Draft

201  Locke PGR HFPEF

201.1 Summary

  • If everyone has HFpEF, does anyone?
  • Patient:
  • 2 arguments why HFpEF at pulmonary GR
  • Aims
  • True or False: CPET is gold standard for diagnosing HFpEF?
  • CPET in CHF
  • Abnormalities on TTE are required to diagnose HFpEF?
  • HF2PEF (2022 ACC/AHA CPG)
  • You are evaluating a patient you think has HFpEF. They do not have crackles. How does this change the likelihood they have congestion?

201.2 Slide outline

201.2.1 Slide 1

  • If everyone has HFpEF, does anyone?
  • B Locke PGR ### Slide 2
  • Patient:
  • 65M with 6 months of dyspnea
  • BMI 36
  • Current smoking and prior inhalational drug use
  • Moderate apical paraseptal emphysema; No obstruction on PFTs
  • TTE with no diastolic dysfunction, mild LVH, mild left atrial enlargement
  • No improvement with LABA/LAMA trial
  • CPET:
  • VO2 max ~45% weight normalized predicted
  • VEVCO2 43
  • Maximum HR 110; Significant metabolic acidosis
  • Normal MVV; Low BR ### Slide 3
  • 2 arguments why HFpEF at pulmonary GR
  • Diagnosis of symptomatic disease
  • 👎: Se (# Patients w/ finding & disease) / (# Patients w/ Finding whether or not they have disease)
  • Consider how we do PFTs
  • Susceptible to subtle spectrum bias
  • 👍: (Likelihood in COPD) / (Likelihood in HFpEF)
  • You have a differential. You want findings that discriminate between the options (NOT findings that separate has disease vs doesn’t have disease)
  • Opinion: 👎 “Reason for Consult: Dyspnea; ….
  • A/P: Not the lungs”
  • If a reason for dyspnea is needed and possible, we should be able to diagnose it regardless where in the chain of respiration the problem occurs.
  • Our expertise is the entire respiratory system
  • Consider Nephrology: Recs re AKI diagnosis
  • COPD
  • PAH
  • HFpEF ### Slide 4
  • Aims
  • Review diagnostic criteria for HFpEF
  • Review notable (or not) findings in HFpEF
  • What’s up with chronotropic incompetence?
  • What’s up with the wedge?
  • What’s up with the pleural pressure? ### Slide 5
  • True or False: CPET is gold standard for diagnosing HFpEF?
  • True
  • False ### Slide 6
  • True or False: CPET is gold standard for diagnosing HFpEF?
  • True
  • False
  • The [ exercise ] RHC directly measures atrial pressures and is considered the criterion standard (100% sensitivity and specificity; C statistic, 1.0) for HFpEF diagnosis
  • We will discuss this more. ### Slide 7
  • CPET in CHF ### Slide 8
  • Abnormalities on TTE are required to diagnose HFpEF?
  • True
  • False ### Slide 9
  • Abnormalities on TTE are required to diagnose HFpEF?
  • True
  • False
  • Requires evidence of increased filling pressures (R atrial pressure, PCWP, or LVEDP) at rest or with exercise. Which can be:
  • TTE
  • Catheterization
  • Or inferred by physical exam/CXR/BNP/H2FPEF score
  • 30% of patients with elevated PCWP have BNP < 100. (“BNP/NT-proBNP assays are insufficient to rule out HFpEF, particularly in younger patients, those with sinus rhythm, and those with obesity and/or normal kidney function.”) ### Slide 10
  • HF2PEF (2022 ACC/AHA CPG)
  • Rest PCWP 15+ OR Exercise PCWP 25+
  • 60% had HFpEF
  • The odds of HFpEF doubled for each 1-unit score increase ### Slide 11
  • You are evaluating a patient you think has HFpEF. They do not have crackles. How does this change the likelihood they have congestion?
  • A lot more likely
  • A little more likely
  • No difference
  • Less likely
  • ”[Congestion can be] inferred from physical exam” ### Slide 12
  • You are evaluating a patient you think has HFpEF. They do not have crackles. How does this change the likelihood they have congestion?
  • A lot more likely
  • A little more likely
  • No difference
  • Less likely
  • ESCAPE Trial: RCT of PA-C guided CHF mgmt vs clinical exam guided.
  • Analysis of the 250 randomized to PA-C
  • Crackles (1/3 of lung field): +LR 1.36, -LR 0.96 for predicting PCWP 22+ mmHg
  • Most patients do not have crackles related to chronic, congested HF. Presence/absence of crackles barely gives any information about congestion.
