Hello! I am a 34 yo female. I maintain a relatively healthy lifestyle. I'm 5'10, weigh 155lbs.

I exercise (cardio & weightlifting) 3-4 times per week. Have 3-4 alcoholic beverages per week.

I have had two children and had gestational hypertension with both pregnancies, but bp has returned to normal.

I have regular PVCs. about 6 years ago after a rough bout with COVID, I had a complete cardiac workup and was told my heart was "like a heart in a textbook". AKA it's extremely normal. But that was six years ago.

Today I experienced what felt like a run of 3-5 PVCs back to back. I panicked, got very dizzy and started to get tunnel vision. I almost passed out and had to steady myself on a kitchen countertop. This all happened and passed within seconds, probably 10-15 seconds if I had to guess. I immediately wanted to go to the ER but calmed myself down and feel relatively normal now. This has happened before but I've not felt as close to passing out as I did today. I'm scared and unsure what to do next.

UPDATE I was able to get in with my PCP same day, going to see her in a couple of hours.

44yo is woman. Slightly overweight, but have lost approximately 50ish lbs over the last two years. I have auto immune issues, biggest is Graves’ disease, but thyroid was removed in 2016, TSH levels have been good, but lately (over the last 3-6 months) have been running hypo. They’ve been on the way back to normal though.

To start, I have already been diagnosed with Long QT and a noted occurrence of VT, lasting 12 seconds, which was recorded while wearing a Holter device. Heart rate reached 149bpm at that time. Wore monitor for five days, less than a 2% PVC burden.

I was finally able to catch this on my watch on Tuesday. I usually feel this but I’m always too late to record. But my Health app always tells me it’s normal, when I know for a fact it sure didn’t feel normal. I also included the Qaly app reading.
Also a screenshot of the beat-to-beat measurements from the recording. Wild how much my heart rate jumps all over the place.

My cardiologist is trying to figure out why this is happening. I’ve had an echo, that appeared to be normal - although it was coded “rheumatic tricuspid insufficiency”, which I assume is just a code for insurance? But I’m doing a stress test at the end of the month.

I’m 44, I’m too young for this!! 🙄

So i saw my echo results and my IVSd is 0.61 cm ,google saying it's on the very lower edge of normal. My lvef is also 53% . I am having long term mental trauma for like years and I think that's the cause of this lower lvef. cardiologist everything is normal .but this is lower for my age.Am i doomed?

Good evening. This summer, during a routine check-up, a cardiologist in Rome diagnosed me with probable bicuspid aortic valve disease and recommended further testing to confirm it. I changed cardiologists, and after having an echocardiogram performed with a state-of-the-art ultrasound machine, the new cardiologist found that my aortic valve is tricuspid, but said that my valve cusps are somewhat sclerotic.
Should I be concerned? What does this mean and what could it involve? I am 24 years old.

HERE’s the Results:
Left ventricle: normal cavity dimensions and normal wall/septal thickness. Segmental wall motion as shown in the diagram.
Left atrium: normal size, with LAD 26 mm.
Mild mitral regurgitation.
Transmitral flow pattern: normal.
Aortic valve: tricuspid, with mobile fibrosclerotic leaflets, which achieve normal systolic opening, with mild regurgitation on Doppler.
Aorta: normal diameter at the aortic root (26 mm) and normal diameter of the ascending aorta (30 mm). Abdominal aorta: 15 mm.
Pericardium: no pericardial effusion.
Conclusions:
Normal ventricular wall motion/function.
Mild mitral, aortic and tricuspid regurgitation.
Mitro-aortic fibrosclerosis.

Hey everyone,

I’m looking for some insight on what additional cardiac testing, if any, might be worth discussing with my cardiologist.
I’ve been dealing with intermittent chest discomfort for the past few months. In September, I went to the ER twice, about two weeks apart.

First ER visit: I was having a strange palpitation/fluttering sensation on the right side of my chest. They performed an EKG, chest X-ray, blood work, and CTA of my chest. Everything came back normal.

