High Blood Pressure: the basics

Hypertension, or high blood pressure, increases the amount of work the heart has to do. It’s like going to the gym and lifting heavier weights. Just like when you lift heavier weights at the gym to get bigger biceps, when your heart beats against a higher pressure it compensates by getting thicker. However, this compensatory mechanism can actually weaken the heart over time making it harder to perfuse the heart with blood and over time increases your risk of heart failure, heart attack, and stroke.

Some of my patients tell me, “but I feel fine”. And that’s the thing- high blood pressure is a silent killer. You can have elevated blood pressure for many years and not even ‘feel’ it. That doesn’t mean it can’t cause serious harm and increase your risk of future heart attack or stroke.


Defining Hypertension (high blood pressure)

A ‘normal’ blood pressure is <120/80. That means both the systolic (top number) and diastolic (bottom number) need to be below 120 and 80, respectively. Some people have lower blood pressures and that can be completely normal. The short and skinny of it is that you want your blood pressure less than 120/80.

Below are the different stages of hypertension. How we treat blood pressure depends on your individual circumstances and medical history. It is based on robust data summarized in a the 2017 ACC/AHA (American College of Cardiology/American Heart Association) guidelines.

If you have a normal blood pressure reading (<120/80) that doesn’t mean you’re off the hook. You should still get a yearly blood pressure reading. Sometimes you just hit a certain age where your blood pressure starts to creep up a little bit. This is a good reminder that having high blood pressure, like many things in medicine, is both genetic predisposition as well as some behavioral and lifestyle choices that can impact it. Having high blood pressure doesn’t mean you did anything wrong. Some of my patients are the healthiest individuals I’ve ever met. Except that hypertension runs in their family. We will get into some behavioral and nutritional choices you can make to help bring down your blood pressure in another post.

Elevated blood pressure is 120-129/<80. Notice the different goals for the systolic and diastolic (i.e. top and bottom numbers). Essentially, if your bottom number goes above 80 you are considered hypertensive. But if your diastolic remains <80 but your systolic is 120-129 we generally recommend rechecking your blood pressure in 3-6 months. This doesn’t mean you need medications but it does mean that we want to ensure you don’t develop high blood pressure. It’s also another chance to make some positive lifestyle habits and nutritional choices that can pay off over time. As many of my patients can attest, one of my favorite sayings is that many of the choices we make today can pay off over time. Like building a strong retirement fund with a good interest rate. In contrast, ignoring high blood pressure is like having bad debt. Either way- the interest is going to compound. So it’s always better to know if you have high blood pressure than to ignore it.

Stage 1 hypertension is either a systolic between 130-139 or a diastolic between 80-89. This is where working with your physician is important. In patients at higher risk of heart disease, like those who already have clinical evidence of atherosclerotic cardiovascular disease (i.e. prior stroke, heart attack) we often will initiate both lifestyle modifications and treatment with blood pressure medications. If you are a low risk patient we can consider lifestyle modifications alone and rechecking your blood pressure in a few months. If lifestyle modifications do the trick and bring down your blood pressure we can avoid using medications. But if you are doing all the right things and your blood pressure won’t budge then you likely will require medications to lower your blood pressure. Regardless, patients with stage 1 hypertension should be reassessed in 1 month.

Stage 2 hypertension is either a systolic >140 or a diastolic >90. In these patients we often jump to use medications while also initiating lifestyle modifications because the degree that lifestyle modifications will impact your blood pressure likely won’t be enough. Just like how you wouldn’t ignore a leak under your sink you should also not ignore high blood pressure-both will cause damage over time. This is where talking with your physician is important because not all patients are alike. If you want to avoid using medications I certainly don’t think it’s unreasonable to hold off if you are right on the borderline of stage 1 and stage 2 of hypertension as long as we have a plan in place and you continue to follow up. However, a blood pressure of 142/88 for instance is very different than a blood pressure of 180/100. For latter blood pressure (i.e. 180/100) would likely require initiation of medications right away. All patients with stage 2 hypertension should be also reassessed in 1 month (just like those with stage 1 hypertension).

The more uncontrolled your blood pressure is and the greater the period of time that it remains uncontrolled the greater your risk of heart disease (e.g. heart attack, stroke). Just because you have high blood pressure doesn’t mean you will have a heart attack and just because we treat your high blood pressure doesn’t mean you won’t. It’s all about decreasing that intrinsic risk.


Why you should check your blood pressure at home

In my clinical practice I like when my patients take their blood pressure at home for a few reasons. First, if you’ve ever been to a doctor’s office you know it can be a little anxiety inducing. That’s why I never make drastic changes based on a single blood pressure reading. Some patients can have white coat hypertension– when the blood pressure readings at your doctor’s office are always elevated but when you take them at home they are normal. These patients don’t need to be treated for high blood pressure!

Second, you can only go the doctor’s office so many times. Taking your blood pressure at home gives us additional data points to use to estimate your average blood pressure. Generally, I care the most about the your blood pressure trend. Let’s look at two patients as an example. ‘Patient 1’ consistently gets systolic blood pressure readings in the 140-150’s but occasionally gets a systolic blood pressure of 118. ‘Patient 2’ on the other hand gets consistent systolic blood pressure readings in the 120’s but occasionally gets a systolic blood pressure reading in the 140’s. In both patients I won’t ignore the occasionally high or low reading but I care more about where your blood pressure average tends to be.


How to take your blood pressure at home

Type of blood pressure cuff

Generally, arm cuffs are better than wrist cuffs. However the most important thing is that you use an appropriately sized cuff. Using the wrong size blood pressure cuff can give you falsely high or falsely low readings (shown below).

If you want to be accurate, the American Heart Association recommends a cuff bladder width 40% of the arm circumference and a bladder length 80% of the arm circumference. Use the middle part of your arm to check the circumference (shown below).

How to actually measure your blood pressure

If you don’t like reading I made a short TikTok video explaining how to actually check your blood pressure (shown below). The following tips aren’t to torture you- they are so we get accurate readings. The important things to remember are:

  • Blood pressure cuff should be bare to skin (not over clothing)
  • Keep your arm supported (don’t elevate it in the air)
  • Keep your feet flat on the ground
  • Don’t cross your legs
  • 30 minutes before taking your blood pressure do not smoke, drink caffeine, or exercise (life hack- take it first thing in the morning before your first cup of coffee or if you smoke before your first cigarette)
  • You can repeat the reading after waiting 5 minutes. I typically tell patients to take it once in the morning and once in the evening
  • WRITE DOWN YOUR READINGS IN YOUR PHONE OR NOTE PAD AND BRING THE READINGS TO YOUR NEXT DOCTOR’S VISIT

Don’t forget to bring your readings to your next doctor’s appointment

Every day after work when I leave the hospital I put my hospital identification card in my car. That way I don’t have to remember to take it with me to work the next day. Because believe me there’s nothing worse than getting to work and having to turn around and drive home to pick up your ID badge. Similarly, remove road blocks from bringing your blood pressure readings to your next doctor’s appointment by putting the information directly into your phone. This way you don’t have to remember to bring the notepad you’ve been writing your blood pressure readings in. If you choose to do it the old fashioned way with pen and paper that is perfectly fine. Just remember to bring it to your next visit. Remember to document both the top and bottom number in addition to your heart rate. Lastly, please do not rely on your memory to serve as a blood pressure log. I want to know what blood pressure readings you are getting at home and not just that it was ‘high’ or ‘normal’.


If you found this helpful then:

High Yield Board Review for Cardiology Fellows: Vascular Diseases

Below are some of my high yield notes for the general cardiology board examination focusing on vascular diseases with easily sharable supplemental articles and tables my reference.

Aortic Aneurysm

  • Bentall procedure for surgical aortic aneurysm repair
  • Elephant trunk for surgical aortic aneurysm repair
  • thoracic endovascular aortic aneurysm repair

Location:

  • Ascending aorta/root: 60%
  • Descending aorta: 40%
  • Both thoracic and abdominal aorta: 5-10%

Surgical Indications for Thoracic Aortic Aneurysm Repair

ConditionSize Threshold
Aneurysm≥5.5 cm
Bicuspid AV (BAV)≥5.5 cm
BAV with risk factors + low surgical risk≥5 cm
BAC with AVR>4.5 cm
Marfan syndrome≥5 cm
Marfan syndrome + risk factors>4.5 cm
Loeys-Dietz syndrome4 – 4.5 cm
Familial thoracic aortic aneurysm syndromes (TAAD)4.5 – 5 cm
*Abdominal aortic aneurysm≥5.5cm
*Abdominal aortic aneurysm>0.5 in 1 year
  1. Patients with infrarenal or juxtarenal AAAs measuring ≥5.5 cm should undergo repair to eliminate the risk of rupture. (Level of Evidence B)
  2. Infrarenal or juxtarenal AAAs measuring 4.0 to 5.4 cm in diameter should be monitored by ultrasound or computed tomographic scans every 6 to 12 months to detect expansion. (Level of Evidence A)

US Screening for Abdominal Aortic Aneurysm

Patient Level of Evidence
Men 65-75 who have ever smokedB
Men 65-75 who never smokedC
Women 65-75 who have ever smokedI
Women who never smokedD
*B: high certainty of moderate net benefit
*C: selectively offer given moderate certainty of small benefit
*D: no net benefit or possible harm
I: insufficient evidence

Surveillance Imaging in Known Aortic Aneurysm

Abdominal Aneurysm SizeFrequency
25-29 mm4 years
30-39 mm3 years
40-44mm2 years
*≥45 mmYearly
Class IIa, LOE B
*Yearly in both thoracic and abdominal aneurysms if ≥45mm. Otherwise repeat thoracic imaging q2-3 years


Peripheral Vascular Disease

  • Risk factors and odds ratio (95% CI): CAD/CVD 2.27, smoker 2, former smoker 1.87, DM1 1.68, HTN 1.47, age 1.39
  • Clinical Presentation of PAD (i.e. angina of the legs): 50% asymptomatic, 33% atypical limb symptoms, 15% typical intermittent claudication, 2-3% critical limb ischemia
  • Patients at risk of PAD who should be screened (IIa rec): (1) age ≥65yo, (2) Age 50-64 with risk factors (DM2, smoking history, HLD, HTN) or FH of PAD, and (3) age <50 with DM2 and 1 additional risk factor for atherosclerosis
Location of claudicationLocation of disease
CalfFemoral-popliteal ±aorto-iliac
Buttock & calfAorto-iliac
ButtockInternal iliac

Ankle Brachial Index (ABI)

ABIResult
>1.4Non-compressible
1-1.4Normal
0.91-0.99Borderline abnormal
≤0.9Abnormal
*If borderline and good story for claudication: can perform stress ABI (exercise or reactive hyperemia) to augment blood flow through stenosis
** If >1.4: perform toe-brachial index. 20-30% increase is normal. >20 mmHg drop is abnormal
How to perform: use HIGHEST value from DP or PT

Screening for PAD

Treatment of PAD

Acute Limb Ischemia (ALI)


Medium and Large Vessel Vasculitis

ClassificationDiagnosisEtiologyManifestationsTreatment
Large-vessel vasculitisTakatasu arteritis
Age <50, > women, Asain, B-sypmtoms, ±erythema nodosum)– 70% aortic lesions
– Vascular inflammation ➡️ stenosis (long and tapering i.e. rat-tailing) ±aneurysm
– Arm/leg claudication, mesenteric ischemia, stroke, renovascular HTN
– Diastolic murmur, bruit, absent pulses
Steroids, IL-6i, TNFai
Large-vessel vasculitisGiant cell arteritisAge >50, >women, caucasian– HA, jaw claudication, visual disturbances, stroke
– ±Polymyalgia rheumatica (40-60%): stiffness, proximal muscle pain (RF, anti-CCP antibodies)
– Subclavian, axillary stenosis/aneurysm, carotid/vertebral involvement
Steroids

Tocilizumab
Medium-vessel vasculitisPolyarteritis nodosa
Men, ~age 50, rare, associated with HBV infection

Diagnosed clinically
B-symptoms, neurologic complaints (peripheral neuropathy), renal involvement, GI involvement, orchitis, cardiomyopathy, pericarditis, coronary involvementSteroids

±Cyclophosphamide or azathioprine

Antivirals if associated with active HBV infection
Medium-vessel vasculitisKawasaki disease<5yo, Asain children (>Japanese),5 days fever, BL conjunctivitis, mucositis, rash, erythma, or desquamation of hands/feet, cervical lymphadenopathyUntreated: ~25% develop coronary aneurysms

Acute: IVIG ± aspirin. Sometimes steroids

±Anticoagulation if large aneurysms
Variable vessel vasculitisBehçet’s disease
Variable vessel vasculitisCogan syndrome
Single-organ vasculitisIsolated aortitis
Vasculitis associated with probable etiologyInfectious aortitis: syphillis, mycobaterial aortitis, suppurative/mycotic infectious aortitis

Rheumatologic disease: IgG4-related disease, antineutrophil cytoplasmic antibody-associated vasculitis (ANCA), spondyloarthritis, Erdeim-Chester disease, relapsing polychondritis, sarcoidosis

Coronary CT for Cardiology Fellows

The basics of cardiac CT imaging

My notes on coronary computerized tomography (CT).

