Tag Archives: heart Disease

Myocardial Infarction- Third Universal definition and classification

Definition of myocardial infarction

Criteria for acute myocardial infarction :

The term acute myocardial infarction (MI) should be used when there is evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischaemia. Under these conditions any one of the following criteria meets the diagnosis for MI:

Detection of a rise and/or fall of cardiac biomarker values [preferably cardiac troponin (cTn)] with at least one value above the 99th percentile upper reference limit (URL) and with at least one of the following:

  1. Symptoms of ischaemia.
  2. New or presumed new significant ST-segment–T wave (ST–T) changes or new left bundle branch block (LBBB).
  3. Development of pathological Q waves in the ECG.
  4. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.
  5. Identification of an intracoronary thrombus by angiography or autopsy.

•Cardiac death with symptoms suggestive of myocardial ischaemia and presumed new ischaemic ECG changes or new LBBB, but death occurred before cardiac biomarkers were obtained,or before cardiac biomarker values would be increased.

• Percutaneous coronary intervention (PCI) related MI is arbitrarily defined by elevation of cTn values (>5 x 99th percentile URL) in patients with normal baseline values (≤99th percentileURL) or a rise of cTnvalues >20% if the baseline values are elevated and are stable or falling. Inaddition,either(i)symptoms suggestiveof myocardialischaemia or (ii) new ischaemic ECG changes or (iii) angiographicfindings consistent with a proceduralcomplication or (iv) imaging demonstration of new loss of viable myocardium or new regional wall motion abnormality are required.

• Stent thrombosis associated with MI when detected by coronary angiography or autopsy in the setting of myocardial ischaemia and with a rise and/or fall of cardiac biomarker values with at least one value above the 99th percentile URL.

• Coronary artery bypass grafting (CABG) related MI is arbitrarily defined by elevation of cardiac biomarker values (>10 x 99th percentile URL) in patients with normal baseline cTn values (≤99th percentile URL). In addition, either (i) new pathological Q waves or new LBBB,or (ii) angiographic documented new graft or new native coronary artery occlusion, or (iii) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.

Criteria for prior myocardial infarction

Any one of the following criteria meets the diagnosis for prior MI:

• Pathological Q waves with or without symptoms in the absence of non-ischaemic causes. • Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract,in the absence of a non-ischaemic cause.

• Pathological findings of a prior MI

 UNIVERSAL CLASSIFICATION OF MYOCARDIAL INFARCTION

Type 1: Spontaneous myocardial infarction

Spontaneous myocardial infarction related to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus in one or more of the coronary arteries leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis. The patient may have underlying severe CAD but on occasion non-obstructive or no CAD.

Type 2: Myocardial infarction secondary to an ischaemic imbalance

In instances of myocardial injury with necrosis where a condition other than CAD contributes to an imbalance between myocardial oxygen supply and/or demand, e.g.coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachy-/brady-arrhythmias, anaemia, respiratory failure, hypotension, and hypertension with or without LVH.

Type 3: Myocardial infarction resulting in death when biomarker values are unavailable

Cardiac death with symptoms suggestive of myocardial ischaemia and presumed new ischaemic ECG changes or new LBBB, but death occurring before blood samples could be obtained, before cardiac biomarker could rise, or in rare cases cardiac biomarkers were not collected.

Type 4a: Myocardial infarction related to percutaneous coronary intervention (PCI)

Myocardial infarction associated with PCI is arbitrarily defined by elevation of cTn values >5 x 99th percentile URL in patients with normal baseline values (£99th percentile URL) or a rise of cTn values >20% if the baseline values are elevated and are stable or falling. In addition, either (i) symptoms suggestive of myocardial chaemia, or (ii) new ischaemic ECG changes or new LBBB, or (iii) angiographic loss of patency of a major coronary artery or a side branch or persistent slow- or no-flow or embolization, or (iv) imaging demonstration of new loss of viable myocardium or new regional wall motion abnormality are required.

Type 4b: Myocardial infarction related to stent thrombosis

Myocardial infarction associated with stent thrombosis is detected by coronary angiography or autopsy in the setting of myocardial ischaemia and with a rise and/ or fall of cardiac biomarkers values with at least one value above the 99th percentile URL.

Type 5: Myocardial infarction related to coronary artery bypass grafting (CABG)

Myocardial infarction associated with CABG is arbitrarily defined by elevation of cardiac biomarker values >10 x 99th percentile URL in patients with normal baseline cTn values (£99th percentile URL).In addition,either (i) new pathological Q waves or new LBBB,  or (ii) angiographic documented new graft or new native coronary artery occlusion, or (iii) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality

Revised Jones Criteria for Acute Rheumatic Fever – 2015 guideline

Acute rheumatic fever remains a serious healthcare concern for the majority of the world’s population despite its decline in incidence in Europe and North America. This statement reviews the historic Jones criteria used to diagnose acute rheumatic fever in the context of the current epidemiology of the disease and updates those criteria to also taking into account the use of Doppler echocardiography in the diagnosis of carditis as a major manifestation of acute rheumatic fever.

1. Epidemiology:

1. It is reasonable to consider individuals to be at low risk for ARF if they come from a setting or population known to experience low rates of ARF or RHD (Class IIa; Level of Evidence C).
2. It is reasonable that where reliable epidemiological data are available, low risk should be defined as having an ARF incidence <2 per 100 000 school-aged children (usually 5–14 years old) per year or an allage prevalence of RHD of ≤1 per 1000 population per year (Class IIa; Level of Evidence C).
3. Children not clearly from a low-risk population are at moderate to high risk depending on their reference population (Class I; Level of Evidence C).

2. Clinical Manifestations of ARF:

Generally, the clinical profile of ARF in low- and middle-income countries closely resembles that of high-income countries. Universally, the most common major manifestations during the first episode of ARF (the “major criteria” for diagnosis) remain
carditis (50%–70%) and arthritis (35%–66%). These are followed in frequency by chorea (10%–30%), which has been demonstrated to have a female predominance, and then
subcutaneous nodules (0%–10%) and erythema marginatum (<6%), which remain much less common but highly specific manifestations of ARF.

3.Carditis: Diagnosis in the Era of Widely Available Echocardiography:

Classically, as discussed in the 1992 AHA revised Jones criteria statement, carditis as a major manifestation of ARF has been a clinical diagnosis based on the auscultation of typical murmurs that indicate mitral or aortic valve regurgitation, at either valve or both valves. Numerous studies over the past 20 years have addressed the role of echocardiography (compared with purely clinical assessment) in the diagnosis of ARF. More than 25 studies have reported echocardiography/Doppler evidence of mitral or aortic valve regurgitation in patients with ARF despite the absence of classic auscultatory findings. This writing group concludes the following:

1. Echocardiography with Doppler should be performed in all cases of confirmed and suspected ARF (Class I; Level of Evidence B).
2. It is reasonable to consider performing serial echocardiography/ Doppler studies in any patient with diagnosed or suspected ARF even if documented carditis is not present on diagnosis (Class IIa; Level of Evidence C).
3. Echocardiography/Doppler testing should be performed to assess whether carditis is present in the absence of auscultatory findings, particularly in moderate- to high-risk populations and when ARF is considered likely (Class I; Level of Evidence B).
4. Echocardiography/Doppler findings not consistent with carditis should exclude that diagnosis in patients with a heart murmur otherwise thought to indicate rheumatic carditis (Class I; Level of Evidence B).

