The Gastrocardiac Syndrome

Roemheld syndrome (RS) or gastric-cardiac syndrome, is a complex of gastrocardiac symptoms where issues with gut are found to be associated with cardiac symptoms like arrhythmias and benign palpitations. Despite a full workup, when the cause of symptoms is not found then this condition is one of the possible diagnosis. These are the patients who are often labeled as  "Non-Cardiac Chest Pain' or "MSK related CP" in the Emergency Department. 

Possible reasons for Gastrocardiac Syndrome

• Anatomical close proximity between the stomach and the heart (GERD, Hiatus Hernia)
• Same nerve supply - Vagus Nerve (Compressed by distended stomach leaading to bradycardia and occasionally arrythmias)
• PPIs (Often used for GERD/Peptic ulcer) leading to HypoMg leading to ectopic beats

Due to pressure in the epigastric and left hypochondrium, the diaphragm is elevated and displaces the heart. This reduces the heart's ability to fill and increases the contractility of the heart causing palpitations/dizziness/anxiety. Typically, there are no changes/abnormalities related in the EKG detected. 

Symptoms can be variable and include a whole list of GI and Cardiovascular symptoms:  They are usually seen after eating a meal.

• Sinus Bradycardia
• Shortness of Breath
• Chest tightness, Anxiety
• Muscle crampiness
• Dizziness
• Palpitations
• Belching, nausea

Conditions that come under the spectrum of RS:

• GERD
• Hiatus Hernia
• Lactose intolerance
• Gall Bladder disease
• Intestinal Disorders 

RS in an ED diagnosis and our workup must include ECGs and troponins. Extensive GI and Cardiac workup are needed before calling this condition. Therefore, the diagnosis is made based on symptoms in the absence of heart abnormalities. 

Management

Ruling out another diagnosis such as peptic ulcer, bowel cancer, GB disease, ACS is the priority. Treatment is based on symptoms relief. Medications that have found to help include Anticholinergics, Antacids, Beta-Blockers, Anti-convulsants and simethicone. 

Take Home:

Gastrocardiac Syndrome is not an ED diagnosis. Always think of ACS first but beware of close proximity between stomach and heart.

References:

1. Gastrocardiac syndrome: A forgotten entity; Saeed, Mohammad et al. The American Journal of Emergency Medicine , Volume 0 , Issue 0
2. Jervell, O. and Lødøen, O. (1952), THE GASTROCARDIAC SYNDROME. Acta Medica Scandinavica, 142: 595-599. doi:10.1111/j.0954-6820.1952.tb13409.x
3. The effect of the lateral decubitus position on vagal tone. Chen GY, Kuo CD. Anesthesia. 1997 Jul;52(7):653-7. Department of Medicine, Provincial Tao-Yuan General Hospital, Republic of China.

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

Acute Aortic Syndromes

Background

Acute aortic dissection is part of a spectrum of diseases referred to as Acute Aortic Syndromes which basically encompasses 3 related conditions: 

(1) Aortic dissection
(2) Intramural hematoma (lacks blood flow in the false lumen or its lack of an intimal flap or entry point. Believed to originate from a rupture of the vasa vasorum within the medial layer; or from microscopic intimal tears )
(3) Penetrating atherosclerotic ulcer (typically seen in older population and often found incidentally, may progress to intramural hematoma)

The pathology, diagnosis, and treatment of these three entities are similar

Presentation
While aortic dissection usually presents with severe pain, its presentation can be more subtle and should be considered in anyone with chest pain, back pain or abdominal pain and pain with either syncope or focal neurological deficits.  Aortic dissection can also present as an acute stroke. There are 2 main anatomic classification systems: 

Stanford type B dissections are further classified as:
1. Complicated - Radiographic evidence of thoracic aortic rupture (eg, blood outside the aortic wall); ischemia involving the viscera, kidneys, spinal cord, or lower extremities; persistent pain; or rapid expansion in the distal arch or proximal descending aorta to a total aortic diameter of > 4.5 cm. These findings require immediate intervention due to the threat to life and limb.
2. Uncomplicated


The dissection creates a new false lumen, which separates the media from the adventitia and can extend either anterograde or retrograde involving the aortic root, arch, or any of the main aortic branches. The false lumen may compress the true lumen and compromise blood flow to distal arteries and causing ischemic complications such as renal failure, stroke, spinal infarction, limb ischemia, and myocardial events.

Classically, aortic dissection will present with abrupt chest or back pain, but about  5% of patients with an acute aortic dissection will have no pain. 

