiologist. Endomyocardial

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biopsy is much more essential in this subset of patients but it is so often overlooked. The prognosis after procedures is so well described in this class of patients, but they are hardly the guiding lights before performing a procedure.

In case of hypertrophic cardiomyopathy (HCM), there are stringent guidelines for both medications as well as procedures.3 Genetic testing of a patient as well as his family members is a must, however it is hardly taken care of. The risk stratification for sudden cardiac death (SCD) is an essential component of the management of a patient of HCM and should always be a priority of the treating cardiologist.4 The guidelines for pacing are very structured in patients of HCM and they are so often flouted just to satisfy vested interests. Alcohol Septal Ablation (ASA), septal myomectomy and the indications of ICD are extensively discussed and mentioned in the ACC guidelines, however these are dictated by the free will of a cardiologist.

ARRHYTHMIAS

The guidelines for arrhythmia management are specifically important to be understood and practiced.

While performing radiofrequency ablation (RFA), it is important to be sure of the type of arrhythmia and to dictate the procedure as per the type of arrhythmia and not the convenience of the cardiologist.5 The decision to take up a patient for electrophysiological studies should also be based on, the recurrence of an arrhythmia. It may be necessary to take up the patient urgently for RFA in some cases while in others, it may have to be carried out only after drug failure is documented. All these need to decided as per the standard guidelines.

These days CARTO system is being used for better management of arrhythmias. CARTO is the brandname of this medical system which is used in cardiac electrophysiology. The CARTO 3 EP navigation system helps to visualise the real-time calculated position and orientation of a specialised RF ablation catheter within the cardiac chamber.6 The goal of this technology is to minimise radiation exposure during fluoroscopy, and to increase the accuracy of targeted RF ablation and reacquisition of pacing sites for re-ablation.7

CONGENITAL HEART DISEASE (CHD)

In taking decisions regarding congenital heart disease, it is important to ensure that guidelines regarding suitability of device closure or surgical intervention should be explored in depth and decision should be guided by principle and not by mere intuition.

While taking any decision, it is also important to see that the degree of pulmonary hypertension and its severity are also accounted for. A procedure which takes care of these factors together with the definitive management of the lesion should be chosen rather than a procedure which minimally improves pulmonary hypertension vis–avis the anatomical improvement in the lesion. Hence we see that the type of CHD as well as the associated abnormalities have to be kept in mind while taking a final decision.

DEVICES FOR CONGESTIVE HEART FAILURE (CHF)

Protocols and guidelines are especially important while taking up a patient for cardiac resynchronization therapy (CRT), as the cost of treatment is high but the change in ejection fraction is less. However, even a mild increment in ejection fraction is sufficient to provide great symptomatic relief.8 As per the ACC/AHA class I indications for CRT, it is indicated in patients who have an ejection fraction of ≤ 35%, who are in sinus rhythm with a QRS duration of ≥ 150 msec and NYHA class II, III or ambulatory IV symptoms.9 Similarly for implantable cardioverter defibrillator (ICD) implantation in CHF, it is also important to stratify patients who are at risk of SCD and also to select patients who are expected to live for more than one year.10 In another new development, heart transplantation might become arbitrary owing to the high cost of the procedure and hence guidelines need to be strictly followed for the benefit of the patient and the care-givers.

CONCLUSION

Guidelines are for evidence based rational treatment.

Sometimes cardiologists can read in between lines as per the clinical scenario and there a deviation from protocols is justified. But a deviation which is far from the original guidelines and getting involved into corrupt practices for commercial gains is not only unethical but criminal with serious legal ramifications.

REFERENCES

1.

Lee WW, So Y, Kim K B, Lee DS. Impaired coronary flow reserve is the most important marker of viable myocardium in the myocardial segment-based analysis of dual-isotope gated myocardial perfusion single-photon emission computed tomography.

2. Bose A, Kandala J, Upadhyay GA, et al. Impact of myocardial viability and left ventricular lead location on clinical outcome in cardiac resynchronization therapy recipients with ischemic cardiomyopathy. J Cardiovasc Electrophysiol 2014; 25:507-13.

3.

Perry M. Elliott, Aris Anastasakis, Michael A Borger. et al. 2014 ESC Guidelines on diagnosis and management of hypertrophic cardiomyopathy. European Heart Journal Advance Access published August 29, 2014.

4.

Imke Christiaans; Klaartje van Engelen; Irene M. van Langen; Erwin Birnie; Gouke J. Bonsel; Perry M. Elliott; Arthur A.M. Wilde. Risk Stratification for Sudden Cardiac Death in Hypertrophic Cardiomyopathy: Systematic Review of Clinical Risk Markers. Europace 2010; 12:313-321.

5.

Scheinman M, Calkins H, Gillette P, Klein R, Lerman BB, Morady F. NASPE policy statement on catheter ablation: personnel, policy, procedures, and therapeutic recommendations. Pacing Clin Electrophysiol 2003; 26:78999. [Medline].

6. Shpun S, Gepstein L, Hayam G, et al. Guidance of radiofrequency endocardial ablation with real-time threedimensional magnetic navigation system. Circulation 1997; 96:2016–2021. [PubMed] 7.

Rotter M, Takahashi Y, Sanders P, et al. Reduction of fluoroscopy exposure and procedure duration during

ablation of atrial fibrillation using a novel anatomical navigation system. Eur Heart J 2005; 26:1415–1421. [PubMed] 8.

Nelson GS, Curry CW, Wyman BT, Kramer A, Declerck J, Talbot M, Douglas MR, Berger RD, McVeigh ER, Kass DA. Predictors of systolic augmentation from left ventricular preexcitation in patients with dilated cardiomyopathy and intraventricular conduction delay. Circulation 2000; 101:2703–2709.

9.

Oliver Turschner; Guido Ritscher; Helge Simon; Criteria for Patient Selection in Cardiac Resynchronization Therapy.

Future Cardiol 2010; 6:871-880.

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10. Gabriel Gregoratos, Melvin D. Cheitlin, Alicia Conill. ACC/ AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: Executive Summary.

Circulation 1998; 97:13.

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ECG in Non-cardiac Conditions

INTRODUCTION

Since its discovery in 1902 by William Einthoven, the electrocardiogram (ECG) has served as the most cost effective investigation. Its usefulness in cardiac conditions, both in coronary and non coronary heart disease is well established. However, most often it is believed that the ECG is a cardiac investigation, utilised only for diagnosing cardiac condition. The beauty of ECG is that it can provide valuable information in variety of non-cardiac conditions also. In this article we explore the usefulness of ECG in many non cardiac situations.

M Chenniappan, Kader Sahib

ischemia rather than coronary artery disease which also indicates a bad prognosis.

Pulmonary Thrombo Embolism

There are many ECG signs described in pulmonary thromboembolism. The most important and common ECG

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

This ECG is very useful in COPD to assess the prognosis. A peculiar ECG sign in COPD is ‘Lead I sign’ or ‘Schamroth sign’ which is low voltage P, QRS, T in LI because of vertical axis of all the vectors1 (Figure 1). The ECG may also show right ventricular hypertrophy and right axis deviation which are the signs of cor pulmonale where the prognosis is bad. In addition to this, the symmetrical T inversion in chest leads may be due to right ventricular

Fig. 3: ECG mimicking anterior MI in a patient with skeletal abnormalities

Fig. 1: ECG showing Schamroth sign (Arrow)

Fig. 2: ECG in acute pulmonary embolism showing symmetrical T inversion in V1 –V4

Fig. 3a: The patient showing skeletal abnormality whose ECG is shown in Fig 3.

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Fig. 4: Deep broad T inversion with prolonged QT interval in SAH

CHAPTER 13 Fig. 6: A patient with esophageal spasm showing transient ST elevation due to transient coronay spasm Calcium influx

Slow K + efflux

Fig. 5: ECG in a patient with acute pancreatitis showing ST coving mimicking acute coronary syndrome sign is symmetrical inversion of T wave in anterior chest leads2 (Figure 2). This is due to right ventricular ischemia and dilatation where Right ventricle occupies region of V1-V3. This ECG sign in appropriate clinical setting not only establishes the diagnosis but also indicates poor response to treatment as well as poor prognosis.

SKELETAL ABNORMALITIES

ECG may be abnormal due to skeletal abnormalities such as kyphoscoliosis. The common ECG sign is non progression of R wave in chest leads due to shifting of the heart (Figure 3 & 3a) Non progression of R wave is defined as R wave less than 3mm in V3 when chest electrodes are correctly placed. In this situation, taking ECG one space below or above may increase the R wave voltage in V3 in which case anterior MI as the cause of non-progression of R wave is unlikely.

CENTRAL NERVOUS SYSTEM DISORDERS (CNS)

ECG can be abnormal in certain CNS disorders. Sub arachnoid haemorrhage (SAH) and some cases of stroke usually produce deep, broad T inversion (Figure 4). CAD also produces deep T inversion in chest leads. But in SAH, T inversion is deep; broad with prolonged QT interval3 (Figure 4). Rarely in SAH, ECG may show ST elevation mimicking acute ST elevation MI. This is due to excessive catecholamines released from brain producing extensive myocardial injury. Thrombolysis here is disastrous. In some patients with vertebro basilar insufficiency, atrial fibrillation can occur.

GASTRO INTESTINAL DISORDERS (GID)

Some GID may also produce ECG changes. Acute

Fast K + efflux

Fig. 7: Relationship between action potential, movement of ions and ECG. pancreatitis can sometimes produce ECG changes mimicking acute coronary syndrome (Figure 5) The ECG changes in pancreatitis are due to proteolytic enzymes released by pancreas injuring the myocardium.

The clinical correlation with ECG interpretation in this situation is crucial as the treatment given for Acute Coronary Syndrome will worsen pancreatitis. In some patients, oesophageal disorders not only mimic CAD but can also produce ECG changes4 due to associated coronary spasm known as ‘Linked Angina’ (Figure 6)

ELECTROLYTE DISTURBANCES

Electrolyte disturbance can cause significant ECG changes. The relationship between active potential and ECG is shown Figure 7. The QRS corresponds to sodium entry, calcium to ST segment and potassium to T wave.

Potassium

Hyperkalaemia initially produces Tall T waves (Figure 8), with increasing levels producing P and QRS changes5. The ECG changes appear beyond 6mEq/L. When hyperkalaemia produces tall T waves, it may be mistaken for acute subendocardial ischemia (Figure 9).

Hyperkalaemia produces Tall T with narrow base and

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CARDIOLOGY

Fig. 11: ECG showing short QT due to shortened ST segment interval due to hypercalcemia Fig. 8: ECG showing hyperkalaemia - Tall T with a narrow base and sharp apex

Fig. 12: ECG showing Prolonged ST segment due to hypocalcaemia

Fig. 9: ECG showing tall T waves due to sub endocardial ischemia. (Broad base with blunt apex) Fig. 13: Hypothermia showing Osborn Wave. (Arrow).This hypothermia was due to paracetamol poisoning there is a low voltage T wave, one should look for ‘u’ wave to rule out hypokalaemia. When K is less than 1.7 mEq./L, it produces significant ST depression, low voltage T and prominent U mimicking acute coronary syndrome5(Figure 10).The apparent QT prolongation in hypokalaemia differentiates it from acute myocardial injury.

Calcium

Fig. 10: ECG in severe hypokalaemia showing down sloping ST depression, low voltage T wave and prominent U extending into next P wave sharp apex; acute ischemia produces Tall T waves with wide base and blunt apex.