Evolving role of echogardiography in acute rheumatic fever

Evolving role of echogardiography in acute rheumatic fever

4.Specific doppler criteria for diagnosis of rheumatic valvulitis

Pathological mitral regurgitation (all 4 criteria met)
1.Seen in at least 2 views
2.Jet length ≥2 cm in at least 1 view
3.Peak velocity >3 m/s
4.Pansystolic jet in at least 1 envelope

Pathological aortic regurgitation (all 4 criteria met)
1.Seen in at least 2 views
2.Jet length ≥1 cm in at least 1 view
3.Peak velocity >3 m/s
4.Pan diastolic jet in at least 1 envelope

Morphological Findings on Echocardiogram in Rheumatic Valvulitis

Acute mitral valve changes
Annular dilation
Chordal elongation
Chordal rupture resulting in flail leaflet with severe mitral regurgitation
Anterior (or less commonly posterior) leaflet tip prolapse
Beading/nodularity of leaflet tips

Chronic mitral valve changes: not seen in acute carditis
Leaflet thickening
Chordal thickening and fusion
Restricted leaflet motion
Calcification

Aortic valve changes in either acute or chronic carditis
Irregular or focal leaflet thickening
Coaptation defect
Restricted leaflet motion
Leaflet prolapse

5.Evidence of preceding Streptococcal infection:

Because other illnesses may closely resemble ARF, laboratory evidence of antecedent group A streptococcal infection is needed whenever possible, and the diagnosis is in doubt when such evidence is not available.

Any one of the following can serve as evidence of preceding infection:
Increased or rising anti-streptolysin O titer or other streptococcal antibodies (anti-DNASE B) (Class I, Level of Evidence B). A rise in titer is better evidence than a single titer result.
A positive throat culture for group A β-hemolytic streptococci (Class I, Level of Evidence B).
A positive rapid group A streptococcal carbohydrate antigen test in a child whose clinical presentation suggests a high pretest probability of streptococcal pharyngitis (Class I, Level of Evidence B).

6. Diagnosis of Acute rheumatic fever:

For all patient populations with evidence of preceding GAS infection

Diagnosis: initial ARF: 2 Major manifestations or 1 major plus 2 minor manifestations
Diagnosis: recurrent ARF: 2 Major or 1 major and 2 minor or 3 minor

Major and minor criteria for diagnosis of Acute rheumatic fever

Major and minor criteria for diagnosis of Acute rheumatic fever


Flow charts for diagnosis of rheumatic fever

Flow charts for diagnosis of rheumatic fever

 

7.Rheumatic Fever Recurrences

As stated in the 1992 guidelines, patients who have a history of ARF or RHD are at high risk for “recurrent” attacks if reinfected with group A streptococci. Such an attack is considered
a new episode of ARF, but one in which the complete set of Jones criteria, even as revised, may not be completely fulfilled.

The guideline recommendations for diagnosing rheumatic fever recurrences are:
1. With a reliable past history of ARF or established RHD, and in the face of documented group A streptococcal infection, 2 major or 1 major and 2 minor or 3 minor manifestations may be sufficient for a presumptive diagnosis (Class IIb; Level of Evidence C).
2. When minor manifestations alone are present, the exclusion of other more likely causes of the clinical presentation is recommended before a diagnosis of an ARF recurrence is made (Class I; Level of Evidence C).

8.“Possible” Rheumatic Fever

In some circumstances, a given clinical presentation may not fulfill these updated Jones criteria, but the clinician may still have good reason to suspect that ARF is the diagnosis.
This may occur in high-incidence settings. In such situations the clinicians should use their discretion and clinical acumen to make the diagnosis that they consider most likely and manage the patient accordingly.

1. Where there is genuine uncertainty, it is reasonable to consider offering 12 months of secondary prophylaxis followed by reevaluation to include a careful history and physical examination in addition to a repeat echocardiogram (Class IIa; Level of Evidence C).
2. In a patient with recurrent symptoms (particularly involving the joints) who has been adherent to prophylaxis recommendations but lacks serological evidence of group A streptococcal infection and lacks echocardiographic evidence of valvulitis, it is reasonable
to conclude that the recurrent symptoms are not likely related to ARF, and discontinuation of antibiotic prophylaxis may be appropriate (Class IIa; Level of Evidence C).

Summary:

Jones criteria needed revision to meet current technological advances and clinical needs. Strict application of echocardiography/Doppler findings may be used to fulfill the major criterion of carditis, even in the absence of classic auscultatory findings, providing that ambient loading conditions are taken into consideration. In addition, monoarthritis or polyarthralgia could be accepted as fulfilling the major criterion of arthritis, but only in moderate- to high-risk populations. For low-risk populations, monoarthritis is not included, and polyarthralgia remains a minor criterion. Similarly, the requirement for the presence of fever can be fulfilled with oral, tympanic, or rectal temperature documented at 38°C in moderate- to high-risk populations, but only at ≥38.5°C in others.

Refernce:

1. http://circ.ahajournals.org/content/early/2015/04/23/CIR.0000000000000205.abstract

Top 10 Cardiology Articles of the week

Top 10 Cardiology Articles of the week (02.03.2015-08.03.2015)

1. Low-Level Transcutaneous Electrical Vagus Nerve Stimulation (LLTS) Suppresses Atrial Fibrillation

Conclusion: LLTS suppresses AF and decreases inflammatory cytokines in patients with paroxysmal AF. The results support the emerging paradigm of neuromodulation to treat AF.

2. Implantable Cardioverter-Defibrillator Therapy in Brugada Syndrome:A 20-Year Single-Center Experience

Background: Patients with Brugada syndrome and aborted sudden cardiac death or syncope have higher risks for ventricular arrhythmias (VAs) and should undergo implantable cardioverter-defibrillator (ICD) placement. Device-based management of asymptomatic patients is controversial. ICD therapy is associated with high rates of inappropriate shocks and device-related complications.

Objectives: The objective of this study was to investigate clinical features, management, and long-term follow-up of ICD therapy in patients with Brugada syndrome.

Methods: Patients presenting with spontaneous or drug-induced Brugada type 1 electrocardiographic findings, who underwent ICD implantation and continuous follow-up at a single institution, were eligible for this study.

Results A total of 176 consecutive patients were included. During a mean follow-up period of 83.8 ± 57.3 months, spontaneous sustained VAs occurred in 30 patients (17%). Eight patients (4.5%) died. Appropriate ICD shocks occurred in 28 patients (15.9%), and 33 patients (18.7%) had inappropriate shocks. Electrical storm occurred in 4 subjects (2.3%). Twenty-eight patients (15.9%) experienced device-related complications. In multivariate Cox regression analysis, aborted sudden cardiac death and VA inducibility on electrophysiologic studies were independent predictors of appropriate shock occurrence.

Conclusions: ICD therapy was an effective strategy in Brugada syndrome, treating potentially lethal arrhythmias in 17% of patients during long-term follow-up. Appropriate shocks were significantly associated with the presence of aborted sudden cardiac death but also occurred in 13% of asymptomatic patients. Risk stratification by electrophysiologic study may identify asymptomatic patients at risk for arrhythmic events and could be helpful in investigating syncope not related to VAs. ICD placement is frequently associated with device-related complications, and rates of inappropriate shocks remain high regardless of careful device programming.

