74yo woman, with a history of CAD and hyperlipidemia, presents to your office with a 6-month history of leg pain and swelling. She states that it seems to be worse when she is on her feet and improves when she can put her legs up. She denies worsening pain with activity or walking, but has recently developed a “rash” on her legs that is worrying her (see below). Physical examination reveals warmth to the feet and legs with scattered, thin hair. You appreciate 1+ DP and PT pulses bilaterally.
What are some bedside maneuvers or tests you can perform to differentiate between arterial and venous insufficiency?
Definition – collection of electrical conduction cells of the heart that transmit impulses from the AV node to the ventricles
Clinical Significance – this bundle of cells is responsible for communication contraction impulses from the atria to the ventricles. Any damage to this area can result in varying degrees of heart block and conduction abnormalities
History – Named after Wilhelm His Jr. (1863-1934), a Swiss-born cardiologist and anatomist who received his medical doctorate from the University of Leipzig in 1889. The son of the equally famous Basel anatomist Wilhelm His Sr., he would become professor extraordinaire at his alma mater 6 year after graduating. He also went on to be physician-in-chief at the Friedrichstadt Hospital in Dresden, chair of internal medicine in Berlin, and advisory internist for several armies during World War I. He would describe his eponymous bundle as an assistant professor in 1893.
References
Firkin BG and Whitwirth JA. Dictionary of Medical Eponyms. 2nd ed. New York, NY; Parthenon Publishing Group. 1996.
Bartolucci S, Forbis P. Stedman’s Medical Eponyms. 2nd ed. Baltimore, MD; LWW. 2005.
Yee AJ, Pfiffner P. (2012). Medical Eponyms (Version 1.4.2) [Mobile Application Software]. Retrieved http://itunes.apple.com.
His Jr, W. Die Tätigkeit des embryonalen Herzens und deren Bedeutung für die Lehre von der Hezbewegung beim Menschen. Arbeiten aus der medidizinischen Klinik zu Leipzig, 1893: 23.
Review of the Electrical Conduction System of the Heart
Cardiac cells specialized to initiate and distribute electrical impulses in an orderly and sequential manner
Sinoatrial Node
Located in superior region of the crista terminalis
SVC feeds into the right atrium
Pacemaker of the heart and initiates the heartbeat
Starts in the node, spreads down the walls of the atria, until it reaches the AV node, stimulating contraction of the myocardium
Arterial Supply – SA nodal artery via the RCA
Atrioventricular Node
Located in interatrial septum above the coronary sinus near the attachment of the septal cusp of the tricuspid valve (Triangle of Koch)
Passes SA node impulse to the AV bundle (Bundle of His)
Arterial Supply – AV nodal artery via the RCA (80-90%) or LCx (10-20%)
AV Bundle (Bundle of His)
Arises from the AV node and descends along the membranous portion of the interventricular septum, where it divides at the upper border of the muscular portion of the interventricular septum into the left and right bundles suppling their respective ventricles
Transmits AV nodal impulses through the interventricular septum to the left and right bundle branches, which gives rise to the Purkinje fibers that ultimately distribute the ventricular myocardium
Bundle Branch Blocks Pearls
R-wave = depolarization going TOWARDS the lead
S-wave = depolarization going AWAY from the lead
RBBB = delay in conduction is oriented to the RIGHT and ANTERIOR
QRS = Positive V1 and negative V6
LBBB = delay in conduction is oriented to the LEFT and either ANTERIOR or POSTERIOR
QRS = Negative V1 and positive V6
Wide QRS complex > 120 ms
Delay in conduction due to the block
Secondary Repolarization (ST-T) Abnormalities
T-wave discordance with last deflection of QRS
Causes
RBBB
More common in patients without structural heart disease
Congenital
ASD
Cardiac
Valvulopathies, ischemic heart disease
Pulmonary
Pulmonary HTN, PTE
LBBB
4 main underlying conditions
Coronary disease
Hypertensive heart disease
Aortic valve disease
Cardiomyopathies
RBBB EKG Diagnostic Criteria
QRS > 120 ms
If all other criteria met but QRS < 120 ms, it is termed incomplete RBBB
rSR’ pattern in V1 and V2
Slurred S-wave in lateral leads (I, aVL, V5, V6)
ST depression and T-wave inversion in V1-V3
LBBB EKG Diagnostic Criteria
QRS > 120 ms
Dominant S-wave in V1-V3
Moving away from the leads
Broad, monophasic (M-shaped or notched) R-wave in lateral leads (I, aVL, V5, V6)
Moving towards the leads
Appropriate discordance
ST-segment and T-wave are in OPPOSITE direction to the main vector of the QRS complex