Anatomy

  • Coronary artery segmentation
  • Normal coronary course
  • Normal anatomy on CT
  • Common anomalous coronary arteries
  • Common anomalous coronary arteries

Classification of anomalous coronary arteries

  1. Anomalies of:
    1. Origin (>LCX from right coronary sinus most common)
    2. Course
    3. Intrinsic anatomy
    4. Termination
  2. Hemodynamic consequence: non/significant
  3. Coronary fistula
  4. Complete myocardial bridging (>LAD most common)
  5. Association with higher risk of sudden cardiac death (SCD)

Normal Anatomy

  • A normal CTCA has a high negative predictive value (98– 100%) for excluding CAD
  • Indications for CTCA:
    • Low-to-intermediate risk patients with acute chest pain and non-diagnostic ECG and serum biomarkers
    • Low-to-intermediate probability of CAD and unable to exercise or with inconclusive functional test results

Malignant Anatomy: associated with chest pain, myocardial ischemia, or sudden cardiac death

  1. RCA arising from left sinus
  2. Left main coronary artery (LMCA) arising from right coronary sinus
  3. LMCA arising from the pulmonary artery

RCA arising from left side- generally better prognosis

  • Right coronary artery originating from the left coronary sinus. RCA in red, Left main coronary artery yellow. The proximal RCA's acute angle take off passes through the pulmonary trunk and aortic root causing moderate compression.
  • Myocardial bridging of the mid LAD
  • Pulmonary trunk level showing LMCA originating from pulmonary artery (red asterisk)
  • Aorta gives rise to RCA. Pulmonary artery gives rise to LMCA, now dilated
  • Again showing aorta gives rise to RCA. Pulmonary artery gives rise to LMCA, now dilated
  • Again showing aorta gives rise to RCA. Pulmonary artery gives rise to LMCA, now dilated
  • Anomalous left coronary from the pulmonary artery (ALPACA or Balnd-White-Garland syndrome)

Ischemic Cardiomyopathy (ICM)

High risk calcification features associated with higher event rates:

  • Low attenuation plaque: <30 Hounsfield units
  • Positive remodeling: lesion with vessel area >10% larger than a proximal normal reference site (remodeling index >1.1)
  • Napkin-ring sign: low-attenuation core surrounded by a rim-like area of higher attenuation (but less than 130 HU)
  • Spotty calcification: <3 mm length calcifications comprising <90°
  • CTA plaque phenotype features
  • CTA plaque phenotype features
  • CAD-RADS scoring and modifiers

Coronary artery calcium score (CACS) of 0

  • Asymptomatic, independent of Framingham risk score: very low risk of events (0.10% per year), safety window of at least 5 years
  • No benefit from aspirin for primary prevention
  • Patients with abnormal lipid profile but CACS 0 have little benefit from statin
  • Stable symptomatic patients with low-to-intermediate pretest likelihood of CAD, a CACS 0 can safely exclude flow-limiting coronary disease
  • CACS of 0
  • CACS of 0. Minimal calcium in the aortic root and aortic valve

Abnormal coronary artery calcium score (CACS)

  • Symptomatic patients with CACS> 400 are at high risk of events (>2% per year), independent of risk factors and functional tests.
  • CACS>1000, even if normal stress testing, have significantly higher risk of major adverse events
  • CACS 1832
  • Bicuspid AV with aortic dilation, and non-obstructive mixed plaque with evidence of positive remodeling`
  • pLAD, mLAD, dLAD in cross section
  • Obstructive CAD in LAD

Coronary Dissection

  • Linear low-density intraluminal image suggestive of focal dissection
  • Moderate ostial RCA stenosis. PRedominantly non-calcified eccentric lesion with low-attenuation core
  • Moderate ostial RCA stenosis. PRedominantly non-calcified eccentric lesion with low-attenuation core

LAD calcification

  • Calcified LAD with severe dLAD lesion
  • Severe focal, eccentric, predominantly non-calcified lesion in mid-to-distal LAD with low attenuation core, positive remodeling, and napkin ring sign

CTO of LCX with RCA collaterals in patient with discordant normal SPECT but abnormal ECG stress (2mm ST-depressions) sent for CTCA to evaluate coronary anatomy

  • Diffuse calcification of D1 and CTO of LCX

ECG Reference Guide For Medical Trainees

A quick reference guide for diagnostic ECG criteria with examples. Will continue to update regularly.


P-Wave Abnormalities

Right atrial enlargement (RAE)

  • 2 things help me remember RAE. First, the normal P-wave on an ECG typically represents the left atrium because the right atrium is typically smaller and it’s electrical current is typically hidden in the left atrium’s electrical signal. Second, the SA node sits in the right atrium. So when the right atrium gets enlarged we start to see it on the ECG. The P-wave gets BIGGER! I think of it similar to what we see in left ventricular hypertrophy. Typically, in a normal QRS complex we only see the left ventricle because it’s size and electrical signal is so much larger than the right atrium (similar to our atria). However, in LVH the left ventricle gets even larger. So the electrical signal it puts out is even bigger too. This is just like what happens in RAE. The right atrium is able to be seen in the P-wave which manifests with TALL P-waves. Thus, the diagnostic criterion are:
  • Inferior lead P-waves: >2.5 mm in height (tall positive P-wave because the SA node is superior in the heart so the electrical signal in the inferior leads, the direction the electrical impulse goes toward, will be larger in size)
  • >1.5mm in V1, V2
  • Clinically can be seen in RVH, COPD, pHTN > CHD >>tricuspid stenosis

Left atrial enlargement (LAE)

  • Back to our discussion about P-waves. In normal physiology the SA node in the right atrium fires and then the signal has to travel all the way over the left atrium. We already know that on normal ECG’s that the P-wave represents the left atrium. Thus, if the left atrium gets enlarged you will see LONGER P-waves because it will take more time for that signal to reach the entirety of the left atrium. Or at least that’s how I remember it in my head. Thus, for LAE think “1 box deep, 1 box wide”. If you can fit 1 small box inside the negatively deflected P-wave you should be thinking about LAE. The diagnostic criterion are:
  • Terminal portion V1 > 1mm deep, >40ms duration
  • Inferior leads: notched P-wave > 120ms

Biatrial enlargement (BAE)

You can also have both diagnostic criterion met for both left and right atrial enlargement. In these cases we simply call it biatrial enlargement. Here’s a quick and dirty reference for atrial enlargement:


Ventricular Hypertrophy

Left Ventricular Hypertrophy (LVH)

There are a LOT of criterion for LVH but the most frequent ones that I use in clinical practice are:

  • aVL >11 (Sokolow-Lyon ‘stand alone‘ criteria)
  • Cornell Criteria: R wave in avL + S wave in V3 > 28mm in men/> 20mm in women (Easy way to remember: CorneLL has 2 L’s, aVL has 1 L. Add them together to remember you use lead V3)
  • Sokolow-Lyon Criteria: S wave in V1 + R wave in V5 or V6 > 35mm
  • Delayed intrinsicoid deflection in V5, V6 >50ms (interestingly this is the only non-voltage criteria for LVH)

LVH can also have a ‘strain pattern’ with T-wave inversions (TWI) as seen in the ECG below.

LVH with strain pattern in I, II, V5, V6

Right Ventricular Hypertrophy (RVH)

  1. RAD: mean QRS axis ≥ 100 degrees
  2. Secondary ST-T segment changes (STD, TWI) in right precordial leads
  3. (R/S ratio in V1 > R/S ratio in V5, V6) or (R/S ration in V6 <1) or (R wave > 7mm in V1)

Clinically, Posterior MI can mimic RVH

  • Factors that favor RVH diagnosis: concomitant RAD, TWI in V1-V2
  • Factors that favor posterior MI: presence of inferior Q-waves

Combined Ventricular Hypertrophy

  • Exists when criteria for both isoloated LVH) and RVH are met
  • Should be suspected when criteria for LVH is present but QRS axis is > 90 degrees or criteria for right atrial enlargement exist
  • R/S ratio approximately equal to 1 in both V3 and V4 (Kutz-Wachtel phenomenon)
Diagnosis: Atrial flutter, LAD, LVH, RVH, iRBBB

Intraventricular Conduction

Left Bundle Branch Block (LBBB)

  1. QRS ≥120 ms
  2. Terminal S-wave in V1 (late forces of QRS should be negative)
  3. I, aVL, V5, V6: Broad notched or slurred R-wave. Occasional RS pattern in V5, V6 may be attributed to displaced transition of QRS complex)
  4. No Q-waves in I, V5, V6 but in aVL a narrow Q-wave may be present without myocardial pathology
  5. Delayed onset of intrinsicoid deflection >60 ms from beginning of QRS to peak of R-wave in V5, V6 but normal in V1-V3 when small initial R-wave can be discerned

Left Anterior Fascicular Block (LAFB)

  1. LAD (QRS axis between -45 to -90 degrees) and mean QRS duration < 120 ms
  2. qR complexes in I, aVL
  3. rS complexes in II, III, aVF
  4. Prolonged R wave peak time in aVL > 45ms (from beginning of QRS complex to peak of R wave)
  5. *Absence of other causes of marked LAD such as inferior MI or LVH

Note: The entire left bundle conduction system of the heart is made up of two fascicles, one anterior and one posterior. The left anterior fascicle supplies fibers to the anterior and lateral walls of the left ventricle. The above criteria of left anterior fascicular block do not apply to patients with congenital heart disease in whom left-axis deviation is present in infancy.

Left Anterior Fascicular Block (LAFB)

Left Posterior Fascicular Block (LPFB)

  1. RAD (QRS axis 90 to 180 degrees in adults) with mean QRS duration < 120 ms
  2. rS complexes in leads I and aVL
  3. qR complexes in leads II, III and aVF
  4. *Absence of other causes of right axis deviation including lateral MI, dextrocardia, or RVH

Note: The entire left bundle conduction system of the heart is made up of two fascicles, one anterior and one posterior. The left posterior fascicle is shorter and thicker than the left anterior, and receives dual blood supply from both the left and right coronary arteries. Multivessel coronary artery disease is the most common cause of left posterior fascicular block.