3.Evaluation and Treatment of Patients With Lower Extremity Peripheral Artery Disease

The lack of consistent definitions and nomenclature across clinical trials of novel devices, drugs, or biologics poses a significant barrier to accrual of knowledge in and across peripheral artery disease therapies and technologies. Recognizing this problem, the Peripheral Academic Research Consortium, together with the U.S. Food and Drug Administration and the Japanese Pharmaceuticals and Medical Devices Agency, has developed a series of pragmatic consensus definitions for patients being treated for peripheral artery disease affecting the lower extremities. These consensus definitions include the clinical presentation, anatomic depiction, interventional outcomes, surrogate imaging and physiological follow-up, and clinical outcomes of patients with lower-extremity peripheral artery disease. Consistent application of these definitions in clinical trials evaluating novel revascularization technologies should result in more efficient regulatory evaluation and best practice guidelines to inform clinical decisions in patients with lower extremity peripheral artery disease.

4. Long-Term Survival Benefit of Revascularization Compared With Medical Therapy in Patients With Coronary Chronic Total Occlusion and Well-Developed Collateral Circulation

Objectives: The purpose of this study was to compare the long-term clinical outcomes of patients with chronic total occlusion (CTO) and well-developed collateral circulation treated with revascularization versus medical therapy.

Background: Little is known about the clinical outcomes and optimal treatment strategies of CTO with well-developed collateral circulation.

Methods: 2,024 consecutive patients with at least 1 CTO detected on coronary angiogram were screened. Of these, data was analyzed from 738 patients with Rentrop 3 grade collateral circulation who were treated with medical therapy alone (n = 236), coronary artery bypass grafting (n = 170) or percutaneous coronary intervention (n = 332; 80.1% successful). Patients who underwent revascularization and medical therapy (revascularization group, n = 502) were compared with those who underwent medical therapy alone (medication group, n = 236) in terms of cardiac death and major adverse cardiac events (MACE), defined as the composite of cardiac death, myocardial infarction, and repeat revascularization.

Results: During a median follow-up duration of 42 months, multivariate analysis revealed a significantly lower incidence of cardiac death (hazard ratio [HR]: 0.29; 95% confidence interval [CI]: 0.15 to 0.58; p < 0.01) and MACE (HR: 0.32; 95% CI: 0.21 to 0.49; p < 0.01) in the revascularization group compared with the medication group. After propensity score matching, the incidence of cardiac death (HR: 0.27; 95% CI: 0.09 to 0.80; p = 0.02) and MACE (HR: 0.44; 95% CI: 0.23 to 0.82; p = 0.01) were still significantly lower in the revascularization group than in the medication group.

Conclusions In patients with coronary CTO and well-developed collateral circulation, aggressive revascularization may reduce the risk of cardiac mortality and MACE.

5.Percutaneous Circulatory Assist Devices for High-Risk Coronary Intervention

A unifying definition of what constitutes high-risk percutaneous coronary intervention remains elusive. This reflects the existence of several recognized patient, anatomic, and procedural characteristics that, when combined, can contribute to elevating risk. The relative inability to withstand the adverse hemodynamic sequelae of dysrhythmia, transient episodes of ischemia-reperfusion injury, or distal embolization of atherogenic material associated with coronary intervention serve as a common thread to tie this patient cohort together. This enhanced susceptibility to catastrophic hemodynamic collapse has triggered the development of percutaneous cardiac assist devices such as the intra-aortic balloon pump, Impella (Abiomed Inc., Danvers, Massachusetts), TandemHeart (CardiacAssist, Inc., Pittsburgh, Pennsylvania), and extracorporeal membranous oxygenation to provide adjunctive mechanical circulatory support. In this state-of-the-art review, we discuss the physiology underpinning their application. Thereafter, we examine the results of several randomized multicenter trials investigating their use in high-risk coronary intervention to determine which patients would benefit most from their implantation and whether there is a signal to delineate whether they should be used in an elective pre-procedure, standby, rescue, or routine post-procedure fashion.

6.Porcelain Aorta: A Comprehensive Review

Calcification of the thoracic aorta is often associated with valvular and coronary calcification, reflecting an underlying atherosclerotic process. It has been found to be associated with an increased rate of mortality and cardiovascular disease. Porcelain aorta (PA) is extensive calcification of the ascending aorta or aortic arch that can be completely or near completely circumferential. This entity is rare in the general population, but it has an increasing incidence in older patients and in patients with coronary artery disease (CAD) or aortic stenosis (AS). The clinical relevance is based on the fact that it can complicate surgical aortic valve replacement (SAVR) for the treatment of severe AS by preventing safe access via the ascending aorta. PA is associated with increased morbidity and mortality, especially as a result of increased perioperative stroke risk. Recently, transcatheter aortic valve replacement (TAVR) has emerged as a less invasive and feasible treatment option in patients at high risk for conventional SAVR. In some series, ≈20% (5%–33%) of patients undergoing TAVR were diagnosed with PA. Inconsistencies in the definition and the use of different diagnostic modalities contribute to this wide range of PA prevalence. This article reviewed the available published data to seek a consistent, clinically relevant definition based on contemporary imaging, a firm understanding of the pathogenesis and associations, and the clinical implications of this disease entity.

7.Digoxin use in patients with atrial fibrillation and adverse cardiovascular outcomes: a retrospective analysis of the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF)

Conclusion: Digoxin treatment was associated with a significant increase in all-cause mortality, vascular death, and sudden death in patients with AF. This association was independent of other measured prognostic factors, and although residual confounding could account for these results, these data show the possibility of digoxin having these effects. A randomised trial of digoxin in treatment of AF patients with and without heart failure is needed.

8.Diagnosis of atrial fibrillation after stroke and transient ischaemic attack: a systematic review and meta-analysis

Background:Among patients with atrial fibrillation, the risk of stroke is highest for those with a history of stroke; however, oral anticoagulants can lower the risk of recurrent stroke by two-thirds. No consensus has been reached about how atrial fibrillation should be investigated in patients with stroke, and its prevalence after a stroke remains uncertain. The authors did a systematic review and meta-analysis to estimate the proportion of patients newly diagnosed with atrial fibrillation after four sequential phases of cardiac monitoring after a stroke or transient ischaemic attack.

Methods: The authors searched PubMed, Embase, and Scopus from 1980 to June 30, 2014 and included studies that provided the number of patients with ischaemic stroke or transient ischaemic attack who were newly diagnosed with atrial fibrillation. They stratified cardiac monitoring methods into four sequential phases of screening: phase 1 (emergency room) consisted of admission electrocardiogram (ECG); phase 2 (in hospital) comprised serial ECG, continuous inpatient ECG monitoring, continuous inpatient cardiac telemetry, and in-hospital Holter monitoring; phase 3 (first ambulatory period) consisted of ambulatory Holter; and phase 4 (second ambulatory period) consisted of mobile cardiac outpatient telemetry, external loop recording, and implantable loop recording. The primary endpoint was the proportion of patients newly diagnosed with atrial fibrillation for each method and each phase, and for the sequential combination of phases. For each method and each phase, they estimated the summary proportion of patients diagnosed with post-stroke atrial fibrillation using random-effects meta-analyses.