Left axis deviation
Poor R-wave progression
SPECIAL CONSIDERATIONS
Fascicular Blocks
Anterior
Pathology
When blocked, the conduction to the high lateral portion of the ventricle is delayed
Spreads to the intact posterior fascicle and RBB
Causes left axis deviation
Criteria for left anterior fascicular block
QRS normal to slightly prolonged
Left axis deviation WITHOUT other reasons
Small R-wave and large S-wave in inferior leads (II, III, aVF)
Small Q-wave with large R-wave in lateral leads (I, aVL)
Posterior
Pathology
When blocked, the conduction to the inferior portion of the ventricle is delayed
Spreads to the intact anterior fascicle and RBB
Causes right axis deviation
Criteria for left posterior fascicular block
QRS normal to slightly prolonged
Right axis deviation WITHOUT other reasons
Small R-wave and large S-wave in lateral leads (I, aVL)
Small Q-wave and large R-wave in inferior leads (II, III, aVF)
Sgarbossa’s Criteria
Used in the presence of LBBB or paced rhythm to uncover potential ischemia
Original (1996)
Concordant ST elevation > 1mm in leads with a positive QRS complex (5 points)
Concordant ST depression > 1mm in V1-V3 (3 points)
Excessively discordant ST elevation > 5mm in leads with a negative QRS complex (2 points)
Score ≥ 3 has a specificity of 90% for detecting concomitant ischemia
Smith-Modified Sgarbossa Criteria (2012)
≥ 1 lead with ≥ 1mm of concordant ST elevation
≥ 1 lead of V1-V3 with ≥ 1mm of concordant ST depression
≥ 1 lead ANYWHERE with ≥ 1mm ST elevation AND proportionally excessive discordant ST elevation
Defined as ≥ 25% of the depth of the preceding S-wave
1893 Cottage Physician
References
Heart. In: Morton DA, Foreman K, Albertine KH. eds. The Big Picture: Gross Anatomy, 2e. McGraw-Hill; Accessed January 17, 2021.
Jaffar A. Anatomical Structure of the Heart. In: Elmoselhi A. eds. Cardiology: An Integrated Approach. McGraw-Hill; Accessed January 17, 2021.
Goldberger AL. Electrocardiography. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 20e. McGraw-Hill; Accessed January 17, 2021.
Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) Investigators. N Engl J Med. 1996; 334(8):481-7. [pubmed]
Smith SW, Dodd KW, Henry TD, Dvorak DM, Pearce LA. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified Sgarbossa rule. Ann Emerg Med. 2012; 60(6):766-76. [pubmed]
Meyers HP, Limkakeng AT Jr, Jaffa EJ, et al. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. Am Heart J. 2015; 170(6):1255-64. [pubmed]
62yo man, with a history of COPD and 52-pack-year history of smoking, presents to your office to establish care. His shortness of breath has been manageable using tiotropium daily with albuterol 2-3x per month for exacerbation. He denies angina, chest pain, or unreasonable dyspnea with exertion. An EKG was performed and is below.
What does it show?
What are the diagnostic criteria present?
Answer
The EKG reveals a right bundle branch block most likely due to his underlying COPD and pulmonary hypertension.
Diagnostic criteria for RBBB are:
Wide QRS > 120 ms
RSR’ pattern in V1-2 (“rabbit ears”) with R’ > R
Wide, slurred S wave in I, aVL, or V5-6
Other common findings, though not always associated, is ST depression and T wave inversion in the right precordial leads (V1-3)
Clinical Significance – although not seen in every patient with cardiac tamponade, it is a common question on boards and certification examinations. These include: 1) hypotension, 2) JVD, and 3) muffled/distant heart sounds.
History – Named after Claude Schaeffer Beck (1894-1971), an American cardiac surgeon who recieved his medical doctorate from Harvard University in 1921. He would attend surgical residency at Case Western University, where he would spend his entire career. He developed a novel re-circulation technique for cardiac ischemia called the Beck Procedure, where pectoral muscle was implanted in the pericardium, and later placing a vein graft between the aorta to the coronary sinus. He also pioneered the first successful use of a defibrillator in 1947 to restore ROSC in a 14yo patient he was operating on for a congenital heart defect. His eponymous triad was first described in 1935 in an article entitled “Two cardiac compression triads” in the Journal of the American Medical Association.
References
Firkin BG and Whitwirth JA. Dictionary of Medical Eponyms. 2nd ed. New York, NY; Parthenon Publishing Group. 1996.
Bartolucci S, Forbis P. Stedman’s Medical Eponyms. 2nd ed. Baltimore, MD; LWW. 2005.
Yee AJ, Pfiffner P. (2012). Medical Eponyms (Version 1.4.2) [Mobile Application Software]. Retrieved http://itunes.apple.com.