Right Bundle Branch Block (RBBB)

  1. QRS ≥ 120 ms
  2. V1, V2: RSR’ with secondary R-wave usually wider than initial R-wave
  3. Minority of patients may have a wide and often notched R wave pattern in lead V1 and/or V2
  4. S wave duration > than R wave or > 40 ms in leads I and V6
  5. Normal R peak time in leads V5 and V6 but > 50 ms in lead V1

Of the above criteria, the first 3 should be present to make the diagnosis. When a pure dominant R wave with or without a notch is present in V1, the 4th criteria should be satisfied

ECG Right Bundle Branch Block RBBB 5

Incomplete Right Bundle Branch Block (iRBBB)

  1. Same criteria for RBBB but QRS < 120ms but > 100ms

Non-specific inter-ventricular conduction delay

  1. QRS ≥ 110 ms
  2. Specific criteria for RBBB, LBBB not met

Quick and dirty reference to compare LBBB and RBBB:

Bundle Branch Block : Mnemonic | Epomedicine

Atrial Rhythms

Sinus Rhythm

In medical school we are taught this incorrectly. The correct way to tell that a P-wave is of sinus origin is that they are:

  1. Upright in the inferior leads (remember the sinus node is in the right atrium so the electrical wave will go from the top down and thus be positive inferiorly)
  2. Biphasic in V1
  3. Axis between 0 to 75 degrees (i.e. upright in the inferior leads)

The number of P-waves before every QRS complex is irrelevant. You can have sinus rhythm but be in complete heart block. Or have sinus rhythm but have second degree type I or type II heart block. Generally however they should have the same morphology. A single P-wave with a different morphology can indicate a premature atrial complex (PAC) but if you have multiple different P-wave morphologies then you might be dealing with wandering atrial pacemaker (WAP) or multifocal atrial tachycardia (MAT). I think of WAP and MAT as the same rhythm across a spectrum ranging from a normal heart rate (WAP) to a fast heart rate (MAT).

Sinus Arrhythmia

Diagnostic criteria:

  • Normal P wave axis (0 to 75 degrees; i.e. upright in leads I and II)
  • P-P interval varies by > 10% or 0.16 seconds

tl;dr normal sinus P-waves (as above) but P-P interval varies by >10% or 160ms (4 little boxes). ECG intervals can vary with respiration but they shouldn’t vary by more than 10%. Often incidental without major clinical significance

High Yield Board Review Notes for Cardiovascular Disease Fellowship

The following are iterative notes that I take while studying for my general cardiology, echocardiography, and nuclear cardiology board exams. Making them public so I can access them on the go and help out anyone else looking for similar information.


Valvular Heart Disease

Aortic Insufficiency/Regurgitation (AI/AR)

Severe AI, indications for surgery

  1. Asymptomatic: EF ≤55%
  2. Asymptomatic: EF >55% + LVESD >50mm or LVESDi >25mm/m2
  3. Asymptomatic: EF >55% with progressive decline in EF to low-normal (55-60%) with LVEDd >65mm
  4. Symptomatic
  5. Other concurrent cardiac/aortic surgery

  • Severe AI surgical indications
  • Accurate measurements
  • Severe AI via echo
  • Chronic sever eaortic regurgitation (AI/AR) symptom progression
  • Severe AI: survival and LV function
  • Severe AI: survival and NYHA class

Aortic Stenosis

  • Prostehtic AV algorithm

Low-Flow Low-Gradient AS (LF-LG AS)

  • LFLG algorithm 2

Bicuspid Aortic Valve

  • Bicuspid AV algorithm
  • Frequency of bicuspid anatomy
  • Screening guidelines
  • Bicuspid AV imaging surveillance guidelines
  • Bicuspid aortic valve surgical intervention guideline recomendations

Surgical indications for dilated aortic root/ascending aorta

Aorta sizeIndicationClass recomendation
≥ 5.5 cmRisk factors for dissection (FH, growth rate >0.5cm/year, bicuspid AV)I
> 5.0 cmRisk factors and low surgical risk <4% (FH of dissection, growth 3-5mm/year, aortic coarctation, small stature)IIa
> 5.0 cmLow risk, experienced surgeon, expert centerIIa
> 4.5 cmBicuspid AV planning for surgical AVR for AS/AIIIa

*Aortic root measured at sinus of Valsalva

ACC Guideline: Aortic Surgery for Bicuspid AV

Mitral Regurgitation

  • Simplified asymptomatic severe primary MR algorithm
  • Primary mitral regurgitation (MR) algorithm
  • Qualitative and quantitative MR by echocardiography (TTE)
  • Mitral valve anatomy
  • Etiologies of chronic mitral regurgitation (MR)- acute and chronic
  • Pathophysiology of acute and chronic MR
  • Qualitative assessment of MR
  • Clinical workflow for diagnosis and management of MR
  • MR algorithm
  • Qualitative and quantitative MR by echocardiography (TTE)
  • Medical therapy for chronic MR
  • Surgical interventions for asymptomatic chronic primary MR
  • Surgical interventions for asymptomatic chronic primary MR
  • Surgical interventions for asymptomatic chronic primary MR
  • Transcatheter edge-to-edge repair (TEER) for severe primary MR

Mitral valve prolapse and flail

Carpentier Classification of MR

  • Type 1: normal leaflet mobility (primary: endocarditis, perforation, clefts; secondary: dilated annulus)
  • Type 2: excessive leaflet mobility (prolapse, flail)
  • Type 3: restricted leaflet motion
    • 3a: in systole and diastole (Fibrosis of subvalvular apparatus: rheumatic, radiation, drug-induced injury, inflammatory conditions)
    • 3b: only in systole (Leaflet or chordal tethering: ICM, NICM causing LV dilation)

Mitral Valve Regurgitation Review Article

Chronic MR Algorithms

  • Qualitative and Quantitative Assessment of MR severity by echo
  • Recommended Treatment of severe secondary MR
  • Severe MR Algorithm
  • Recommended Treatment of severe secondary MR
  • Algorithm for Eligibility of Transcatheter Edge-to-Edge Repair (TTER) in severe MR
  • Semiquantitative parameters in MR
  • Quantitative measures for severe MR by PISA png
  • Pulsed Doppler Volumetric Quantification of severe MR
  • Indications for exercise stress testing in MR
  • Routine monitoring of MR via echo
  • MR treatment algorithm

Indications for TTE, TEE in MR

  1. Initial evaluation if suspicious for MV disease or MVP
  2. Initial evaluation of known ur suspected MR
  3. Annual evaluation in severe MR
  4. Reevaluation of MR with change in clinical status
  5. TEE to determine mechanism of MR and suitability of valve repair
  6. *Inappropriate: routine evaluation of MVP with (1) no or mild MR and (2) no change in clinical status

Mitral Valve Prolapse (MVP)

Arrhythmic MVP

  • Non-invasive markers associated with sudden cardiac death (SCD) despite not having severe MR
  • High density of PVCs, inferior TWI, spiked systolic high-velocity signal on echo (Pickelhaube sign), myocardial/papillary scar on MRI
  • Pickelhaube sign: peak systolic lateral mitral annular velocity ≥16 cm/s. More likely to have malignant arrythmia in those with myxomatous bileaflet MVP (‘B’ in image below)
Non-invasive markers associated with SCD in MVP

Acute Severe MR

  • Rapid equalization of pressure across LA/LV may only cause a short, unimpressive murmur (may only appear as mild MR)
  • *Suspect in acute heart failure with normal LV systolic function
  • *Suspect in decreased LVOT VTI despite hyperdynamic LV EF (suggestive of low forward flow- consistent with severe MR)

Mitral Stenosis

  • Stages of mitral stenosis (MS)
  • Stages of mitral stenosis (MS)
  • Wilkins Score for rheumatic mitral stenosis (MS)
  • Mitral stenosis (MS) pressure half-time
  • Mitral stenosis (MS) pressure half-time 2
  • Mitral stenosis (MS) mean gradient (MG)
  • Mitral stenosis (MS) PISA
  • Continuity equation for mitral stenosis (MS)
  • Mitral valve area via LHC
  • Gorlin formula: mitral valve area via LHC
Typical appearance of rheumatic mitral stenosis

2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease


Invasive Hemodynamics Review


Classic Valvular Murmurs

LesionTimingQualityRadiationSeverity
ASCrescendo-decrescendo

Gap between S1, murmur, and S2
Harsh, noisy
MRHolosystolic through S2

Starts with S1 through S2
Blowing, high pitchedAnterior prolapse/flail: axilla, left intrascapular area

Posterior: anteriorly along aortic outflow in left parasternal area (can be confused with SEM)
Weak correlation between intensity and severity

S3: increase in diastolic flow across MV orifice during rapid filling phase  

Increased P2 intensity: pHTN   Enlarged, displaced LV impulse: LV dilation
Post PVCMR changes little: high gradient between LA/LV in SR and post-PVC*AS murmur increases post-PVC as SV after PVC is greater (more flow)  
MVPEarly, mid-systolic click ➡️ systolic murmur±High pitched, ‘whoop’ sound Maneuvers on click and murmur:
– ⬇️ LV volume/preload (Valsalva, squat to stand): murmur/click occur earlier in systole
– ⬆️ LV afterload (squatting): murmur/click occur later in systole
Severe MVP: holosystolic murmur 
Differentiating AS from MR

Prosthetic Valves

Prosthetic Aortic Valves

Pressure recovery: due to small aorta causing falsely elevated mean gradient readings and thus low AVA

Prosthetic Valve Thrombosis

Prosthetic Valve Guidelines from JASE (Journal of American Society of Echocardiography)


Heart Failure

Non-Ischemic Cardiomyopathy (NICM)

2022 AHA/ACC/HFSA Guidelines

Abnormalities in Hepatic Vein Flow on Doppler

Amyloidosis

Diagnostic algorithm for diagnosis of amyloidosis

Figure 2.
99mTechnetium-pyrophosphate imaging for transthyretin cardiac amyloidosis

Treatment for ATTR amyloidosis

Medical therapies for amyloid

  • Tafamadis: amyloidosis but not NYHA IV
  • Patisiran: for ‘papa’- familial amyloid neuropathy

Pulmonary Hypertension (pHTN)

Peak TR jet velocity (m/s)Presence of other echo ‘PH Signs’TTE probability of pHTN
≤2.8 or not measurableNoLow
≤2.8 or not measurableYesIntermediate
2.9-3.4NoIntermediate
2.9-3.4YesHigh
>3.4Not requiredHigh

Echo Findings in Pulmonary Hypertension (pHTN)

VentriclesPulmonary ArteryIVC, RA
RV/LV basal diameter ratio >1RVOT acceleration time (AT) <105ms ±midsystolic notchingIVC >21mm, <50% inspiratory collapse with sniff (or <20% with quiet inspiration)
IVS flatteningEarly diastolic PI velocity >2.2m/sRA size >18cm2 at end-systole
PA diameter >25mm

Chagas Cardiomyopathy

Hypertrophic Cardiomyopathy (HCM)