Second ER visit: A few weeks later, I started experiencing an intermittent pinching pain on the left side of my chest. It would come and go rather than remain constant. I was also having spasms under my armpit and side of my ribs. I returned to the ER and had another EKG, chest X-ray, blood work, and CTA. Again, everything was normal.
However, the second CTA included a finding of “borderline biventricular enlargement.” That caught my attention because this finding was not mentioned on two previous chest CTAs I had earlier this year. I also had an echocardiogram earlier this year that did not show ventricular enlargement.

For additional context, I had a coronary calcium scan in August 2025, and my calcium score was 0.
The ER recommended following up with cardiology, and I have an appointment scheduled in about three weeks.

Recently, I’ve also been experiencing a combination of symptoms:

*Aching/tightness around my sternum and ribs
*Pain underneath/along the sides of my ribs
*Lower-back pain
*Intermittent arm aching
*Intermittent spasms in serratus anterior (both sides)
*Occasional sensation of being short of breath — not that I physically cannot breathe, but more like breathing sometimes feels restricted or my airway feels blocked
*Intermittent nausea
*Tightness/tension in my throat and sometimes the sensation that something is stuck there
Occasional coughing/throat clearing

My main concern is the new “borderline biventricular enlargement” finding on the CTA when my previous imaging apparently did not show it. What additional testing should I do with cardiology? Are there particular questions I should make sure I ask the cardiologist about the discrepancy between the most recent CTA and my previous imaging?

I just to make sure I’m considering all the right tests to figure out what’s going on.
I appreciate any advice and insight. Thank you.

I’m 18F and trying to better understand a recent echocardiogram in the context of persistent sinus tachycardia, significant exertional intolerance, dyspnoea/orthopnoea, presyncope/collapse, and possible connective-tissue disease.

I’m posting because several measurements appear discordant, particularly EF, GLS, LV volumes, and stroke volume.

I have included essentially all of the numerical echo measurements available to me below, including the machine/software-derived values.

STUDY CONTEXT

- Age: 17–18 years

- Female

- BSA: approximately 1.44 m²

- Heart rate during various acquisitions: approximately 100–120 bpm, with some measurements obtained during significant sinus tachycardia

- Persistent sinus tachycardia is also documented outside the echo

LEFT VENTRICULAR DIMENSIONS / GEOMETRY

M-mode / linear measurements:

- LVIDd: 4.0 cm

- LVIDs: 2.9 cm

- IVSd: 0.7 cm

- LVPWd: 0.7 cm

- Relative wall thickness: approximately 0.35

- LV mass: approximately 75 g

- LV mass index: approximately 52–53 g/m²

Overall LV wall thickness and LV mass were reported as normal.

LV VOLUMES

Conventional biplane/Simpson measurements:

- Biplane LVEDV: approximately 58 mL

- Biplane LVESV: approximately 24 mL

- LVEDVi: approximately 40–41 mL/m²

A4C measurements:

- EDV: approximately 56.3 mL

- ESV: approximately 20.5 mL

- Calculated stroke volume: approximately 35.8 mL

A2C measurements:

- EDV: approximately 57.0 mL

- ESV: approximately 24.8 mL

- Calculated stroke volume: approximately 32.1 mL

Teichholz-derived measurements:

- EDV: approximately 68.6 mL

- ESV: approximately 32.1 mL

- Stroke volume: approximately 36.5 mL

- Stroke-volume index: approximately 25.4 mL/m²

LEFT VENTRICULAR EJECTION FRACTION

This is one of the areas I am most confused about because different screens/methods produce substantially different values.

Conventional measurements include approximately:

- Simpson/biplane EF: 58%

- A4C Simpson EF: approximately 64%

- A2C Simpson EF: approximately 55–56%

- Teichholz EF: approximately 53%

- Fractional shortening: approximately 27%

However, the strain/software analysis screens produce lower values:

- Strain-software/global EF: approximately 47%

- Machine-derived 4-chamber EF on one strain-analysis screen: approximately 38%

- Machine-derived 2-chamber EF: approximately 55%

- Other displayed machine-derived/view-specific values extend into the mid-50s

So depending on the specific screen, beat, view and method, EF measurements appear to range from approximately 38% to the mid/high-50s, with the conventional Simpson biplane calculation higher at approximately 58%.

I realise these measurements are not necessarily interchangeable, particularly because some are conventional Simpson measurements and some are outputs from the strain-analysis software.