Findings:  The systematic review returned 28 290 studies, of which 50 studies (comprising 11 658 patients) met the criteria for inclusion in the meta-analyses. The summary proportion of patients diagnosed with post-stroke atrial fibrillation was 7·7% (95% CI 5·0–10·8) in phase 1, 5·1% (3·8–6·5) in phase 2, 10·7% (5·6–17·2) in phase 3, and 16·9% (13·0–21·2) in phase 4. The overall atrial fibrillation detection yield after all phases of sequential cardiac monitoring was 23·7% (95% CI 17·2–31·0).

Interpretation: By sequentially combining cardiac monitoring methods, atrial fibrillation might be newly detected in nearly a quarter of patients with stroke or transient ischaemic attack. The overall proportion of patients with stroke who are known to have atrial fibrillation seems to be higher than previously estimated. Accordingly, more patients could be treated with oral anticoagulants and more stroke recurrences prevented.

9.Comparative Outcomes of Catheter-Directed Thrombolysis Plus Anticoagulation Versus Anticoagulation Alone in the Treatment of Inferior Vena Caval Thrombosis

Conclusions—There has been a steady increase in the use of CDT in the treatment of patients with inferior vena cava thrombosis in the United States. This observational study showed no significant difference in mortality between CDT versus anticoagulation alone; however, the bleeding events and resource utilization were higher in the CDT group. Adequately powered randomized controlled trials are needed in this area.

10.Drug-eluting stents versus bare metal stents prior to noncardiac surgery

DES implantation was not associated with higher adverse events after NCS. Moreover, the incidence of adverse events following NCS was lower when NCS was performed >90 days post-DES implantation suggesting that it may not be necessary to wait until 12 months post PCI with DES before NCS.

Calculation of heart rate from ECG

Calculation of heart rate from ECG

In my last post I have enumerated the points for studying an ECG.

The first step is to check the calibration and paper speed. Then comes the calculation of heart rate. There are various methods of calculating the heart rate from ECG. We will discuss about the most commonly used and authentic methods of calculation.

ALL THESE METHODS ARE APPLICABLE FOR PAPER SPEED OF 25MM/SEC.

No.1 and 2 are applicable for a regular heart rhythm. No.3 is applicable for irregular heart rhythm

No.1: Calculate the number of large boxes

Figure 1

Figure 1

Count the number of large boxes between two consecutive R-R waves. 300 divided by the number of large boxes between two consecutive R-R waves is the heart rate. In figure 1 there are 3 large boxes between two consecutive R-R waves, so the heart rate is 300/3 =100/minute.

No.2: Calculate the number of small boxes

Count the number of small boxes between two consecutive R-R waves. 1500 divided by the number of small boxes between two consecutive R-R waves is the heart rate. In figure 1 there are 16 small boxes between two consecutive R-R waves, so the heart rate is 1500/16 = 94/min. This method is more accurate than the previous method.

No.3: Calculate the total number of R-waves in the rhythm strip

This method is applicable when the heart rate is irregular e.g. in patients with atrial fibrillation, frequent VPCs etc. At a paper speed of 25 mm/sec the duration of a 12-lead ECG is 10 seconds. So count the total number of R-waves in the rhythm strip (the long lead II at the bottom of the ECG ) and multiply it by 6 to get the heart rate. In the example shown below there are frequent VPCs.

2011.11.8The total number of R-waves is 12. So the heart rate is 12×6 = 72/min

I suggest you practice all the methods in the beginning so that after sometime you will be well habituated to use a method as needed.

Next week we will discuss about analyzing rhythm from ECG.

Top 10 Cardiology Articles of the week

Top 10 Cardiology Articles of the week (17.11.14-23.11.14)

1. A Polypill Strategy to Improve Adherence:Results From the FOCUS Project
Compared with the 3 drugs given separately, the use of a polypill strategy met the                   primary endpoint for adherence for secondary prevention following an acute MI

2. Six-month versus 24-month dual antiplatelet therapy after implantation of drug eluting    stents in patients non-resistant to aspirin: ITALIC, a randomized multicenter trial 
The ITALIC trial showed that rates of bleeding and of thrombotic events were not significantly different according to 6- versus 24-month DAPT after PCI with new-generation DES in good aspirin responders.

3.  First-in-Man Transseptal Implantation of a “Surgical-Like” Mitral Valve Annuloplasty Device for Functional Mitral Regurgitation

4.  Pressure-Wire-Guided Percutaneous Transluminal Pulmonary Angioplasty

5.  AVOIDing Oxygen in Suspected STEMI Tied to Smaller Infarcts, Less Recurrent MI

6.  Percutaneous Left Atrial Appendage Closure vs Warfarin for Atrial Fibrillation. A Randomized Clinical Trial

7.  Meta-analysis Questions One-Size-Fits-All Anticoagulant Strategy in STEMI Patients

8.  Periprocedural Complications and Long-Term Outcome After Alcohol Septal Ablation Versus Surgical Myectomy in Hypertrophic Obstructive Cardiomyopathy

9.  Spontaneous Coronary Artery Dissection Revascularization Versus Conservative Therapy

10.  Surgical Treatment of Moderate Ischemic Mitral Regurgitation

cpr

Sudden cardiac death

What is sudden cardiac death (SCD) ?

Sudden cardiac death is defined as natural death from cardiac causes, heralded by abrupt loss of consciousness within 1 hour of the onset of an
acute change in cardiovascular status. Related terms are sudden cardiac arrest and cardiovascular collapse. Sudden cardiac arrest means abrupt cessation of cardiac
mechanical function, which may be reversed by prompt intervention but will lead to death in its absence. Cardiovascular collapse means sudden loss of effective
blood flow due to cardiac and/or peripheral vascular such as cardiac arrest or syncope.

What is the relation to heart disease?

preexisting heart disease may or maynot have been known to be present. The mode of death is natural rapid and unexpected.

What are the symptoms?

Prodromes occuring weeks or months before an event are not very accurate to predict SCD. Sudden onset of chest pain, dyspnea, palpitation, lightheadedness
often precede the onset of cardiac arrest and eventual death.

How big is the problem?

For an adult population 35 years of age and older, the overall incidence of sudden cardiac death is 0.1% to 0.2% per year (that means in a country like India
12,00,000 to 24,00,000 people die suddenly from natural cardiac causes each year). Among people who have disease of coronary arteries of heart around 50% die
suddenly and unexpectedly. Even in developed countries where there is a decrease in total number of deaths due to coronary artery disease, the proportion of
deaths that are sudden and unexpected has remained same. These examples highlight the extent of the problem.

Who are at increased risk?