Surgical options and complicationsSeptal myectomy –> LBBB
Alcohol septal ablation —> RBBB
DysopyramideQT-prolongation
Physical exam maneuversLouder murmur with Valsalva (decreased preload)Softer murmur with hand grip
High risk features for SCD1. First degree relative SCD
2. IVSd ≥30mm (IIa indication: ICD for primary prevention)
3. Unexplained syncope in past 6 months
4. LV apical aneurysm
5. EF <50%
6. NSVT: children (IIa), adults (IIb)
7. Extensive LGE on CMR (IIb)
8. Exercise induced NSVT or abnormal BP response to (drop ≥20mmHg) + high risk features (IIa- it is IIb if no high risk features)
HCM family screening in 1st degree relatives

Echo following septal myectomy for HCM with edge-to-edge (Alfieri) repair of the mitral valve

  • Anterior and posterior leaflets are sutured together in the mid portion giving the typical appearance of a double-orifice mitral valve
  • The color jet that can be seen on the septal wall represents flow from a coronary-LV fistula, a common benign finding after septal myectomy procedures
  • May lead to functional mitral stenosis (MS) requiring surgical interventions following edge-to-edge repair

Coronary Artery Disease

Guidelines/Review Articles

CABG (coronary artery bypass graft) Guidelines

UA/NSTEMI

  • TIMI risk score for UA/NSTEMI: predicts all-cause mortality, new/recurrent MI, severe recurrent ischemia requiring urgent revascularization through 14 days
  • GRACE score for UA/NSTEMI: predicts in-hospital mortality and death or MI
  • Risk stratification into ischemia guided, immediate invasive

NSTEMI: Early invasive strategy (within 24 hours) if:

  1. Elevated troponin
  2. Dynamic ST-changes
  3. Recurrent angina
  4. EF <40%
  5. Recent PCI
  6. Prior CABG
  7. DM
  8. Intermediate/high risk score (GRACE >140)

ACS Medications and Anti-Platelet Agents

NTg and PDE5i interaction

  • NTg contraindicated 24 hours of last use of sildenafil (Viagra, Revatio)
  • NTg cointraindicated 48 hours of last use of tadalafil (Cialis)

Coronary Microvascular Dysfunction

  • Coronary flow reserve (CFR) <2.5 indicative of microvascular disease in the absence of obstructive epicardial CAD
  • Treatment: ± beta blockers, CCB but not definitive guideline

Coronary Flow Reserve

  • iFR ≤0.89 or FFR <0.8

STEMI

  • RCA vs. LCX: STE III >II indicates RCA

Spontaneous Coronary Artery Dissection

  • Risk factors: fibromuscular dysplasia (FMD), postpartum status, multiparity, connective tissue disorders, systemic inflammatory conditions, and hormonal therapy
  • FMD screening: screen for extracoronary disease from brain to pelvis with CTA or contrast-enhanced MRA for aneurysms, dissections, and other areas of FMD
  • Renal aneurysms: treat when >2cm
  • Renal stenosis: balloon angioplasty > stenting. Stent reserved for procedural complications (i.e. dissection)


General Cardiology

Guideline Indications

TreatmentIndication
EntrestoHFrEF (≤40%) and NYHA II, III
IvabridineHFrEF (≤35%) at max tolerated dose of bb in SR with HR ≥70bpm
IV iron sucrose or ferric carboxymaltoseNYHA II, III and at least 1 of the following: 1. Ferritin <100 ng/mL2. Ferritin 100-299 ng/mL but iron sat <20%
PatisiranFamilial amyloid neuropathy
ICD, primary prevention1. EF ≤35%, NYHA II, III due to N/ICM
2. EF ≤30%, NYHA I, II, III
CRT indications1. LBBB with QRS ≥150 msec
2. EF ≤35%
3. NYHA II, III or ambulatory type IV
4. Already on GDMT
(LOE A for NYHA class III, IV and LOE B for NYHA class II)

ICD Indications

EFNYHAEtiologyClass Indication
≤35%II-IIIN/ICMI
≤35%INICMIIb
≤30%IICMI
≤40%Inducible VT/VF on EPSICMI
>55%Inducible VT/VF on EPS with extensive scarring on PET/MRIBrugadaIIb
>55%Inducible VT/VF on EPS with extensive scarring on PET/MRISarcoidIIa

Hypertension (HTN)

TypeDefinition
Resistent HTN≥130/80 on 3 meds for ≥ 1 month
Refractory HTNNot adequately controlled on 5 meds
PseudoresistentWhite coat HTN
MaskedNormal in office, high at home

Genetics

MutationAssociated Disease
Lamin A/CSkeletal muscle dystrophies
Notch 1Bicuspid AV, early AV calcification
T-box 5Holt-Oram syndrome (abnormal thumbs, ASD, VSD, HCM, conduction disease)
FBN1Fibrillin-1. 90% AD for Marfan syndrome
COL3A1Collagen- Ehlers-Danlos syndrome

Long QT-Syndromes

SyndromeGeneFunctional EffectAssociationInheritance
LQTS 1KCNQ1⬇️ IKSSwimmingAD; AR, ~30-35%
LQTS 2KCNH2⬇️ IKRStartleAD, ~25-30%
LQTS 3SCN5A⬆️ INASleepAD, ~5-10%
JLNS 1, 2KCNQ1, KCNE1⬇️ IKRDeafnessAR, very rare

Genetic Screening

  • Start with index family member with unknown or uncertain patterns (athletes with LVH or apical hypertrophy)
  • Idiopathic dilated cardiomyopathy without known mutation in family: first degree relatives TTE q3-5 years

Physical Exam

MurmurLesionLocation Best Heard
Fixed split S2ASD 
Single 2nd heart soundTOF 
Absent A2AS 
Absent P2Pulmonary stenosis 
Loud P2pHTN 
Worsens with ValsalvaHOCM (decreased preload) 
Diastolic murmur?Subaortic membrane 
Early systolic clickBicuspid AV (stiff but mobile)Left 2nd IC space, apex
Mid-systolic clickMVPLeft lower sternal border
Diastolic opening snapMS (and diastolic rumble)Left lower sternal border in LLD position

JVD Physical Exam Findings

DiagnosisJVD Finding
Constrictive pericarditisProminent Y descent, ±prominent X descent
TamponadeProminent X descent, absent Y descent
RV infarctionAbsent X and Y descent
VT, CHBVariable size A-waves (‘cannon A-wave’)

Vascular Diseases

Abdominal Aortic Aneurysm (AAA)

Society for Vascular Surgery recommendations, surveillance intervals for asymptomatic AAA:

  1. >2.5 cm but <3.0 cm, rescreen after 10 years
  2. 3.0-3.9, repeat imaging every 3 years
  3. 4.0-4.9, repeat imaging in 12 months
  4. 5.0-5.4, repeat imaging in 6 months

Indications for elective repair of an asymptomatic AAA include:

  1. >2.5 cm but ≤5.5 cm
  2. rapid expansion
  3. AAA associated with peripheral arterial aneurysms or peripheral artery disease.

May-Thurner Syndrome

PathophysiologyAnatomical variant: right common iliac artery overlies and compresses the left common iliac vein against lumbar spine
Risk factorsLeft lower DVT
Scoliosis
Female sex
OCP use or recent pregnancy
Left lower extremity swelling in absence of DVT
Clinical presentationYoung adult woman with left leg swelling and DVT
Diagnostic testMagnetic resonance venography of the pelvis
References
1. Peters M, Syed RK, Katz M, et al. May-Thurner syndrome: a not so uncommon cause of a common condition. Proc (Bayl Univ Med Cent) 2012;25:231-3.
2. Baglin T, Gray E, Greaves M, et al.; British Committee for Standards in Haematology. Clinical guidelines for testing for heritable thrombophilia. Br J Haematol 2010;149:209-20.
3. Society for Vascular Medicine. Five Things Physicians and Patients Should Question (Choosing Wisely website). 2015. Available at: http://www.choosingwisely.org/wp-content/uploads/2015/02/SVM-Choosing-Wisely-List.pdf. Accessed 03/22/2019.
May-Thurner Syndrome

Electrophysiology (EP)

CRT Indications

Antiarrhythmic Medications

*DFT: defibrillator threshold
SyndromeGeneMiscellaneous
ARVCPKP-2Plakophillin-2Intracellular calcium signaling abnormality
ARVCDSPDesmoglein-2Intracellular calcium signaling abnormality
ARVCDSC2Desmocollin-2Intracellular calcium signaling abnormality
ARVCJUPPlakoglobinIntracellular calcium signaling abnormality
MarfanFBN1Fibrillin-1Associated with aortic aneurysm, dissection
Ehlers-DanlosCOL3A1Collagen type 3, a1Associated with aortic aneurysm, dissection
Loeys-DietzTGFB1, 2Transforming growth factorAssociated with aortic aneurysm, dissection
CPVT1RYR-2Ryanodine receptorAD (>70% of cases, intracellular Ca-signaling)
CPVT2CASQ2CalsequestrinAR inheritence
LQTS1KCNQ1K current IKsbb (nadalol > propanalol)
***Associated with SCD while swimming
LQTS2KCNH2K current IKrK-supplementation (IIb rec)
LQTS3SCN5Aalpha-unit of INa±Mexilitine (IIb rec)
GAIN of function mutation
BrugadaSCN5ALOSS of function mutation
Hereditary PAHBMPR-2Bone morphogenic protein receptorAssociated with >70% of inherited pulmonary arterial HTN
DCMLamin A/C± skeletal muscle dystrophy
T-box5Holt-Oram (hand heart, ASD)
Notch 1Bicuspid AV, premature AV calcification
Genetic mutations associated cardiac conditions
Cardiac Genetics Chart

Supraventricular Tachycardia (SVT)

  • Focal AT- ongoing treatment options

Early Afterdepolarization (EAD) and Delayed Afterdepolarization (DAD)

Localizing VT Origin: LVOT vs. RVOT

  • Step 1: V1
    • LBBB: anterior to posterior- RVOT
    • RBBB: posterior to anterior- LVOT
  • Step 2: concordance
    • Positive: originates near base
    • Negative: originates near apex
  • LVOT VT
  • RVOT VT
  • RVOT: later R-wave transition (≥V3)
  • LVOT: earlier R-wave transition, LBBB, inferior axis

Bidirectional Ventricular Tachycardia (aka CPVT or catecholaminergic polymorphic VT)

  • Also known as Familial polymorphic VT
  • Inheritance: RyR2 gene mutation is AD, CASQ2 gene mutation is AR
  • Treatment: Nadolol (non-selective β1 and β2 agonist)
  • Dose: 0.8 mg/kg of nadolol ~ 1 mg/kg of metoprolol SR
  • Flecainide also used (ask EP)
Source: Leren, I., Saberniak, J., Majid, E., Haland, T., Edvardsen, T., & Haugaa, K. (2016). Nadolol decreases the incidence and severity of ventricular arrhythmias during exercise stress testing compared with β1-selective β-blockers in patients with catecholaminergic polymorphic ventricular tachycardia. Heart Rhythm13(2), 433-440. doi: 10.1016/j.hrthm.2015.09.029

2:1 AV Block

AV nodeHPS
Type of BlockMobitz I >> Mobitz IIMobitz II > Mobitz I
Conducted QRSNarrow (unless preexisting BBB)Wide (except intra-His block)
Escape rhythmReliable (narrow QRS)Unreliable (wide QRS)
PR on conducted beatsLongNormal
*Carotid sinus pressure Block worsensBlok improves
*Exercise/atropineImproves blockBlock worsens
Characteristics to identify site of block in 2:1 AVB

Stroke (CVA) Management

Blood Pressure

  1. If tPA used: BP should be lowered <180/110 prior to tPA administration
  2. After tPA: <180/105 for at least 24 hours post-tPA
  3. No tPA: only treat if >220/120
  4. Can treat if no tPA plus other reason to treat (Aortic dissection, pre/eclampsia, unstable CAD, acute HF)