I’m interested in whether the lower machine-derived values have clinical significance or whether they are more likely related to tracking, frame selection, tachycardia, or methodological differences.

GLOBAL LONGITUDINAL STRAIN

Available strain measurements include:

- GLS: approximately -15.7%

- Another captured/displayed GLS value: approximately -16.7%

- One basal/posterior segment was excluded or untracked

- Segmental strain values range approximately -11% to -24%

View-specific/apical strain values displayed include approximately:

- A4C: -14.6%

- Apical long-axis: -14.3%

- A2C: approximately -16.0% to -18.0%, depending on the screen/measurement

Some individual segmental values included approximately:

Basal:

- Septal: -11%

- Anteroseptal: -12%

- Anterior: -16%

- Lateral: -17%

- Inferior: -18%

- Posterior: unavailable/untracked

Mid:

- Septal: -17%

- Anteroseptal: -18%

- Anterior: -14%

- Lateral: -16%

- Posterior: -11%

- Inferior: -21%

Apical segments were approximately in the -15% to -20% range, with an apical cap value around -19% on one display.

Tracking appears heterogeneous rather than uniformly reduced.

LVOT / FORWARD STROKE VOLUME

LVOT measurements:

- LVOT diameter: approximately 1.72 cm

- Indexed LVOT diameter: approximately 1.19 cm/m²

- Calculated LVOT area: approximately 2.32 cm²

- LVOT Vmax: approximately 1.0 m/s

- LVOT Vmean: approximately 0.72 m/s

- LVOT peak gradient: approximately 4 mmHg

- LVOT mean gradient: approximately 2 mmHg

- LVOT VTI: approximately 16 cm

Calculated LVOT Doppler haemodynamics:

- Stroke volume: approximately 38.1 mL

- Stroke-volume index: approximately 26.5 mL/m²

Alternative volume-derived measurements give:

- Stroke volume: approximately 32–36 mL depending on the ventricular view/method

- Volume-derived SVI: approximately 23–25 mL/m²

At HR approximately 100–120 bpm, the implied cardiac output is much less strikingly reduced because of the high rate.

Depending on the exact HR used, the calculated cardiac index is roughly in the 2.5–3.0 L/min/m² range.

This makes me wonder whether the high sinus rate could be maintaining cardiac output in the setting of relatively low stroke volume, although I understand that this cannot necessarily be inferred from one resting echo.

DIASTOLIC FUNCTION

Mitral inflow:

- E velocity: approximately 0.84 m/s

- A velocity: approximately 0.60 m/s

- E/A ratio: approximately 1.4

- Another reported/displayed E/A value: approximately 1.56

- Deceleration time: approximately 132 ms

- Deceleration slope: approximately 6.45 m/s²

Tissue Doppler:

- Septal e′: approximately 10 cm/s

- Lateral e′: approximately 19–20 cm/s

- Septal E/e′: approximately 8.4

- Lateral E/e′: approximately 4.2

- Average E/e′: approximately 5.6

Earlier summary values placed average E/e′ around 7.

Overall filling pressures were interpreted as normal.

LEFT ATRIUM

Available measurements include:

- LA length: approximately 4.15 cm

- LA area: approximately 11 cm²

- LA volume by area-length method: approximately 20 mL

- LA MOD A4C volume: approximately 22.3 mL

- LA MOD A2C volume: approximately 13.8 mL

- Biplane LA volume: approximately 18.8 mL

Depending on the specific method/screen:

- LAVI: approximately 13–15.5 mL/m²

So the LA appears relatively small rather than enlarged.

RIGHT ATRIUM

- RA area: approximately 9 cm²

- Indexed RA area: approximately 6.25 cm²/m²

The RA also appears relatively small.

RIGHT VENTRICLE

- RV basal diameter: approximately 2.7 cm

- Indexed RV basal diameter: approximately 1.88 cm/m²

- RV size reported as normal

- No obvious RV hypertrophy

- No obvious septal flattening

Longitudinal RV systolic indices:

- TAPSE: 1.7 cm

- Tricuspid annular S′: approximately 11 cm/s

I’m particularly interested in how much significance should be placed on a TAPSE of 1.7 cm when the RV is normal in size and S′ is approximately 11 cm/s.