Hypokalaemia: Hypokalaemia produces low voltage T waves with prominent U waves. Usually the ECG changes occur when potassium is <2.7mEq/l. Whenever

The abnormalities in calcium produce ST changes.

Hypercalcemia produces short QT interval due to a short ST segment and hypocalcaemia produces prolonged QT interval due to a prolonged ST segment5 (Figures 11, 12).

Digoxin produces short QT interval due to shortening of ST segment because of intracellular hypercalcemia.

HYPOTHERMIA

Hypothermia is defined as core body temperature below 95° Fahrenheit. ECG changes appear below 90° F and when the temperature approximates 86° F, 80% of patients show an extra deflection at the end of QRS which

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Fig. 15: ECG after the relief of Pneumothorax .Please note progression and good voltage of R wave in left sided leads

Fig. 16: ECG showing sinus tachycardia, wide QRS and tall R in avR due to tricyclic antidepressant toxicity is known as Osborn wave6 (Figure 13). This change which was described by Dr.John Osborn is due to the gradient of potassium current between epicardial and endocardial surfaces.

PNEUMOTHORAX

Diagnosis of pneumothorax is purely clinical. ECG changes are due to shifting of the heart which gets normalised immediately after the relief of pneumothorax.

(Figure 14, 15).

DRUG TOXICITY

Many non-cardiac drugs produce ECG changes at their toxic levels. Tricyclic antidepressant toxicity typically produces wide QRS, sinus tachycardia and terminal R in avR. Terminal R wave in avR more than 3mm, QRS duration more than 100m.sec and sinus tachycardia are

CHAPTER 13

Fig. 14: ECG showing sinus tachycardia, low voltage and nonprogression of R wave in chest leads due to Pneumothorax on left side shifting the heart to right side.

Fig. 17: ECG showing diffuse T inversion due to CO monoxide poisoning which is an indication for hyperbaric therapy

Fig. 18: ECG showing diffuse ST elevation due to ALP poisoning.

(See text) bad prognostic signs7 (Figure 16). Many chemotherapeutic drugs especially anthracyclines cause cardiac dysfunction and induce changes of myocardial ischemia.

POISONING

Cardiac toxicity is a common finding in patients who have been poisoned with wide variety of chemical agents.

Carbon monoxide (CO) poisoning typically produces ischemic changes in ECG due to inhibition of cellular respiration8 (Figure 17).

Organo phosphorous poisoning, cyanide poisoning and heavy metal poisoning produce arrhythmias and ECG changes. One of the common insecticides which are used in South India is Aluminium Phosphide (ALP). ALP poisoning produces cellular hypoxia due to inhibition of cytochrome oxidase in mitochondria. This may produce diffuse ST elevation mimicking Acute Myocardial Infarction (Figure 18).

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Fig. 19: ECG showing Parkinson tremor mimicking Torsade de Pointes. Note that LII which is simultaneously recorded with LI and LIII does not show same ECG changes confirming STA Fig.20 b. Correctly recorded ECG showing actual inferior MI

Fig. 20: Right arm and left arm lead reversal leading to positive complexes in lead aVR and negative complexes in lead I

Fig. 21: ECG changes in pregnancy

Table 1: Pathologic changes in ECG in pregnancy Sinus Bradycardia A.V. Blocks (New onset) Complex Premature beats Atrial Fibrillation Significant chamber enlargements (LA,LV,RV) Ischemic changes(deep T inversion, ST elevation or depression)

Fig. 20a: ECG showing High lateral MI like picture because of upper limb, lower limb lead reversal

TREMORS

Tremors due to various reasons especially Parkinsonism produce somatic tremor artefacts (STA). This STA will mimic arrhythmias such as atrial flutter, Torsade de pointes and may be wrongly treated with powerful antiarrhythmic agents and DC shock9. The clinical examination during the arrhythmia will show disparity between pulse and ECG. The ECG in Parkinsonism is shown in Fig.19, which exactly looks like Torsade de pointes. Careful examination of L II which is simultaneously recorded with other leads did not show the arrhythmia, confirming the diagnosis of tremors. Further careful examination of limb leads confirm that the leads using left arm such as L1, L III, and avL showed the ECG changes and not L II which is not using left upper limb indicating the tremor is maximum

in left upper limb. So the ECG can be utilized not only to diagnose tremors but also the limb of tremors!

LEAD MISPLACEMENT

Upper arm lead reversal is well known to cause technical dextrocardia where limb leads show the evidence of dextrocardia (P, QRS negative in L I and positive in avR) but chest leads show normal R wave progression (Figure 20).

Less well known is the reversal of electrodes between upper and lower limbs10. In Figure 20a & b upper, lower limb lead reversal actually changes site of infarction. The actual inferior wall MI is shown as high lateral MI due to upper, lower limb lead reversal.

PREGNANCY

Pregnancy produces a lot of ECG changes such as Sinus tachycardia, nonspecific ST T changes, short PR, rare

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Fig. 22: ECG in erect posture;compare the ECG in lying posture (Fig. 22a)

CONCLUSION

Most often, whenever there are ECG changes it is presumed, it is due to cardiac disease. It should be realised that many non cardiac conditions can produce significant ECG changes which are mistaken for cardiac disease and wrongly treated especially in critical care settings. The clinical correlation, careful study of ECG and awareness of ECG changes in non cardiac conditions will prevent many such therapeutic disorders.

REFERENCES

1.

Harrigan RA, Jones K. ABC of clinical electrocardiography.

Conditions affecting the right side of the heart. BMJ 2002; 324:1201-4.

2. Panos RJ, Barish RA, Depriest WW, et al. The electrocardiographic manifestations of pulmonary embolism. J Emerg Med 1988; 6:301–307.

3.

premature beats and minor axis deviation towards left due to elevation of diaphragm11 (Figure 21).

Di Pasquale G, Andreoli A, Lusa M, et al. Cardiologic complications of subarachnoid hemorrhage. J Neurosurg Sci 1998; 42(suppl 1):33–36

4.

The pathological changes in ECG during pregnancy are listed in Table 1.

Baldi F, Ferrarini F. Non-cardiac chest pain: a real clinical problem. Eur J Gastroenterol Hepatol 1995; 7:1136–1140.

5.

Surawicz B. Electrolytes, hormones, temperature, and miscellaneous factors: electrophysiologic basis of ECG and cardiac arrhythmias. Baltimore, MD: Williams & Wilkins, 1995; 426–453

6.

Gussak I, Bjerregaard P, Egan T, et al. ECG phenomenon called the J wave. J Electrocardiol 1995; 28:49–58.

7.

Groleau G, Jotte R, Barish R. The electrocardiographic manifestations of cyclic antidepressant therapy and overdose: a review. J Emerg Med 1990; 8:597–605.

8.

Marius-Nunez AL. Myocardial infarction with normal coronary arteries after acute exposure to carbon monoxide.

Chest 1990; 97:491–494.

9.

Knight BP, Pelosi F, Michaud GF, et al. Clinical consequences of electrocardiographic artifact mimicking ventricular tachycardia. N Engl J Med 1999; 341:1270–1274.

Fig. 22a: ECG of the same pt. in fig .22 in lying posture

POSTURE

Changes in posture itself can produce significant ECG changes. Standing may produce T wave changes and axis shift (Figure 22 a & b); so when interpolating ECG it is important to know in which position the ECG has been taken.

RENAL DISEASE

ECG in chronic kidney disease (CKD) usually shows LVH, Left Atrial Enlargement and most often hyperkalemia12.

Sometimes combination of electrolyte abnormalities may produce some typical ECG changes which are diagnostic of chronic renal diseases. The combination of hypocalcaemia and hyperkalaemia show prolonged ST segment (hypocalcaemia) and peak T waves (hyperkalaemia) (Figure 23). Although in this ECG, T wave is not typical of hyperkalaemia because of decreased amplitude, one must suspect associated hyperkalaemia because of T waves with a sharp apex.

10. Peberdy MA, Ornato JP. Recognition of electrocardiographic lead misplacements. Am J Emerg Med 1993; 11: 403–405.

11. L.Feldman, Harold H.Hill. Electrocardiogram of the normal heart in pregnancy. American Heart Journal 1934; 10:110–117.

12. Chijioke A, Makusidi AM. Electrocardiographic abnormalities among dialysis naïve chronic kidney disease patients in Ilorin Nigeria. Ann Afr Med 2012; 11:21-6.

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Fig 23: ECG in a CKD patient with hypocalcaemia and hyperkalaemia

C H A P T E R

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Palpitations as a symptom is a common cause for consultation in general, casualty and cardiology practice.

The term Palpitation has its roots in the Latin verbs ‘palpare’, ‘palpitare’ meaning patted or touch gently. The diagnostic and therapeutic management of palpitations is often frustrating and confusing both to practitioner and patient. This is because of myriad causes of this symptom and poor reproducibility. From the management point of view causes could range from psychosomatic disorders to life threatening arrhythmias.1-3 Palpitation has been defined as a disagreeable sensation of pulsation or movement in the chest and/or adjacent areas. In resting conditions one does not usually perceive heartbeat. During intense physical or emotional stress it is quite normal to be aware of one’s own cardiac activity making them physiological. Outside of these situations palpitations are abnormal.

Palipitations are a frequent clinical presentation accounting for upto 15-20% of general practice and second to chest pain in cardiology setups. Palpitations originate from a variety of causes, cardiac related in approximately 43% of cases, psychosomatic in 30% and unknown/miscellaneous cause in 27%4-8. Arrhythmias cause palpitations often but significant number of patients with arrhythmias don’t report palpitation as a symptom.

There is every need to have a evidence based structured evaluation of patients presenting with palpitations to help us identify patients with more serious conditions.

Palpitations are perceived with still less understood sensory afferent pathways with receptors in myocardial, pericardial or peripheral receptors. These stimuli are transmitted to sub cortical areas and base of frontal lobes9.

Receptors could be triggered for a variety of reasons as listed in Table 1.

Table 1: Triggers of Arrhythmias Variation in heart rate

Arrhythmias (Tachy and Brady), Sinus tachycardia (systemic illness fever, thyrotoxicosis, anxiety etc)

Increase in intensity of contraction

Large increase in stroke volume secondary to Regurgitantvalvular lesions, congenital Shunt lesions, Arteriovenous malformation, hyperdynamic states(pregnancy, anemia etc)

Altered perception of heartbeat

Psychosomatic disorders

Practical Approach to the Patient with Palpitations MS Aditya, K Sarat Chandra

To evaluate a particular patient it is important to known the potential causes of palpitations. Possible aetiologies10-16 have beenlisted in Figure 1.

CLINICAL EVALUATION OF PALPITATIONS

As in any clinical situation a thorough history and examination will help to arrive at an appropriate diagnosis.

For the purpose of clinical clarity four types of palpitations have been identified in practice. Though no clear differentiation is possible four types have been identified17-18 Figure 2.

Extrasystolic palpitation are usually sudden in onset perceived as a skipped or jumped beat usually interspersed with normal periods.

Tachycardiac palpitations are perceived as rapid flapping movements over the chest could be irregular or regular and be associated with angina, syncope and fatigue.

Anxiety related palpitations are usually associated with slight increase in heart rates and associated with tingling sensations in hands and feet, atypical chest pain etc.