CHA2DS2-VASc

  • 2 points: age ≥ 75 years and history of stroke/TIA/thromboembolism

Contraindications (CI) to tPA

AbsoluteRelative
History of hemorrhagic stroke or stroke unknown originTIA in prior 6 months
CVA within previous 6 monthsOral anticoagulation
CNS neoplasmPregnancy or first post-partum week
Major trauma, surgery, or head injury in past 3 weeksNon-compressible puncture site
Bleeding diathesisTraumatic resuscitation
Active bleedingRefractory HTN (sBP > 180)
Advanced liver disease
Infective endocarditis
Active peptic ulcer

Pulmonary Embolism


Cardiac Oncology

  • Dexrazoxane: prevent anthracycline-induced cardiotoxocity
  • Anthracycline cardiotoxicity: risk if >250mg/m2

Congenital Heart Disease (CHD)

D-Loop Transposition of the Great Arteries (D-TGA)

  • Atrio-ventricular concordance and ventricular arterial discordance
  • 2nd most common cyanotic congenital lesion (#1 is ToF)
  • Associated defects: VSD (~40%), pulmonic stenosis (PS), coronary artery anomalies
  • D-TGA anatomy
  • D-TGA Surgical Corrections
  • D-TGA surgical correction complications
  • Complications of arterial switch
  • Event free survival following atrial switch
  • Apical 4 chamber view showing anterior transposed aortic valve with posterior pulmonary valve behind it

Complications Following D-TGA Surgical Correction: Arterial Switch (Mustard/Senning Procedure)

  1. Arrhythmia: sinus node dysfunction, frequent SVT
  2. Systemic RV: 25% develop heart failure in their 30’s
  3. Tricuspid regurgitation (TR): functional due to annular dilation

Complications Following D-TGA Surgical Correction: Atrial Switch

  1. Supravalvular AS, pulmonic stenosis (AS), PPS (pulmonary artery stenosis)
  2. Coronary stenosis at re-implantation site
  3. Branch pulmonary artery stenosis
  4. Neo-aortic dilation and AI

L-TDA (or congenitally corrected-TGA)

  • Double-discordance (RA to LV to PA, LA to RV to aortia)
  • Non-cyanotic
  • Treat severe TR like severe MR in normal patients
  • Complications: TR, RV dysfunction, CHB (complete heart block)
  • L-TDA (ccTGA)
  • Complications of L-TGA


Biostats

TermDefinitionExample
Relative risk reduction (RRR)Rate in treatment/rate in placebo10%/20%=0.5
Absolute risk reduction (ARR)(Rate in placebo)-(rate in treatment)20%-10%=10% or 0.1
Number needed to treat (NNT)1/(ARR)1/(0.1)=10 so treat 10 patients over 2 years to prevent 1 event
Example: over a 2 year period therapy A has an event rate of 10% and placebo has an event rate of 20%

Echocardiography

Physics

Speed of sound propagation through tissue: 1540 m/s

Mitral Valve Leaflets on TEE

MV Leaflets on TEE

Stress Testing

Duke Treadmill Score= minutes of exercise – (5 x mm of ST-depression) – (4 x anginal index)

  • Anginal index: 0 for no angina, 1 for non-limiting angina, 2 for having to stop exercise due to angina
  • Positive score is good. Possible to get a negative score
  • Score ≤ -11 is high risk (79% survival at 5 years), -10 to +4 is medium risk (95% survival at 5 years) ≥5 is low risk (99% 5 year survival)
  • Consider LHC for high risk patients (≤ -11)

Nuclear Cardiology

Occupational Dose Limits

1 Rem = 0.01 Sv (international standard unit)

LocationRemSv
Whole body (organs)5 Rem0.05 Sv
Skin50 Rem0.5 Sv
Lens of eye15 Rem0.15 Sv
Pregnant workers
(Over gestation period)
500 mRem5 mSv
Fetus
(non-occupational worker)
500 mRem5 mSv
General public100 mRem1 mSv

Shielding

Alpha particles

Particle typeShield requirement
Alpha particlesSheet of paper
Beta particlesPlastic/clothing
Gamma raysInches/feet of concrete or lead

Common artifacts

  • LBBB: anterior septum (occurs least frequently with NM stress)

Abnormal TID (~1.36, exercise ≥1.29) with normal perfusion: special considerations

  1. HTN with LVH
  2. Difference in HR between rest and stress
  3. Technical difficulties in image acquisition

Most Commonly Used Tools Cardiologists Use For Palpitations

Palpitations are one of the most common reasons that I see patients in the inpatient and outpatient setting. Palpitations are abnormal the sensation of your heart beating. I explain them briefly in this TikTok video:

@marckatzmd

What are palpitations and other questions explained in greater detail on my 15min YouTube video #Cardiology #MedicalTikTok #Cardiologist #Palpitations

♬ original sound – Marc Katz, M.D.

Depending on the underlying diagnosis they can be completely benign or potentially life-threatening. I go into much greater detail in a much longer separate YouTube video here:


To understand the common tools we use to diagnose and treat palpitations you have to find out how frequently they occur. So let’s review the most common tools cardiologists use to evaluate palpitations.

If they’re happening right now- get an ECG! Sometimes an Apple Watch can even diagnose some abnormal heart rhythms like atrial fibrillation. But if palpitations are not happening when you get the ECG then you will not catch the rhythm. In the inpatient setting we often also use telemetry. This also underpins the importance of talking to patients to evaluate how frequent palpitations occur as different tools can be used for different durations of time. Sometimes even when we diagnose certain abnormal heart rhythms we use the next few tools to quantify the ectopic burden (how many extra beats are there) as this may influence treatment.

Holter Monitor: 24 – 48 hours

Holter Monitoring - SND Hospital Ropar

Holter monitors are 24-48 hour mini ECG’s, as depicted above. Patients wear them and document when they feel symptoms and we correlate the information we collect from the monitor. This can also help quantify how frequently someone is having a known abnormal heart rhythm to help guide other treatment choices.

ZioPatch Event monitor: 1 – 2 weeks

How Zio works | iRhythm

Event monitors are the next step up in duration. They can be worn for extended period of time, typically for 1-2 weeks. My favorite is the ZioPatch, shown above. It can be worn for weeks at a time (again, typically 1-2) and is small, goes on the chest, and records everything while being worn, and patients can even shower with this device. They click a button on the device to note when symptoms occur and then we go back to see what rhythm was happening at that time when we receive the report. It does not get transmitted in real time. Instead, as shown below, patients actually take it off at home and send it back to the company in the mail who then forward a report to the ordering physician.

The wireless future of medicine | zhiyaobme

Implantable Loop Recorder: up to 3 years

Implantable Loop Recorder

Lastly are implantable loop recorders (ILR). ILRs are less than 2 inches long and quite thin, as depicted below.ILRs are the only monitoring device that is actually implanted under the skin on the chest. They record everything and have up to a 3 year battery life! The ILR automatically records certain fast and slow rhythms but patients can also use an activator to save rhythms if they’re having symptoms. We often use these when the palpitations are infrequent or if we have a high suspicion of an underlying arrhythmia without a documented diagnosis that might change management. For example, I frequently use these in tandem with neurologists in stroke patients in whom we suspect but have not diagnosed atrial fibrillation (AF). If we see AF on an ILR then we would start a blood thinner but sometimes don’t want to treat empirically.  The location these are placed is shown below and often can be safely removed.

Just like any test these tools aren’t perfect. First, patients can have palpitations a few days a week but for whatever reason don’t have any symptoms when wearing the monitor. Depending on the clinical scenario sometimes we will redo the test. Second, these monitors should not be ordered unless clearly indicated. If you were to place Holter monitors on 100 random individuals you are certain to find some abnormal heart rhythms that are completely benign. Thus ordering unnecessary cardiac monitoring for patients can lead to unnecessary follow up procedures, testing, and possible harm.


If you found this helpful:

Lyme Carditis | How Lyme Disease Can Involve the Heart

I’m starting a new section on my blog and YouTube channel bringing you some cool cardiology related topics that you might not have heard about. To kick things off I wanted to talk about Lyme disease- and more specifically a possible complication of Lyme disease known as Lyme carditis. And if you prefer videos to reading check out my YouTube video on the topic and be sure to give it a like and subscribe!

Background: what is Lyme Disease?

Lyme disease is caused by the bacterium Borrelia burgdorferi (and rarely Borrelia mayonii). It is transmitted to humans through the bite of an infected tick, as depicted below.

Lyme Disease: Borrelia burgdorferi - YouTube

Why is it called Lyme Disease?

Lyme disease got it’s name from the small coastal town in Connecticut back in 1977 when Yale researchers identified clusters of what they initially called Lyme arthritis but then changed the name 2 years later to Lyme disease (1).

What are typical symptoms?

Classic Lyme disease typically causes a ‘bullseye-like rash’ on the skin on average 7 days after the initial tick bite but can happen anywhere between 3-30 days after the initial tick bite known. The medical term for this is erythema migrans. Erythema migrans can manifest differently, as below (2). It is rarely itchy or painful and can have a variable appearance. Additionally in dark skinned individuals it can be difficult to appreciate or visualize well.

Other symptoms that can happen anywhere from days to months after the initial tick bite include headache, neck stiffness, and severe joint pain and swelling that normally involve the knees and other large joints. So why is a cardiology fellow talkign about Lyme disease? Because a potentially serious and life threatening complication of Lyme disease is Lyme carditis.

What is Lyme carditis?

Lyme carditis occurs when the bacterium infects the heart tissue and disrupts the normal electrical conduction system of the heart. This can have a variable clinical expression. The most serious complication is complete heart block.

What is complete heart block?

To understand the complete heart block let’s look at what normal conduction of the heart looks like. To create a coordinated heart beat your heart conducts electrical impulses down a network of nerves. It goes from the SA (sino-atrial) node to the AV (atrio-ventricualar) node, then down to both ventricles, as below.

In complete heart block the top and bottom chambers of the heart are unable to communicate with one another and beat independently. This is also why complete heart block is also referred to as third degree AV block because the electrical impulses are unable to get through the AV node.

Why is complete heart block a big?

Normally the top chamber of the heart is in charge. It sends impulses down the electrical system of the heart and the ventricle does as its told. So what happens when the ventricle never receives any of those electrical signals? Your heart has a backup system for these very instances but it is far from perfect. This back-up system is normally inhibited by electrical impulses received from the SA or AV node but when it never receives those impulses it generates a ventricular rate of about 20-40 beats per minute. This means that you might only be able to sustain a heart rate of about 20-40 beats per minute! Additionally this back-up system isn’t always 100% and in Lyme carditis can lead to a fatal arrhythmia. It is serious and should be treated in the hospital.

What are the symptoms of complete heart block?

A slow heart rate also explains symptoms of complete heart block. Think about what happens everyday of your life when you stand up to walk around- your heart beats faster. If your heart can’t increase the rate that your ventricle beats then your brain is not going to get enough blood and you will feel faint, lightheaded, dizzy, and could even pass out. Passing out, or syncope, is your body’s way of making the heart not have to work against gravity but can also seriously hurt you or somebody else depending on how you fall. Other symptoms of complete heart block can include symptoms severe shortness of breath, palpitations, or chest pain.

How do we treat Lyme carditis?

The first thing we do is treat empirically for Lyme disease with antibiotics. The confirmatory lab tests can take a while to get back and some people don’t develop antibodies until a few weeks after infection. So we don’t waste any time and start treating as the benefit fo treatment often far outweigh the risk of the antibiotics. In the hospital we typically use Ceftriaxone and then switch to oral Doxycycline for a typical duration of about 21 days.