Aortic dissection should always be considered in the differential diagnosis of patients with suspected acute coronary syndromes or pulmonary embolism. 

Atypical presentations can also occur. 

• Syncope has been reported in up to about 20% of patients
• Acute neurological deficits or coma occur in 30% of patients presenting with an acute type A dissection. Neurological findings can be associated with aortic dissections secondary to the extension of the dissection into the aortic branches. These branches can be occluded by either expansion of the false lumen occluding the true lumen or by emboli from an expanding thrombus. Deficits may occur from insults to the brain or spinal cord.

• Patients may be hypertensive (49%), normo- tensive (35%) orhypotensive (8%), or in shock (8%). The presence of hypotension or shock is an ominous finding. 
• Blood pressure discrepancy can occur when a dissection extends into a branch of the aorta occluding the subclavian artery. A difference of 20 mm Hg between arms is considered positive and can be suggestive of an aortic dissection (this finding cannot be used to rule out dissection); however, 20% of the population will have a blood pressure differential without an aortic dissection.
• A pulse deficit is defined as having weak or no pulse on the affected side. However, data from the IRAD database of 2538 patients founda pulse de cit or blood pressure differential in only 20% of patients.
• An aortic dissection may extend retrograde and involve the aortic valve or coronary arteries. A diastolic murmur can be heard in about 1/3rd of patients with an aortic dissection and may represent severe aortic regurgitation but the presence of a diastolic murmur is neither sensi- tive nor specific for aortic dissection.
• 2-5% of patients with aortic dissections will have concurrent myocardial ischemia. Proximal aortic dissections can dissect into the right coronary artery, causing occlusion, and can present with a STEMI. If clinical suspicion for aortic dissection is present, other diagnostic modalities should be used to evaluate for proximal aortic dissection prior to anticoagulation or thrombolytics. 

Risk Factors

• Poorly controlled hypertension
• Connective tissue disorders (eg, Marfan syndrome, Ehlers-Danlos syndrome)
• Congenital valvular disorders (eg, bicuspid aortic valve)
• Aortic coarctation
• Homocystinuria
• Previous cardiac surgery
• Familial aortic dissections, aortic aneurysms
• Pheochromocytoma
• inflammatory vasculitis
• Sympathomimetics (eg, cocaine)
• Cardiac surgery (eg, aortic valve replacement, coronary artery bypass grafting) or percutaneous catheter placement (eg, cardiac catheterisation),

Diagnosis

D-Dimer
More and more evidence is accumulating in support of the use of D-dimer as a screening tool for aortic dissection but currently, only a few small studies have looked at the sensitivity of D-dimer in ruling out aortic dissection (need further validation). Also, Intramural hematoma or aortic dissections with a thrombosed false lumen can have a false negative D-dimer. If there is sufficient clinical suspicion for an acute aortic dissection, advanced imaging is indicated. 

A Negative D-dimer cannot rule out Aortic Dissection

Imaging Modalities for Acute Aortic Syndrome

CXR
Chest radiography can suggest an aortic dissection. Abnormalities are seen in approxi- lately about 88% of patients. A widened mediastinum is commonly associated with aortic dissection and is seen in approximately 60% of patients. 

A normal CXR cannot rule out an aortic dissection.

Treatment

• ABCs
• Adequate Pain Relief (Morphine or Fentanyl)
• Target HR< 60 beats/min and Target SBP  between 100-120 mm Hg. Always start with Beta Blockers first (not vasodilators)
• In case of cocaine toxicity, use benzodiazepines to decrease the sympathetic drive.
• Type and Screen
• If hypotensive with poor perfusion then use inotropes (can potentially worsen dissection due to increase in shearing forces) or consider pericardicentesis in cases of tamponade (poor prognosis)

• Emergent Vascular Surgery Consultation - Type A acute aortic dissections require prompt surgical treatment. Definitive treatment of type B acute aortic dissections is unclear. Uncomplicated distal dissections have traditionally been treated with blood pressure control. Surgery has been reserved for patients who have persistent pain, uncontrolled hypertension, occlusion of a major arterial trunk, frank aortic leaking or rupture, or development of a localized aneurysm. 

Rationale for Beta-Blockers First: Aortic wall stress is directly affected by the velocity of ventricular contraction over time (dP/dt). Initiation of treatment to decrease these shear forces should occur as soon as the diagnosis is made or suspected.intravenous narcotics should also be given and titrated to pain control.  Beta-blocker therapy should be given prior to initiating intravenous vasodilators to prevent reflex tachycardia. However, in cases of severe aortic regurgitation, use of intravenous beta blockers or calcium-channel blockers with caution.  