Beck CS. Two Cardiac Compression Triads. JAMA. 1935;104(9):714-716. [link]
Theruvath P, Ikonomidis JS. Historical perspectives of The American Association for Thoracic Surgery: Claude S. Beck (1894-1971). JTCVS. 2015;149(3):655-660. [link]
62yo man, with a history of COPD and 52-pack-year history of smoking, presents to your office to establish care. His shortness of breath has been manageable using tiotropium daily with albuterol 2-3x per month for exacerbation. He denies angina, chest pain, or unreasonable dyspnea with exertion. An EKG was performed and is below.
Definition – low-pitched, rumbling, mid-to-late diastolic murmur heard best at the apex
Clinical Significance – this murmur is associated with severe aortic regurgitation and is due to two distinct mechanisms. First, the aortic jet flow impinging on the mitral valve causing vibrations from premature closing and second, turbulence of two columns of blood from the left atrium to left ventricle and aorta to left ventricle.
History – Named after Austin Flint I (1812-1886), an American physician who received his medical doctorate from Harvard University in 1833. He would practice in Boston, Buffalo (where he would help found the Buffalo Medical College, and New York City, where he was professor of medicine at the famed Bellevue Hospital. A proponent of European diagnostic methods (as he was mentored by James Jackson at Harvard, who was a follower of Laënnec), he advocated and popularized the use of the binaural stethoscope in physical diagnosis. He was a prolific writer and researcher with his Treatise on the Principles and Practice of Medicine considered as a classic medical text. He is also recognized as having coined the term “broncho-vesicular breathing” in lung auscultation. He would publish the first detailed description his eponymous murmur in 1862 in the American Journal of Medicine Sciences in an article entitled “On cardiac murmurs”.
References
Firkin BG and Whitwirth JA. Dictionary of Medical Eponyms. 2nd ed. New York, NY; Parthenon Publishing Group. 1996.
Bartolucci S, Forbis P. Stedman’s Medical Eponyms. 2nd ed. Baltimore, MD; LWW. 2005.
Yee AJ, Pfiffner P. (2012). Medical Eponyms (Version 1.4.2) [Mobile Application Software]. Retrieved http://itunes.apple.com.
62yo man, with a history of pseudotumor cerebri, presents to your clinic with progressive headache and vision changes. You would like to confirm an increased intracranial pressure before sending him to the neurologist.
What are two (2) ways at the bedside you can confirm and what are the thresholds for positive findings?
Answer
The old and busted bedside way to determine if a patient has increased intracranial pressure is the fundoscopic examination. What you are looking for specifically is the cup:disc ratio of the optic nerve. Normal is around 0.3, or 1/3rd. If it is increased, it suggests increased intracranial pressure.
2. The new, hotness is using bedside POCUS to measure the optic nerve directly. Using the high frequency linear probe with a tegaderm placed over the patient eye, place a generous amount of gel over the globe and measure the optic nerve 3mm from the retina. A normal optic nerve should be < 5mm in diameter and anything over than suggests increased intracranial pressure
Definition – bedside test to evaluate hearing loss using a 512hz tuning fork
Clinical Significance – this maneuver is performed by vibrating a 512hz tuning fork and placing it on the mastoid process. The patient then informs the provider when they no longer can hear the ringing, at which point the tuning fork is moved in front of the canal. In normal hearing, the patient should still be able to hear the ringing (although it can also occur in sensorineural hearing loss). If conductive hearing loss is present, bone conduction is greater than air conduction.
History – Named after Heinrich Adolf Rinne (1819-1868), a German otologist who received his medical doctorate from the University of Göttingen. He would practice here for the majority of his career exploring the diseases of the ears, nose, and throat. He first described his eponymous test in 1855, but did not get widespread recognition for it until 1881 when it was further publicized by otologists Bezold and Lucae
References
Firkin BG and Whitwirth JA. Dictionary of Medical Eponyms. 2nd ed. New York, NY; Parthenon Publishing Group. 1996.
Bartolucci S, Forbis P. Stedman’s Medical Eponyms. 2nd ed. Baltimore, MD; LWW. 2005.
Yee AJ, Pfiffner P. (2012). Medical Eponyms (Version 1.4.2) [Mobile Application Software]. Retrieved http://itunes.apple.com.