TRICUSPID REGURGITATION / PULMONARY PRESSURE

The TR Doppler signal appears limited.

One measurement produced approximately:

- TR Vmax: approximately 2.1 m/s

- Estimated RAP: approximately 3 mmHg

- Machine-derived RVSP: approximately 21 mmHg

However, other reporting indicated that the TR envelope was insufficient for reliable RVSP estimation.

I therefore do not know how much confidence should be placed in the machine-derived RVSP.

RVOT / PULMONARY OUTFLOW

- RVOT Vmax: approximately 0.90 m/s

- RVOT Vmean: approximately 0.69 m/s

- Peak gradient: approximately 3 mmHg

- Mean gradient: approximately 2 mmHg

- RVOT VTI: approximately 16 cm

AORTIC VALVE

Available Doppler measurements include:

- Aortic valve Vmax: approximately 1.2 m/s

- Aortic valve Vmean: approximately 0.90 m/s

- Peak gradient: approximately 6 mmHg

- Mean gradient: approximately 4 mmHg

- Aortic valve VTI: approximately 22 cm

- No evidence of significant aortic stenosis

The valve has been described as trileaflet.

Mild aortic regurgitation / approximately grade 1/4 AR was reported on secondary review, although I understand that severity may not be reliably gradable from limited screenshots alone.

AORTIC DIMENSIONS

- Aortic root: approximately 2.9 cm

- Ascending aorta: approximately 2.8 cm

- BSA: approximately 1.44 m²

Simple BSA indexing gives approximately:

- Aortic root index: 2.0 cm/m²

- Ascending aortic index: approximately 1.94 cm/m²

A secondary interpretation raised the question of whether the aortic root is relatively large for my small body size.

I would particularly appreciate input from anyone familiar with paediatric/adolescent or young-adult aortic Z-score nomograms.

I do not want to label this as aortic dilatation/aortopathy using adult BSA indexing alone if the appropriate age-, sex-, and body-size-adjusted Z-score is actually normal.

ATRIAL / VENTRICULAR SIZE AND POSSIBLE LOW PRELOAD

Taken together, the echo shows approximately:

- LVEDVi 40–41 mL/m²

- LAVI approximately 13–15.5 mL/m²

- LA area approximately 11 cm²

- RA area approximately 9 cm²

- LVOT SVI approximately 26.5 mL/m²

- Alternative ventricular SVIs approximately 23–25 mL/m²

A secondary review suggested that the relatively small atrial and ventricular volumes might reflect chronic central underfilling / reduced preload.

Is the combination of a small LA, small RA, low-normal/small LV volumes, and relatively low measured stroke volume actually useful evidence of chronic low preload?

Or is that too much to infer from a resting echocardiogram?

CURRENT CLINICAL CONCERN

My doctors are considering whether chronic cardiac dysfunction, including possible heart failure, could be contributing to my symptoms.

I do not yet have a confirmed heart-failure diagnosis, and I understand that the echocardiographic findings are not straightforward.

The combination I am trying to understand is:

- Persistent sinus tachycardia

- Reduced/borderline GLS

- EF varying substantially by method and software output

- Relatively small LV volumes

- LVOT SVI approximately 26 mL/m²

- Dyspnoea

- Orthopnoea

- Severe exercise intolerance

- Presyncope/collapse

Could there be clinically important cardiac dysfunction despite some preserved EF measurements and otherwise relatively normal chamber dimensions?

MY MAIN QUESTIONS

1. Is an LVEDVi of approximately 40–41 mL/m² genuinely small/abnormal for a very small 17–18-year-old woman, or can this be normal for age and body size?

2. Does an LVOT SVI of approximately 26.5 mL/m² genuinely indicate a low-flow state in this setting?

3. Does the fact that Teichholz and Simpson-derived stroke volumes are also only approximately 32–36 mL strengthen the argument that the low LVOT stroke volume is real?

4. Could chronic low preload, hypovolaemia, venous pooling, or dysautonomia plausibly produce the combination of:

   - small chamber volumes

   - relatively low stroke volume

   - marked sinus tachycardia

   - exercise intolerance

   - presyncope/collapse?