Not everyone who develops Lyme carditis develops complete heart block. There are varying degrees of heart block. About 4-10% of patients with Lyme disease develop some form of Lyme carditis (3). Out of the 4-10% of patients who develop Lyme carditis, about 90% of those only develop 1st degree atrioventricular block (AVB). 1st degree AVB is a benign form of AV block and can often be seen in normal otherwise healthy patients in the general population. However patients who develop new 1st degree AVB in the setting of Lyme disease infection should be watched in the hospital on continuous cardiac telemetry monitoring because it is a good predictor of those who might develop complete heart block.

If you develop hemodynamically significant heart block we often use a temporary pacemaker to ensure that your heart rate is adequate. We place place these through the jugular vein and depending on the type of temporary pacemaker that your receive are either floated to sit in the right ventricle or are screwed into the heart to ensure adequate electrical transmission. Depending on the type, temporary pacemakers are only able to stay in place between 2-7 days and are not a permanent solution.

The good news is that most people who develop complete heart block due to Lyme carditis fully recover with antibiotics and do not require a permanent pacemaker.

How do you prevent Lyme disease and where is it found?

The last teaching point I’ll make for is the importance of checking for ticks after you leave a heavily wooded area. Lyme disease is endemic to the northeast, north-central, and mid-Atlantic regions of the US but can be found elsewhere, as below.

U.S. map reported cases of Lyme Disease at a county-wide level

How do you remove a tick safely?

Now let’s say you notice a tick attached to you. What do you do? Try to get a small tweezers if you can and grasp it from as close to your skin surface as you can, as below.

Unfortunately if you just grab it from the body you can potentially rip off the body and leave its mouth stuck on you. The goal is to get the tick off you ASAP! So don’t use remedies like paints, nail polish, or petroleum jelly to wait for it to fall off. After you remove the tick you can flush it down the toilet, kill it in alcohol, or drop it in a sealed bag.

Then call your doctor

Questions we will ask will attempt to narrow the timeline of when the tick attached to you. Interestingly it takes about 36 hours being attached to you for the tick to transmit the bacterium to you. The reason for this is that the bacteria lives inside the tick gut and it takes about 36 hours for the tick to get so engorged on your blood that it actually vomits and in doing so transmits the bacteria before detaching and falling off.

So technically if you went hiking and noticed a tick one hour later then you might not need any treatment for Lyme disease. The reason why it’s important to call your doctor is that a prophylactic treatment for Lyme disease is a single dose of oral doxycycline which typically outweigh the risks of possible contracting and developing complications of Lyme disease.

Works Cited

  1. Delaware, T. (2020). Lyme Disease Information – Delaware Health and Social Services – State of Delaware. Retrieved 28 July 2020, from https://www.dhss.delaware.gov/dhss/dph/epi/lyme.html#:~:text=Lyme%20disease%20gets%20its%20name,the%20attention%20of%20Yale%20researchers
  2. Lyme disease rashes and look-alikes | CDC. (2020). Retrieved 28 July 2020, from https://www.cdc.gov/lyme/signs_symptoms/rashes.html
  3. Scheffold N, Herkommer B, Kandolf R, May AE. Lyme carditis–diagnosis, treatment and prognosis. Dtsch Arztebl Int. 2015;112(12):202-208. doi:10.3238/arztebl.2015.0202

I hope you guys enjoyed this post. If you liked this post drop a comment below and subscribe so you don’t miss my next post or drop a comment below if there’s something cardiology related that you think would make a cool post or YouTube video and I’ll see if I can make one for yah.

Echo Cheat Sheet For First Year Cardiology Fellows

When my co-fellow and started our cardiology fellowship we wish we had an echocardiography reference value cheat sheet. So we decide to make one for our new first year fellows! Our hope is that by having all of the reference values organized in one easily accessible place online that we can ease any new cardiology fellow into their new role. Instead of making it a Word document or PDF we wanted to share it with any other fellows who may find this useful. We will continue to update it with useful educational links, images, and videos over time. *Please only use this as a reference. The most reliable sources of information are ASE guideliens*

Echocardiography Reference Values

Normal Values for Aorta via 2D echo (Indexed to BSA)

Normal intervalIndexed interval
Aortic annulus20-31 mm12-14 mm/m2
Sinus of Valsalva29-45 mm15-20 mm/m2
Sinotubular junction22-36 mm13-17 mm/m2
Ascending aorta22-36 mm13-17 mm/m2
Aortic arch22-36 mm
Descending aorta20-30 mm

Aortic annulusSinus of ValsalvaSinotubular junctionAscending aortaAortic arch
AgeMenWomenMenWomenMenWomenMenWomenMenWomen
<3011.4 ± 1.211.4 ± 1.115.3 ± 1.815.5 ± 1.512.7 ± 2.313.5 ± 1.414.3 ± 1.615.1 ± 1.610.1 ± 1.310.7 ± 1.0
30-3911.4 ± 1.111.7 ± 1.015.7 ± 1.316.5 ± 1.613.3 ± 1.314.3 ± 1.514.5 ± 1.416.4 ± 1.810.8 ± 1.311.6 ± 1.6
40-4911.5 ± 0.911.7 ± 1.016.6 ± 1.516.8 ± 1.414.1 ± 1.514.6 ± 1.215.5 ± 1.516.4 ± 1.411.3 ± 1.311.5 ± 1.2
50-5911.5 ± 0.912.0 ± 0.916.8 ± 1.717.9 ± 1.614.1 ± 1.515.7 ± 1.316.2 ± 1.618.0 ± 1.411.3 ± 1.212.7 ± 1.1
60-6912.1 ± 1.011.7 ± 1.117.8 ± 1.617.5 ± 1.715.1 ± 1.614.7 ± 1.617.3 ± 1.717.6 ± 1.712.0 ± 1.112.5 ± 1.4
>7012.0 ± 1.011.6 ± 1.118.1 ± 1.718.2 ± 1.914.7 ± 1.615.5 ± 2.017.5 ± 1.418.2 ± 3.312.2 ± 1.312.7 ± 1.2
All11.6 ± 1.011.7 ± 1.016.6 ± 1.817.0 ± 1.913.9 ± 1.814.7 ± 1.715.7 ± 1.816.9 ± 2.311.2 ± 1.411.9 ± 1.5
Aortic Root Dimensions

Aortic Regurgitation

Primary Parameters
MildModerateSevere
Vena contracta (cm)< 0.30.3 – 0.6> 0.6
PHT (ms) – CW doppler> 500200-500< 200
Diast flow rev – PW desc AortaIf present, early diastolicEarly diastolicHolodiastolic
Primary Parameters

Quantification of Jet
MildModerateSevere
Jet-width / LVOT-width< 0.250.25 – 0.64> 0.64
Jet-area / LVOT-area< 0.050.05 – 0.59> 0.59

Qualitative Parameters
MildModerateSevere
Jet areaSmallVariableLarge if central, variable if eccentric
Coaptation defectMildModerateSevere
CW-profileWeakViableDense
LA sizeNormalNormal or enlargedEnlarged
LV sizeNormalNormal or enlargedEnlarged

PISA Parameters
MildModerateSevere
EROA (cm2)< 0.10.1 – 0.29≥ 0.30
Regurgitant volume (ml/beat)< 3030 – 59≥ 60
Regurgitant fraction (%)< 3030 – 49≥ 50

Aortic Stenosis

Disease Defining Parameters
MildModerateSevere
Valve area (cm2)> 1.51.0 – 1.5< 1.0
Indexed valve area (cm2/ m2)> 0.850.6 – 0.85< 0.6
Measured Parameters
MildModerateSevere
Mean gradient (mmHg)< 2020 – 40> 40
Peak gradient (mmHg)< 3535 – 65> 65
Peak velocity (m/s)2.6 – 2.93.0 – 4.0> 4.0
Dimensionless index (LVOT/AV)> 0.50.5 – 0.25< 0.25

Bioprosthetic Aortic Valve Stenosis

EOA (effective orifice area) index
  • Mild PPM: EOA ⩽ 0.85 cm2/m2
  • Moderate PPM: EOA 0.65–0.85 cm2/m2
  • Severe PPM: EOA < 0.65 cm2/m2
Practice Questions | Echocardiographic Evaluation of Aortic Valve Prosthesis
Prosthesis‐patient mismatch: definition, clinical impact, and prevention

Visual Assessment of LV RWMA 

Type of motionDefinitionWall Motion Score
Normal Normal thickening (>30% thickening end-systole to end-diastole)1
Hypokinesia Reduced thickening (10-30%)2
Akinesia Markedly reduced thickening (<10%)3
Dyskinesia Paradoxical thinning and/or outward motion during systole4
Aneurysmal Diastolic deformation5

LV Dimension and Volume

LV Dimension
 Women Men 
 Normal Mild Moderate Severe Normal Mild Moderate Severe 
Diastolic diameter 3.9-5.3 5.4-5.7 5.8-6.1 >6.2 4.2-5.9 6.0-6.3 6.4-6.8 >6.9 
Diastolic diameter/BSA cm/m22.4-3.2 3.3-3.4 3.5-3.7 >3.8 2.2-3.1 3.2-3.4 3.5-3.6 >3.7 

LV Volume
 Women Men 
 Normal Mild Moderate Severe Normal Mild Moderate Severe 
Diastolic volume, mL 56-104 105-117 118-130 >131 67-155 156-178 179-201 >201 
Diastolic volume/BSA mL/m235-75 78-86 87-96 >97 35-75 76-86 87-96 >97 
Systolic volume, mL 19-49 50-59 60-69 >70 22-58 59-70 72-83 >83 
Systolic volume/BSA 12-30 31-36 37-42 >43 12-30 31-36 37-42 >43 

LV Ejection Fraction (EF %)

Women Men 
Normal Mild Mod Severe Normal Mild Mod Severe 
54-74 41-53 30-40 <30 52-72 41-51 30-40 <30 

Right Ventricle Dilation

Base (RVD1)> 42mm
Mid (RVD2)> 35mm
Longitudinal dimension (RVD3)> 86mm
RV focused apical 4 chamber
PLAX Distal RVOT (left side)> 30 mm
PSAX Proximal RVOT (middle)> 35 mm
PSAX Proximal RVOT (right side)> 27 mm

RV dimensions
 Normal Dilated Moderate Severely 
RV diameter (RVD 1) 2.0-2.8 2.9-3.3 3.4-3.8 ≥3.9 
RV diameter (RVD 2) 2.7-3.3 3.4-3.7 3.8-4.1 ≥4.2 
Base-to-apex length 7.1-7.9 8.0-8.5 8.6-9.1 ≥9.2 

RV diameter
 Normal Mild Moderate Severely 
Above aortic valve 2.0-2.8 2.9-3.3 3.4-3.8 ≥3.9 
Above pulmonic valve 2.7-3.3 3.4-3.7 3.8-4.1 ≥4.2 

PA diameter
 Normal Mild Moderate Severe
Below pulmonic valve 1.5-2.1 2.2-2.5 2.6-2.9 ≥3.0 

RV size and function
 Normal Mild Moderate Severe
RV diastolic area, cm2 11-28 29-32 33-37 ≥38 
RV systolic area, cm2 7.5-16 17-19 20-22 ≥23 
RV fractional area change, % 32-60 25-31 18-24 ≤17 