Septal branch of the superior labial branch of the facial artery
Posterior
Woodruff’s Plexus
Posteriorlateral branches of the sphenopalatine artery
Posterior inferior turbinate
Epidemiology
Up to 60% of population will experience a significant nosebleed each year
Only 10% need to seek attention
Common ENT admission condition, but rarely needs surgical intervention
Bimodal age distribution
Before 10 years or between 45-65 years
Male predominance before the age of 49, then equalizes
Estrogen has been shown to protective for mucosa
Anterior bleeds are significantly more common (>90%) and resolve with minor interventions
Posterior bleeds can result in significant hemorrhage
Etiologies
Nose picking
Low environmental moisture
Mucosal hyperemia of viral or allergic rhinitis
Trauma
Foreign body
Anticoagulation
Coagulopathies
Osler-Weber-Rendu, von Willebrand, hemophilias
Connective tissue disease
Aneurysm development
Neoplasm
Squamous cell, inverted papilloma
Hypertension
Debated as a cause, but has shown to prolong bleeding
Nasal medications
Steroids, oxymetazoline
Heart failure
Patient Assessment
Primary
Airway assessment
RR, O2
Cardiovascular stability
HR, BP
Secondary
History
Medications
Anticoagulation, aspirin, nasal medications
PMH
Bleeding disorders, HTN, liver disease
Recent trauma
History of nosebleeds
How often, how long do they last, ever been admitted for one
Diagnostic Studies
Coagulation studies should NOT be routinely ordered
Should be in patients on anticoagulation
In patients with prolonged bleeds:
CBC
Type and cross
Examination
Have patient blow nose to remove clots and blood
Examine nasal cavity to see if you can see the bleeding site
Otoscope, nasal speculum
Don’t have patient tilt head back
Nasopharynx lies in anteroposterior plane and this will obscure the majority of the cavity from view
Interventions
Initial (Woodpecker/Walrus technique)
Have patient blow nose to remove clots
In a small basin mix any or all of the following:
Oxymetazoline
Lidocaine with epinephrine
Tranexamic acid
If available, soak GelFoam/Surgicel in this fluid and place BEFORE the sponge sticks
Trim two oral sponge swabs to better fit in the nasal cavity and soak in the fluid
Make a nasal bridge clamp by taping two tongue depressors together on one end
Place swabs in nasal cavities and apply nasal clamp for 10-15 minutes
Ice pack can also be used
Cautery
If the bleeding site can be visualized on direct examination
Apply topical anesthetic
Silver nitrate sticks
Start from periphery and roll to center of bleeding
No more than 10 seconds
A white eschar should form
Nasal packing
Use if cautery fails
Ensure topical anesthesia
Soak in sterile water
Insert by sliding along the floor of the nasal cavity PARALLEL to floor
Insufflate the balloon with air
Nasal Balloon Catheters
For posterior bleeds
Follow same steps for nasal packing
Insufflate posterior balloon FIRST and apply gently traction
Then insufflate the anterior balloon
Foley Catheters
If you don’t have a prefabricated nasal balloons, a foley catheter can work
Insert the catheter until you can see it in the posterior oropharynx
Insufflate with 5-10cc of water
Apply traction to seat balloon in posterior choana
Add additional water to tamponade
Clamp catheter with umbilical clamp or c-clamp from NG tube
Disposition and Follow-up
For simple nasal packing, patients should be evaluated by ENT within 24-48 hours
Discuss with consultant need for antibiotic prophylaxis
No good evidence supports routine use, but ENT often prefers
Amoxicillin-Clavulanate is most commonly used
Clindamycin or trimethoprim/sulfamethoxazole should be used if concern for nasal carrier of MRSA
Posterior bleeds should be immediately assessed by ENT for potential surgical intervention
Endoscopic sphenopalatine artery ligation
Anterior ethmoid artery ligation
Open or endoscopic
1893 Cottage Physician
References
Kucik CJ, Clenney T. Management of epistaxis. Am Fam Physician. 2005; 71(2):305-11. [pubmed]
Villwock JA, Jones K. Recent Trends in Epistaxis Management in the United States JAMA Otolaryngol Head Neck Surg. 2013; 139(12):1279-84. [pubmed]
Kotecha B, Fowler S, Harkness P, Walmsley J, Brown P, Topham J. Management of epistaxis: a national survey. Ann R Coll Surg Engl. 1996; 78(5):444-6. [PDF]
Fishpool SJ, Tomkinson A. Patterns of hospital admission with epistaxis for 26,725 patients over an 18-year period in Wales, UK. Ann R Coll Surg Engl. 2012; 94(8):559-62. [PDF]
Min HJ, Kang H, Choi GJ, Kim KS. Association between Hypertension and Epistaxis: Systematic Review and Meta-analysis. Otolaryngol Head Neck Surg. 2017; 157(6):921-927. [pubmed]
Shakeel M, Trinidade A, Iddamalgoda T, Supriya M, Ah-See KW. Routine clotting screen has no role in the management of epistaxis: reiterating the point. Eur Arch Otorhinolaryngol. 2010; 267(10):1641-4. [pubmed]
Lin G, Bleier B. Surgical Management of Severe Epistaxis. Otolaryngol Clin North Am. 2016; 49(3):627-37. [pubmed]