Pulsation is a feeling felt after strong contraction of the heart following increased contractility or stroke volume.

History should be focused and directed to achieve reasonable success in arriving at possible diagnosis.

SITUATIONS LEADING TO PALPITATIONS

•

Functional state -sleep, during sport or normal exercise, change inposture, after exercise.

•

Positional variation or trigger.

•

Precipitating factors -emotion, exercise, squatting.

•

Onset of palpitations-Abrupt or slowly arising.

•

Premonitory symptoms -Angina, dyspnea, vertigo, fatigue.

TYPE OF PALPITATIONS

Regular, rapid or permanent.

ASSOCIATED SYMPTOMS

Chest pain, syncope or near syncope, sweating, pulmonary edema, anxiety, nausea, vomiting.

TERMINATION EVENTS

Deceleration or sudden, urination, change in other symptoms.

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Cardiac structural anomalies

Cardiac arrhythmias

1. Venticular/supraventricular tachyarrhythmias 2. Bradyarrhythmias-sinus bradycardia,sinus pause,AV blocks 3. Pacemaker mediated

Systemic causes 1.

2.

3.

4.

5.

6.

Drugs and others

Hyperthyroidism Fever Anemia Orthostatic syndromes Pheochromocytoma Pregnancy

1. Sympathomimetic agents in inhalers 2. Anticholinergics 3. Alcohol, cocaine, caffeine,nicotine 4. Anorexics 5. Psychosomatic

Fig. 1: Aetiology of Arrhythmias rhythm or sinus tachycardia, to evaluate the presence of systemic disease.

Extrasystolic

Anxiety

Palpitations

In the absence of palpitations, signs of structural heart disease thatcould explain the etiology (murmur, clicks, hypertension, valvular heart disease, signs of heart failure).

Tachycardiac

Systematic analysis of clinical clues help to get idea into the nature of palpitations they are summarized in Figure 3:19-21

INVESTIGATIONS

Pulsation

Fig. 2: Types of palpitations Spontaneously or with vagal maneuvers or drug administration.

PAST HISTORY

Age onset of symptoms, frequency, cardiac disease, psychosomatic disorders, systemic diseases, thyroid disorders, family history of cardiac disease, tachycardia or sudden cardiac death, medications at the time of palpitations drug abuse.

EXAMINATION

Goal is to evaluate the tolerance of a arrhythmia (blood pressure, pulmonary edema, etc), and in case of a sinus

ECG

ECG remains the most appropriate investigation to assess a patient of palpitation. During an episode of arrhythmia ECG provides useful information on rate, rhythm and suitably temporally done also onset and offset. Vagal maneuvers or pharmacological tests with adenosine or other drugs under ECG monitoring provide valuable insights into mechanism and triggers of arrhythmia.

In the absence of arrhythmia ECG provides valuables clues about structural heart disease, arrhythmic substrates and chanellopathies.

ECG CLUES TO CAUSE OF PALPITATIONS

Short PR interval-AVRT, Atrial fibrillation P-wave abnormalities, Atrial premature complexes-Atrial fibrillation

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Palpitations

1. Severe Aortic,Mitral regurgitation 2. Mitral valve proplapse 3. Shunt lesions like VSD/ASD/PDA 4. Ebsteins anomaly 5. Dilated,Hypertrohiccardiomyo pathy

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AVNRT/AVRT

AF

AT/AFL

Sudden onset. Exercise or posture induced, regular in nature. Onset of symptoms from childhood

Continuous or paroxysmal. Paroxoysmal or Effort, alcohol or meal continuous.Regular in induced. Irregular in nature except in AV block nature

Polyuria &frog sign Vagal maneuver termination

Polyuria

VT Effort induced, regular in nature Hemodynamic compromise

Fig. 3: AVRT- atrio-ventricular reentrant tachycardia; AT- Atrial tachycardia, AF- Atrial flutter; VT- Ventricular tachycardia

CARDIOLOGY

* Right bundle branch block with coved type/saddle type ST segment elevation in the right precordial ECG leads. #epsilon wave and/or T-wave inversion with QRSduration >110 ms in the right precordial ECG leads seen in ARVDArrhythmogenic right ventricular dysplasia

ECG MONITORING DEVICES

When symptoms are infrequent and inconclusive it makes sense to use devices which can record and transmit/archive ECG. Devices can record ECG data on a continuous basis or be switched on at the onset of palpitation.

Holter-Recorders connected to the patient by means of skin electrodes; these recorders are able to perform continuousbeat-to-beat electrocardiographic monitoring via several leads. Monitoring is usually limited to 1-2 days, useful when palpitations are daily occurrence, cumbersome installation may limit patient activity eliminating several triggers Figure 4.

EVENT RECORDERS

Fig. 4: Holter monitoring

Portable devices applied to skin when symptoms are experienced by patient, single lead data is recorded and/or transmitted. Useful for palpitations whose onset happens weekly or more and last long enough till trigger is switched on. ECG quality may not be good, triggers are not recorded, not suitable when hemodynamic impairment occurs (Figure 5).

EXTERNAL LOOP RECORDER

Fig. 5: Event recorder Left ventricular hypertrophy-Ventricular tachycardia, Atrial fibrillation

Connected to the patient on a continuous basis and equipped with a memory loop which can be triggered by patient or automatically. ECG record before the trigger and after is recorded. Useful when palpitations occur weekly or less frequently. Useful for short lasting palpitations and those with hemodynamic impairment.

Asymptomatic arrhythmias can be recorded with automatic triggering. Long term usage is inconvenient and less tolerated, Figure 6.

IMPLANTABLE LOOP RECORDERS

Large voltages in precordial leads, T wave changesHOCM

When symptoms are less frequent that is monthly or yearly and associated with hemodynamic compromise and all other modalities fail to give definite clue implantable recorders are used. The trigger to record could be externally activated by patient or automatically by device itself22-25 Figure 7.

A-V block, tri- or bifascicular block-Complete heart block, brady- dependent polymorphic ventricular tachycardia

Echocardiography provides a structural and functional

Pathological Q wave, epsilon wave(ARVD) , brugadapattern*-Ventricular tachycardia/fibrillation #

Long or short QT-Polymorphic ventricular tachycardia

ECHOCARDIOGRAPHY

71

Fig. 7: Implantable loop recorder

Suggested diagnostic workup for palpitations ILR-implantable loop recorder, EPS-Electrophysiological study, AECG-Ambulatory electrocardiogram assessment of the heart, valvular heart disease such as mitral valve prolapse, mitral and aortic regurgitation.

Congenital shunt lesions, left ventricular function, features of ARVD etc provide useful corroborative evidence towards possible etiology of palpitations.

STRESS TESTING

Treadmill or pharmacological stress testing may sometimes be used to identify presence of inducible ischemia as a cause of palpitations, as well as catecholamenergic

tachyarrhythmias. The sympathetic state associated with stress identifies triggers to a particular arrhythmia and provides valuable clues to diagnosis. Hemodynamic tolerance to a particular arrhythmia could also be studied during stress testing.

MRI

MRI is emerging as a useful investigation in diagnosing a variety of structural and functional cardiac diseases.

Its utility is proven in the diagnosis of arrhythmogenic

CHAPTER 14

Fig. 6: External loop recorder

72

right ventricular dysplasia which is an important cause of Ventricular tachycardia. It is also useful to identify various lesions like sarcoid granulomas, tumors and tissue characterize them, which in turn could cause various ventricular arrhythmias.

CARDIOLOGY

ELECTROPHYSIOLOGICAL STUDY

Electrophysiological studies are usually the last resort, after exhausting all other diagnostic tools. Various pacing and entrainment protocols are delivered to the heart to trigger and consequently diagnose the nature of arrhythmia. EPS also allows for potential ablative therapy of a wide range of tachyarrhythmias.

TREATMENT OF PALPITATIONS

Therapy is focused on the cause (treatment of cardiac arrhythmias, structural heart diseases, psychosomatic disorders, or systemic diseases. When a clear cause is known and a low-risk curative therapy is available (e.g. supraventricular arrhythmias), this is the treatment of choice. In many benign arrhythmias (e.g. premature beats), a number of general factors may influence and modulate the frequency and severity of the symptoms. changes in lifestyle (e.g. reducing coffee or alcohol) or noncardiologic therapies (e.g. anxiolyticdrugs or psychiatric counselling) may be useful to control symptoms and should be considered. Reassurance of the patient on the benign nature of the disorder can markedly reduce symptoms.

Patients with palpitations may sometimes need to be hospitalized for diagnostic and therapeutic purpose.

Diagnostic indications may include structural heart disease for the purpose of cardiac catheterization and hemodynamic assessment, EPS, in hospital telemetry studies etc.

More serious indications to hospitalize include brady arrhythmias requiring pacemaker, ventricular arrhythmias, supraventricular arrhythmias with hemodynamic compromise, pacemaker/ICD malfunctions, signs and symptoms of heart failure and severe structural cardiac abnormality.

CONCLUSIONS

Palpitations are a common clinical presentation with wide ranging etiology. Thorough history and physical examination is required to arrive at an appropriate clinical diagnosis and follow with relevant investigations.

Potentially life threatening causes should be ruled out before more benign conditions are attributed as cause of palpitations. Newer tools are increasingly available especially for ambulatory ECG monitoring improving diagnostic yield and accuracy. Simple tools like handheld devices, phones etccould prove useful in the future .

REFERENCES

1.

2.

Kroenke K, Arrington ME, Mangelsdroff AD. The prevalence of symptoms in medical outpatients and the adequacy of therapy. Arch Intern Med 1990; 150:1685–9.

Knudson MP. The natural history of palpitations in a family practice. J FamPract 1987; 24:357–60.

3.

Zimetbaum P, Josephson ME. Evaluation of patients with palpitations. New EnglJMed 1998; 338:1369–73.

4.

Weber BE, Kapoor WN. Evaluation and outcomes ofpatients with palpitations. Am J Med 1996; 100:138-48.

5.

Knudson MP. The natural history of palpitations in afamily practice. J Fam Pract 1987; 24:357-60.

7. Barsky AJ. Palpitations, arrhythmias, and awareness ofcardiac activity. Ann InterChignon JM, Lepine JP, Ades J. Panic disorder in cardiac outpatients. Am J Psychiatry 1993; 150:780-5.

8. Barsky AJ, Cleary PD, Coeytaux RR, Ruskin JN. Psychiatricdisorders in medical outpatients complaining of palpitations. n Med 2001; 134:832-7.

9.

Malliani A, Lombardi F, Pagani M. Sensory innervation of the heart. In: CerveroF, Morrison JFB (eds). Progress in Brain Research. vol. 617. New York: Elsevier; 1986.p39–48.

10. Cryer PE, Gerich JE. Glucose counterregulation, hypoglycemia, and intensive insulin therapy in diabetes mellitus. N Engl J Med 1985; 313:232–41.

11. Klein I. Thyroid hormone and the cardiovascular system.

Am J Med 1990; 88:631–7.

12. Bravo EL, Giford RW. Pheocromocitoma: diagnosis, localization and management. N Engl J Med 1984; 311:1298– 303.

13. Rosenthal DS, Braunwald E. Hematological–oncological disorders and heart disease. In: Braunwald E (ed.). Heart Disease: A Textbook of Cardiovascular Medicine.4th ed.

Philadelphia: W.B. Sanders; 1992. p1742–4.