Left Atrial Size and Volumes

Atrial dimensions
 Women Men 
 Normal Mild Mod Severe Normal Mild Mod Severe 
LA diameter 2.7-3.8 3.9-4.2 4.3-4.6 ≥47 3.0-4.0 4.1-4.6 4.7-5.2 ≥5.3 
LA diameter/BSA 1.5-2.3 2.4-2.6 2.7-2.9 ≥3.0 1.5-2.3 2.4-2.6 2.7-2.9 ≥3.0 
RA minor axis, cm 2.9-4.5 4.6-4.9 5.0-5.4 ≥5.5 2.9-4.5 4.6-4.9 5.0-5.4 ≥5.5 
RA minor-axis/BSA (cm/m21.7-2.5 2.6-2.8 2.9-3.1 ≥3.2 1.7-2.5 2.6-2.8 2.9-3.1 ≥3.2 

LA area (cm2)
Women Men 
Normal Mild ModSevere Normal Mild ModSevere 
<20 20-30 30-40 >40 <20 20-30 30-40 >40 

Atrial volumes
 Women Men 
 Normal Mild ModSevere Normal Mild ModSevere 
LA volume 22-52 53-62 63-72 ≥73 18-58 59-68 69-78 ≥79 
LA volume/BSA 22±6 29-33 34-39 ≥40 22±6 29-33 34-39 ≥40 

Mitral Regurgitation

Primary parameters
 Mild ModSevere 
Vena Contracta <0.3 0.3-0.69 ≥0.7 
EROA (cm2) <0.2 0.2-0.39 ≥0.4 
Jet size <4 cm2 or <20% of atrial size 4-10cm 2 or 20-40% of atrial size >10cm 2 or >40% of atrial size 
Jet orientation Central Variable Eccentric 
Pulmonary vein flow S-dominant Reduced S-wave Systolic flow reversal 

Qualitative parameters
 Mild Mod Severe 
Mitral valve apparatus Normal-mildly abnormal Often abnormal Abnormal, possibly flail 
CW-profile Weak Variable Dense 
Shape CW-profile Parabolic Variable Early peak, triantriangular 
LA sizeNormalNormal or dilatedDilated

Additional PISA-parameters
     Mild Mod Severe 
Regurgitation volume (mL/beat) <30 30-59 ≥60 
Regurgitation volume (EROA x TV)   
Regurgitation fraction (%) <30 30-49 ≥50 
PW-doppler A-dominant Variable High E values 

Miscellaneous parameters
    Mild Moderate Severe 
PW-doppler A-dominant Variable High E values 

Mitral Stenosis

Primary parameters
   Mild Mod Severe 
Valve area>1.5cm21.5-1.0m2<1.0cm2
Mean gradient<5mmHg5-10mmHg>10mmHg
PAP<30 mmHg30-50>50

Pulmonary Regurgitation

 MildModSevere
Pulmonary valve morphologyNormalNormal/abnormalAbnormal
Density CW-dopplerWeak, slow decalVariableDense, steep deceleration, early termination of diastolic flow
Jet width color DopplerSmall, <10 mm length, narrow originVariableLarge, wide origin
Ratio pulmonic to aortic flowNormalVariableSignificantly increased

Pulmonary Stenosis

 MildModSevere
Peak velocity (m/s)<33-4>4
Peak gradient (mmHg)<3636-64>64

Tricuspid Regurgitation

 MildModSevere
PISA radius<0.60.6-0.9>0.9
Vena contracta (cm_Not defined<0.7>0.7
Liver vein flowS-dominantReduced S-waveSystolic flow reversal, jet reaching liver vein

Additional Quantitative Parameters
 Mild Moderate Severe 
Jet size<5 cm25-10 cm2>10 cm2
IVC size<2.1cm, compressibleIn between>2.1cm, not compressible
 
Additional Qualitative Parameters 
 Mild Moderate Severe 
Coaptation defectMildModSevere
RV sizeNormalNorma/enlargedEnlarged
RA sizeNormalNormal/enlargedEnlarged
CW-profile tricuspid regurgitationWeak VariableDense
Shape CW-profile TRParabolicVariableEarly peak, triangular

Tricuspid Stenosis

Mean PG≥ 5 mmHg
Valve area ≤ 1cm2
VTI of TV inflow>60cm
Pressure half time≥190 ms
RASeverely enlarged
IVCElnarged

Pulmonary Artery Pressure

 RA pressure
IVC <2.1cm, >50% sniff3 mmHg
All others or if not visualized8 mmHg
>2.1cm, sniff <50%15 mmHg

Pulmonary HTN (pHTN)

Mild30-50 mmHg
Moderate51-65 mmHg
Severe> 65mmHg

LV Region Identification

Diastolic Function

Mitral Valve Leaflets on TEE

https://thoracickey.com/role-of-transesophageal-echocardiography-in-mitral-valve-repair/

Useful Websites

How To Interpret Inpatient Cardiac Telemetry

Continuous cardiac telemetry monitoring, or ‘tele’ colloquially, is how we remotely monitor patients’ heart rhythms while in the hospital. When it is used appropriately it is a valuable diagnostic tool that assists in diagnosing and managing specific abnormal heart rhythms. I use it everyday for post-myocardial infarction patients (those who just suffered a heart attack) to monitor for ventricular ectopic beats caused by ischemic myocardium (dead heart tissue). Unfortunately tele review is one of those lessons thrown into the hidden curriculum of medical training where people are often taught it on the fly without much guidance. Electrocardiogram, or ECG, interpretation is outside the scope of this post. Instead I will focus on a few helpful tips to help improve your ability to understand and utilize tele in a more meaningful and intentionally manner for any nurse, physician assistant, nurse practitioner, intern, resident, or incoming cardiology fellow. Lastly, don’t forget to subscribe so you don’t miss future posts!

1. Not everyone needs tele

Rule number one in medicine is ‘primum non nocere’ or ‘first do no harm’. Exposing patients to unnecessary monitoring can lead to further unnecessary testing and in turn possible harm. Not only is ordering unnecessary tele potentially harmful to patients but it is also costly. The average hospital bed is more expensive if telemetry is added on. It also can harm healthcare professionals through alarm fatigue. Think about how frequently those things beep along with every other alarm in the hospital. Not to mention how annoying actually wearing a tele monitor can be for patients (1). Inappropriate tele use is such a widespread issue in the United States that it is one of the cornerstones of the Choosing Wisely campaign from the Society of Hospital Medicine (2). Tele should be treated like any other imaging study and only be ordered for specific patients when indicated.

2. Evidence behind tele

No large randomized control trials have established standards of care for cardiac telemetry. However as the old adage goes you don’t need an RCT to prove that a parachute is useful when jumping out of an airplane. There are guidelines established by the AHA/ACC but they are just that- guidelines. In the end, you have to use your clinical judgement when ordering or discontinuing tele. Some of the obvious clinical scenarios when telemetry is useful include

  1. Syncope of unexplained origin (meaning if the patient has obvious vasovagal syncope then you don’t need tele!)
  2. Uncontrolled or unstable arrhythmias (AF RVR, VT)
  3. Following a STEMI
  4. ICU monitoring

3. Common reasons for inappropriate tele use

In residency I attempted to combat inappropriate tele use through a quality improvement project. While partially successful I found that there were a few common diagnoses that accounted for a majority of inappropriate tele use. In the New England Journal of Medicine (NEJM) Journal Watch, Dr. Winawer summarized my thoughts quite well in his post detailing top 10 reasons he has anecdotally seen over his career for inappropriate tele monitoring (5). Remember that these are anecdotes for tele use on the general medicine wards and exclude critical care units. Here are 5 of the most common reasons I see patients inappropriately placed on tele.

  • 1. Abnormal electrolyte derangements. You should not be using tele as a surrogate marker for electrolyte abnormalities. You should be managing the patient with frequent BMP’s. If they have ECG manifestations then they should not be on the general medicine floor and should be in a higher level of care. This include patients with End-Stage Renal Disease (ESRD) with chronically abnormal potassium levels without ECG changes.
  • 2. Low-risk chest pain. If you rule out ACS with negative serial troponin you can DC tele.
  • 3. Non-cardiac syncope. If a patient has a syncopal episode due to hypoglycemia or a seizure then tele has zero utility.
  • 4. Sinus tachycardia. Sometimes patients are admitted for non-cardiac issues and are found to have appropriate sinus tachycardia. This could be due to a fever, pain, anemia, or dehydration. Tele is sometimes used as a surrogate for ‘closer patient monitoring’. If a patient needs to be monitored more closely then they should be upgraded to a higher level of care. Tele is not an adequate replacement.
  • 5. History of atrial fibrillation. If a patient has a history of AF but is rate controlled they do not require tele monitoring. This often happens with patients admitted for something non-cardiac like cellulitis and placed on tele despite being hemodynamically stable.

4. Evaluate the need for tele daily

It is far harder to stop a medication than it is to start one. Same thing is true for tele. So each day that you check your patient’s tele remember to ask yourself if it is even necessary in the first place. This is a responsibility of everyone who interacts with the patient from bedside nurses to the advanced practitioner PA or NP, to both the primary physician and consulting physicians. Everyone has the ability to contribute to more meaningful tele use in the hospital- even our patients!

5. How to look at tele systematically

Okay, okay, okay. I get it. Only order tele when it’s indicated and discontinue it when appropriate to do so. So let’s say we have a patient on tele. Where do we start?

  1. Look at the live feed. See what rhythm your patient is in right now.
  2. Look at events. The computer typically will flag preset rhythms based on an algorithm. It has a high sensitivity so it often flags things that aren’t real arrhythmias. So you have to open each one to evaluate them. When in doubt print out the telemetry strip to have with you to review with your attending physician
  3. Look at the timing of the events. Did your patient have a run of atrial fibrillation last night? Look at the timing of the arrhythmia and ask your patient if they felt it. Similarly if your patient complains of chest pain or palpitations see if there are any events on tele that correlate with that timing.

6. Confirm with an ECG

Tele is great but sometimes it isn’t all that accurate. Always get a confirmatory ECG to compare the rhythm in question.

7. Print out the tele strip in question

I once had a patient who had an abnormal arrhythmia in the ICU. Unfortunately by the time we were able to see the patient they got transferred out of the unit to the floor. When this happened their telemetry data didn’t get transferred with them. So whenever you see something abnormal make sure you print it out and get it uploaded into the patient chart so we can see it in the future. This is also why I like to get an ECG to confirm abnormal rhythms so I make sure it gets uploaded to the EMR.

8. Call for help if you need it

This should go without saying but if you are concerned about a rhythm that doesn’t look right then call for help. If you are an intern and aren’t sure what to make of the tele strip then print them out, discuss with your senior, and on rounds. If you area a nurse then print out the strips and speak to the primary team.

9. But first evaluate the patient clinically

I understand that not everyone is a cardiologist but we are all medical professionals. It is not good enough to simply pass the buck and say ‘I called cardiology about it’. For instance, I’ve gotten calls to say “the patient’s heart rate is 40. What do you want to do?’. Well, it depends! Is the patient fast asleep, hemodynamically stable, and has had normal heart rate trends in sinus rhythm all day? Because a heart rate of 40 could simply be vagal tone brought on by sleep. Or is this a patient who just had a right coronary artery myocardial infarction and is now in complete heart block, feeling dizzy, and becoming hypotensive? My point is that one piece of isolated information is more valuable when put in the context of a clinical situation.


Now let’s go over some real life examples

This is the real meat and potatoes of this blog post. The following case presentations are not based on a single patient and are instead a culmination of many common threads I’ve experienced first hand. So let’s pretend you are a first year cardiology fellow and you are called to evaluate the following patients.