The conditions increasing the risk of sudden cardiac death are

  1. Coronary artery disease- Myocardial infarction, Angina etc
  2. Myocardial diseases and heart failure- e.g. dilated cardiomyopathy, ischemic cardiomyopathy etc
  3. Hypertrophy of ventricular myocardium – hypertrophic cardiomyopathy, left ventricular hypertrophy due to hypertension, etc
  4. Inflammatory diseases of heart- viral myocarditis, sarcoidosis, amyloidosis,
  5. Arrhythmogenic right ventricular dysplasia
  6. Diseases of cardiac valves- Aortic stenosis/insufficiency, mitral valve prolapse
  7. Electrical diseases of heart – long QT syndrome, Brugada syndrome, idiopathic ventricular fibrillation etc.
Mechanism of Sudden death

In 80% of cases sudden cardiac death is caused by ventricular tachycardia (VT) or ventricular fibrillation (VF) and in 20% of cases
SCD is caused by bradycardia. Patients having tachycardia have a relatively better outcome and chances of survival than those having bradycardia.

Management

The acute management of cardiac arrest is cardiopulmonary resusitation. More information about latest guidelines of CPR can be found
here

Prevention

Prevention of SCD is divided into two parts: Secondary prevention and Primary prevention. Secondary prevention means preventing further cardiac arrest
in people who have survived one cardiac arrest. Primary prevention means preventing cardiac arrest in people who have rish factors for cardiac arrest
but so far haven’t suffered a cardiac arrest.
Implantable cardioverter-defibrillator(ICD) is a device shown to be effective in secodary and primary prevention of SCD. This device is implanted like
a pacemaker and it gives an electrical shock from inside of the heart to abort an episode of VT or VF. It also has pacing function to support when the
heart rate falls.
Clinical trials like AVID, CASH, CIDS have shown effectiveness of ICD in secondary prevention of SCD. Clinical trials like MADIT, CABG-Patch, MUSTT, DEFINITE and
SCD-HeFT have shown benefit odf ICD in SCD.
Many modifications of the device has come like- subcutaneous ICD and wearable ICD.

Electrophysiological study
EPS and radiofrequency ablation can be done in selected patients to prevent further episodes of cardiac arrest.

Summary: sudden cardiac death is a devastating event resulting in rapid, unexpected and natural death due to cardiac causes. It can occur in persons
with known or unknown heart disease. Effective therapies are available. Increasing awareness about the condition and early therapy can result in
reduction of risk of sudden cardiac death
Keyword: Sudden cardiac death, sudden cardiac arrest, implantable cardioverter defibrillator (ICD), coronary artery disease, heart failure, heart disease, cardiology.

Coronary artery disease

Coronary artery disease

The heart like any other organ in the body needs constant supply of blood to survive. Blood reaches different parts of the heart through the coronary arteries.  Coronary arteries are of vital importance for the sustenance of life.

The different  normal functions of the coronary arteries include:

1. Carrying blood to different  parts of the heart

2. Regulating  blood supply to the heart in the face of varying blood pressure

3. Increasing blood supply to the heart in the face of increased cardiac demand like during exercise.

The coronary arterial system:  Can be divided into four parts

1. Left main coronary artery (LMCA)

        Which divides into

2. Left anterior descending artery  (LAD) And

3. Left circumflex artery (LCX)

4. Right coronary artery (RCA)

LMCA

Left main coronary artery, left anterior descending and left circumflex coronary artery

RCA

Right coronary artery

What is coronary artery disease (CAD)

Any disease which involves coronary arteries is CAD. Usually the most common form is reduction in the size of the coronary arteries. Many disease conditions can result in coronary artery disease but the most common cause of CAD is atherosclerosis. Other diseases like autoimmune diseases, congenital diseases can result in CAD.

Why CAD occurs?

CAD occurs due to a variety of reasons, which are called risk factors. You can read more about risk factors here.

What are the types of CAD?

CAD is a septum of diseases and it is divided to two categories

1. Chronic stable angina (CSA): In CSA there is a pattern of chest discomfort associated with exertion or emotional excitability. The occurrence of angina is after a predictable amount of work.

2. Acute coronary syndromes ( ACS)

ACS are are again divided into three types

A. Unstable angina: When there is new onset angina, worsening of previous angina, rest angina, it is called unstable angina

B. Non-ST elevation myocardial infarction

C. ST elevation myocardial infarction – the classic heart attack

This classification is important for the point of view of management and the aggressiveness of treatment.

What are the symptoms of coronary artery disease?

 A. Angina : Chest pain or discomfort .

B. Angina equivalents – fatigue , dyspnoea (shortness of breath) , eructations, palpitation

C. Sudden onset acute severe chest pain

D. Cold sweating

Read more about symptoms of heart disease here.

What to do?

First of all see your doctor for evaluation and treatment. Some of the general management modalities are discussed here.

Investigations

For the diagnosis of CAD the following investigations may be needed:

A. ECG – is of central importance in CAD. ECG in many occasions shows changes suggestive of reduced myocardial blood flow

B. Stress test – Different types of stress tests are available like treadmill test, nuclear stress  tests. A stress test can be done by performing exercise on a treadmill or by giving drugs in patients who are unable to do exercise. It is done when the symptoms are not typical and ECG changes are not typical.

C. Echocardiography – is for assessment of structure and function of heart

D. CT coronary angiography – It  is a noninvasive imaging modality for the diagnosis of CAD. It is like any other CT scan. Contrast injections are given to visualize the coronary arteries

E. MRI coronary angiography – Not very widely used for imaging of coronary arteries

F. Coronary angiography – this is the gold standard for the diagnosis of coronary artery disease and any percutaneous treatment for CAD can be done in the same setting

Treatment:

A. Risk factor control – Risk factor control is one of the most effective interventions for reducing the impact of coronary heart disease.  Proper control of blood pressure, diabetes, quitting smoking, treatment of abnormalities of cholesterol are some of the steps that greatly reduce the incidence and prevalence of CAD.

B. Medications- Patients with CAD will on some medications indefinitely (usually life long). For chronic stable angina, the first line of treatment is usually medical management. Even  patients who undergo coronary artery stenting or bypass surgery need to take medicines life long.

C. Coronary angiography and percutaneous coronary interventions are usually advised for patients who have more serious symptoms or for whom symptoms are not easily controlled with medicines. In presence of certain high risk factors patients should undergo early angiography and intervention or surgery

D. Coronary artery bypass grafting (CABG)

Drugs used in treatment of CAD:

1. Anti- platelets e.g. Aspirin, Clopidogrel, Prasugrel, ticagrelor, etc

2. Statins e.g. rosuvastatin, atorvastatin etc

C. Beta blockers (metoprolol, bisoprolol etc)

D. Ace inhibitors or angiotensin receptor blockers

E. Anticoagulants (heparin)

F. Nitrates

G. Nikorandil

H. Ranolazine

I. Trimetazadine

H. Therapies for refractory angina

Details about each class of drug I will post each week( Monday )

So please follow up

Cardiac interventions for CAD:

Known as percutaneous coronary intervention(PCI). In this procedure coronary angiography is done and then stenting is done as required.

Coronary artery bypass grafting:

CABG may be needed where PCI is not feasible or doesn’t give optimum results.

Finally there are a spectrum of patients who have drug refractory angina who are not suitable for PCI or CABG. They have refractory angina and the treatment options are limited in such patients.

Conclusion: Coronary artery disease is the leading cause of death and suffering in the world. The most common symptoms include chest pain, shortness of breath. It is diagnosed by ECG, stress tests, coronary angiography etc. The treatment include risk factor reduction, medical management and PCI or bypass surgery as needed.