14. Elkayam U. Pregnancy and cardiovascular disease.

In Braunwald E (ed.). HeartDisease: A Textbook of Cardiovascular Medicine. 4th ed. Philadelphia: W.B.Sanders; 1992. p1790–3.

15. Dinardello CA, Wolff SM. Fever. In: Mandell GL, Douglas RG, Bennett JE (eds). Principles and Practices of Infectious Diseases. 3rd ed. New York: Curchill Livingstone;1990. p464–7.

16. Holman E. Abnormal arteriovenous communications.

Great variability of effectswith particular reference to delayed development of cardiac failure. Circulation 1966; 32:1001–8.

17. Moya A, Sutton R, Ammirati F, Blanc JJ, Brignole M, Dahm JB et al. Guidelines forthe diagnosis and management of syncope. The Task Force for the Diagnosis andManagement of Syncope of the European Society of Cardiology (ESC).

Developedin collaboration with European Heart Rhythm Association (EHRA),Heart Failure Association (HFA), and Heart Rhythm Society (HRS). Eur HeartJ 2009;30:2631–71.

Hlatky MA. Approach to the patient with palpitations.

In Goldman L,Braunwald E (eds). Primary Cardiology.

Philadelphia: W.B. Saunders; 1998.p122–8.

18. Zipes DP, Miles WM, Klein LS. Assessment of patients with cardiac arrhythmia.In Zipes DP, Jalife J (eds). Cardiac Electrophysiology: From Cell to Bedside. Philadelphia:W.B. Saunders; 1995. p1009–12 Am J Med 1996; 100:138–48.

19. Thavendiranathan P, Bagai A, Khoo C, Dorian P, Choudhry NK. Does this patientwith palpitations have a cardiac arrhythmia? JAMA 2009; 302:2135–43.

20. Hoefman E, Boer KR, van Weert HCPM, Reitsma JN, Koster RW, Bindels PJE.Predictive value of history taking and physical examination in diagnosing arrhythmiasin general practice. Fam Pract 2007; 24:636–41.

21. Summerton N, Mann S, Rigby A, Petkar S, Dhawan J. New-onset palpitations ingeneral practice: assessing the discriminant value of items within the clinical history. Fam Pract 2001; 18:383â&#x20AC;&#x201C;92 Zimetbaum PJ, Josephson ME. The evolving role ofambulatory monitoring in general clinical practice. Ann Intern Med 1999; 130:848-56.

22. Fogel RI, Evans JJ, Prystowsky EN. Utility and cost ofevent recorders in the diagnosis of palpitations, presyncope,and syncope. Am J Cardiol 1997; 79:207-8.

23. Kinlay S, Leitch JW, Neil A, Chapman BL, Hardy DB,Fletcher PJ, et al. Cardiac event recorders yield more diagnoses and are more cost-effective than 48-hour Holter

monitoring in patients with palpitations. A controlled clinical trial. Ann Intern Med 1996; 124:16-20.

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24. Zimetbaum PJ, Kim KY, Josephson ME, GoldbergerAL, Cohel DJ. Diagnostic yield and optimal duration of continuous-loop event monitoring for the diagnosis ofpalpitations. A cost-effectiveness analysis. Ann InternMed 1998; 128:890-5.

25. Zimetbaum PJ, Kim KY, Ho KK, Zebede J, JosephsonME, Goldberger AL. Utility of patient-activated cardiac recorders in general clinical practice. Am J Cardiol1997; 79:371-2.

CHAPTER 14

C H A P T E R

15

Transcatheter Aortic Valve Implantation (TAVI or TAVR)

Aortic stenosis is narrowing of the aortic valve opening, a common and a slowly progressive disease in the elderly population but with the onset of symptoms, one in two die within a couple of years. In this condition, the aortic valve within the heart undergoes degeneration (wear & tear) due to aging. It is common in old age, as calcium or scarring damages the valve and restricts the amount of blood flowing through the valve, but can occur at a younger age if the valve is abnormal by birth.

Due to aortic stenosis, the heart needs to work harder to pump blood and this eventually weakens heart muscle.

Left untreated, aortic valve stenosis can lead to lifethreatening heart problems. In spite of this fact, many patients especially the older age group, cannot have conventional valve replacement or repair surgery owing to the prohibitively high surgical risk.

Patients having evidence of symptomatic and severe calcific valvular aortic stenosis, but also having high surgical risks when assessed by EURO and STS scores , have a new and minimally invasive option –the TAVR (Transcatheter aortic valve replacement).

TAVR VS OHS

TAVR is the new alternative for select patients for whom traditional open chest surgery has intermediate or high risk. This minimally invasive procedure repairs the narrowed aortic valve without a major surgery. A catheter is placed in the femoral artery (in the groin) similar to

G Sengottuvelu

angioplasty, and guided into the chambers of the heart.

A compressed tissue heart valve is placed on the balloon catheter and is positioned directly inside the diseased aortic valve. A team of interventional cardiologists and imaging specialists, heart surgeons and cardiac anesthesiologists work together, utilizing fluoroscopy and echocardiography to guide the valve to the site of the patient’s diseased heart valve.

A typical patient will get the diagnosis confirmed by his symptoms and echocardiography and his operative risk will be assessed objectively by the EURO score II. Accordingly if TAVR is decided, CT coronary angiogram and an aortogram up to the femorals will be taken to assess the anatomical feasibility of the vessels. If suitable, the patient will be admitted to hospital a day before the planned procedure and will usually undergo the procedure under local anaesthesia. Typically the patient can walk on the second day and can go home by day five.

TAVR has indeed been a boon to many elderly patients even over the age of 75 and has given them a second lease of life and am sharing our experience.

PATIENT 1

Presentation & Evaluation:

Mr P was a 73 years old diabetic, hypertensive and CAD patient who had undergone PCI in 2006 and CABG in 2011. He was a known case of CKD and severe COPD requiring BiPAP at home.

From January 2014 to October 2015, he had spent more than 5 months as inpatient that included three months of Intensive care. In October 2015 he was consulted for inability to wean from ventilation in spite of good care for COPD. Echocardiogram showed critical aortic stenosis and there was severe PAH with preserved bi-ventricular function. CT surgeons refused aortic valve surgery in view of his high risk, co-morbid conditions and previous thoracotomy. His STS score predicted mortality and morbidity for surgical AVR was 23% and 50% respectively signifying very high risk for open surgery. After confirming his patent bypass grafts, CT assessment revealed suitability for core valve implantation.

Procedure

The procedure was performed under short GA through the right femoral artery the native calcified valve was predilated before implanting a 26mm Medtronic core valve. The procedure was truly percutaneous (no cut

75

CHAPTER 15

Fig. 1 : Core Valve being deployed under TEE guidance

Fig. 3 : Core Valve after Complete deployment

Fig. 2 : Core Valve after Complete deployment)

Fig. 4 : As there was a paravalvular leak, its being post dilated

down required) and femoral arterial access site was pre-closed using specialized vascular closure device called the Proglide. There was immediate improvement in the hemodynamics (gradient reduced to normal and pulmonary arterial pressures significantly reduced) and echocardiogram showed normally functioning core valve with no para-valvular leak. Complete hemostasis was achieved in the lab and the whole procedure lasted for an hour and half. The patient was extubated post procedure in the ICU, and was discharged on day 5 (Figures 1 & 2).

Follow up

PAH which was attributed to COPD, also improved significantly to 44 mm of Hg from the initial 82 mm of Hg. This patient symptom improved significantly that he transformed from a state of depressed man requiring recurrent ICU admissions to a cheerful ambulant gentle man riding bi cycle.

PATIENT 2

Presentation & EvaluationÂ

Mrs P was a 55 years old, diabetic, obese, post-menopausal lady, who presented with progressive dyspnoea on exertion over the last few years progressed to class IV in the last few months. She was diagnosed to have severe

Fig. 5 : Final result post dilation aortic stenosis. Her house was a small nursing home with reclinable short beds, a BiPAP machine, oxygen cylinders, walkers and special nurse assistance for day to activities.

Her past history included diabetic foot, lower limb fractures, Infective endocarditis of a bi-cuspid aortic valve and obstructive sleep apnea. Her logistic Euro score was 16 with a predicated mortality and morbidity of 16% and

76

38% respectively for surgical AVR. Her CT scan revealed suitability for TAVR.

CARDIOLOGY

Procedure

In spite of her multiple comorbidities, TAVR was performed under conscious sedation and was truly percutaneous without cut down. After predilatation during rapid ventricular pacing, a 29 mm Evolut-R second generation valve was deployed ( smaller 14 F sized sheath and is retrievable and repositionable up to 80% deployment) (Figures 3, 4 & 5). Her hemodynamics instantly improved. Post procedure echo showed paravalvular leak which improved after post dilation. The access sites were pre-closed and the entire procedure was done in two hours. She was observed in CCU for 2 days, discharged on day 5. She had significant improvement in her symptoms and loss of weight.

Follow up

His symptoms greatly improved and he is fully ambulant, and able to perform his usual activities.

PATIENT 4

Presentation & Evaluation:

Mr. S , 90 years old gentleman is a known diabetic, hypertensive, COPD, CKD and a CAD-S/P CABG patient. Since 2013 he was having recurrent heart failure admissions and was diagnosed with moderate aortic stenosis and severe LV dysfunction. The AS become severe and he progressed to class IV symptoms. In view of surgical risk surgical AVR was ruled out and he was considered for TAVR.

Procedure

Echo showed normally functioning EVOLUT R valve and normal LV function with no para-valvular leak. She had remarkable improvement in her symptoms and also lost 20 kgs in one month.

He underwent TAVI with a 29 mm Evolut R valve percutaneously (Figures 6 & 7). Intra procedure he had a transient asystole and was resuscitated successfully. He was mobilized the second day and discharged the third post procedure day. At one month follow up his renal functions improved to normal and his functional capacity improved to class II.

PATIENT 3

Follow up

Follow up

Presentation & Evaluation:

Mr P, 64 years old diabetic, CKD with coronary artery disease and had undergone PCI in 2006, LV dysfunction and severe AS. He required ICU admission for LRI and worsening CKD. After stabilizing the patient, a low dose dobutamine stress echo showed presence of contractile reserve with mean AVG of 46 mm of Hg and surgical AVR considered to be high risk in view of LV dysfunction and a STS score predicted mortality and morbidity of 6% and 30% respectively. CT confirmed him suitable for TAVR and also his earlier stent was patent.

Procedure

TAVR was done under local anesthesia with 29 mm Evolut R and was truly percutaneous through right femoral access. Post procedure there was no para-valvular leak and no gradient. He developed trifascicular block requiring permanent pacemaker implantation on day 3.

Fig. 6 : Aortogram after valve implantation

His symptoms greatly improved and he is fully ambulant, and able to perform all his usual activities.

PATIENT 5

Presentation & Evaluation

Mr.Sk a 78 years old gentleman with class III NYHA DOE was diagnosed with bi-cuspid aortic valve with severe aortic stenosis and mild LV dysfunction. He was also diagnosed with interstitial lung disease and thrombocytopenia. In view of his moderate risk for surgical AVR he was offered the options of both TAVR and SAVR but patient and attendants opted for TAVI.

Procedure

Accordingly he underwent the procedure under LA using a 29 mm Medtronic Evolut R valve completely percutaneously. Post procedure he was mobilized the

Fig. 7 : Evolut R valve – post deployment

second day and discharged on the third day and clinically he is doing very well.