Case Number 1: it’s 3am and you are called because a patient is reported to be in ventricular tachycardia (VT) and the primary team wants to confirm if they should use 100J or 200J for the synchronized cardioversion. They send you a picture of the tele strip, below, while you’re walking to evaluate the patient. What do you tell them to do?

You can tell them to let you and the patient go back to sleep! Here’s why: on the telemetry strip you can see 3 rhythms strips. I labeled them 1, 2, and 3 in red, below. Strip number 1 on the top looks scary. It could be VT! But at first glance it doesn’t look quite right.

Now let’s just jump down to lead number 3 on the bottom. If you saw this lead all on it’s own you would never think “this is VT”. You can see clear cut narrow QRS-complexes. Now go back and look again at the blue circles.

Sinus rhythm with interference

Notice how the narrow QRS-complexes in the bottom lead are also present in the middle lead. Those are pretty easy to march out. The tough part is noticing that they are also present in the top lead. This brings us to our first major learning point. You cannot have an abnormal rhythm in one lead and a normal rhythm in another. If you have VT it should be present in every lead.

So what’s the above diagnosis? It’s tough to make out the underlying rhythm. It could be atrial flutter or just sinus rhythm with prominent T-waves. In the end however it is definitely not VT. The top lead is likely just interference!

Let’s drive this point home and look at another tele strip. Now that you are an expert at figuring out if it’s VT or just interference take a look at this one below.

This is another example where it can easily be mistaken for VT. But look smack dab in the middle at lead III. You can clearly see a regular rhythm with narrow QRS-complexes. You can also see narrow spikes in other leads that correlate with the timing of those sinus beats. The other leads simply have interference.

Now let’s take a look at another tele strip. What’s the rhythm?

In the above tele strip you can clearly see that there are 5 narrow QRS-complexes followed by 7 wide QRS-complexes. This is finally an example of non-sustained ventricular tachycardia (NSVT). In this tele strip the wide QRS-complexes are found in all 3 leads.

Ventricular tachycardia is a wide QRS-complex originating from the ventricle. It is considered non-sustained ventricular tachycardia (NSVT) when it lasts for ≥3 beats but for ≤30 seconds. The 30 second timing is kind of an arbitrary man made classification. But generally if the VT lasts longer than 30 seconds it is classified as sustained-VT. Sustained VT can be deadly because it can deteriorate into ventricular fibrillation (VF) which can be fatal.

To finish out this lesson lets take a look at a 12 lead ECG, below. This is an example of sustained VT.

Diagnosing and differentiating VT from atrial fibrillation with aberrancy is outside the scope of this post but I really like this Life In The Fast Lane blog post on this topic if you’re looking for more information.

Case number 2: you are consulted for ‘runs of sinus tachycardia’. What do you do?

Well first off (*using sassy cardiology fellow attitude*) tell them to try and figure out what the actual rhythm is first and then have them call you back . Okay okay, just kidding..kind of. Let’s dive into why you can’t have a ‘run of sinus tachycardia’.

First off, what should every primary team have done first before calling cardiology about actual sinus tach? The basic work up includes addressing underlying reasons for a patient to be tachycardic. This includes:

  1. Dehydration
  2. Acute anemia
  3. Pain
  4. Fever
  5. Hyper/hypothyroidism
  6. Holding a patient’s beta blocker

Fever tangent: What is Liebermeister’s rule?

Liebermeister’s rule is the appropriate increase in heart rate in response to a fever. In general for every degree abvoe 100F the heart rate should increase by about 10. So a fever of 101 can cause a heart rate of 110. A fever of 102 can cause a heart rate of 120, etc.

Conversely, what is the unusual diagnostic association of fever with bradycardia and what can it indicate? It is known as Faget sign. Faget sign can be seen with intracellular bacterial infections like legionella or mycoplasma pneumoniae as well as many other infections including yellow fever, typhoid fever, tularemia, brucellosis, and Colorado tick fever.

Now let’s say you did all of the above and still can’t figure out wyh on tele you are seeing runs of a fast heart rate. Sometimes looking at the graphic trend can help differentiate different rhythms.

First just think about what your normal heart rate does while in sinus rhythm. Throughout the day if you get up and move around your heart rate increases gradually to accommodate for increased cardiac output requirements. Think about when you walk up a flight of stairs or two. Your heart rate increases slowly. It doesn’t suddenly jump from 60 beats per minute to 150. It slowly climbs up to 65, then 70, then 75, then 80 and so on. Then in recovery after you finish climbing the stairs your heart rate similarly will slowly trend down and decrease slowly from 150 to 145 to 140 and so on. Below is an example of a patient who is in normal sinus rhythm without any arrhythmias.

The above graphic trend is for a 24-hour period. So the small spikes that you see are actually happening over a longer period of time. If we were to zoom in you would see a gradual upslope and then gradual down slope.

Now don’t get fooled. This can also happen in atrial fibrillation. Patient’s can be rate controlled pretty well and have gradual increases in their graphic trends. So just because the graphic trend is gradual it does not mean that it is sinus rhythm. Don’t forget the rules of telemetry. Get an ECG or check the rhythm yourself to figure out what you are dealing with.

Now our patient in question was having ‘runs’ of tachycardia, as seen below.

Above is the graphic trend over an 8 hour period. These bursts of fast heart rhythms are starting SUDDENLY and stopping SUDDENLY. This should not happen in sinus rhythm and indicates that you are likely dealing with some type of abnormal heart rhythm. Arrhythmias that can commonly do this include atrial flutter, atrial fibrillation, and atrial tachycardia.

The learning point here is that the graphic trend can be used to help guide your diagnosis. You cannot solely rely on the graphic trend to make a final diagnosis. You still have to go inside the event strip and FD, or full disclosure, strip in order to figure out what rhythm you are dealing with. When in doubt, print it out! And then call your friendly neighborhood cardiology fellow for some help to figure it out together.

Overnight I got called again abotu this patient’s heart rhythm. The primary team thought it was an SVT so they used adenosine to break the rhythm. Below is what they saw (sorry for blurry image).

In the above image the patient was going in a fast rhythm and adenosine was administered. Adenosine slows AV-nodal conduction. So all that it does it stops the atria from communicating with the ventricle. It does not necessarily stop whatever rhythm is happening inside the atria. In the above strip you can see that after the 5th narrow QRS-complex there is long pause until the next QRS-complex comes in. During that extended time period you can still see about 8 P-waves. This is highly suggestive of atrial tachycardia and is the first thing that comes to my mind when a patient is having ‘runs of sinus tachycardia’.

Atrial tachycardia can look like sinus rhythm, suddenly start, and suddenly stop. Again the full treatment of atrial tachycardia is outside the scope of this blog post but if you want to read more about it I like this LITFL blog post on atrial tachycardia.

Lastly, let’s take a look at another graphic trend, below.

Notice how this rhythm also suddenly goes fast and then suddenly goes slower. This is indicative of an underlying arrhythmia. I would be impressed if someone called me with a consult with this information at hand for assistance in rhythm identification. This is some ‘upper level senior resident who is interested in cardiology’ level of knowledge!

Again, graphic trends can be a valuable tool to help guide your ECG diagnosis but always get a 12 lead to confirm! And if rhythms and ECG’s are still tough for you then don’t worry because I still get them wrong at times. Medicine requires lifelong learning so use every one of your patient’s ECG’s as practice!

If you think this blog post helped then comment below and I hope be sure to subscribe so you don’t miss the next blog post!

Works Cited

  1. Henriques-Forsythe MN, Ivonye CC Jamched U, Kamuguisha LKK, Onwuanyi AE. Is telemetry overused? Is it as helpful as thought? Cleve Clin J Med [Internet]. 2009 Jun [cited 2012 Sep 4];368-372.
  2. SHM – Avoid continuous telemetry monitoring | Choosing Wisely. (2020). Choosingwisely.org. Retrieved 22 May 2020, from https://www.choosingwisely.org/clinician-lists/society-hospital-medicine-adult-continuous-telemetry-monitoring-outside-icu/
  3. When Should Hospitalists Order Continuous Cardiac Monitoring?. (2020). The-hospitalist.org. Retrieved 22 May 2020, from https://www.the-hospitalist.org/hospitalist/article/122074/when-should-hospitalists-order-continuous-cardiac-monitoring
  4. Drew BJ, Califf RM, Funk M, et al. Practice standards for electrocardiographic monitoring in hospital settings: an American Heart Association scientific statement from the Councils on Cardiovascular Nursing, Clinical Cardiology, and Cardiovascular Disease in the Young: endorsed by the International Society of Computerized Electrocardiology and the American Association of Critical-Care NursesCirculation. 2004;110(17):2721-2746.
  5. NEJM Journal Watch: Summaries of and commentary on original medical and scientific articles from key medical journals. (2020). Jwatch.org. Retrieved 23 May 2020, from https://www.jwatch.org/na44560/2017/07/06/dos-and-donts-telemetry-monitoring-telemetry-directors-top

Racial Disparities in Treatment of Heart Failure

Given existing disparities in access to health care the growing burden of heart failure in the US could disproportionately impact the African-American and minority community (1). 

Regardless of race or ethnicity, patients with heart failure (HF) have better outcomes when cared for by cardiology specialists than other specialties (e.g. internal medicine) (2,3).

However, prior studies on patients admitted for decompensated heart failure found those with lower incomes or patients who were AA were ‘significantly less likely to receive cardiology care when compared with younger, Caucasian, and more educated patients. Even after adjusting for severity of illness, social factors were strongly associated with receiving care from a cardiologist’ (4). 

In a larger database study published in 2018 of over 100k patients including over 20k AAs the authors found that Caucasians were 40% more likely to receive cardiology care than AAs(5).

As an editorial commented ‘can we continue to blame the disparity in care to lack of access or insurability? Is it not time to consider preconceived notions of access and inherent, although unrecognized, racial bias and stereotyping that lead to racial health disparities?’ (5).

I won’t pretend to be an expert in racial issues or healthcare policy but it is evident that generations of racial and socioeconomic disparities manifest in poor health and that we must recognize and challenge our own bias both personally and professionally.

For now, you can also head to https://justiceforgeorgefloyd.com/ or sign a petition to help get #JusticeForGeorgeFloyd.

Works Cited

  1. Piña, I. (2018). If It Is Not Health Care Access or Insurance Coverage, Then Why Do Racial Disparities Persist?. JACC: Heart Failure, 6(5), 421-423. doi: 10.1016/j.jchf.2018.03.013
  2. Uthamalingam S., Kandala J., Selvaraj V., et al. (2015) Outcomes of patients with acute decompensated heart failure managed by cardiologists versus noncardiologists. Am J Cardiol 115:466–471.Google Scholar
  3. Selim A.M., Mazurek J.A., Iqbal M., Wang D., Negassa A., Zolty R. (2015) Mortality and readmission rates in patients hospitalized for acute decompensated heart failure: a comparison between cardiology and general-medicine service outcomes in an underserved population. Clin Cardiol 38:131–138.Google Scholar
  4. Auerbach A.D., Hamel M.B., Califf R.M., et al. (2000) Patient characteristics associated with care by a cardiologist among adults hospitalized with severe congestive heart failure. SUPPORT Investigators. Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments. J Am Coll Cardiol 36:2119–2125.FREE Full TextGoogle Scholar
  5. Breathett K., Liu W.G., Allen L.A., et al. (2018) African Americans are less likely to receive care by a cardiologist during an intensive care unit admission for heart failure. J Am Coll Cardiol HF 6:413–420.Google Scholar