142. HF part 11: The Role of the Clinical Examination in Patients With Heart Failure – with Dr. Mark Drazner

CardioNerds Amit Goal, Daniel Ambinder, & Dr. Alex Pipilas (FIT, Boston University) discuss the clinical examination in patients with heart failure with Dr. Mark Drazner, professor of medicine, clinical chief of cardiology, and medical director of the LVAD and Cardiac Transplantation Program at UT Southwestern. In this pearl laden episode, they discuss how the exam can be used to non-invasively assess a patient’s hemodynamic status, risk stratify and inform prognosis, and guide management. They also discuss ways to master the evaluation of the JVP and categorize patients based on their RA:PCWP ratio.

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PearlsNotesReferencesGuest ProfilesProduction Team

Pearls – Clinical Examination in Heart Failure

  • Begin hemodynamic assessment with the evaluation of congestion (“wet” vs “dry”) and perfusion (“cold” vs “warm”). In a 2×2 table, this breaks patients into 4 broad hemodynamic profiles
  • The most sensitive markers of congestion (PCWP > 30) are JVP >12 with an OR of 4.6 and the presence of orthopnea with an OR of 3.6
  • “If you are cold, you are cold, if you are warm, you can still be cold”. Sensitivity for clinical markers of low cardiac index is very poor. Consider a low output state in patients with poor response to what are thought to be appropriate therapies
  • Most patients with acute on chronic heart failure have an RA:PCWP ratio of 1:2. These patients are the so called “concordant” phenotype. There are two other sub-phenotypes:
    • The “RV equalizer group” have an elevated RA:PCWP ratio
    • The “RV compensated” group have a lower RA:PCWP ratio
  • Clinical congestion at the time of hospital admission as well as discharge portends a poor prognosis for patients with heart failure

Show notes – Clinical Examination in Heart Failure

Heart Failure Clinical Examination
Figure 1

1. What is the physical exam important in patients with heart failure?

  • Important to view the physical exam as a diagnostic test with strengths and limitations
  • It is a noninvasive way to assess hemodynamics and risk stratify patients
  • Can provide information on prognosis
  • May enhance the provider-patient relationship

2. How might we classify hemodynamics noninvasively?

  • Framework begins with the “Stevenson” Classification, developed by Dr. Lynne Stevenson
  • Classifies patients along two axes: congestion and perfusion
  • Congestion is the assessment of overall volume status and estimation of right and left sided filling pressures, broadly broken up into “wet” or “dry”:
    • “Wet”, PCWP >15mmHg
    • “Dry”, PCWP <15mmHg
  • Perfusion is the assessment of the adequacy of cardiac output to provide oxygen to peripheral tissues, broken up into “warm” (i.e adequate perfusion) or “cold” (i.e poor perfusion):
    • “Warm”, Cardiac index >2.2
    • “Cold”, Cardiac index <2.2
  • You then develop a 2×2 table to begin hemodynamic assessment (Figure 1 – above)