High surgical morbidity as assessed by Euroscore and STS scores.

Follow up

What are the valve types?

He has recovered and feels well. According to him “This is my first hospitalization in my life and was very scared before and realized it is a simple procedure and now I am able to walk more without any symptoms”

CONCLUSION

“TAVR is the treatment of choice for high risk patients with severe AS. Even in intermediate risk in elderly patients over 75 years, its safety and efficacy have been established and can be considered after assessment by a heart team.”

FAQS

There are two types of valves commonly used , the self expanding Medtronic Core/Evolut R Valve and the balloon expandable Edwards Sapien 3 valve.

How are the patients selected for the procedure ?

For selection of patients for the procedure a detailed clinical evaluation, routine lab values chest xray, trans thoracic echo, PFT, carotid ultrasound , coronary angiography and CT Angiography of the aortic valve, chest, abdomen and pelvis. The CT angio is done to assess the aorto iliac patency, calcification and tortuosity. This is of utmost importance because the presence of occlusive PAD, small vessels and excessive torsuosity would preclude a trans femoral approach.

What are the methods of implantation?

The commonest site of implant is through the femoral route. The other less frequently employed route is subclavian and direct aortic. The newer valves are advantageous because of its smaller delivery system (1418F).

When to refer a patient for TAVR?

What is TAVR ?

TAVR is transcatheter aortic valve replacement which today is the alternative for surgical aortic valve replacement (AVR).

Patients having evidence of calcific severe valvular aortic stenosis who are symptomatic can be referred to TAVR if the surgical morbidity as assessed by EURO and STS score is high.

How is it different from surgical AVR

Are all aortic stenosis patients eligible for TAVR?

TAVR as its name goes is aortic valve implantation done as percutaneous based catheter implantable valves as opposed to an open surgical implant.

Advantages of TAVR versus surgical AVR - The major advantage of TAVR is the fact that owing to its minimum invasive nature it can be done in patients who are too surgically moribund to undergo open surgery. In comparison TAVR is shown to have similar 30day and 1 year mortality and similar 30 day stroke rate.

What are the indications for TAVR?

Patients with severe symptomatic valvular aortic stenosis with an echo derived mean gradient >40mmhg

Patients having severe symptomatic, calcific valvular aortic stenosis who are surgically moribund and are deemed to be at very high surgical risk currently are the candidates eligible for TAVR. The promising results of TAVR have promted to expand its purview to intermediate risk candidates as well.

How many TAVR procedures have been performed? What is the current status in India?

Since the initial TAVR in 2002, over 2,50,000 procedures have been performed worldwide. Few centres in India including ours have already performed TAVR and TAVR is expected to grow in India.

CHAPTER 15

TAVR as its name goes is aortic valve implantation done as percutaneous based catheter implantable valves as opposed to an open surgical implant. The major advantage of TAVR versus surgical AVR is the fact that owing to its minimum invasive nature it can be done in patients who are too surgically moribund to undergo open surgery. In comparison, TAVR is shown to have similar 30 day and 1 year mortality and similar 30 day stroke rate to open surgery.

77

Practical Approach to a Person with Chest Pain

C H A P T E R

16

Suresh V Sagarad, Swetha A Biradar, NS Javali, AB Patil

ABSTRACT

Chest pain is the common reason for presentation in hospital emergency department and outpatient clinic.

Some patients presenting with chest pain will have serious life threatening illness with a high short term risk of mortality. The rapid identification of cause of acute chest discomfort and early specific treatment protocol decreases the risk. Cardiac, pulmonary, gastro intestinal, musculoskeletal, abdominal and psychological reasons are the underlying causes of chest pain. Patients with Acute coronary syndromes, pulmonary embolism, aortic dissection and tension pneumothorax can rapidly deteriorate and hence should be identified as early as possible. Regardless of clinical setting, a stepwise approach should be applied. Clinical examination important to assess hemodynamic stability, may point towards a specific diagnosis. ECG is the first and most often used investigation to identify ST elevation myocardial infarction and to initiate reperfusion therapy. Chest radiography, echocardiography, CT and MRI will aid in arriving definitive diagnosis. High sensitive troponin measurements are useful in evaluation of suspected acute coronary syndromes other than ST elevation MI. In most of the cases with clinical, biochemical and imaging the diagnosis can be reached in emergency department and treatment can be initiated.

KEY WORDS

Chest pain, Emergency, Symptom, Electrocardiogram, protocol

INTRODUCTION

Acute chest pain is one of the most common symptom with which patients present to emergency department (ED) or to out-patient clinics. It accounts for 7 million ED visists annually in USA.1 The evaluation of non traumatic chest pain is often challenging and may include life threatening situations.2,3 Rapid identification and triage of life threatening situation is priority, however, routine and liberal use of testing carry potential for adverse effects.

EPIDEMIOLOGY

In the USA, chest pain is the third leading reason for visit to ED and accounts for 6 to 7 million visits each year.

Less than 40% are not admitted or observed, however, significant proportion of patients require hospitalization and further evaluation. In most of the series of unselected population 5 to 15% of admitted patients are diagnosed as having acute coronary syndromes. Other life threatening cardiopulmonary conditions are noted in around 10%.

Most common cause is attributable to gastro intestinal tract.4 In significant proportion of cases diagnosis remains unknown, however, the prognosis is good in these cases.

In 2 to 6 % of cases who were discharged from ED as non ischemic cause were later found to have had ischaemic injury. These patients with missed diagnosis had worse prognosis. They had 30 day mortality risk double that of hospitalized patients.

ETIOLOGY OF CHEST DISCOMFORT

Cardiac cause (Table 1)

Myocardial causes: Myocardial ischemia is the life threatening chest discomfort. Myocardial ischemia is precipitated by an imbalance between myocardial oxygen requirement and supply. Myocardial oxygen consumption may be elevated by increases in heart rate, ventricular wall stress, and myocardial contractility.

Myocardial oxygen supply is determined by coronary blood flow and coronary arterial oxygen content.

Coronary artery disease (CAD) is commonly due to atherosclerosis which is a gradual process. Chronic stable angina is characterized by ischemic episodes that are typically precipitated by increase in oxygen demand like exertion, tachyarrhythmia, hypertension etc. The episode is typically relieved upon resting. Rupture or erosion of atherosclerotic plaque leads to unstable coronary syndrome. Acute coronary syndrome is characterized by ST segment elevation in STEMI and either ST depression or T wave changes or none in NSTEMI. Documentation of myocardial injury or necrosis by troponin or other cardiac biomarker establishes the diagnosis of myocardial infarction (MI). Unstable coronary symptoms may also occur because of increased myocardial oxygen demand

Table 1: Causes of chest pain3 Causes of chest discomfort

%

Gastrointestinal

42

Ischaemic heart disease

31

Chest wall syndrome

28

Pericarditis

4

Pleuritis

2

Pulmonary embolism Lund cancer

2 1.5

Aortic aneurysm

1

Aortic stenosis

1

Herpes zoster

1

79

Acute chest pain

Assess vitals clinical evaluation

Stable Suggestive cardiac cause

Unstable Stabilize Life threatening?

11 had ECG

CHAPTER 16

Other Pericarditis / Metabolic / Pulmonary embolism

Start reperfusion therapy

Additional biochemical / imaging studies

Non cardiac cause

NSTEMI

CXR

USG / Endoscopy / Others

Pneumothorax

Start NSTEMI Therapy Access hs Troponin Pneumonia

Mediastinal widening

TEE / CT / MRI

Aortic dissection

Cause not determined

Psychogenic emotional

Musculoskeletal cause

Fig. 1: Algorithm to evaluate and manage acute chest pain or because of decreased oxygen delivery due to anemia, hypoxia, or hypotension. Though atherosclerosis is the underlying cause of ischemia in most of the cases, there are variety of non atherosclerotic cause - Congenital anomalies, myocardial bridging, arteritis, radiation arteriopathy etc. Also non vascular causes like aortic valve disease, cardiomyopathies may cause coronary ischemic symptoms.

Pericardial: Pericarditis due to infective or non infective causes can produce acute chest discomfort. Most of the pericardium is insensitive to pain. It is postulated that associated pleurisy is the cause of pain and it typically referred to shoulder and neck due to overlapping supply

of central diaphragm via the phrenic nerve with somatic sensory fibers originating from 3rd and 4th cervical segments.

OTHER CARDIO-PULMONARY CAUSES

Acute aortic syndromes: This includes a spectrum of diseases related to disruption of the media of the aortic wall. Aortic dissection, penetrating ulcer and intramural hematoma are the prototypes of this spectrum. Though less common (estimated annual incidence, 3 cases per lakh population) these can be catastrophic when recognized late or left untreated. Aortic aneurysms can also produce chest discomfort.

Pulmonary disorders: Pleurisy either infective or non

80 Acute chest pain

ECG

CARDIOLOGY

Suggestive of Ischemia

Suggestive of MI

Yes

No

Two or more risk factors

Intermediate risk (8%)

No risk factors

Very low risk (<1%)

Two or more risk factors

High risk (>16%)

Hig (>16%)h risk

One risk factor or None

Intermediate risk (8%)

One risk factor

Low risk (4%)

Fig. 2: Risk stratification in acute cardiac chest pain infective is an important cause of chest discomfort. It is typically knifelike pain that is worsened by inspiration or coughing. Pulmonary embolism may be associated with chest discomfort. The pain may be because of pulmonary infarction with pleurisy, distension of pulmonary artery or RV wall stress and / or RV sub endocardial ischemia.

Pneumothorax may present with chest pain. Most the pulmonary disorders presenting with chest pain are usually associated with other symptoms like dyspnoea, cough, syncope etc.

NON CARDIOPULMONARY CAUSES

GI disorders: This is a most common cause of non traumatic chest pain. The discomfort may mimic serious conditions like MI. GERD, motility disorders of esophagus and tear should be considered in evaluation of chest pain.

Hepatobiliary disorders like cholecystitis and biliary colic may also mimic acute coronary syndromes.

Musculoskeletal and others: Musculoskeletal disorders are an important cause of chest pain. Pain may be due to involvement of chest wall, nerves of the chest wall or upper limbs. Costochondritis and cervical radiculitis may produce acute or chronic pain. Herpes zoster before the eruptions may confuse with other causes.

Emotional and psychological causes: Significant proportion of patients presenting ED may have emotional or psychological cause for chest pain. There may be other clues to suggest psychological origin, however, at times it may be difficult differentiate it from common organic causes.

Approach to chest pain (Figure 1): As there are many causes of chest pain it is challenging in the ED to triage patients with chest pain. The most important questions to be answered on arrival are clinical stability of the patient and likelihood of a underlying cause of chest to life threatening. The high risk life threatening conditions

include ACS, aortic syndromes, tension pneumothorax, pulmonary embolism. A rapid targeted assessment for a serious cardiopulmonary cause is of particular relevance for patients with acute ongoing chest pain. Mortality for patients with AMI differs greatly between admitted and discharged patients (6% vs 25%).6 Missed MI accounts for 20% of US emergency medicine related litigation dollars.7 Task force report on the management of chest pain is available.8 Following questionnaire is useful in the assessment of acute chest pain.

or movement are more likely to be musculoskeletal.

Pain getting worsened in supine and relieved by sitting upright or leaning forward suggest pericarditis. GERD symptoms are also aggravated by supine position and may be relieved by sitting. Angina during stable patients are noted during exertion and are relieved by rest. The similar discomfort at rest may suggest life threatening ACS. Post prandial angina also suggest severe underlying CAD.

