Most likely explanation: catecholamine excess (pheochromocytoma/paraganglioma) until proven otherwise

• Catecholamine surges cause episodic hypertension, tachycardia, headache, and diaphoresis.
• Between surges (or after abrupt catecholamine washout, especially if the patient is volume-contracted from chronic vasoconstriction, or has been given an alpha/beta blocker without prior volume expansion), patients can swing into significant hypotension - this paradox of hypertensive-crisis-then-hypotension is well described.
• Chronic catecholamine excess produces pressure-overload/toxic cardiomyopathy that echoes as concentric LVH, sometimes with associated diastolic dysfunction.

Other differentials to actively rule out

1. Autonomic failure / dysautonomia (diabetic autonomic neuropathy, Parkinson disease, multiple system atrophy/Shy-Drager): a well-recognized pattern is supine hypertension alternating with orthostatic hypotension - "Supine hypertension is common in patients with orthostatic hypotension due to autonomic failure, affecting >50% of patients in some series... orthostatic hypotension may present after initiation of therapy for hypertension" (Harrison's Principles of Internal Medicine, 22e). Diaphoresis can occur as a compensatory autonomic response. Longstanding hypertension explains the concentric LVH independently. A tilt-table test and formal autonomic testing would clarify this.
2. Drug-related hypotension: Telmisartan (ARB) can unmask volume depletion, superimposed diuretic use, or additive effect with other antihypertensives/nitrates - review the full medication list and volume status.
3. Adrenal insufficiency (Addisonian crisis) - can cause hypotensive episodes with diaphoresis, though it doesn't explain the pre-existing hypertension/LVH; check cortisol/ACTH if suspected, especially if hyponatremia/hyperkalemia coexist (note: your labs actually show Na 148 - high - which argues against classic Addisonian crisis).
4. Intermittent bradyarrhythmia or heart block causing drop attacks with reflex diaphoresis - your ECGs show sinus rhythm with voltage criteria consistent with LVH (deep S in V1/V2, tall R in V5/V6) but no obvious high-grade block on the strips provided; a 24-48 hour Holter would help capture a transient arrhythmia coinciding with a hypotensive episode.
5. Baroreflex failure (rare - seen after neck surgery/irradiation or carotid body tumor) - produces labile BP swings with diaphoresis and tachycardia.
6. Sepsis/vasodilatory shock superimposed on chronic hypertensive heart disease - diaphoresis plus hypotension from an acute infective/inflammatory process, with the pre-existing concentric LVH simply reflecting long-standing hypertension. This is worth actively excluding given the blood gas below.

Important flag from the ABG you shared

• flash pulmonary edema / acute decompensated heart failure precipitated by a hypertensive surge (fits with concentric LVH -> diastolic dysfunction), or
• a respiratory arrest/severe hypoventilation event (sedation, aspiration, severe pneumonia) that itself caused the hypotension, or
• a peri-arrest/shock state from sepsis.

Bottom line

• reviewing/adjusting the antihypertensive regimen and volume status,
• screening for autonomic dysfunction if metanephrines are negative,
• placing a Holter for arrhythmia correlation, and
• urgently addressing the critical ABG abnormality, which suggests the patient may have been in respiratory failure/shock at the time of one of these episodes and needs immediate bedside reassessment (airway, oxygenation, hemodynamics) if this hasn't already been acted on.

Reframed differential: hypotension + diaphoresis in a patient with hypertensive heart disease (concentric LVH)

1. Septic shock - fits best with your ABG

2. Cardiogenic component from his existing concentric LVH

3. Relative/absolute adrenal insufficiency

4. Autonomic dysfunction / orthostatic hypotension

5. Medication contribution

6. Arrhythmia

7. Don't forget hypoglycemia

Priority actions given your data

• Treat the ABG as an emergency first - pO2 28.6/SaO2 43.6% with pCO2 60 is critical hypoxemic-hypercapnic respiratory failure; secure oxygenation/ventilation before anything else.
• Septic screen: lactate, blood cultures, CXR, CBC, CRP/procalcitonin.
• Cardiac screen: troponin, BNP, repeat/continuous ECG or Holter.
• Endocrine screen: random cortisol, glucose, TSH.
• Medication reconciliation and volume status assessment.