3. What is the role of the clinical exam in the assessment of congestion: “Wet” or “Dry”

  • Signs:
    • Elevated jugular venous pressure. The JVP is one of the two most sensitive markers for congestion such that a JVP > 12 predicts PCWP > 30 with an OR of 4.6 (Drazner, 2008).
    • Rapidly developing ascites or edema
    • Square wave test. The square wave test takes advantage of an abnormal response to Valsalva in patients with low systolic function and elevated filling pressures. In those with congestion, the MAP fails to fall with decrease in RV and LV preload from the Valsalva maneuver due to preexisting high filling pressures. This is likely the best evidence that the patient has elevated filling pressures and may help to identify patients with the discordant hemodynamic phenotypes.
  • Symptoms:
    • Orthopnea: one of the two most sensitive markers for congestion such that the presence of orthopnea predicts PCWP > 30 with an OR of 3.6 (Drazner, 2008).
    • Bendopnea: the sensation of feeling breathless within 30 seconds of bending over. Bendopnea is associated with higher filling pressures and low cardiac index (Thibodeau JT T. A.-M., 2014), with increased risk of short term heart failure admission ( (Thibodeau JT J. B., 2017), and with elevated VE/VCO2 (more advanced HF marker from CPET) (Dominguez-Rodriguez A, 2016). Relief of bendopnea during hospitalization is associated with greater fall in median NT-proBNP.
  • The following are less helpful for identifying patients with acute on chronic  HF
    • Rales have a low sensitivity and specificity for acute on chronic decompensated heart failure. If rales are present in chronic HF patients, consider looking for pulmonary pathology. This doesn’t apply for patients with acute MI or flash pulmonary edema.
    • Weight may be misleading as heart failure is a cachexia promoting illness such that variation in weight may not be referred to fluid status alone. Volume overload often leads to appetite changes and weight loss as well as fluid retention which together can lead to net negligible weight change. Additionally once patients are euvolemic and clinically improved, they might gain true caloric weight which makes tracking “dry weights” difficult. Weight may be helpful over the short term i.e with a report of 10lbs of weight gain within the past week + significant stigmata of overload. With these considerations, we must be cautious regarding targeting a fixed “dry” weight over long periods of time given true changes in body weight.
  • Adjunctive data may help adjudicate the bedside assessment of congestion:
    • Prognosis is better with down trending natriuretic peptides but no data clearly suggests benefit from tailoring therapy based on these levels.
    • Echo parameters such as the PASP, mitral inflow pattern, and IVC size may be helpful in the right context.
    • Implantable PA sensors (i.e. CardioMems) may be helpful. A large RCT looking at this, Guide-HF, trial is still enrolling. 

4. What are some tips & tricks for measuring the JVP?

  • We are not looking for venous structure, but rather referred pulsating waves, which are usually better seen than felt.
  • Look on both sides of the neck!
  • Carotid vs Jugular vein – if you compress BELOW the pulsation and it goes away then it is a VENOUS pulsation. If not, then it is likely carotid. Venous pulsation (not carotid pulsation) will change in height as you adjust the degree of patient’
  • If unable to see the pulsation, sit the patient upright and assess. It may be too high to see when recumbent
  • Can use the EJ if it is respirophasic. If it isn’t then the high level could be due to a valve in the vein in which case we need to be cautious with interpretation.

5. What is the connection of the JVP (i.e estimated RA pressure) to left sided filling pressures (i.e PCWP/LVEDP) (Drazner 2008)?

  • The RAP:PCWP ratio is ~1:2 (“concordant”) in 70-75% of patients in acute on chronic heart failure from ESCAPE trial data.  Importantly, this relationship does not hold in all groups of patients including those with acute MI or other conditions which may cause discordance between right- and left-sided filling pressures like primary pulmonary hypertension, significant valvular disease, etc.
  • This relationship does not hold ~25-30% of the time, where the RAP and PCWP are “discordant.” The two sub-phenotypes to think about are:       
    • Right/left equalizers: high RAP:PCWP ratio (ratio ~≥ 2:3). Clinically, a high JVP may overestimate the overall fluid status. They may run into hypotension and worsening renal function because left sided pressures are lower than you would estimate by the JVP. These tend to be sicker patients with a generally worse prognosis (Grodin JL, 2015).
    • Compensated RV group: low RAP:PCWP ratio (ratio ~≤ 1:3). In contrast to the right/left equalizers, those with a “compensated RV” may have a JVP which underestimates the overall fluid status since the RAP is lower for a given PCWP. Consider this phenotype in those with classic left sided HF symptoms despite a relatively low or normal JVP.
  • There are no clear clinical makers to identify patients who are in the discordant phenotypes but if the clinical course is not what you expect, consider exploring if a patient’s hemodynamics fall within these discordant phenotypes.
  • If a patient has had a RHC in the past, you can use their previous RA:PCWP ratio to estimate left sided filling pressures with JVP during subsequent encounters
    • There is some data to suggest that a given patient us unlikely to move from one extreme to another, at least over a short period of time (i.e move from right/left equalizers to compensated RV ect)
    • More likely, a patient may move from extremes to the middle with either progression of disease or improvement