  • Se + Sp 100% > adds no information ### Slide 13
  • Why?
  • Stage 1: interstitial fluid (can be up to 500mL with minimal extra pressure). No crackles.
  • Stage 2 Crescentic filling of the alveoli
  • Stage 3 Alveolar Flooding. Crackles
  • Stage 4 Froth in air passages ### Slide 14
  • Pulmonary Edema: Interstitial & Alveolar
  • Endothelial (vessels-interstitium) Gradient & Permeability: interstitial edema?
  • Epithelial (interstitium-alveoli) Gradient & Permeability: alveolar edema?
  • Inflammation? ### Slide 15
  • In normal conditions, most fluid returns to the capillaries by starling forces, 18% by lymphatics
  • In edematous states, lymphatics increase 8-10 fold
  • Precapillary vasoconstriction -> divert blood flow away from portions of lung with high fluid flux. This has significant inter-individual variation that may contribute to individuals “prone-ness” to edema formation.
  • Derangements/loss of protective factors can be regional: imaging findings can be “geographic” even when “cardiogenic”
  • Time constant of alveolar flooding: 3 minutes
  • Presentation of HF w Alveolar Edema / HF w/o Alveolar Edema ### Slide 16
  • The mechanism of dyspnea in HFpEF is that PCWP increases with exertion
  • True
  • False ### Slide 17
  • HR response to exercise is reduced in patients with HFpEF
  • This was generally considered pathologic
  • Chronotropic incompetence inability to meet predicted maximum heart rate
  • Patients with HFpEF and chronotropic incompetence having a PM implanted were randomized to “Fast” vs ”Regular” pacing with exercise. ### Slide 18
  • TODO: No text extracted from this slide. ### Slide 19
  • single-blind, randomized (to nitro or placebo) cross-over trial.
  • Invasive CPET in 30 patients with HFpEF
  • Upright cycling at 20W (not maximal intensity exercise) ### Slide 20
  • no decrease in PVR from Nitro ### Slide 21
  • “These findings have important clinical implications and indicate that lowering PCWP does not decrease DOE in patients with HFpEF; rather, lowering PCWP exacerbates DOE, increases ventilation-perfusion mismatch, and worsens ventilatory efficiency during exercise in these patients. This study provides compelling evidence that a high PCWP is likely a secondary phenomenon rather than a primary cause of DOE in patients with HFpEF,”
  • Things that might cause dyspnea in patients with HFpEF:
  • Poor V/Q matching -> increased ventilation requirement
  • Poor circulation -> stagnant hypoxemia -> hyperventilation -> increased ventilation requirement
  • Elevated PCWP -> congestion -> increased respiratory system loads
  • How long does it take for the interstitial edema to change?
  • The combination of these two study suggests:
  • The slow heart rate is probably not often a cause of dyspnea
  • The high filling pressures are (acutely) required for two purposes:
  • They allow for maintenance of CO by allowing for adequate preload
  • They allow for V/Q matching (loss of blood flow to apices?) in the setting of congestion ### Slide 22
  • If the elevated PCWP is a epiphenomena or a consequence of whatever causes the dyspnea…
  • Adaptive?
  • How often is HFpEF an incidental finding? (They are congested and SOB, but they are not causally related)
  • Traditional Paradigm ### Slide 23
  • Should RHC measurements be adjusted for intrapleural pressure for HFpEF?
  • Yes/No/Maybe?
  • Notably, more than 80% of patients with HFpEF are obese ### Slide 24
  • Review: what did the study do? ### Slide 25
  • What did they find?
  • More obese patients would be candidates for vasodilators
  • More obese patients would not be labeled as having PH.
  • Many obese patients who previously were post-capillary will be undifferentiated (PVR > 2 but < 3, PA > 20, PCWP < 12. ### Slide 26
  • Lowing afterload (diuretics) aren’t likely to help 1 and 3.
  • Patient (Q3 for all)
  • PAm
  • PCWP (ref atm)
  • Ppl
  • PCWPcorr
  • PVR
  • PAH Class Old
  • PAH Class New
  • 1 – high pl, low rv afterload
  • Low lv preload
  • 35
  • 20
  • 10
  • 5
  • Group 2