Key words: Patient information, Coronary artery disease, heart disease, coronary angiography, ECG, Angina, CAD, PCI, CABG

APPROACH TO SYNCOPE

APPROACH TO SYNCOPE
History taking in cardiology cont.
Syncope has been defined by the European society of cardiology as “A transient loss of consciousness due to transient global cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous recovery.”
Syncope is a common problem, it causes significant agony and apprehension and may result in serious injury to the patient. Analysing and making an etiologic diagnosis of syncope is a difficult problem and even after investigations a significant number of patients still remain unexplained.
A detailed history is of paramount importance in the evaluation of syncope. Because all evaluation is usually retrospective. We will discuss in this article an approach to syncope and how to make a probable diagnosis from history.

STEPS IN THE EVALUATION OF SYNCOPE:
Patients present with the complain of loss of consciousness. From here we have to proceed in a systematic fashion to make a diagnosis. We will approach syncope under two headings
1. Taking the history of the episode
2. Analysing the history to reach at a diagnosis

RECORDING THE HISTORY OF SYNCOPE:

Below is a sample questionnaire for recording the history
WHAT WERE THE CIRCUMSTANCES JUST PRIOR TO THE ATTACK?

• The physical position of the patient is important. Inquire whether the patient was supine, sitting or standing.

• Activity related to syncope episode (rest. change in posture, during or after exercise, during or immediately after urination, defecation cough, or swallowing)
• Predisposing factors (e.g. crowded or warm places, prolonged standing. post-prandial period) and of precipitating events (e.g. fear, intense pain, neck movements)

HOW THE ATTACK STARTED ?
• Nausea, vomiting, abdominal discomfort, feeling of cold, sweating, aura, pain in neck or shoulders, blurred vision, dizziness
• Palpitations

QUESTIONS ABOUT THE ATTACK (EYEWITNESS)
• Way of falling (slumping or kneeling over), skin color (pallor, cyanosis, flushing), duration of loss of consciousness, breathing pattern (snoring) movements (tonic, clonic, tonic-clonic, minimal myoclonus or automatism), duration of movements, onset of movement in relation to fall, tongue biting
HOW THE ATTACK ENDED?
• Nausea, vomiting, sweating, feeling of cold, confusion, muscle aches, skin color, injury, chest pain, palpitations, urinary or fecal incontinence
BACKGROUND HISTORY OF THE PATIENT
• Family history of sudden death, congenital arrhythmogenic heart disease or fainting
• Previous cardiac disease
• Neurological history (Parkinsonism, epilepsy, narcolepsy)
• Metabolic disorders (diabetes, etc.)
• Medication (antihypertensive, antianginal, antidepressant agent, antiarrhythmic, diuretics, and QT-prolonging agents) or other drugs including alcohol
• In the case of recurrent syncope, information on recurrences such as the time from the first synopal episode and on the number of spells

ANALYSIS OF HISTORY
Once the history is recorded, the next step is to differentiate syncope from other causes of transient loss of consciousness.
Causes of transient loss of consciousness (T-LOC)

1. Syncope – we will discuss
2. Neurologic or cerebrovascular disease – e.g. seizure, posterior circulation TIA
3. Metabolic syndromes and coma – e.g. hypoglycaemia, drug or alcohol intoxication, hypoxia, hypocapnea
4. Psychogenic syncope- anxiety disorders, panic disorders, somatization disorders
DIFFERENTIATING SYNCOPE FROM OTHER CAUSES OF T-LOC
Following questions help in differentiating syncope from other causes of T-LOC
(1) Did the patient experience a complete loss of consciousness?
(2) Was the loss of consciousness transient with rapid onset and short duration?
(3) Did the patient recover spontaneously, completely, and without sequelae?
(4) Did the patient lose postural tone?
If the answer to one or more of these questions is negative, other nonsyncopal causes (as listed above) of transient loss of consciousness should be evaluated.
ESTABLISHING THE CAUSE OF SYNCOPE
Features of some of the common causes of syncope

Neutrally mediated syncope Arrhythmia Seizure Psychogenic
EpidemiologyAnd clinical setting Female>malesYounger age (<55)Frequent episodes(>2)

Prolonged standing, extreme emotions, hot humid surrounding

 

Structural heart diseaseMales>femalesOlder age (>55 years)

Lesser episodes(<3)

In supine position or during exertion

Family history of sudden cardiac death

Younger age (<45yrs)Any clinical situation Females>malesOccurs in others presenceYoung age (<40 yrs)

Many episodes (many episodes in a day)

No definite trigger

 

Premonitory symptoms Longer duration(>5s)PalpitationsBlurred vision

Nausea

Warmth

Diaphoresis

Light-headedness

Shorter duration(<6s)Palpitation less common Sudden onsetBrief aura (déjà vu, olfactory, gustatory, visual Usually absent
During the episode Pallor & diaphoresisDilated pupilHypotension

Bradycardia

Urine and fecal incontinence

Brief clonic movements may occur

 

Cyanosed not paleIncontinenceClonic movements may occur Cyanosed, no pallorTongue bitingFrothing at mouth

Prolonged syncope(>5 mins)

Hypertension

Tachycardia

Horizontal eye deviations

Tonic-clonic movements

Normal colourNormal pulse and BPProlonged duration

No incontinence

Eyes closed

Residual symptoms CommonFatigueOriented Residual symptoms uncommon (unless prolonged unconsciousness) CommonMuscle achesDisorientation

Fatigue

Headache

Slow recovery

uncommon

 

Salient features of syncope due to less common causes

Cause of syncope Salient features
  1. Vascular steal syndromes (subclavian steal syndrome)

 

 

Syncope in association with symptoms of brain stem ischemia (i.e.,diplopia,tinnitus,focal weakness or sensory loss, vertigo, dysarthria.
  1. Migraine associated syncope
Throbbing unilateral headache, scintillating scotomata, nausea, vomiting, photophobia, phonophobia
  1. Orthostatic hypotension
History of orthostatic symptoms and syncope, features of autonomic failure and other neurological symptoms (e.g.,parkinsonism, disturbances of bowel, bladder , thermoregulatory and sexual function, ataxia)-volume depletion-drug and alcohol induced
  1. Carotid sinus hypersensitivity
Common in elderly, relationship to specific neck positions (neck collar, shaving etc.), carotid sinus massage reproduces symptoms or bradycardia
  1. Situational syncope
Related to specific situations ( cough, defecation, laugh, swallow, after food, sneeze, micturition etc.)
  1. Glossopharyngeal syncope
Associated with glossopharyngeal neuralgia

 

These tables provide enough information to help in diagnosis. Clinical history and physical examination has around 25% sensitivity for etiologic diagnosis of syncope. Most of these patients need further evaluation.

Special note for students about to appear in exams:
Remember the structural heart diseases which result in syncope. Important ones
1. LVOTO- aortic stenosis, HCM, coarctation of aorta
2. RVOTO – pulmonary stenosis
3. Pulmonary hypertension
4. Atrial myxoma
These conditions will have a lot of other cardiac symptoms which will help in making a clinical diagnosis. You will have to remember the natural history of important structural heart diseases and exam cases.

This article is part of the series about history taking in cardiology and is intended primarily for medical students. Physicians and practitioners are referred to ESC guideline on evaluation and management of syncope (http://www.escardio.org/guidelines-surveys/esc-guidelines/guidelinesdocuments/guidelines-syncope-ft.pdf).