6. What is the role of the clinical exam in the assessment of perfusion: “Warm” or “Cold”?

  • “If they are cold, they are cold. If they are warm, they still may be cold.” In other words, the sensitivity of the clinical evaluation is poor for the diagnosis of poor perfusion, but the specificity is high.
  • Signs:
    • Narrow pulse pressure
      • Sensitivity is 10%, specificity is 96%
    • SBP <90 mmHg
      • Sensitivity 12%, specificity 86%
    • Cool lower extremities
      • Sensitivity of 20%, specificity of 88%
    • Consider low output if there is poor response to appropriate diuretic administration (Drazner, 2008) (Thibodeau JT D. M., 2018)
  • Symptoms:
    • Lethargy – likely signifies a more advanced low output state, though not specific to heart failure

7. How does the hemodynamic profile guide initial management strategies?

  • Profile A, “warm and dry”: compensated heart failure, if symptomatic, then consider heart failure mimics such as pulmonary or hematologic disease.
  • Profile B, “warm and wet”: IV diuretics. If they do not respond as expected, then consider discordant RAP:PCWP groups or low output state.
  • Profile C, “Cold and wet”, sick patients: IV diuretics, Inotropes, vasodilators, mechanical support.
  • Profile L, “Cold and dry”, often very sick, tailored to situation.

8. What is the connection between the hemodynamic status and prognosis?

  • Congestion portends a poor prognosis.
    • The occurrence of a heart failure hospitalization marks a steep inflection point in a patient’s prognosis (Drazner MH R. J., 2001).
    • The occurrence of clinical congestion and decompensation is a marker for increased mortality in the patient with heart failure.
    • The reason for the poor prognosis of heart failure decompensation is not clear. Is decompensation indicative of poor cardiorespiratory reserve or is it causal in some way? Reasons for the poor prognosis may include: neurohormal activation, ischemia, etc. More research is needed.
  • Admission Congestion = increased risk of adverse event (Guillem Caldentey, 2014).
    • Unclear what the pathway is from clinical congestion to adverse outcomes.
      • Part could be renal congestion, cardiac cachexia and liver dysfunction.
  • Discharge congestion = increased risk of adverse events when compared to patients who are discharged without congestion (Ambrosy, 2013).
  • If you are UNABLE to congest someone or if re-congestion occurs within 1 year (i.e 2 hospitalizations in one year) this suggests a sick patient that may need to be considered for advanced therapies.