1.

Could the chest pain be due to potentially life threatening conditions?

2.

Could the chest pain be due to a chronic condition likely to lead to serious complications?

3.

Could the chest pain be due to an acute condition that warrants specific treatment?

4.

Could the chest pain be due to another treatable condition?

Presence of associated symptoms may indicate specific diagnosis. Diaphoresis, dyspnea, nausea, fatigue, pre syncope or syncope may accompany angina chest pain.

Hemo dynamically significant pulmonary embolism is associated with dyspnea and / or syncope. Hemoptysis suggest paranchymal pathology, pulmonary edema, pulmonary embolism. Predominant nausea, vomiting and eructation generally indicate gastro intestinal pathology.

Clinical examination: General and systemic examination may reveal the origin of chest pain.

Quality of pain

Tightness or pressure is consistent with typical presentation of myocardial ischemic pain. However, many times patients may have atypical chest discomfort.

Pain similar to earlier angina episodes points towards ACS. Tearing or ripping pain is often noted in aortic dissection. A burning quality may suggest acid reflux or peptic ulcer disease but may occur with MI. Esophageal spasm is usually severe squeezing type. Pleurisy is typically described as a knife like pain.

Location and radiation

A substernal location with radiation to neck, jaw, or arms is typical of myocardial ischemia. Highly localized pain are unlikely angina episodes. Esophageal disorders most commonly present with substernal pain. Severe pain radiating to back should suggest aortic dissection.

Radiation to ridge of trapezius is characteristic of pericarditis. Hepatobiliary, pancreatic and peptic ulcer pains are predominantly epigastric.

Pattern of pain

Many patients present to ED repeatedly with severe very short lasting migratory pain. This is unlikely to be of ischemic origin. Myocardial ischemic discomfort usually builds over minutes. Constant and prolonged pains are also unlikely to represent ACS. They are more likely to due to hepatobilaiary or pancreatic in origin.

Aggravating and relieving factors

Alteration in the severity of pain with changes in position

Associated symptoms

General physical examination and vital signs

Patients with ACS are generally anxious, uncomfortable, pale, cyanotic or diaphoretic. Levineâ&#x20AC;&#x2122;s sign (clenched fist against the sternum) suggest angina pain.

Hyperventilation is sign of psychological origin.

Peripheral signs of shock are hallmark of severe organic pathology and needs emergent attention. Hypertension and pulse asymmetry are noted in aortic dissection.

Hypoxemia indicating severe nature may occur both in pulmonary and cardiac conditions. Evidence of DVT should arose strong suspicion of pulmonary embolism.

There may be tell tale signs of peripheral arterial disease.

Chest

Specific signs like pleural rub (pleurisy), bronchial breathing (pneumonia), absent lung sounds (pneumothorax), basal rales (pulmonary edema) are useful in arriving clinical diagnosis.

Cardiovascular system

Third heart sound indicate heart failure, fourth sound is common in hypertension and MI. Murmurs due to valvular pathology and VSD are important clinical indicators of cardiac pathology. Pericardial friction rub indicate pericardial inflammation.

Abdomen

Organomegaly and local signs point towards local causes. Congestive hepatomegaly may be significant in congestive heart failure.

Investigations

Rapid access to investigative tools is a key while triaging patients with acute chest.

Electrocardiography

The ECG should be recorded as early as possible.

Guidelines recommend that an ECG be obtained within 10 minutes of presentation. The ECG is an excellent tool for identifying ACS especially STEMI. It is highly specific

CHAPTER 16

HISTORY AND CLINICAL EVALUATION

Careful history is useful aid in diagnosis of chest pain.

Past history of MI may point towards ACS while history suggestive connective tissue disorders or Marfanâ&#x20AC;&#x2122;s syndrome may indicate aortic dissection or pneumothorax. Risk factors for atherosclerosis may be present. Past history of cholelithiasis or evidence of peptic ulcer on previous endoscopy may help in arriving diagnosis.

81

CARDIOLOGY

82

(77 to 100%) depending on the criteria used. However, the sensitivity of ECG is poor (28 to 54%) in the first 12 hours.7,9 Presence of a normal ECG neither excludes MI nor provides sufficient assurance to discharge the patient from ED. Reperfusion therapy is mainly based on recognition of STEMI on ECG. ST segment depression and symmetric T wave inversions at least 0.2 mV in depth are useful for detecting myocardial ischemia in the absence of STEMI and are also indicative of higher risk of death or recurrent ischemia. Serial ECGs is recommended in the ED for suspected ACS. ST and T wave changes may be seen in variety of non ischemic conditions like pericarditis, myocarditis, metabolic abnormalities, pulmonary embolism, hyperventilation, ventricular hypertrophy etc.

Chest Radiography

Chest radiograph is useful in evaluating chest pain due to pulmonary causes. It may reveal pneumonia, pneumothorax, pleural effusion. Mediastinal widening may be present in acute aortic syndromes. Hampton’s hump or Westermark’s sign in pulmonary embolism or pericardial calcification in chronic pericarditis are some specific findings.

Cardiac biomarkers

Assessment of cardiac biomarkers is vital during the initial and subsequent evaluation of patient with chest pain suggestive of ACS. Elevated biomarkers indicate myocardial injury and high risk. These are circulating proteins released from injured myocardial cells and the rise is proportional to degree of injury. However, owing to the time necessary for the release, initial evaluation may reveal normal range of biomarkers despite extensive STEMI. Over the years cardiac specific troponin assessment has become gold standard in the evaluation of ACS patients. High sensitivity troponin assay are available to rule in or rule out MI based on serial assay.

High sensitivity assay have revolutionized evaluation of ACS patients. This permits earlier detection of myocardial injury and enhanced overall accuracy and improved risk stratification. The diagnosis of MI should be reserved for acute myocardial injury as shown by a rising and / or falling pattern with at least on value exceeding 99th percentile of reference limit due to ischemia.

D-dimer assessment is useful in the evaluation of suspected pulmonary embolism. It has a very high negative predictive value. NT-proBNP is useful in diagnosis and prognostication of heart failure.

Echocardiography

Trans-thoracic echocardiography is widely available now. It is useful tool to assess overall ventricular function, valvular morphology, presence of regional wall motion abnormality, pericardial effusion etc. Trans-esophageal echocardiography can accurately detect acute aortic syndromes. Mechanical complications of MI like mitral regurgitation, VSD or cardiac tamponade can be quickly appreciated by echocardiography. Right sided chamber assessment can reveal possibility of pulmonary embolism.

CT angiography

The technology is very useful in certain subgroup of patients when diagnosis in uncertain. CT coronary angiography can detect presence or absence of significant obstructive coronary artery disease. CT pulmonary angiography can identify pulmonary embolism. CT angiography is very useful in evaluating aortic dissections. CT scan can detect other pulmonary paranchymal or pleural pathology.

MRI imaging

Cardiac MRI (CMR) can accurately predict structural and functional abnormalities of heart and vasculature.

Gadolinium enhanced CMR can provide early detection of MI. MR angiography is very accurate in detecting aortic dissections.

Clinical decision making

Clinical decision making can be challenging in ED. The most important is to identify life threatening conditions and to start early interventions specific to diagnosis.

Several clinical algorithms are available as decision aids in ED. Goldman and Lee developed one of the first such decision aids, using only the ECG and risk indicators – hypotension, pulmonary rales, and known CAD – to categorize patients into four risk categories ranging from a <1% to a > 16% probability of a major CV complications.

The Acute Cardiac Ischemia Time-Insensitive Predictive Instrument (ACI-TIPI) combines age, sex, chest pain presence, and ST –segment abnormalities to define a probability of ACS. Heart Score and North American Chest pain Rule can also be used as decision aids.

Treatment of acute chest pain: Acute chest pain treatment depends on the diagnosis made after initial clinical evaluation, ECG, biochemical and other imaging modalities. ACS, pulmonary embolism, aortic dissection and tension pneumothorax which have high morbidity and mortality should be treated early as per the standard guidelines. Low risk group can be discharged from the ED and can be followed on out-patient basis (Figure 2).

CONCLUSIONS

Acute chest pain is the commonest symptom for attending emergency and out-patient departments. Acute chest pain can be manifestation of a life threatening situation.

However, it can also be a manifestation insignificant cause.

Clinical, biochemical and other investigations should be used to diagnosis of chest pain as early as possible.

Early initiation of targeted therapy reduces mortality and morbidity. Although it is essential to identify all patients with serious conditions, it is also important to control costs and not to subject to unnecessary investigations, in patient care and resultant psychological stress.

REFERENCES

1.

Sabastine MS, Cannon CP Approach to the patient with chest pain in Braunwald’s Heart Disease A text book of cardiovascular medicine, 9th edition Bonow RO, Mann DL, Zipes DP, Libby P, Elsevier Inc 2012.

2.

Marrow DA. Chest discomfort in Harrison’s principles of Internal Medicine 19th ed Kasper DL, Fauci AS, Hauser SL,

Longo DL, Jameson LJ, Loscalzo J. Mc Graw Hill, Health Professionals division 2015 3. Parsonage WA, Cullen L, Younger JF. The approach to patients with possible cardiac chest pain. MJA 2013 doi:10.5694/mja12.11171 P Fruergaard, Launbjerg J, Hesse B, Jorgenesen F, Petri A, Eiken P et al The diagnosis of patients admitted with acute chest pain bur without myocardial infaection Eur Heart J 1996;17:1028-34

5.

Lee TH, Rouan GW, Weisberg M, Brand DA, Acampora D, Stasiulewicz C et al Clinical characteristics and natural history of patients with acute myocardial infarction sent home from the emergency department. Am J Cardiol 1987; 60:219-24.

Karcz A, Holbrook J, Burke MC, Doyle MJ, Erdos MS, Friedman M et al Massachusetts Emergency Medicine closed malpractice claims:1988-90. Ann Emerg Med 1993; 22:553-9.

7.

Herren KR, Mackway-Jones K. Emergency management of cardiac chest pain: a review. Emerg Med J 2001; 18:6-10.

8.

Erhardt L, Herlitz J, Bossaert L, Halinen M, Keltai M, Koster R, Marcassa C et al. Task force on the management of chest pain. Eur Heart J 2002; 23:1153-76.

9.

Brush JE, Brand DA, Acampora D, Chalmer B, Wackers FJ et al. Use of the initial electrocardiogram to predict in hospital complications of acute myocardial infarction. N Engl J Ned 1985; 312:1137-41.

83

CHAPTER 16

4.

6.

Practical Approach to a Patient with ECG Changes

C H A P T E R

17

Shirish MS Hiremath

The ECG is the oldest cardiologic test, but even 100 years after its inception, it continues as the most commonly used cardiologic test.

Historical milestones in ECG1 1887: Augustus Desire Waller, recorded electric current preceding cardiac contraction.

1903: Einthoven, developed string galvanometer.

1911: Sir Thomas Lewis published his pioneering work on ECG 1929: Dock, use of cathode ray oscilloscope for ECG 1932: Wolferth CC and Wood CC, introduced chest leads 1942: Goldberger E, Introduced unipolar limb leads.

ECG in emergency room: Despite the advent of expensive and sophisticated alternatives, ECG dictates the timely diagnosis and management in acute coronary syndrome (ACS) and arrhythmias.