Keywords : history taking in cardiology, medical students, syncope, symptoms of heart disease, analysis of symptoms

APPROACH TO PALPITATION

APPROACH TO PALPITATION

History taking in cardiology contd…

Palpitation is a common symptom in cardiac patients as well as in patients with a variety of other diseases, sometimes even without diseases. History taking represents a major part of evaluation of patients with palpitation as most patients by the time they visit a physician have no palpitation and the diagnosis has to be made retrospectively.

Before embarking on the understanding of palpitation we should know what palpitation is. As defined by EHRA (European heart rhythm association) “Palpitations are a symptom defined as awareness of the heartbeat and are described by patients as a disagreeable sensation of pulsation or movement in the chest and/or adjacent areas.”

Even though palpitation is a very common symptom it is a difficult problem to evaluate and to make a definitive diagnosis.

Below is given a list of the possible etiologies of palpitation. Take a careful look into the list  so that you understand what we are looking for while taking history of palpitation.

Etiologies of palpitation:

  1. Cardiac arrhythmias

Supraventricular/ventricular extrasystoles

Supraventricular/ventricular tachycardias

Bradyarrhythmias: severe sinus bradycardia, sinus pauses, second and

third-degree atrioventricular block

Anomalies in the functioning and/or programming of pacemakers and ICDs

  1. Structural heart diseases

Mitral valve prolapse

Severe mitral regurgitation

Severe aortic regurgitation

Congenital heart diseases with significant shunt

Cardiomegaly and/or heart failure of various aetiologies

Hypertrophic cardiomyopathy

Mechanical prosthetic valves

  1. Psychosomatic disorders

Anxiety, panic attacks

Depression, somatization disorders

  1. Systemic causes

Hyperthyroidism, hypoglycaemia, postmenopausal syndrome, fever,

anaemia, pregnancy, hypovolaemia, orthostatic hypotension,

postural orthostatic tachycardia syndrome, pheochromocytoma,

arteriovenous fistula

  1. Effects of medical and recreational drugs

Sympathicomimetic agents in pump inhalers, vasodilators,

anticholinergics, hydralazine

Recent withdrawal of b-blockers

Alcohol, cocaine, heroin, amphetamines, caffeine, nicotine, cannabis,

synthetic drugs

Weight reductions drugs

Now lets go to the history taking proper. Here we will have our standard step-wise approach to history taking and analysis (as mentioned in approach to chest pain)

Step 1: describe the symptom in detail

Step2: localize the symptom to an anatomical system

Step 3: localize the palpitation to an organ/mechanism

Step 4: etiology of palpitation

As described in history taking in cardiology , always begin by noting down the premorbid functional status of the patient. Any change in functional status should be noted.

Step 1.Recording the history of palpitation:

Given here is a scheme of question to ask while taking history of palpitation

  1. Circumstances prior to the beginning of palpitations

Activity (rest, sleeping, during sport or normal exercise, change in

posture, after exercise)

Position (supine or standing)

Predisposing factors (emotional stress, exercise, squatting or

bending)

  1. Onset of palpitations

Abrupt or slowly arising

Preceded by other symptoms (chest pain, dyspnoea, vertigo, fatigue,

etc.)

  1. Episode of palpitations

Type of palpitations (regular or not, rapid or not, permanent or not)

Associated symptoms (chest pain, syncope or near syncope,

sweating, pulmonary oedema, anxiety, nausea, vomiting, etc.)

  1. End of the episode

Abrupt or slowly decreasing, end or perpetuation of accompanying

symptoms, duration, urination

Spontaneously or with vagal manoeuvres or drug administration

  1. Background

Age at the first episode, number of previous episodes, frequency

during the last year or month

Previous cardiac disease

Previous psychosomatic disorders

Previous systemic diseases

Previous thyroid dysfunction

Family history of cardiac disease, tachycardia or sudden cardiac

death

Medications at the time of palpitations

Drug abuse (alcohol and/or others)

Electrolytes imbalance

Step 2:

Once the history of palpitation has been recorded, next step is to localize whether it is cardiac or noncardiac in origin (please refer to the Etiology list for cardiac and noncardiac causes). It may be less reliable to differentiate a cardiac from noncardiac cause of palpitation based on history only. For that associated symptoms really help. Someone who has other symptoms of cardiac disease has more likelihood of having cardiac cause of palpitation.

Step 3:

Among cardiac cause of palpitation our aim is to differentiate arrhythmic from nonarrhythmic causes.

Features which suggest arrhythmic palpitations are

Structural heart disease

Primary electrical heart disease

Abnormal ECG

Family history of sudden death

Advanced age

Tachycardiac palpitations

Palpitations associated with haemodynamic impairment

Below are listed description of some common types of palpitation.

Type ofpalpitation  Subjectivedescription  Heartbeat Onset andtermination  Triggersituations  Possible associated symptoms
Extrasystolic ‘Skipping/missing a beat’, ‘sinking of the heart’ Irregular, interspersed withperiods of normal heartbeat  Sudden Rest
Tachycardiac ‘Beatingwings’ in the chest Regular or irregular, markedly accelerated Sudden Physical effort, cooling down Syncope,dyspnoea,fatigue,chestpain
Anxiety-related Anxiety, agitation Regular,slightly accelerated Gradual Stress,Anxiety attacks

 

Tingling in the hands and face, lump in the throat,atypical chest pain,sighing dyspnoea 
Pulsation Heart pounding Regular,normal frequency Gradual Physicaleffort Asthenia

 

Some features also help to differentiate the different types of arrhythmic palpitations:

Type of arrhythmia Heartbeat Trigger situation Associated symptoms Vagal manoeuvres
AVRT, AVNRT Sudden onset regular with periods of elevated heart rate Physical effort, changes in posture Polyuria, frog sign Sudden interruption
Atrial fibrillation Irregular with variable heart rate Physical effort, cooling down,post meal, alcohol intake Polyuria Transitory reduction in heart rate
Atrial tachycardia and atrial flutter Regular (irregular if A-V conduction is variable) with elevated heart rate Transitory reduction in heart rate
Ventricular tachycardia Regular with elevated heart rate Physical effort Signs/symptoms of hemodynamic impairment No effect

 

These tables will help to delineate the cardiac cause of palpitation.

 

Step 4:

This the final step where all the above discussion culminates in a list of differential diagnosis. The differential diagnosis will look something like this

  1. Arrhythmic palpitation
  2. Structural heart disease e.g.
    1. Valvular regurgitation
    2. Congenital or acquired shunt lesions
  3. Heart failure    etc..

 

In the exams it is a bit difficult to make  differential diagnoses based on palpitation only. There evaluate other cardiac symptoms very carefully. Once all the cardiac symptoms have been analysed then forming differential diagnoses is a bit easy. Yes one more thing read the natural history of cardiac diseases. I will post articles on natural history of cardiac diseases once this discussion on history taking is over.

This outlines the approach to palpitation. I hope it fulfils your purpose. All these articles are intended for medical students and exam goings. For professional there are a few references listed below for further reading.

Further readings:

  1. Weber BE, Kapoor WH. Evaluations and outcomes of patients with palpitations.

Am J Med 1996;100:138–48.