References – Clinical Examination in Heart Failure

  1. Ambrosy, A. P., Pang, P. S., Khan, S., Konstam, M. A., Fonarow, G. C., Traver, B., Maggioni, A. P., Cook, T., Swedberg, K., Burnett, J. C., Grinfeld, L., Udelson, J. E., Zannad, F., & Gheorghiade, M. “Clinical course and predictive value of congestion during hospitalization in patients admitted for worsening signs and symptoms of heart failure with reduced ejection fraction: Findings from the EVEREST trial.” European Heart Journal (2013): 835-43.
  2. Dominguez-Rodriguez A, Thibodeau JT, Abreu-Gonzalez P, Ayers CR, Jimenez-Sosa A, Aranda JM Jr, Drazner MH. “Association Between Bendopnea and Key Parameters of Cardiopulmonary Exercise Testing in Patients With Advanced Heart Failure.” Journal of Cardiac Failure (2016): 163-165.
  3. Drazner MH, Rame JE, Stevenson LW, Dries DL. “Prognostic importance of elevated jugular venous pressure and a third heart sound in patients with heart failure.” New England Journal of Medicine (2001): 574-81.
  4. Drazner MH, Velez-Martinez M, Ayers CR, Reimold SC, Thibodeau JT, Mishkin JD, Mammen PP, Markham DW, Patel CB. “Relationship of right- to left-sided ventricular filling pressures in advanced heart failure: insights from the ESCAPE trial.” Circulation Heart Failure (2013): 264-70.
  5. Drazner, M. H., Hellkamp, A. S., Leier, C. V., Shah, M. R., Miller, L. W., Russell, S. D., Young, J. B., Califf, R. M., & Nohria, A. “Value of clinician assessment of hemodynamics in advanced heart failure: the ESCAPE trial. .” Circulation. Heart failure (2008): 170-177.
  6. Grodin JL, Drazner MH, Dupont M, Mullens W, Taylor DO, Starling RC, Tang WH. “A disproportionate elevation in right ventricular filling pressure, in relation to left ventricular filling pressure, is associated with renal impairment and increased mortality in advanced decompensated heart failure.” American Heart Journal (2015): 806-812.
  7. Guillem Caldentey, Paul Khairy, Denis Roy, Hugues Leduc, Mario Talajic, Normand Racine, Michel White, Eileen O’Meara, Marie-Claude Guert. “Prognostic Value of the Physical Examination in Patients With Heart Failure and Atrial Fibrillation: Insights From the AF-CHF Trial.” JACC Heart Failure (2014): 15-23.
  8. Thibodeau JT, Drazner MH. “The Role of the Clinical Examination in Patients With Heart Failure.” JACC Heart Failure (2018): 543-551.
  9. Thibodeau JT, Jenny BE, Maduka JO, Divanji PH, Ayers CR, Araj F, Amin AA, Morlend RM, Mammen PP, Drazner MH. “Bendopnea and risk of adverse clinical outcomes in ambulatory patients with systolic heart failure.” American Heart Journal (2017): 102-107.
  10. Thibodeau JT, Turer AT, Gualano SK, Ayers CR, Velez-Martinez M, Mishkin JD, Patel PC, Mammen PP, Markham DW, Levine BD, Drazner MH. “Characterization of a novel symptom of advanced heart failure: bendopnea. .” JACC Heart Failure (2014): 24-31.

Guest Profiles

Dr. Mark Drazner
Dr. Mark Drazner

Mark Drazner, M.D., is a Professor in the Department of Internal Medicine at UT Southwestern Medical Center. He specializes in treating patients with cardiomyopathy and advanced heart failure, including those who undergo a heart transplant or implantation of a ventricular assist device to help the heart pump blood. He is the Clinical Chief of Cardiology at UT Southwestern and the Medical Director of the Left Ventricular Assist Device (LVAD) and Cardiac Transplant Program. He holds the James M. Wooten Chair in Cardiology.

Dr. Drazner earned his medical degree at Washington University in St. Louis. He completed a residency in internal medicine at UT Southwestern Medical School, where he was Chief Resident. He received advanced training in cardiology through a fellowship at Duke University and then further specialized training in heart failure/cardiac transplantation through a fellowship at Brigham and Women’s Hospital. He also earned a Master of Science in epidemiology at Harvard University School of Public Health.

Dr. Drazner was one of the first physicians in North Texas to be certified by the American Board of Internal Medicine in the new subspecialty of advanced heart failure and transplant cardiology.

He has been at the forefront of research in heart failure and cardiac transplantation and has published numerous academic articles in top medical journals.

Dr. Drazner is a member of several professional organizations, including the American Heart Association, the American College of Cardiology, the Heart Failure Society of America, and the International Society for Heart and Lung Transplantation.

He has been selected as a Best Doctor by D Magazine, a Super Doctor by Texas Monthly, a Best Doctor in America by Best Doctors Inc., and a Top Doctor by Castle Connolly on numerous occasions.

Dr. Alexandra Pipilas - CardioNerds
Dr. Alexandra Pipilas

Alexandra Pipilas (@apipilasMD) is a cardiology fellow at Boston Medical Center. She completed her undergraduate training at Boston University before leaving for a short stint in Chicago for medical school. She then returned to Boston for internal medicine residency and chief residency at Boston Medical Center. Outside of the hospital, she is enjoys attempting to climb the peloton leaderboard and spending time with friends and family.

CardioNerds Heart Failure Production Team

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