In a suspected case of ACS, ECG should be acquired and interpreted promptly (i.e. target within 10 min) after clinical presentation, and initial ECG is non-diagnostic then serial ECG should be acquired (15-20 minute interval) to catch the dynamic changes.3 R

PR

T wave

J

P

P

QRS 1

V= Vulnerable period

2

0

Phase

Isoelectric line: horizontal level between cardiac cycles

ST segment

Cell cytoplasm Na+ K+ K+K+ Na+ – – + + + + – – – – + + K+ Na+ Na+ Na+ K+ Na+ influx Efflux K+ – +

ST elevation

ST depression and T wave changes

New ST elevation at the J point in two contiguous leads with the cut-points: ≥0.1 mV in all leads other than leads V2–V3 where the following cutpoints apply: ≥0.2mVinmen≥4 0years;≥0.25mVinmen <40 years,or ≥0.15 mV in women.

New horizontal or downsloping ST depression ≥0.05 mV in two contiguous leads and/orT inversion ≥0.1 mV in two contiguous leads with prominent R wave or R/S ratio >1.

3 Phase 4

K+ – +

Coronary artery size and distribution of arterial segments, collateral vessels, location, extent and severity of coronary stenosis, and prior myocardial necrosis can all impact ECG manifestations of myocardial ischaemia.

Electrocardiographic evidence of myocardial ischaemia in the distribution of a left circumflex artery is often overlooked and is best captured using posterior leads at the fifth intercostal space (V7 at the left posterior axillary line, V8 at the left mid-scapular line, and V9 at the left paraspinal border). A cut-point of 0.05 mV ST elevation is recommended in leads V7–V9; specificity is increased at a cut-point ≥0.1 mV ST elevation and this cutpoint should be used in men, 40 years old. ST depression in leads V1–V3 may be suggestive of infero-basal myocardial ischaemia (posterior infarction), especially when the terminal T wave is positive (ST elevation equivalent), however this is non-specific. In patients with inferior and suspected right ventricular infarction, right pre-cordial leads V3R and V4R should be recorded, since ST elevation ≥0.05 mV (≥0.1 mV in men , 30 years old) provides supportive criteria for the diagnosis (ref Fig---). Other ECG signs associated with acute myocardial ischaemia include cardiac arrhythmias, intraventricular and atrioventricular conduction delays, and loss of precordial R wave amplitude. Coronary artery size and distribution of arterial segments, collateral vessels, location, extent and severity of coronary stenosis,

Table 1: ECG manifestations of acute myocardial ischaemia (in absence of LVH and LBBB)4

QT

K+ – +

Acute or evolving changes in the ST– T waveforms and Q waves, when present, potentially allow the clinician to time the event, to identify the infarct-related artery, to estimate the amount of myocardium at risk as well as prognosis, and to determine therapeutic strategy. Various algorithms predict the IRA in case of STEMI, though this correlation is not valid in NSTEMI.

– – + +

–

Cell membrane

Fig. 1: The action potential, and the electrocardiogram2

85

ST-segment elevation in V1, V2 and V3

ST-segment elevation in V1 (>2.5 mm) or right bundle-branch block with Q wave or both

ST-segment depression (>1 mm) in II, III, and aVF

Proximal left anterior descending artery Sensitivity 34% Specificity 98% Positive predictive value 93% Negative predictive value 68%

Distal left anterior descending artery Sensitivity 66% Specificity 73% Positive predictive value 78% Negative predictive value 62%

Fig. 2: Algorithm for identifying IRA in anterior wall MI5 Inferior Wall AMI (ST elevation II, III, aVF) LCx vs RCA

ST ä ≥ 1 mm POS T – WAVE

PROXIMAL OCCLUSION RCA

NO ST ä : POS T – WAVE

DISTAL OCCLUSION RCA

NEG T – WAVE

OCCLUSION CX

ST segment elevation III > II No

Yes ST segment elevation VI

LCX or Distal RCA No

Yes

Proximal RCA and RV Infarction

ST elevation V4R Yes

Proximal RCA with RV involvement

No Mid RCA, No RV involvement

Fig. 3: Algorithm for identifying IRA in inferior wall MI6 and prior myocardial necrosis can all impact ECG manifestations of myocardial ischaemia.

When the patient has LBBB on admission and recent previous ECGs do not show LBBB, the patient is presumed to have new-onset LBBB, which many investigators and current guidelines accept as the equivalent of electrocardiographic findings supportive of AMI.8,9 When the patient has LBBB on arrival and no preexisting ECG is available for comparison, then there are specific ECG criteria which could distinguish between patients with new injury or infarction and those without. Sgarbossa et al. proposed specific electrocardiographic criteria for the diagnosis of AMI in the presence of LBBB applied to patients in GUTO-I trial.10 But this criteria performed

Fig. 4: Value of ST-T changes in acute infero-posterior MI poorly because of a low sensitivity of 10%, although the specificity was high at 82%.

Using a criterion of twice the upper limit of normal value for serum troponin as the ‘gold standard’ for confirmation of myocardial injury, the investigators in the Wong et al.11 study demonstrate a high specificity for the criteria.

Acute pericarditis very closely resembles acute coronary syndrome in terms of symptoms and the ECG changes.

The two classical ECG findings of acute pericarditis are ST elevation (most sensitive and consistent) and PR depression (most specific). Characteristic ST-elevation of acute pericarditis is concave upwards and it is present in the majority of the standard ECG leads, except in leads AVR and V1 where the ST segment is always depressed.

This ST-elevation is often transient and are sometimes followed (after a variable time) by diffuse T-wave inversions.

Event ECG at the time of palpitation is of foremost importance in diagnosis and management of arrhythmia.

For evaluation of arrhythmia, traditional step-wise assessment of event-ECG should be followed i.e. rate, rhythm, axis, tachycardia cycle-length, QRS morphology, p-wave morphology, p-QRS relationship. ECG during asymptomatic period has equal importance in diagnosis i.e. p/QRS-morphology, QRS duration (QRSd), QT-

CHAPTER 17

Proximal left anterior descending artery Sensitivity 12% Specificity 100% Positive predictive value 100% Negative predictive value 61%

ST-segment depression (≤1 mm) or ST-segment elevation in II, III, and aVF

86

Table 2: Differential diagnosis of ST-elevation7 1.

Ischemia/myocardial infarction Noninfarction, transmural ischemia (Prinzmetal’s angina, and probably Tako-Tsubo syndrome, which may also exactly simulate classical acute infarction) Acute myocardial infarction

CARDIOLOGY

Postmyocardial infarction (ventricular aneurysm pattern) 2.

Acute pericarditis

3.

Normal variants (including “early repolarization” patterns)

4.

Left ventricular hypertrophy/left bundle branch block

5.

Other (rarer) Acute pulmonary embolism

Fig. 5: An electrocardiogram in acute pericarditis.

Brugada patterns (right bundle branch block–like pattern with ST elevations in right precordial leads)

Narrow QRS tachycardia (QRS duration less than 120 ms)

Class 1C antiarrhythmic drugs

Regular tachycardia?

DC cardioversion Hypercalcemia Hyperkalemia

Atrial fibrillation Atrial tachycardia/flutter with variable AV conduction MAT

Atrial rate greater than ventricular rate?

Myocarditis Tumor invading left ventricle Trauma to ventricles

Table 3: Sgarbossa criteria for diagnosis of AMI in LBBB (score ≥3 have high specificity)10 ECG criteria

Yes

No

Atrial flutter or atrial tachycardia

Analyze RP interval

Short (RP shorter than PR)

Score

1.

ST-segment elevation ≥1 mm and concordant with QRS complex

5

2.

ST-segment depression ≥1 mm in lead V 1 V2V3

3

3.

ST-segment elevation ≥5 mm and discordant with QRS complex

2

pre-excitation,

Visible P waves?

Yes

Nonischemic myocardial injury

interval, presence of pathological q-wave.

No

No

Hypothermia [J (Osborn) waves 6.

Yes

presence

RP shorter than 70 ms

RP longer than 70 ms

AVNRT

AVRT AVNRT Atrial Tachycardia

Long (RP longer than PR)

Atrial tachycardia PJRT Atypical AVNRT

Fig. 6: Algorithm for diagnosis of a narrow QRS tachycardia12 of

First step in assessment of tachycardia is QRSd, less than 120msec is defined as narrow-complex tachycardia (NCT) and ≥120msec is defined as broad complex tachycardia (BCT). With few exceptions NCT is almost always supraventricular in origin therefore less likely to be life-threatening. With few exceptions BCT is almost always ventricular in origin therefore more likely to be life-threatening.

Initial step in assessment of NCT is regularity of R-R interval, as AV-junctional tachycardias are always regular.

In management of NCT, rate control in emergency room

can be done with intravenous beta-blocker, calcium channel blocker or adenosine. Long-term management largely depends on number of recurrences and underlying structural heart disease. For tachycardia involving AVjunction (AVRT/AVNRT) electrophysiological study with radiofrequency ablation is highly effective, with more than 95% curing rate in long-term and very low risk of recurrence.

For atrial tachycardias (Afib, Aflutter and ATach), rate control versus rhythm control strategy depends on age of the patient and underlying structural heart disease.

Ventricular tachycardia (VT) arises distal to the bifurcation of the His bundle in the specialized conduction system,

87

Wide QRS-complex tachycardia (QRS duration greater than 120 ms)

Regular or irregular?

Regular

Irregular

Vagal maneuvers or adenosine

Previous myocardial infarction or structural heart disease?

If yes, VT is likely

Atrial fibrillation Atrial flutter/AT with variable conduction and a) BBB or b) antegrade conduction via AP

1 to 1 AV relationship?

No

Yes or unknown

QRS morphology in precordial leads

Typical RBBB or LBBB

SVT

V rate faster than A rate

A rate faster than V rate

VT

Atrial tachycardia Atrial flutter

Precordial leads • Concordant* VT • No R/S pattern • Onset of R to nadir longer than 100 ms

RBBB pattern • qR, Rs or Rr1 in V1 • Frontal plane axis range from +90 degrees to –90 degrees

VT

LBBB pattern • R in V1 longer than 30 ms VT • R to nadir of S in V1 greater than 60 ms • qR or qS in V6

Fig. 7: Algorithm for diagnosis of a wide QRS tachycardia12 ventricular muscle, or combinations of both tissue types.

Mechanisms include disorders of impulse formation (enhanced automaticity or triggered activity) and conduction (reentry). In patient without underlying structural heart disease, prognosis of VT is good, but with underlying heart disease there is high risk of sudden cardiac death. Differentiating VT from SVT with aberrant conduction is very important, though may be difficult at times.

Various algorithms are available for early diagnosis of VT in emergency room. Of these, Brugada’s algorithm is the most commonly used.13

After acute management of sustained VT, the goal of long-term therapy is to prevent sudden cardiac death and recurrence of symptomatic VT. Patients with structural heart disease especially LV systolic dysfunction (ejection fraction ≤35%) are at highest risk of recurrence of VT and subsequent SCD. Idiopathic VT is defined as monomorphic VT in patients without any structural heart disease or coronary disease.