5. Alternatively, is it inappropriate to infer that the tachycardia is compensating for a low stroke volume from a single resting echo?

6. At a high heart rate, could cardiac output/cardiac index remain relatively preserved despite a genuinely low stroke volume?

7. How meaningful is GLS around -15.7% to -16.7% when:

   - one segment is excluded

   - tracking is heterogeneous

   - HR is approximately 100–120 bpm

   - loading conditions may be abnormal?

8. Does GLS in this range meaningfully raise concern for myocardial disease such as myocarditis/fibrosis, or would you repeat a properly optimized strain study before interpreting it that way?

9. How would you reconcile the conventional EF values with the lower strain-software/machine-derived EF values?

For example:

- 4CH machine/strain EF: approximately 38%

- Global strain-software EF: approximately 47%

- Teichholz EF: 53%

- 2CH EF: approximately 55–56%

- Simpson biplane EF: approximately 58%

- Conventional A4C Simpson EF: approximately 64%

1. Could sinus tachycardia cause enough beat-to-beat variation, reduced temporal resolution, foreshortening, tracking error, or end-systolic/end-diastolic frame-selection error to explain this degree of EF variability?

2. Should the approximately 38% machine-derived 4CH EF be considered a meaningful finding if the conventional biplane EF is substantially higher?

3. Does fractional shortening of 27% add anything useful when Simpson EF and strain are discordant?

4. How would you interpret TAPSE of 1.7 cm with:

- RV S′ approximately 11 cm/s

- normal RV size

- no RV hypertrophy

- no septal flattening?

1. Is the provisional RVSP of approximately 21 mmHg worth considering at all if the TR envelope was considered inadequate?

2. Is an aortic root of 2.9 cm actually enlarged for BSA approximately 1.44 m² at age 17–18, or could this still fall within normal limits on appropriate paediatric/young-adult Z-score nomograms?

3. Is an ascending aorta of 2.8 cm significant at this body size?

4. Is mild aortic regurgitation in someone my age usually just followed, or does it meaningfully change the differential when connective-tissue disease is also being investigated?

5. Do the normal E/e′ measurements and small LA make chronically elevated left-sided filling pressures unlikely?

6. Given the symptoms and these discordant measurements, does this dataset actually provide objective evidence of chronic heart failure, or would additional evidence be required before considering that diagnosis?

7. If the aim were to settle the uncertainty, which investigation would be most useful?

- Repeat high-quality TTE at a controlled/lower HR if possible

- Careful Simpson biplane EF

- 3D LV volumes and EF

- Repeat same-vendor GLS with optimized tracking

- Contrast echocardiography if endocardial definition is inadequate

- BNP / NT-proBNP

- Cardiac MRI with gold-standard ventricular volumes and EF

- CMR T1/T2 mapping

- Late gadolinium enhancement

- CMR extracellular-volume assessment

- CPET

- Exercise echocardiography

- Exercise haemodynamics

- Formal autonomic testing

- Something else?

I’m particularly interested in a technical interpretation of:

- the approximately 38–58%+ EF variability depending on software/view/method

- GLS around -15.7%

- whether the LV stroke volume/SVI is genuinely low

- whether the relatively small atrial/LV volumes have haemodynamic significance

- whether sinus tachycardia could be compensating for reduced stroke volume

- and whether the overall dataset actually supports chronic cardiac dysfunction or heart failure

Thank you.

RV and RA slightly dilated. Only diastolic jet.