  1. Thavendiranathan P, Bagai A, Khoo C, Dorian P, Choudhry NK. Does this patient

with palpitations have a cardiac arrhythmia? JAMA 2009;302:2135–43.

  1. Hoefman E, Boer KR, van Weert HCPM, Reitsma JN, Koster RW, Bindels PJE.

Predictive value of history taking and physical examination in diagnosing arrhythmias

in general practice. Fam Pract 2007;24:636–41.

  1. Managing patients with palpitation. Europace (2011) 13, 920–934

Approach to chest pain

History taking in cardiology cont..

Chest pain is a common symptom of a variety of diseases. Developing a clear and thorough approach to chest pain is immensely important for your day to day practice and also for students for their assessments and exams. The spectrum of diseases producing chest pain range from innocuous conditions like muscle aches to life threatening myocardial infarction and aortic dissection.

Developing an approach to chest pain:

I will discuss in detail the approach which will be applicable for case presentation in exams and also for day to day practice.

The approach to chest pain can be divided into four steps

Step-1: this should include a thorough description of the symptom. Characterize the pain in the best possible detail

Step-2: localization of the pain to the different anatomic systems in the chest like – respiratory system, cardiovascular system, musculoskeletal system, gastrointestinal tract, hepato-pancreato-biliary system, neurological system.

Step-3: since we are mainly concerned with the cardiovascular system, the next step is localization of the chest pain to different cardiac structures – pericardium, coronary arteries, myocardium, endocardial structures and aorta.

Step-4: And finally etiology of chest pain.

A thorough understanding of each step is of paramount importance. At the end of history you should be able to form a list of etiologic differential diagnoses ranked according to priority.

Does this sound too much? Its not actually as you will discover as you read further.

Step-1: describing the chest pain

Describe the chest pain in the following headings

  1. Quality of pain – the common terms used to describe different types of chest pain are deep, boring, chest discomfort, tightness, heaviness, uneasiness, pricking, choking, sharp, shooting, ripping pain etc
  2. Location of pain- try to elicit the exact location by asking the patient to point to point to the site of maximum pain
  3. Radiation of pain
  4. Onset of pain- acute onset or insidious onset
  5. Tempo of progression
  6. Duration of symptoms
  7. Aggravating factors
  8. Relieving factors
  9. Positional variation in pain
  10. Any associated symptoms
    1. Other cardiac symptoms – shortness of breath, palpitation, fatigue, syncope, dizziness, cyanosis
    2. Respiratory symptoms- cough, expectoration, wheezing, hemoptysis, shortness of breath etc
    3. Gastrointestinal symptoms- nausea, vomiting, relation to food, dysphagia, odynophagia,
    4. Any neurological symptoms
    5. Any pain, redness or swelling at site of pain

Once this characterization part is over move to step-2

Step-2: Localization of pain to different organ systems:

The key to localization of the symptom to a particular system is the above characterization of pain. Below is a table of the salient features of each system.

SYSTEM SYNDROME CLINICAL DESCRIPTION KEY DISTINGUISHING FEATURES
Cardiac Angina Retrosternal chest pressure, burning, or heaviness; radiating occasionally to neck, jaw, epigastrium, shoulders, left arm Precipitated by exercise, cold weather, or emotional stress; duration 2-10 min, relieved by rest or nitrates
Rest or unstable angina Same as angina, but may be more severe Typically <20 min; lower tolerance for exertion; crescendo pattern
Acute myocardial infarction Same as angina, but may be more severe Sudden onset, usually lasting ≥30 min; often associated with shortness of breath, weakness, nausea, vomiting
Pericarditis Sharp, pleuritic pain aggravated by changes in position; highly variable duration Pericardial friction rub
Vascular Aortic dissection Excruciating, ripping pain of sudden onset in anterior of chest, often radiating to back Marked severity of unrelenting pain; usually occurs in setting of hypertension or underlying connective tissue disorder such as Marfan syndrome
Pulmonary embolism Sudden onset of dyspnea and pain, usually pleuritic with pulmonary infarction Dyspnea, tachypnea, tachycardia, signs of right heart failure
Pulmonary hypertension Substernal chest pressure, exacerbated by exertion Pain associated with dyspnea and signs of pulmonary hypertension
Pulmonary Pleuritis and/or pneumonia Pleuritic pain, usually brief, over involved area Pain pleuritic and lateral to midline, associated with dyspnea
Tracheobronchitis Burning discomfort in midline Midline location, associated with coughing
Spontaneous pneumothorax Sudden onset of unilateral pleuritic pain, with dyspnea Abrupt onset of dyspnea and pain
Gastrointestinal Esophageal reflux Burning substernal and epigastric discomfort, 10-60 min in duration Aggravated by large meal and postprandial recumbency; relieved by antacid
Peptic ulcer Prolonged epigastric or substernal burning Relieved by antacid or food
Gallbladder disease Prolonged epigastric or right upper quadrant pain Unprovoked or following meal
Pancreatitis Prolonged, intense epigastric and substernal pain Risk factors including alcohol, hypertriglyceridemia, medications
Musculoskeletal Costochondritis Sudden onset of intense fleeting pain May be reproduced by pressure over affected joint; occasionally, swelling and inflammation over costochondral joint
Cervical disc disease Sudden onset of fleeting pain May be reproduced with movement of neck
Trauma or strain Constant pain Reproduced by palpation or movement of chest wall or arms
Infectious Herpes zoster Prolonged burning pain in dermatomal distribution Vesicular rash, dermatomal distribution
Psychological Panic disorder Chest tightness or aching, often accompanied by dyspnea and lasting 30 minutes or more, unrelated to exertion or movement Patient may have other evidence of emotional disorder

 

This table provides a lot of information. Once you go through the table a list of differential diagnoses can be made and appropriate investigations ordered.

The next discussion is for case presentation in exams

Step-3: the above table also helps in localizing the cardiovascular structures causing the pain.

Step-4: Etiology of cardiovascular cause of chest pain:

Finally you have to think of the Etiology of the cardiac chest pain. Now we will examine the common etiologies of chest pain and try to differentiate them clinically.

  1. Coronary artery disease: there will be history of angina as described in the table
  2. Left ventricular outflow tract obstruction (LVOTO): the symptoms of LVOTO are remembered by the letters – ASD- Angina, Syncope and Dyspnea. RVOTO also has similar symptoms. They may have additional features of right heart failure like- peripheral edema, ascites, right upper quadrant pain, neck pulsations, cyanosis etc
  3. Mitral stenosis and less commonly mitral regurgitation can have chest pain. But the predominate symptoms in case of
    1. Mitral stenosis: dyspnea
    2. Mitral regurgitation: fatigue and palpitation
  4. Pulmonary arterial hypertension: can have angina. The predominant symptoms will be dyspnea, fatigue. Associated symptoms can be palpitation, syncope.

This will cover some of the common cardiac causes of chest pain for exam case presentation.

Conclusion: Chest pain is a common symptom with a wide spectrum of presentation. Attention to the details of history will help to narrow down the possible conditions giving rise to the chest pain.

Your comments, suggestions and corrections are most welcome and will greatly help me to improve my articles.

Thank you

Dr. Anupam Jena
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