There are three distinct entities with characteristic ECG pattern, based on the location of the VT—outflow tract tachycardia, annular tachycardia, and fascicular tachycardia. These type of VTs have very favourable

CHAPTER 17

Is QRS identical to that during SR? If yes, consider: • SVT and BBB • Antidromic AVRT†

Cumulative Sensitivity for VT

Cumulative Specificity for VT

1. Absence of an RS complex in all precordial leads

21%

100%

2. Precordial RS interval >100 ms

66%

98%

3. VA dissociation

82%

98%

4. Morphological criteria for VT

99%

97%

High-risk subgroup Prior coronary event EF < 30%; heart failure

0

QS in V6

Cardiac arrest survivor

AVID, CIDS, CASH

Arrhythmia risk markers, post-myocardial infarction

MADIT I, MUSTT

30

0

150,000 300,000 ABSOLUTE NUMBER

Any Q V6

Any Q in V6

Fig. 8: Brugada’s morphological criteria13 prognosis and RF catheter ablation effectively eliminates tachycardia in symptomatic patients.

Right ventricular outflow tract (RVOT) VTs have a characteristic electrocardiographic appearance of a left bundle branch block contour in V1 and an inferior axis in the frontal plane. It responds best to vagal maneuvers, beta-blocker. Most probable mechanism is cyclic adenosine monophosphate–triggered activity resulting from early or delayed afterdepolarizations. ECG of LV outflow tract VT mimics RVOT-VT with presence of an S wave in lead I and an early precordial R wave transition (V1-V2).

For mitral annular VT, the ECG pattern is typically right bundle branch block pattern (transition in V1 or V2), S wave in V6, and monophasic R or Rs in leads V2 through V6. For tricuspid annular VT, the foci generally originate in the septal region, and thus the typical ECG pattern is left bundle branches block pattern (Qs in lead V1), an early transition in precordial leads (V3), and narrower QRS complexes.

Left fasicular VT is characterized by a right bundle branch block contour, those originating from posterior fascicle have right-ward axis and those originating from anterior fascicle have left-ward axis. Re-entry is the probable mechanism, so they very well respond to calcium channel blockers (verapamil/diltiazem) and highly amenable to radiofrequency ablation.

Bradyarrhythmias are arbitrarily defined as a heart rate below 60 beats/min. Bradyarrhythmias can be categorized

30

to rs]

ac

su sk

ris

-ri gh

tip ral

ne Ge

io

lat

pu

po

ear 5y

3 n>

er [1 p

e

f ag

so

ul

hi al

[1 per 100,00]

20

kf

bg

ro u

p

[1 per 4-10]

00]

-1,0

500

k subgroup Individual low-ris [0-1 risk factor]

Usual causes: • Coronary atherosclerosis • Dilated cardiomyopathy • Infiltrative heart diseases • Valvular heart disease

Adolescents/young adults

AGE (years)

[M

du vi

Usual causes: • Myocarditis • Hypertrophic CM • Long-QT syndromes • Right ventricular dysplasia • Anomalous coronary artery • brugada syndrome • Idiopathic VF

di

B

Advanced heart disease

le

LBBB configuration

In

RS < 1 in V6

20

SCD-HeFT

Fig. 9: Impact of population subgroups and time from events on the clinical epidemiology of Sudden cardiac death (SCD)14

QRS width > 160 ms, right axis

(A) Initial R in V1 > 30 ms (B) Slurring or notching of the downstroke of the S– A wave in V1–2 (C) Begin QRS-nadir S– C Rabbit ear in V1 wave > 70 ms in V1–2

10

MADIT II

PERCENT

0.001%/year

R in V1

Events

General population

QR, R, RSr’ complex in V1

qR in V1

Population segment

10-25%/year

RBBB configuration QRS width > 140 ms, left axis

Incidence

0.1%/year

ECG criteria

CARDIOLOGY

SUDDEN CARDIAC DEATH - INCIDENCE AND TOTAL EVENTS

Table 4: Brugada Algorithm: Steps13

INCREASING RISK

88

40

50

60

Fig. 10: Age-related and disease-specific risk for SCD on the basis of the level of disturbance in the hierarchy of the normal impulse generation and conduction system (from sinus node to AV node to His-Purkinje system).

Sinus bradycardia is defined as sinus rhythm at a rate slower than 60 beats/min. P waves have a normal contour and occur before each QRS complex, usually with a constant PR interval longer than 120 milliseconds. Sinus arrhythmia often coexists.

Sick sinus syndrome is a term applied to a syndrome encompassing a number of sinus nodal abnormalities, like persistent spontaneous sinus bradycardia inappropriate for the physiologic circumstance; sinus arrest or exit block; combinations of SA and AV conduction disturbances; alternation of paroxysms of rapid regular or irregular atrial tachyarrhythmias and periods of slow atrial and ventricular rates (bradycardia-tachycardia syndrome). Sick sinus syndrome can occur in the absence of other cardiac abnormalities. The course of the disease is frequently intermittent and unpredictable because it is influenced by the severity of the underlying heart disease.

An AV block exists when the atrial impulse is conducted with delay or is not conducted at all to the ventricle when the AV junction is not physiologically refractory.

The conduction disturbance is classified by severity into three categories. Most common cause is age-related degenerative AVB followed by congenital, post-operative.

Serum potassium (mEq/L)

J Point

ST segment monitoring; monitoring: reference points Fig. 11: Automated ST-segment

P QRS T U

10

Ventricular fibrillation

9

Auricular standstill, intraventricular block

8

Prolonged PR interval, depressed ST segment, high T wave

7

High T wave

sign-wave appearance

4D5

CHAPTER 17

PR Point Isoelectric point

Normal

ST Point

Hyperkalemia

ST Segment

89

Normal

2

Electrolyte imbalance

0 3 4

K+

K+

Ca2+

K+

outward

Hypokalemia

1

inward

3.5

Low T wave

3

Low T wave, high U wave

2.5

Roller-coaster Low T wave, high U wave, sign low ST segment

Camel-hump sign

Fig. 13: ECG changes in hyperkalemia Na+

Purkinje system. Type II AV block, particularly in association with a bundle branch block, is localized to the His-Purkinje system.

Fig. 12: A ventricular action potential with a schematic of the ionic currents flowing during the phases of the action potential Depending on severity and level of block, there 3 types of AVB. 1.

First degree: During first-degree AV block, every atrial impulse conducts to the ventricles and a regular ventricular rate is produced, but the PR interval exceeds 0.20 second in adults, mostly with no QRS aberration. Clinically important PR interval prolongation can result from a conduction delay in the AV node (A-H interval), in the His-Purkinje system (H-V interval), or at both sites.

2.

Second-degree: Blocking of some atrial impulses conducted to the ventricle at a time when physiologic interference is not involved constitutes seconddegree AV block. Electrocardiographically, typical type I second-degree AV block is characterized by progressive PR prolongation culminating in a nonconducted P wave , whereas in type II seconddegree AV block, the PR interval remains constant before the blocked P wave. In both cases, the AV block is intermittent and generally repetitive. Type II AV block often antedates the development of Adams-Stokes syncope and complete AV block, whereas type I AV block with a normal QRS complex is generally more benign and does not progress to more advanced forms of AV conduction disturbance. Type I AV block with a normal QRS complex almost always takes place at the level of the AV node, proximal to the His bundle. Type I AV block in a patient with a bundle branch block can be caused by a block in the AV node or in the His-

3.

Third degree (complete AVB): Third-degree or complete AV block occurs when no atrial activity is conducted to the ventricles and therefore the atria and ventricles are controlled by independent pacemakers, thus there is complete AV dissociation.

The ventricular rate in acquired complete heart block is < 40 beats/min but can be faster in congenital complete AV block. Complete AV block can result from block at the level of the AV node (usually congenital), within the bundle of His, or distal to it in the Purkinje system (usually acquired).

ECG in intensive care unit: For patients admitted in medical or surgical ICU continuous ECG monitoring is very essential for early recognition of myocardial ischaemia, electrolyte disturbances, and dysarrhythmias.

Myocardial ischaemia: For ischaemia monitoring, commonly applied standard criteria suggested by Ellestad and colleague includes horizontal or down sloping depression of more than 1 mm at 60 msec from the ‘J’ point (‘J’ point is where QRS complex changes its slope) lasting for at least 60 seconds.6 This has been accepted by American college of cardiology.

On ECG monitor, single best lead, for detection of myocardial ischaemia is V5. V4, II, V3 and V6 are in decreasing order of sensitivity. Chances of ischaemia detection among combined leads is; V5 & II in 80%, V4 & V5 in 90%, V4 , V5 & II in 96% and II & V2 -V5 in 100% of cases.8 Electrolyte disturbances in ICU: Potassium and calcium

90

are essential for maintenance of transmembrane potential and propagation of action potential, so changes in these electrolytes are reflected in resting ECG. But ECG changes don’t always correlate with serum level.

CARDIOLOGY

ECG changes in hypokalemia are due to delayed repolarisation so the changes are seen in ST-segment, T-wave and U-wave. These are most marked when serum K+ is < 2.7 mmol/L. Hyperkalemia is a medical emergency because it leads to cardiac arrhythmias, increase in plasma K+ concentration depresses intracardiac conduction, with progressive prolongation of the PR and QRS intervals.

Severe hyperkalemia results in loss of the P wave and a progressive widening of the QRS complex.

Extracellular calcium is important for transmembrane action potential so changes in serum ionised calcium level affects conduction time leading to changes in QT interval (no changes in QRS-T duration). Hypercalcemia causes shortening and in severe cases absence of ST-segment, conversely in hypocalcemia there is prolong ST-segment.

Marked QT prolongation, sometimes with deep, wide T-wave inversions, may occur with intracranial bleeds, particularly subarachnoid haemorrhage (“CVA T-wave” pattern). Systemic hypothermia also prolongs repolarization, usually with a distinctive convex elevation of the J point (Osborn wave). Similar J-point elevation is also seen in severe Hypercalcemia, called as nonhypothermic Osborn wave.

REFERENCES

1. R S Atkinson, G B Rushman, J Alfred Lee. Notes on Physiology. A Synopsis of Anaesthesia. Bombay: K M Varghese Company, 1987; 51–52.

2.

Khan, M. Gabriel: On Call Cardiology, 3rd ed., Philadelphia, 2006, WB Saunders, Elsevier Science

3. Thygesen K, Alpert JS, White HD, Joint ESC/ACCF/ AHA/WHF Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction.

Eur Heart J 2007; 28:2525–2538.

4.

ThygesenK, AlpertJS, JaffeAS. Third universal definition of myocardial infarction. European Heart Journal 2012; 33:2551–2567.

5.

Engelen DJ, Gorgels AP, Cheriex EC, De Muinck ED, Ophuis AJ, Dassen WR, et al. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol 1999; 34:389-95.

6.

Gorgels AP, Engelen DJ, Wellens HJ. The electro cardiogram in acute myocardial infarction. In: Hurst’s the Heart. 11th edition, Fuster V, Alexander RW, O’Rourke RA (Eds.), McGraw-Hill: New York 2004:p.1351-60.

7.

Braunwald E, Bonowro, Mann DL, Zipes DP Et Al, Editors.

Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 9th Ed. Saunders, An Imprint Of Elsevier 2012

8.

Edhouse JA, Sakr M, Angus J, et al. Suspected myocardial infarction and left bundle branch block: electrocardiographic indication of acute ischemia. J Accid Emerg Med 1999; 16:331–5.

9.

Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with STelevation myocardial infarction—executive summary: a report of the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients with Acute Myocardial Infarction).

Circulation 2004; 110:588–636.

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