1. VBG vs ABG - different normal ranges (my earlier read assumed arterial)

2. Can it be a technical/pre-analytical error - yes, quite possibly

• Delayed analysis without icing - red cells and white cells keep metabolizing glucose and consuming oxygen inside the syringe after the draw. If the sample sits at room temperature for more than a few minutes before being run, this "in vitro glycolysis" artificially lowers pO2/sO2 and raises pCO2 - "the rate of in vitro oxygen consumption is so high that it results in spuriously low pO2 unless blood is analyzed immediately... blood should be sampled into a pre-cooled syringe, kept on ice and analyzed within a few minutes if bedside analysis is not feasible" (acutecaretesting.org). This is sometimes called "leukocyte larceny" when white cell counts are high.
• Prolonged tourniquet time / sluggish draw from a poorly perfused limb - if the sample was drawn from an arm during or right after a hypotensive episode (cold, vasoconstricted, poor flow), the stagnant local blood gets over-extracted of oxygen by the tissue before it's even drawn, giving an exaggerated low saturation that doesn't reflect the patient's true central/systemic status.
• Air bubble contamination would actually push values the other way (pO2 up toward ~150, pCO2 down, pH up), so that's an unlikely explanation for this particular pattern - you can reasonably rule that one out here.
• Excess liquid heparin dilution tends to falsely lower pCO2, not raise it, so also doesn't fit.

Bottom line / what I'd do

How to rule out adrenal insufficiency in this patient

Step 1 - Screening test: 8 AM serum cortisol (plus plasma ACTH)

• ≥16.3 mcg/dL rules out adrenal insufficiency (99.2% sensitive)
• ≤3.6 mcg/dL establishes the diagnosis (98.4% specific)
• 3.6-16.3 mcg/dL is indeterminate - proceed to a cosyntropin (ACTH) stimulation test

Step 2 - Confirmatory test if indeterminate: cosyntropin (ACTH) stimulation test

• Give 250 mcg cosyntropin IM/IV, measure serum cortisol at 0, 30, and 60 minutes.
• A peak cortisol <18 mcg/dL (cortisol fails to rise appropriately) = positive test, confirms adrenal insufficiency (Tietz Textbook of Laboratory Medicine; Frameworks for Internal Medicine).
• If he's on any hydrocortisone already, hold the morning dose before testing - it can be given right after the samples are drawn.

Step 3 - Localize with plasma ACTH

• High ACTH + low cortisol = primary AI (Addison disease - adrenal gland itself failing; look for autoimmune adrenalitis, TB, hemorrhage, metastatic infiltration).
• Low/normal ACTH + low cortisol = secondary/tertiary AI (pituitary/hypothalamic disease, or - most common in practice - exogenous steroid use/recent steroid withdrawal). Ask specifically about any chronic oral, inhaled, topical, or intra-articular steroid use - this is the single most common cause of secondary AI and easy to miss.

Step 4 - Supportive labs and clues specific to your case

• Electrolytes: primary AI classically shows hyponatremia + hyperkalemia (aldosterone deficiency) plus sometimes mild hypoglycemia and eosinophilia. Note that his sodium was actually 148 (high), not low - this argues against a classic primary Addisonian crisis, though it doesn't fully exclude secondary AI (which spares aldosterone and may not cause the same electrolyte pattern).
• If primary AI is suspected on labs: 21-hydroxylase (adrenal) antibodies for autoimmune Addison's, and CT adrenals for hemorrhage/infiltration/TB.
• If secondary AI is suspected: pituitary MRI and check other pituitary axes (TSH/free T4, LH/FSH, prolactin).

Step 5 - Don't delay treatment for the workup if he's unstable

Practical summary for this patient

1. 8 AM (or random, given acute instability) cortisol + ACTH - drawn before any steroid.
2. If indeterminate -> cosyntropin stimulation test.
3. ACTH level to classify primary vs secondary.
4. Correlate with Na/K, glucose, and steroid-use history.
5. Treat empirically with IV hydrocortisone if clinically unstable rather than waiting on results.

24-hour vs 48-hour Holter - how to decide

If he's currently admitted

If outpatient monitoring is being planned instead

• Episodes happening daily or near-daily ("multiple hypotensive episodes" suggests fairly frequent): a 48-hour Holter is the better default over 24-hour. It doubles the capture window for essentially the same logistics/cost, and extended monitoring consistently picks up more arrhythmic events than a single 24-hour run - "a 24- or 48-hour Holter monitor [is] useful for documenting arrhythmias that occur with sufficient frequency" (Washington Manual of Medical Therapeutics).
• Episodes every few days to weekly: 24-48h Holter will likely miss it. Step up to a 7-14 day event/patch monitor - "event monitoring is at least as effective as Holter monitoring for detection of symptomatic arrhythmias... event monitoring also has the advantage of less frequently recording asymptomatic arrhythmias" (Pfenninger and Fowler's Procedures for Primary Care).
• Episodes are rare (monthly or less): neither Holter option is adequate. Braunwald's Heart Disease notes "use of an implantable loop recorder for 1 year is more likely to identify the mechanism of syncope than is a conventional approach that uses Holter or event monitors" - so an implantable loop recorder becomes the right tool for infrequent events.

Practical recommendation for this patient