  • Group 1
  • 2 – low pl, high rv afterload, high lv preload
  • 0
  • Group 2 (CPC)
  • 3 - high pl, normal RV afterload, low LV preload
  • 25
  • 1.8
  • Group 2 (IPC)
  • No PH [or, presumably HFpEF] ### Slide 27
  • Pulmonary Hypertension: Do we care about transmural or dynamic pressures? DebatableFor Heart Failure: We care about transmural pressures (for both preload and afterload) ### Slide 28
  • Does ↑PCWP predict pathology or response?
  • If there is heterogeneity in all of:
  • The pathology leading to symptoms [surrogate for future treatment/research]
  • Response to current treatments for that disease
  • Diuretics will NOT help patients with elevated PCWP due to pleural pressure for e.g.
  • Prognosis for people with the disease
  • Then actually “” is just a bad disease definition
  • What else are disease definitions supposed to accomplish? ### Slide 29
  • 2 new studies
  • https://x.com/docBLocke/status/1681703444074348544?s20
  • https://x.com/docBLocke/status/1666505807939117060?s20 ### Slide 30
  • Takeaways:
  • Review diagnostic criteria for HFpEF: elevated filling pressures and dyspnea
  • Review notable (or not) findings in HFpEF: crackles minimally helpful
  • What’s up with chronotropic incompetence? Incidental?
  • What’s up with the wedge? Adaptive? Not causal to dyspnea
  • What’s up with the pleural pressure? Transmural pressures diverge
  • Elevated filling pressures and dyspnea is the definition of HFpEF, but it’s not a great definition
  • Disparate pathologies lead to this (obesity, renal disease, OSA…)
  • The elevated filling pressures are probably NOT the cause of symptoms, but an epiphenomenon or adaptive mechanism
  • Symptom/Sign Interpretation: Chronic HF is not a disease of crackles; Diurese then diagnose re: CT abnormalities. ### Slide 31
  • Patient:
  • CPET:
  • VO2 max ~45% weight normalized predicted; low AT
  • VEVCO2 43
  • Maximum HR 110; Significant metabolic acidosis
  • VE achieved > (normal) MVV; Low (negative) BR; no obstruction pre or post.
  • Interpretation:
  • He has ventilatory limitation due to a high ventilation requirement (inefficient ventilation; probably from HFpEF and emphysema)… but minimal excess respiratory system loads.
  • He has chronotropic incompetence
  • I tried taking of the BB (no indication for it) and some evidence withdrawal helps
  • Maybe an SGLT2 inhibitor (improves QoL and Exertional Capacity in HFpEF)
  • He needs to quit smoking and lose weight… but inhalers? ### Slide 32
  • There are no pharmacologic treatments that improve dyspnea in HFpEF? T/F
  • True
  • False ### Slide 33
  • There are no pharmacologic treatments that improve dyspnea in HFpEF? T/F
  • True
  • False
  • Empagliflozin and Dapagliflozin (2 trials; 12,000 patients) reduced HR of re-hospitalization (HR ~0.7) and improved Kansas CM score + 6MW in Dapa case.
  • similar impact on the rate of HF hospitalizations or cardiovascular death regardless of age, sex, EF, presence of diabetes, body mass index, or kidney function (range allowed in the trials: estimated glomerular filtration rate >20-25 mL/min/1.73 m2)
  • Also cardiac rehab. ### Slide 34
  • TODO: No text extracted from this slide.

201.3 Learning objectives

  • If everyone has HFpEF, does anyone?
  • Patient:
  • 2 arguments why HFpEF at pulmonary GR
  • Aims
  • True or False: CPET is gold standard for diagnosing HFpEF?

201.4 Bottom line / summary

  • If everyone has HFpEF, does anyone?
  • Patient:
  • 2 arguments why HFpEF at pulmonary GR
  • Aims
  • True or False: CPET is gold standard for diagnosing HFpEF?

201.5 Approach

  1. TODO: Outline the initial assessment or decision point.
  2. TODO: Outline the next diagnostic or management step.
  3. TODO: Outline follow-up or escalation criteria.

201.6 Red flags / when to escalate

  • TODO: List red flags that require urgent escalation.

201.7 Common pitfalls

  • TODO: Capture common errors or missed steps.

201.8 References

TODO: Add landmark references or guideline citations.

201.9 Slides and assets

201.10 Source materials