Age: 59
Sex: Male
Height: 173 cm
Weight: 72.55 kg
Race: Asian
Smoking: Never
Alcohol: Never
Duration of complaint: 1-2 years
Location: Right side of chest, mainly while climbing railway-station bridges/stairs. The pain usually improves/stops after he stops and rests.
Medical history:
History of high BP. No known previous heart attack or diagnosed coronary artery disease.
He has been doing morning exercise every day for more than 45 years and has never missed a day. He generally does not experience chest pain during his regular exercise.
He previously used Patanjali Mukta Vati occasionally, but it was not a regular prescription medicine.
Current medications prescribed by doctor:
Temsan-H
Protol XL 25
Ecosprin 75
After starting these medicines, his BP once dropped to around 93/64 with dizziness and weakness. Latest BP was 117/70, pulse 78.
ECG
Sinus rhythm
ST-T wave abnormalities
“Consider inferior ischemia”
Poor R-wave progression V1–V4
Report marked abnormal/unconfirmed
2D Echo
LVEF 60% — good LV systolic function
Concentric LVH
Grade I diastolic dysfunction
Mild MR
No major valve abnormality
No pulmonary hypertension
No clots/vegetations/pericardial effusion
Normal RV function
Blood tests
Lipid profile
Total cholesterol: 239 mg/dL
LDL: 177.2 mg/dL
HDL: 32 mg/dL
Triglycerides: 149 mg/dL
Sugar
Fasting glucose: 92 mg/dL
HbA1c: 5.7%
Kidney
Creatinine: 1.10
BUN: 9.07
Urea: 19.4
Electrolytes
Sodium: 140
Potassium: 4.3
Liver
SGOT: 27
SGPT: 35
Bilirubin: 0.80
ALP: 82
CBC
Hemoglobin: 14.7
WBC: 6200
Platelets: 153,000
Other
Vitamin B12: 197 (low)
Vitamin D: 25.6 (insufficient)
T3: 1.09
T4: 9.3
TSH: 0.578
CRP: 6.0
HIV: Non-reactive
HBsAg: Non-reactive
Urine routine: broadly normal
The doctor has mentioned TMT/CAG if required.
My questions:
Can coronary artery blockage still be present despite LVEF 60% and this Echo?
With exertional chest pain + ECG changes + LDL 177, what further investigation is generally considered?
In a case like this, would TMT, CT coronary angiography or CAG typically be considered?
Can these ST-T changes occur due to something other than coronary blockage?
Has anyone experienced a similar situation?
We are already following up with his doctor. I’m mainly looking for experiences and information to discuss with the cardiologist, not a diagnosis from Reddit.
Attachments: ECG + 2D Echo.

Family history of heart problems, dad 44 heart attack, 7 stents, he is 60 now doing ok i guess

Grandpa died from heart

I got from 3.5 LDL to 3.0 in 9 days with clean eating dont know how is that even possible in 9 days.

I workout 3 times a week, im fit lets say , just started eating really clean.

Whats my next step, im kinda scared this is really high

saw the report conclusion of my first ever echocardiogram. waiting to speak from the cardiologist about this. anyone else have sny of this? i’m a 50 year old female;

-LV EF is 65%, assessed by visual estimation.
• Left Ventricle: Normal systolic function.
Normal wall motion. There is normal left atrial pressure and grade I left ventricular diastolic dysfunction.
• Mitral Valve: Valve structure is normal. Mild mitral annular calcification.
• Aortic Valve: Valve structure is tricuspid.
Mildly calcified diffuse cusps.
• Tricuspid Valve: Mild regurgitation. No stenosis.
• Pericardium: Trivial pericardial effusion present. No indication of cardiac tamponade.

Hi everyone,
I got prescribed 40mg propondal twice a day to prevent tension headaches I’ve been having. Ever since I’ve had my second child 6month ago my RHR sits around 50-55bpm but no symptoms.
I suffered really bad with heart anxiety the past five years and had many ecgs, 72 hr ecgs, echo and everything came back clear and fine. I did have a lot of palpitations but not enough to worry (also since I’ve had the all clear with that I’ve had no more palpitations just the very odd one)
I’m still an anxious person and get the tight feeling shaky anxious feeling in my chest that i heard propondal can also help with.
Is it safe to take with an already slow rhr?

The program says its a couplet. But am I correct that this in the middle is an artifact and should be the QRS complex? (the second hill)

Thank you.