Chronic Dissection
Patients who present with chronic aortic dissection have already survived their period of greatest mortality risk and are usually treated by blood pressure control and close monitoring unless complications mandate surgery. All patients who have sustained and survived an aortic dissection, regardless of the type of definitive therapy used, require careful long-term surveillance and treatment. 


Documentation:

• Document HPI with pertinent negative findings
• Presence of Absence of risk factors
• Listen for bruits
• Pulsate Mass, BP difference in lies or any pulse deficits
• Neuro Exam and CXR, ECHO findings

Take Home

• Use your gestalt to work up dissections. Read more here on ADvISED Trial.   Currently, no validated clinical decision rule exists to rule out an acute aortic dissection. Historical and physical exam can be used to increase or decrease probability, but atypical presentations are common. 
• Aortic dissection should always be in the differential for patients with chest pain, back pain, or abdominal pain.
  
• Once the diagnosis is made or strongly suspected, ED Management is limited to pain relief, HTN and BP control and urgent Vascular surgery consulnation.
  
• D-dimer and CXR alone should not be used to “rule out” aortic dissection. POCUS can be helpful in unstable patients but it should not be relied upon to rule out an aortic dissection. 
  
  

   References and Further Reading:

1. Friado FJ. Aortic dissection: a 250-year perspective. Tex Heart Inst J. 2011;38(6):694-700. (Review)
2. Hagan PG, Nienaber CA, Isselbacher EM, et al. The Inter- national Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000;283(7):897-903. (Retrospective; 464 patients)
3. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/ STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease: a report of the Ameri- can College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American As- sociation for Thoracic Surgery, American College of Radiol- ogy, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Soci- ety of Thoracic Surgeons, and Society for Vascular Medicine. Circulation. 2010;121(13):1544-1579. (Guideline) 
4. Mancini MC. Aortic dissection. Medscape. Available at: http://emedicine.medscape.com/article/2062452-overview.
5. Accessed June 10, 2013. (Review)
6. Hardie AD, Wineman RW, Nandalur KR. The natural his- tory of acute non-traumatic aortic diseases. Emerg Radiol. 2009;16(2):87-95. (Review) 
7. Collins JS, Evangelista A, Nienaber CA, et al. Differences in clinical presentation, management, and outcomes of acute type A aortic dissection in patients with and without previ- ous cardiac surgery. Circulation. 2004;110(11 suppl 1):II237- II242. (Retrospective; 617 patients) 
8. Bossone E, Rampoldi V, Nienaber CA, et al. Usefulness of pulse de cit to predict inhospital complications and mortal- ity in patients with acute type A aortic dissection. Am J Cardiol. 2002;89(7):851-855. (Retrospective; 513 patients) Rogers AM, Hermann LK, Booher AM, et al. Sensitivity of the aortic dissection detection risk score, a novel guideline- based tool for identi cation of acute aortic dissection at initial presentation: results from the international registry of acute aortic dissection. Circulation. 2011;123(20):2213-2218.
9. Lo BM. An evidence-based approach to acute aortic syndromes. Emergency medicine practice. 2013 Dec 1;15(12):1-23.

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

  

The "qRBBB" pattern

Presence of qRBBB in the setting of acute coronary syndrome signifies proximal occlusion of left descending coronary artery with compromise of circulation in the septal arteries supplying the bundle branches. Anterior STEMi with RBBB is associated with a higher risk of death when compared with that of patients with normal conduction. 

qRBBB with LAFBInstead of the rSR pattern (seen in RBBB), there is qRBBB pattern in V1 because the initial r wave has been knocked off by anterior wall myocardial infarction. 

Due to anterior location of the right ventricle than that of the left ventricle, activation of the right ventricular free wall can neutralize the abnormal septal forces associated with an anteroseptal MI. Therefore, in most patients with an anteroseptal infarction, abnormal Q waves in right precordial leads is mostly manifest during RBBB showing the classical qRBBB pattern, due to delayed activation of the right ventricle. 

Understanding RBBB
RBBB causes delayed depolarisation of right Ventricle as depolarisation spreads across the septum (instead of the Right Bundle) taking longer than usual. This produces characteristic ECG changes described below in the diagnostic criteria. Left Ventricle depolarisation remains normal i.e normal early part of QRS complex. 

