Monthly Archives: April 2014

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

CRT – the expanded indications

FDA Approves Medtronic CRT Devices for Mild HF With AV Block. This approval is based on the  BLOCK-HF trial. The approval expands the labeling on the defibrillating and pacing-only cardiac resynchronization therapy devices (CRT-D and CRT-P, respectively), which until now had been approved only for heart-failure patients with LVEF <35% and prolonged QRS intervals. The BLOCK-HF indications included a different niche of patients, those with first-, second-, or third-degree AV block, NYHA class 1-3 heart failure, and LVEF <50%. Read more @ http://www.medscape.com/viewarticle/823485
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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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The unheard-of symptom – Bendopnea

Characterization of a Novel Symptom of Advanced Heart Failure: Bendopnea

JCHF. 2014;2(1):24-31. doi:10.1016/j.jchf.2013.07.009

Objectives:  This study sought to examine the frequency and hemodynamic correlates of shortness of breath when bending forward, a symptom that has been named by the newly coined term “bendopnea.”

Background:  Many heart failure patients describe bendopnea such as when putting on their shoes. This symptom has not previously been characterized.

Methods: This was a prospective study of 102 subjects with systolic heart failure referred for right-heart catheterization. Time to onset of bendopnea was measured prior to catheterization. Forty-six subjects also underwent hemodynamic assessment when sitting and bending. Hemodynamic profiles were assigned on the basis of whether pulmonary capillary wedge pressure (PCWP) was ≥22 mm Hg and cardiac index (CI) was ≤2.2 l/min/m2.

Results: Bendopnea was present in 29 of 102 (28%) subjects with median (25th, 75th percentiles) time to onset of 8 (7, 11) seconds. Subjects with bendopnea had higher supine right atrial pressure (RAP) (p = 0.001) and PCWP (p = 0.0004) than those without bendopnea but similar CI (p = 0.2). RAP and PCWP increased comparably in subjects with and without bendopnea when bending, but CI did not change. In those with, versus without, bendopnea, there was more than a 3-fold higher frequency of a supine hemodynamic profile consisting of elevated PCWP with low CI (55% vs. 16%, respectively, p < 0.001) but no association with a profile of elevated PCWP with normal CI (p = 0.95).

Conclusions: Bendopnea is mediated via a further increase in filling pressures during bending when filling pressures are already high, particularly if CI is reduced. Awareness of bendopnea should improve noninvasive assessment of hemodynamics in subjects with heart failure.

Antiplatelet Therapy for Stable CAD in AF Patients Taking an Oral Anticoagulant

Background—The optimal long-term antithrombotic treatment of patients with coexisting atrial fibrillation and stable coronary artery disease is unresolved, and commonly, a single antiplatelet agent is added to oral anticoagulation. The study investigated the effectiveness and safety of adding antiplatelet therapy to vitamin K antagonist (VKA) in atrial fibrillation patients with stable coronary artery disease.

Methods and Results—Atrial fibrillation patients with stable coronary artery disease (defined as 12 months from an acute coronary event) between 2002 and 2011 were identified. The subsequent risk of cardiovascular events and serious bleeding events (those that required hospitalization) was examined with adjusted Cox regression models according to ongoing antithrombotic therapy. A total of 8700 patients were included (mean age, 74.2 years; 38% women). During a mean follow-up of 3.3 years, crude incidence rates were 7.2, 3.8, and 4.0 events per 100 person-years for myocardial infarction/coronary death, thromboembolism, and serious bleeding, respectively. Relative to VKA monotherapy, the risk of myocardial infarction/coronary death was similar for VKA plus aspirin (hazard ratio, 1.12 [95% confidence interval, 0.94–1.34]) and VKA plus clopidogrel (hazard ratio, 1.53 [95% confidence interval, 0.93–2.52]). The risk of thromboembolism was comparable in all regimens that included VKA, whereas the risk of bleeding increased when aspirin (hazard ratio, 1.50 [95% confidence interval, 1.23–1.82]) or clopidogrel (hazard ratio, 1.84 [95% confidence interval, 1.11–3.06]) was added to VKA.

Conclusions—In atrial fibrillation patients with stable coronary artery disease, the addition of antiplatelet therapy to VKA therapy is not associated with a reduction in risk of recurrent coronary events or thromboembolism, whereas risk of bleeding is increased significantly. The common practice of adding antiplatelet therapy to oral VKA anticoagulation in patients with atrial fibrillation and stable coronary artery disease warrants reassessment.

Circulation.2014; 129: 1577-1585

MI rates with Ticagrelor (from PLATO)

This article in JACC examines the rates of MI in patients with ACS treated with ticagrelor vs clopidogrel.

The rates of overall MI at 12 months:

1. Ticagrelor- 5.8%

2. Clopidogrel – 6.9%

3. Nonprocedural MI (HR: 0.86; 95% CI: 0.74 to 1.01) and MI related to percutaneous      coronary intervention or stent thrombosis tended to be lower with ticagrelor.

click here to read more

Fetal echocardiography

Congenital anomalies are the leading cause of infant death and congenital heart diseases accounts for 30 to 50 percent of these deaths. As the major cause of the largest single category of mortality, the identification and management of fetal cardiac abnormalities is of paramount importance. Population screening studies have shown that congenital heart disease occurs in 5/1000 to 8/1000 newborns, with about one-half causing major disease and one-half causing minor disease. Fetal echocardiography is a reasonably accurate investigation for the detection of such anomalies. The prospective parents, obstetricians and cardiologists should have some basic concepts about this extremely useful tool.

Indications for fetal echocardiography:

The common indications are divided into three categories: 1. familial 2.maternal 3.fetal. Each is elaborated below

1. Familial risk factors

●First or second degree relatives with congenital heart disease (eg, the fetus’ siblings, parents, and grandparents)

●Syndromes including congenital heart disease (eg, Noonan, tuberous sclerosis, Holt-Oram, velocardiofacial [DiGeorge] syndrome)

2. Maternal risk factors

●Maternal congenital heart disease

●Cardiac teratogen medications (e.g., lithium, methotrexate, thalidomide, drugs for seizure, isotretinoin, paroxetine, warfarin)

●Maternal medical illness (e.g., diabetes, phenylketonuria, anti Ro/SSA or anti La/SSB antibodies)

●Exposure to prostaglandin synthetase inhibitors (can cause premature closure of the ductus arteriosus in the third trimester)

●Rubella infection in the first trimester

●In vitro fertilization

3. Fetal risk factors

●Suspected cardiac anomaly during basic sonogram

●Extracardiac anomaly

●Aneuploidy

●Nonimmune hydrops

●Arrhythmia

●Abnormal fetal situs

●Increased nuchal translucency at 11 to 14 weeks of gestation

●Chromosomal abnormality

●Monochorionic twins, with or without twin-twin transfusion syndrome

What is the timing of fetal echocardiogram?

Usually between 18 to 22 weeks

How accurate is fetal echocardiography for detection of cardiac anomalies?

Studies suggest widely variable sensitivity of fetal echo ranging from 0 to 80%. A reasonable figure would be an accuracy of 40%.

How fetal echocardiography changes the outcome?

Any cardiac anomaly should be properly explained to the parents. Though parents are less interested to know the exact anatomical details of the cardiac problem. What is more important for them is the short-, mid- and long-term prognosis of the child. Also information about place of child birth, and method to be used like- normal labour, LSCS etc. Though fetal cardiac interventions have been tried , they are far from being of routine use in near future.

For doctors it is important to explain the prognosis in clear terms. One study showed that cardiac anomalies which were amenable to biventricular repair had better outcome than single ventricle physiology (Ultrasound Obstet Gynecol. 1997 Oct;10(4):237-41. PMID 9383873)

.

Referral to a maternal-fetal medicine specialist, pediatric cardiologist, geneticist, and/or neonatologist to discuss prognosis, obstetrical and neonatal management, and options is recommended.

Conclusion:

The following interventions are recommended when a fetal cardiac anomaly is suspected:

•Full fetal echocardiography to evaluate cardiac structure and function, arterial and venous flow, and rhythm.

•Detailed scanning of the fetal anatomy to look for associated anomalies, particularly involving the digits and bones.

•Thorough family history to evaluate for familial abnormalities or syndromes.

•Thorough maternal medical history to identify chronic medical disorders, viral illnesses, or medications which are potential teratogens.

•Fetal karyotype, with screening for deletion in 22q11.2 when conotruncal anomalies are present

•Referral to a maternal-fetal medicine specialist, pediatric cardiologist, geneticist, and/or neonatologist to discuss prognosis, obstetrical and neonatal management, and options.

•Delivery at an institution that can provide neonatal cardiac care, if needed.

Dr. Anupam Jena
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Colchicine in Stable Chronic Heart Failure

Heart failure is associated with activation of inflammatory cascades. this trial examines the effects of usig colchicine in Hf.

American College of Cardiology Foundation | JACC: Heart Failure | Anti-Inflammatory Treatment With Colchicine in Stable Chronic Heart FailureA Prospective, Randomized Study.

Natural history of pediatric idiopathic DCM

Natural history studies of pediatric idiopathic dcm are scarce. previous studies have demonstrated heterogenous figures of actuarial survival at 1 year of 63-90%, and at 5 years of 20-80%. this study add to our knowledge of natural history and LV function recovery.

American College of Cardiology Foundation | Journal of the American College of Cardiology | Recovery of Echocardiographic Function in Children With Idiopathic Dilated CardiomyopathyResults From the Pediatric Cardiomyopathy Registry.

REOPEN-AMI Trial

high-dose intracoronary adenosine after thrombus aspiration improves microvascular dysfunction, LV remodelling.

American College of Cardiology Foundation | Journal of the American College of Cardiology | Left Ventricular Remodeling and 1-Year Clinical Follow-Up of the REOPEN-AMI Trial.