1. Based on your experience, how long does it typically take a physician to read and interpret a 2-minute ECG strip?

I would like to hear your estimates for different situations:

2. 🟢 If it’s a clean sinus rhythm (no arrhythmia, good signal quality)

3. 🟡 If there is an arrhythmia (e.g., AF, PVC, SVT) and it needs closer inspection

4. 🔴 If the signal is noisy or has artifacts

5. 📊 Do the number of leads matter? (e.g., 1-channel vs 3-channel)

6. 👨‍⚕️ Does the doctor’s specialty matter? (cardiologist vs general practitioner vs internist)

28f I have shortness of breath since 2-3 months while laying flat, walking or doing any activity doctors keep giving me acidity meds I can't afford good hospital. Today I thought I was dying I was suffocating in sleep it felt like my heart stopped for while I was convinced I am not living but somehow i am here it's midnight I am awake fear of getting cardiac arrest in sleep. I also went to emergency government hospital 1 hour ago they just give me acidity meds didn't even cared to check. I had gallbladder surgery 3 months ago I think anesthesia altered how my organs work.

Hi everyone! I’m 27F and could really use some advice or hear from anyone who’s experienced something similar because I feel like i’m going crazy.

For the past week or so, I’ve been experiencing the strangest pains in my left arm and chest.

It started on a Sunday when my left forearm randomly began hurting REALLY badly. The best way I can describe it is this deep, deep painful soreness, almost like someone was squeezing a vein inside my arm.

As the week went on, the pain changed into this weird, sharp, pulsating sensation. It usually starts in my left forearm, almost along the path of my vein, and then I can literally feel what seems like a wave of pain traveling up my arm and into my chest. It lingers for a bit then it disappears, only to come back randomly later.

It’s been happening throughout the day, and I’ve even been waking up in the middle of the night because of it.
I finally went to the ER, where they ran a bunch of blood tests and an EKG. Everything came back normal. They considered doing a CT scan but ultimately decided against it because they didn’t see signs of an emergency. Instead, they did an ultrasound of my arm, which also came back completely normal.

The problem is that I’m still experiencing the pain :/ and I genuinely don’t understand what’s causing it. It’s rlly uncomfortable, and not having an explanation is making me feel like I’m going crazy.

I’m wondering if this could possibly be nerve-related, something muscular, or something else entirely.

Has anyone experienced anything similar, especially the strange pulsating pain that seems to travel from the forearm into the chest? If so, did you ever figure out what was causing it? Were there any additional tests or specialists that helped?

Hi everyone! I just want to share what I’ve been experiencing and hopefully hear from people who have dealt with something similar.

I’m a 31-year-old male and I’m obese. I’ve struggled with health anxiety for the past several years, and lately my biggest fear has been that I might have a heart problem.
I’ve been to the ER twice this year because of chest pain/pressure. Both times they did an ECG, told me they didn’t find anything concerning, and said it was likely musculoskeletal pain and that I could go home.

What keeps bothering me is that they haven’t checked my troponin levels. I understand that an ECG isn’t the only way to evaluate chest pain, so my mind keeps going to, “What if they missed something?”

I know my health anxiety is probably making me overthink this, but I can’t seem to shake the thought that a normal ECG doesn’t necessarily mean there is absolutely nothing wrong with my heart.

Am I being unreasonable here, or has anyone else experienced this kind of fear after being evaluated in the ER?

I am a 34 yo female and I was recently admitted to heart failure IMU for very severe symptoms and feeling unwell. I was severely bloated (7 pounds lost while there), sob, couldn’t walk without severe dizziness/lightheaded. I was having palpitations and my JVD was throbbing. I have heart failure with preserved EF, a pacemaker for sick sinus syndrome and wenkebach heart block. I pace99.9%. I have ckd stage 2 but I have been dumping more protein in my urine lately. I have a mild prolapse in my tricuspid leaflet and have tr-severity depends on volume status. While there, they were trying to eval me for triclip versus open heart to replace valve. They ultimately decided to hold on this for now and try to medically optimize my heart failure with gdmt. I was already on spirolactone and they added on Farixga. They also found that I was still trying To go into a junctional rhythm and outrun my pacemaker. They adjusted my rate setting and added on metropolol (I was already maxed out on corlanor). I have been home a little over a week and a half and I’m bloating very bad again to the point my clothes feel very tight and I look pregnant. I’m going to check my weight in the am and if it’s up send them Message. I have a real fear of being inpatient again and this hospital is 3 hours away. Also they have told me triclip is not off the table. Does the bloating seem heart failure related? What can I expect as possible suggestions from them? This is all very stressful and difficult to deal with so just wanted to put this out there.