Diagnostic Criteria 

• Broad QRS > 120 ms
• RSR’ pattern in V1-3 (‘M-shaped’ QRS complex) or a broad monophonic r wave or a qR complex
• Wide, slurred S wave in the lateral leads (I, aVL, V5-6
• Delayed intrinsicoid deflection time 

RBBB (Image from LIFTL)

RBBB often shows STD and TWI in V1-3 due to secondary depolarisation abnormalities 

Causes

• Ischemic Heat Disease
• Acute Pulmonary HTN (PE)
• Chronic Pulmonary HTN (Cor Pulmonale)
• Valvular Heart Disease
• Myocarditis
• Degenerative Diseases of conduction system
• Congenital Heart Disease
• Overdose of Na Channel Blockers
• Idiopathic
• Transient and Rate Related 

RBBB should NOT have any ST Elevation. Look for the qRBBB pattern and RBBB with LAFB (Leftward Axis, qR in lead I, aVL, rS in lead III) pattern. 

qRBBB in V1-4 with STE (Image from TheECGinAcuteMI)

Take Home:

• Remember the qRBBB pattern morphology
• RBBB should never have any ST elevation 
• When in doubt, do serial ECGs and screening bedside ECHO to look for RWMA

References and Further Reading:

1. Mishra, V., Sinha, S. K., & Razi, M. (2016). Right Bundle Branch Block: A Masquerader in Acute Coronary Syndrome. North American Journal of Medical Sciences, 8(2), 121–122. http://doi.org/10.4103/1947-2714.177347
2. 2. Widimsky P, Rohác F, Stásek J, Kala P, Rokyta R, Kuzmanov B, et al. Primary angioplasty in acute myocardial infarction with right bundle branch block: Should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy? Eur Heart J. 2012;33:86–95.
3. Ganesan S, Kannan K, Victor A, Selvan KT, Arun R, Majella JC, Kumar RS, Aravind A, Viswanathan N, District V. QRBBB in acute coronary syndrome: Does it matter in modern era? Angiographic correlation. Indian Heart Journal. 2015 Dec 1;67:S38.
4. Wong CK, Stewart RA, Gao W, French JK, Raffel C, White HD. Prognostic differences between different types of bundle branch block during the early phase of acute myocardial infarction: Insights from the Hirulog and Early Reperfusion or Occlusion (HERO)-2 trial. Eur Heart J. 2006;27:21–8. 
5. http://hqmeded-ecg.blogspot.co.uk/2010/01/right-bundle-branch-block-with-subtle.html
6. http://hqmeded-ecg.blogspot.co.uk/2017/04/rbbb-with-transient-st-elevation.html
7. http://hqmeded-ecg.blogspot.co.uk/2010/11/wide-complex-tachycardia-its-really.html
8. http://hqmeded-ecg.blogspot.co.uk/2014/03/elderly-woman-in-shock-ekg-from.html
9. https://emcrit.org/wp-content/uploads/2015/03/Who-to-PCI-by-Smith-and-Weingart.pdf
10. https://lifeinthefastlane.com/ecg-library/basics/right-bundle-branch-block/

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

Firing the Esophagus - GERD in ED

GERD is often listed as a part of Chest Pain differentials in ED. It is caused due to the reflux of gastric contents into the oesophagus and can cause a multitude of symptoms and it can be challenging to differentiate from ACS. A weak lower esophageal sphincter is frequently responsible for reflux. However, asymptomatic reflux several times a day is a normal physiologic phenomenon. 

Causes of GERD

Dysmotiliy

• Achalasia
• Scleroderma

Prolonged Emptying

• Anti-cholinergics
• Gastric Outlet Obstruction
• Diabetic Gastroparesis
• Fat rich diet

Low LES tone

• Ethanol
• Caffeine, Chocolate
• Tobacco Smoking
• Medications (CCBs, Nitrates, Progesterone, Oestrogen)
• Pregnancy

Symptoms
Pain and discomfort with meals indicate GERD. Symptoms might be exacerbated with a head-down position or an increase in intra-abdominal pressure. and are transiently alleviated by antacids. GERD may be accompanied by diaphoresis, pallor, and nausea and vomiting which makes it hard to differentiate from cardiac pain. 

• Heartburn
• Diaphoresis, pallor, and nausea and vomiting (Always rule out Cardiac etiology)
• Odynophagia, dysphagia, Acid regurgitation, and hyper-salivation (Water brash) 
• Asthma exacerbations
• Sore throat and other ENT symptoms
• Dental erosions, gingivitis, halitosis, vocal cord ulcers and granulomas, laryngitis with hoarseness and repeated throat clearing
• Chronic sinusitis
• Chronic cough

Long standing GERD may lead to strictures, dysphagia, and inflammatory esophagitis.  

Radiation into both arms is rarely seen in reflux, whereas it may be present in approximately one quarter of patients with ischemic heart disease. 

Management

GERD is a very common problem. ED management focuses on ruling out the life threats, proving symptomatic relief and arranging follow up care. 

• H2 Blockers or PPIs (PPIs are more effective than H2-blockers in eliminating symptoms and healing mucosal damage)
• Antacids
• Pro kinetics 
• Lifestyle advice (Weight loss, avoid ethanol, caffeine,nicotine, chocolate, fatty foods, sleep with the head of the bed elevated, and avoid eating within 3 hours of going to bed at night)
• Follow up care (esophageal pH monitoring, an upper GI radiographic series, esophageal manometry, or esophagoscopy may be necessary, especially for patients who fail to respond to all of the preceding measures

Further Reading:
https://coreem.net/podcast/episode-74-0/

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

  

Interpreting Elevated Troponins and Types of Myocardial Infarction

Elevations of cardiac biomarkers in the blood reflect injury leading to necrosis of myocardial cells but biomarkers do not indicate the underlying mechanism of this injury. Myocardial injury can be due to ischemic and non-ischemic causes. Therefore, small amounts of myocardial injury with necrosis may be detected, which are associated with CCF, renal failure, myocarditis, arrhythmias, pulmonary embolism and percutaneous or surgical coronary procedures. Troponin elevation in these contexts should not be called as Myocardial Infarction but Myocardial Injury.

Onset of myocardial ischaemia is the initial step resulting from an imbalance between oxygen supply and demand. This can be identified from history and ECG. Possible ischaemic symptoms include various combinations of chest, upper extremity, mandibular or epigastric discomfort or an ischaemic equivalent such as dyspnoea or fatigue (in women). Pain associated with vomiting, worse on exertion, sweating is definitely worrisome. The discomfort with acute MI usually lasts 20 min. In an ideal world, the sequence should be history, physical exam, ECG and troponins. Whenever symptoms recur, it is important to repeat the ECG. If you are ordering trop troponins, you must order serial ECGs as well. remember, ECG is more of a rule in test not a rule out test for ACS.

MI is classified into various types, based on pathological, clinical and prognostic differences, along with different treatment strategies 

References:

1. Roe MT, Harrington RA, Prosper DM, Pieper KS, Bhatt DL, Lincoff AM, Simoons ML, Akkerhuis M, Ohman EM, Kitt MM, Vahanian A, Ruzyllo W, Karsch K, Califf RM, Topol EJ. Clinical and therapeutic profile of patients pre- senting with acute coronary syndromes who do not have significant coronary artery disease. The Platelet glycoprotein IIb/IIIa in Unstable angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial Investigators. Circulation. 2000;102:1101 – 1106.
2. Bugiardini R, Manfrini O, De Ferrari GM. Unanswered questions for manage- ment of acute coronary syndrome: risk stratification of patients with minimal disease or normal findings on coronary angiography. Arch Intern Med 2006; 166:1391 – 1395.
3. Reynolds HR, Srichai MB, Iqbal SN, Slater JN, Mancini GB, Feit F, Pena-Sing I, Axel L, Attubato MJ, Yatskar L, Kalhorn RT, Wood DA, Lobach IV, Hochman JS. Mechanisms of myocardial infarction in women without angiogra- phically obstructive coronary artery disease. Circulation 2011;124:1414 – 1425. 
4. Bertrand ME, LaBlanche JM, Tilmant PY, Thieuleux FA, Delforge MR, Carre AG, Asseman P, Berzin B, Libersa C, Laurent JM. Frequency of provoked coronary arterial spasm in 1089 consecutive patients undergoing coronary arteriography. Circulation 1982;65:1299 – 1306.
5. Suwaidi JA, Hamasaki S, Higano ST, Nishimura RA, Holmes DR Jr, Lerman A. Long-term follow-up of patients with mild coronary artery disease and endothe- lial dysfunction. Circulation 2000;101:948 – 954.
6. Bugiardini R, Manfrini O, Pizzi C, Fontana F, Morgagni G. Endothelial function predicts future development of coronary artery disease: a study on women with chest pain and normal angiograms. Circulation 2004;109:2518 – 2523. 
7. Kristian Thygesen, Joseph S. Alpert, Allan S. Jaffe, Maarten L. Simoons, Bernard R. Chaitman and Harvey D. White: the Writing Group on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction 

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic