DECISION AND ORDER

WILLIAM M. SKRETNY, District Judge.

1. Plaintiff, Yolanda R. Ross, challenges an Administrative Law Judge's ("ALJ") determination that she is not disabled within the meaning of the Social Security Act ("the Act"). Plaintiff alleges that she has been disabled since February 19, 2010, due to degenerative heart disease, depression, anxiety, and foot pain following an ankle injury. Plaintiff contends that her impairments have rendered her unable to work. She therefore asserts that she is entitled to disability and supplemental income benefits under the Act.

2. Plaintiff applied for Disability Insurance Benefits ("DIB") and Supplemental Security Income benefits ("SSI") benefits on August 3, 2010. The Commissioner of Social Security initially denied her applications on December 13, 2010. Pursuant to Plaintiff's request, ALJ William M. Weir held an administrative hearing on June 11, 2012, at which time Plaintiff appeared with counsel and testified. The ALJ considered the case de novo, and on November 5, 2012, he issued a decision denying Plaintiff's application for benefits. On April 10, 2014, the Appeals Council denied Plaintiff's request for review. Plaintiff filed the current civil action on June 10, 2014, challenging Defendant's final decision.1

3. On October 24, 2014, Plaintiff filed a Motion for Judgment on the Pleadings pursuant to Rule 12(c) of the Federal Rules of Civil Procedure. (Docket No. 8). On December 22, 2014, the Commissioner filed a Motion for Judgment on the Pleadings and in Response to Plaintiff's Brief. (Docket No. 10). Plaintiff filed a reply on January 13, 2015 (Docket No. 11), at which time this Court took the matter under advisement without oral argument. For the following reasons, Plaintiff's motion is granted and Defendant's motion is denied.

4. A court reviewing a denial of disability benefits may not determine de novo whether an individual is disabled. See 42 U.S.C. §§ 405(g), 1383(c)(3); Wagner v. Sec'y of Health & Human Servs., 906 F.2d 856, 860 (2d Cir. 1990). Rather, the Commissioner's determination will be reversed only if it is not supported by substantial evidence or there has been a legal error. Balsamo v. Chater, 142 F.3d 75, 79 (2d Cir. 1998); see also Grey v. Heckler, 721 F.2d 41, 46 (2d Cir. 1983); Marcus v. Califano, 615 F.2d 23, 27 (2d Cir. 1979). Substantial evidence is that which amounts to "more than a mere scintilla," and is defined as "such relevant evidence as a reasonable mind might accept as adequate to support a conclusion." Richardson v. Perales, 402 U.S. 389, 401, 91 S.Ct. 1420, 1427, 28 L. Ed. 2d 842 (1971). Where evidence is deemed susceptible to more than one rational interpretation, the Commissioner's conclusion must be upheld. See Rutherford v. Schweiker, 685 F.2d 60, 62 (2d Cir. 1982).

5. "To determine on appeal whether the ALJ's findings are supported by substantial evidence, a reviewing court considers the whole record, examining the evidence from both sides, because an analysis of the substantiality of the evidence must also include that which detracts from its weight." Williams ex rel. Williams v. Bowen, 859 F.2d 255, 258 (2d Cir. 1988). If supported by substantial evidence, the Commissioner's finding must be sustained "even where substantial evidence may support the plaintiff's position and despite that the court's independent analysis of the evidence may differ from the [Commissioner's]." Rosado v. Sullivan, 805 F.Supp. 147, 153 (S.D.N.Y. 1992). In other words, this Court must afford the Commissioner's determination considerable deference, and will not substitute "its own judgment for that of the [Commissioner], even if it might justifiably have reached a different result upon a de novo review." Valente v. Sec'y of Health & Human Servs., 733 F.2d 1037, 1041 (2d Cir. 1984).

6. The Commissioner has established a five-step sequential evaluation process to determine whether an individual is disabled as defined under the Social Security Act. See 20 C.F.R. §§ 404.1520, 416.920. The United States Supreme Court recognized the validity of this analysis in Bowen v. Yuckert, 482 U.S. 137, 140-142, 107 S.Ct. 2287, 2291, 96 L. Ed. 2d 119 (1987), and it remains the proper approach for analyzing whether a claimant is disabled.

7. This five-step process is detailed below:

Berry v. Schweiker, 675 F.2d 464, 467 (2d Cir. 1982) (per curiam); see also Rosa v. Callahan, 168 F.3d 72, 77 (2d Cir. 1999); 20 C.F.R. § 404.1520.

8. Although the claimant has the burden of proof as to the first four steps, the Commissioner has the burden of proof on the fifth and final step. See Bowen, 482 U.S. at 146 n.5; Ferraris v. Heckler, 728 F.2d 582, 584 (2d Cir. 1984). The final step of this inquiry is, in turn, divided into two parts. First, the Commissioner must assess the claimant's job qualifications by considering her physical ability, age, education and work experience. Second, the Commissioner must determine whether jobs exist in the national economy that a person having the claimant's qualifications could perform. See 42 U.S.C. § 423(d)(2)(A); 20 C.F.R. § 404.1520(f); Heckler v. Campbell, 461 U.S. 458, 460-61, 103 S.Ct. 1952, 1954, 76 L. Ed. 2d 66 (1983).

9. At the time of the ALJ hearing, Plaintiff was 39 years old, with an eleventh grade education. (R. 31). She had previously worked as a hotel housekeeper, janitor, and bakery production worker. (R. 31-33). Plaintiff's alleged disability first stems from a work-related accident on February 19, 2010, in which she injured her foot and ankle. (R. 296). She was later diagnosed with plantar fasciitis and tarsal tunnel syndrome. (R. 432). On July 18, 2010, Plaintiff suffered a myocardial infarction, and she underwent double cardiac bypass surgery a few days later. (R. 188). Following the heart attack and surgery, Plaintiff reported related anxiety and depression, for which she began mental health treatment in September 2010. (R. 605). On March 23, 2012, Plaintiff underwent surgery for tarsal tendon release and endoscopic plantar fasciotomy to relieve her lingering foot pain. (R. 461).

10. In this case, the ALJ made the following findings with regard to the five-step process set forth above: (1) Plaintiff has not engaged in substantial gainful activity since February 19, 2010, the onset date of her alleged disability (R. 14)2; (2) Plaintiff's status post myocardial infarction and tarsal tunnel syndrome were "severe" impairments within the meaning of the Act (id.); (3) Plaintiff's impairments do not meet or equal the criteria necessary for finding a disabling impairment under the listed impairments in 20 C.F.R. Part 404, Subpart P, Appendix 1 (R. 17); (4) Plaintiff is unable to perform any of her past relevant work (R. 20); and (5) Plaintiff had the residual functional capacity ("RFC") to perform sedentary work, with the noted limitation that she can climb stairs only occasionally (R. 21). Ultimately, the ALJ determined that Plaintiff was not under a disability, as defined by the Act, at any time from the alleged onset date through November 5, 2012, the date of his decision. (R. 21)

11. Plaintiff asserts that remand is necessary. First, Plaintiff argues that the ALJ failed to consider her cardiac impairment in his RFC determination. She maintains that the ALJ should have sought a medical opinion regarding her cardiac condition because he is not qualified to independently assess its functional impact, and that his ultimate RFC conclusion is not supported by substantial evidence. Second, Plaintiff argues that the ALJ neglected his duty to develop the record on the extent of Plaintiff's impairments from foot pain when he rejected certain "unclear" medical opinions, rather than contacting the treating source for more information. Third, Plaintiff asserts that the ALJ insufficiently explained his credibility analysis, and that he improperly rejected Plaintiff's subjective complaints in favor of relying solely on the objective medical evidence to establish disability. Fourth, Plaintiff argues that the ALJ erred in finding her mental impairments to be non-severe at step two when he primarily relied on opinions given early in Plaintiff's mental health treatment and failed to discuss more serious psychological issues apparent in the record. And further, that he omitted mental status from his RFC determination.

12. Plaintiff's disability period began with her foot injury, and the Court will first address her arguments related to these medical records. Specifically, Plaintiff claims that the ALJ erred when he rejected the opinions of her treatment providers at University Orthopaedic Services because he found their opinions to be unclear. (See R. 19). Plaintiff argues that the ALJ should have requested more information from those providers and, by failing to do so, he neglected his duty to develop the record related to her foot problem before making the RFC determination.

In light of the non-adversarial nature of the benefits proceedings, an ALJ has an obligation to develop the record regardless of whether the claimant is represented by counsel. Shaw v. Chater, 221 F.3d 126, 131 (2d Cir. 2000); Schaal v. Apfel, 134 F.3d 496, 505 (2d Cir.1998). As this Court has recently stated, "the question of whether `the record contains sufficient evidence from which an ALJ can assess the petitioner's residual functional capacity' necessarily dovetails with the `treating physician rule,' which mandates that the opinion of a claimant's treating physician `regarding the nature and severity of [the claimant's] impairments' be given controlling weight if it is `well-supported by medically acceptable clinical and laboratory diagnostic techniques and is not inconsistent with the other substantial evidence in [the] case record.'" Swanson v. Colvin, No. 12-CV-645S, 2013 WL 5676028, at *5 (W.D.N.Y. Oct. 17, 2013), quoting 20 C.F.R. § 404.1527(d)(2); see also Burgess v. Astrue, 537 F.3d 117, 128 (2d Cir. 2008). The Act further provides that the Commissioner "shall make every reasonable effort to obtain from the individual's treating physician (or other treating health care provider) all medical evidence, including diagnostic tests, necessary in order to properly make [a disability determination], prior to evaluating medical evidence obtained from any other source on a consultative basis." 42 U.S.C. § 423(d)(5)(B).

Here, Plaintiff's treating podiatrist, Dr. Davidson, D.P.M., initially described Plaintiff as 30% disabled on March 25, 2010, following her accident, and noted that she rated her pain as 9/10, but walked with a normal and well-balanced gait. (R. 296-297). On April 22, 2010, Dr. Davidson assessed a 50% improvement since Plaintiff's previous visit, but still deemed her 30% disabled. (R. 300-301). On May 6, 2010, he noted Plaintiff was 90% improved since the April 22nd visit, that she rated her pain as 2/10, and changed the disability assessment to 10%. (R. 303-304). Subsequently, however, Dr. Davidson stated in his May 24, 2010 treatment note that Plaintiff was "100% disabled," following her return to work for one week. (R. 305-306). At that visit, Plaintiff reported her pain as 8/10, but Dr. Davidson again noted she walked with normal and well-balanced gait. (R. 305). On August 12, 2010, Dr. Davidson again assessed her as 100% disabled, noted that her gait was "markedly antalgic," and recommended foot surgery. (R. 307-308). Likewise, a physical therapist in the same practice characterized Plaintiff as 10% disabled at her initial visit with him on May 19, 2010 (R. 275), but stated she was 100% disabled at four later visits in June and July of 2010. (R. 265, 267, 269, 271). The ALJ afforded these opinions little weight because "Dr. Davidson and the physical therapists did not attach a narrative statement to explain their opinions, and it is unclear whether these opinions state that the claimant is disabled from her prior work, or all work. Dr. Davidson also did not explain why his opinion changed." (R. 19).

The ALJ similarly disregarded the opinion of consultative examiner George Vasiliadis, D.P.M., because he did not explain his disability finding. (R. 20). On the other hand, the ALJ gave great weight to the opinions of impartial medical examiner Peter Riznyk, D.P.M., who examined Plaintiff on September 17, 2010, and January 24, 2011, in connection with her related worker's compensation claim, and consultative examiner Samuel Balderman, M.D., who examined Plaintiff on November 4, 2010, in connection with her claim for social security benefits. (R. 19).

Although an ALJ is permitted to disregard a treating physician's opinion for "good reason," here, the ALJ gave little weight to Plaintiff's treatment providers with regard to her foot problems for the reason that the records did not contain enough information. (R. 19); see 20 C.F.R. 404.1527(c). While the ALJ properly disregarded the conclusory statements that Plaintiff was 100% disabled, see Snell v. Apfel, 177 F.3d 128, 133 (2d Cir. 1999) (treating physician's statement that claimant is disabled is not itself determinative), he should have sought clarification from Plaintiff's treatment providers in order to complete the record rather rejecting the available opinions entirely. Schaal, 134 F.3d at 505 (rather than rejecting opinions because the clinical findings were inadequate, ALJ had "duty to seek additional information from [the provider] sua sponte"); see Clark v. Callahan, No. 96 CIV. 3020 (SAS), 1998 WL 336653, at *2 (S.D.N.Y. June 22, 1998) (remanding case to develop record seeking a medical explanation, with clinical findings, for why plaintiff's condition deteriorated).

At this juncture, the Court is not convinced that there is overwhelming evidence of disability elsewhere in the record; however, given the non-adversarial nature of the disability proceedings, the Court finds that the undetailed treatment notes create a gap, which the ALJ failed to fill. Shaw, 221 F.3d at 131. Furthermore, in rejecting all of Dr. Davidson's opinions, the ALJ left nothing in the record to which he could properly apply the treating physician rule with regard to Plaintiff's foot problem. See Swanson, 2013 WL 5676028, at *5. Nowhere is it apparent that the ALJ asked for clarification, and because he specifically rejected Plaintiff's podiatrist's and physical therapist's treatment notes for lack of information, the Court finds an error of law and will remand the decision for further development of this portion of the record.

13. Plaintiff also argues that the ALJ assessed Plaintiff's RFC using medical opinions that did not address her cardiac impairment, and that he was not qualified to draw the conclusion that she had "recovered well" from her heart attack and surgery. (See R. 18, 20). Moreover, Plaintiff asserts that the record does not support this assessment because of the restrictions placed on Plaintiff immediately following her heart surgery, consultative examiner Dr. Balderman's note indicating that Plaintiff's echocardiogram and stress test should be reviewed "to assess cardiac function," and numerous treatment notes demonstrating ongoing cardiac symptoms. Therefore, according to Plaintiff, the RFC determination was not based on substantial evidence because the ALJ failed to obtain expert medical opinion regarding the functional limitations caused by her heart problem.

As this Court has recently stated, "it is not per se error for an ALJ to make the RFC determination absent a medical opinion ..., [and] remand is not necessary where `the record contains sufficient evidence from which an ALJ can assess the petitioner's residual functional capacity.'" Lewis v. Colvin, No. 13-CV-1072S, 2014 WL 6609637, at *6 (W.D.N.Y. Nov. 20, 2014), quoting Tankisi v. Comms'r of Social Security, 521 F. App'x 29, 34 (2d Cir. 2013). In addition, the "regulatory language provides ample flexibility for the ALJ to consider a broad array of evidence as `medical opinions.'" Sickles v. Colvin, No. 12-CV-774 MAD/CFH, 2014 WL 795978, at *4 (N.D.N.Y. Feb. 27, 2014), citing 20 C.F.R. § 404.1527 (including "`statements ... that reflect judgments about the nature and severity of [the claimant's] impairment(s), including [ ] symptoms, diagnosis and prognosis,' claimant's capabilities, and any physical or mental restrictions"). Similarly, "where the medical evidence shows relatively little physical impairment, an ALJ permissibly can render a common sense judgment about functional capacity even without a physician's assessment." Walker v. Astrue, No. 08-CV-0828(A)(M), 2010 WL 2629832, at *7 (W.D.N.Y. June 11, 2010) report and recommendation adopted, No. 08-CV-828A, 2010 WL 2629821 (W.D.N.Y. June 28, 2010), quoting Manso-Pizarro v. Sec'y of Health & Human Servs., 76 F.3d 15, 17 (1st Cir. 1996); see also Dumas v. Schweiker, 712 F.2d 1545, 1553 (2d Cir. 1983) ("[the Commissioner] is entitled to rely not only on what the record says, but also on what it does not say").

In support of her argument, Plaintiff highlights the following evidence of "abnormal cardiac functioning," which she claims "demanded further assessment from a medical expert." On December 16, 2010, Plaintiff visited the Buffalo General Hospital Heart and Lung Center, where Dr. Ashish Shukla reviewed her October 26, 2010 2-D echocardiogram and noted an "LVEF of 35%-40% with mild to moderate reduction in the ejection fraction." (R. 566-567). Dr. Shukla also recorded that Plaintiff had shortness of breath that was "consistent with PND and orthopnea."3 (R. 567, 569). On February 10, 2011, Plaintiff again saw Dr. Shukla with complaints of intermittent sharp, stabbing chest pain around the bypass surgery area and mild orthopnea. (R. 564). Plaintiff saw her primary care physician, Dr. Vinod Patel, at UB Family Medicine on April 5, 2011, complaining of on and off chest wall pain. (R. 616). Plaintiff reported to the Heart and Lung Center on May 5, 2011, complaining of pain around her incision site and was assessed with atypical chest pain (R. 562). On July 27, 2011, Plaintiff returned to the Heart and Lung Center, complaining of the same pain. (R. 560). At that visit, Dr. Shukla noted that another 2-D echocardiogram, conducted on April 15, 2011 showed "mild to moderate tricuspid regurgitation and mild mitral regurgitation." (R. 560). On September 19, 2011, Plaintiff saw Dr. Patel at UB Family Medicine, stating she had heart palpitations and episodes of dyspnea.4 (R. 439). On February 6, 2012, at her preoperative assessment for foot surgery, Plaintiff again complained of cutaneous chest discomfort, and cardiologist Dr. Susan Graham noted an abnormal EKG reading. (R. 558).

The cited evidence does not necessarily help Plaintiff because, if supported by substantial evidence, the Commissioner's finding must be sustained "even where substantial evidence may support the plaintiff's position and despite that the court's independent analysis of the evidence may differ from the [Commissioner's]." See Rosado, 805 F.Supp. at 153. Upon reviewing the same treatment notes cited above, the Court finds substantial evidence to support the ALJ's position that Plaintiff had "recovered well." For example, at the December 16, 2010 visit, Dr. Shukla indicated that Plaintiff "denies any chest pain on exertion, or palpitations" and referred her to cardiac rehabilitation. (R. 566-567). On February 10, 2011, Dr. Shukla recorded that Plaintiff denied chest pain and shortness of breath on exertion, and that her pain was likely from her surgery incision. (R. 564). He also noted that a recent stress test "showed no evidence of ischemia"5 and recommended that Plaintiff continue with cardiac rehabilitation. (Id.) On April 5, 2011, the treatment note from UB Family Medicine states that Plaintiff "denied any substernal chest pain" and that her congestive heart failure was "under good control." (R. 616). At the May 5, 2011 visit to the Heart and Lung Center, when Dr. Beck examined Plaintiff's scar area, he assessed the pain was not caused by exertion and that she "feels that is getting better." (R. 562). Dr. Beck also noted that Plaintiff "exercises and ambulates with no problem", and "continues to improve on her exercise tolerance." (R. 562). On July 27, 2011, Plaintiff denied chest pain and shortness of breath at rest or on exertion, denied palpitations, reported that she had not been following up with cardiac rehabilitation, but said that her functional status was good. (R. 560). On September 19, 2011, the note indicates that Plaintiff was "doing well" and denied cardiovascular symptoms. (R. 439). Finally, at the preoperative assessment on February 6, 2012, Plaintiff had no cardiovascular complaints. (R. 558-559). According to Dr. Graham, Plaintiff was "medically stable from a cardiovascular perspective," had "no signs or symptoms of heart failure at this time," and despite a persistently abnormal EKG, it "has improved since 2010." (Id.). Dr. Graham thus cleared Plaintiff for foot surgery. (Id.). Thus, the Court finds substantial evidence in the record supports the ALJ's assessment of Plaintiff's cardiac impairment.

In this instance, the ALJ did not reject any treating physician's opinion in favor of drawing his own differing conclusion. See Rosa, 168 F.3d at 79 (2d Cir. 1999) ("ALJ cannot arbitrarily substitute his own judgment for competent medical opinion"). To the contrary, the ALJ's RFC analysis, albeit brief regarding Plaintiff's heart condition, refers to four selected records that are consistent with the evidence discussed above and representative of the record as a whole. See Cichocki v. Astrue, 729 F.3d 172, 178 (2d Cir. 2013) ("ALJ need not recite every piece of evidence that contributed to the decision, so long as the record permits us to glean the rationale of an ALJ's decision"), citing Mongeur v. Heckler, 722 F.2d 1033, 1040 (2d Cir. 1983). In his decision, the ALJ noted that, following her myocardial infarction and double bypass surgery, on February 13, 2011, Plaintiff complained of shortness of breath, but a chest x-ray was negative. (R. 18). The ALJ also addressed notes discussed herein from Plaintiff's July 27, 2011 visit to the Heart and Lung Center, September 19, 2011 visit with Dr. Patel at UB Family Medicine, and Dr. Graham's February 6, 2012 note clearing Plaintiff for foot surgery. (Id.). While the ALJ may not be qualified to make medical determinations, he is permitted to draw the commonsense conclusion from the record that Plaintiff's cardiovascular disease does not cause any significant limitations for sedentary work. Walker, 2010 WL 2629832, at *7.6 Thus, we cannot say that the ALJ's failure to obtain a medical opinion specifically addressing Plaintiff's limitations due to cardiovascular disease demands remand as a matter of law.

14. Regarding Plaintiff's alleged mental health issues, Plaintiff argues the ALJ erred in determining that her major depressive and anxiety disorders were nonsevere. (See R. 15). Plaintiff further argues that, even if his determination was otherwise based on substantial evidence, the ALJ did not consider her mental impairments when shaping her RFC, therefore, his error is not harmless. See generally Reices-Colon v. Astrue, 523 F. App'x 796, 798 (2d Cir. 2013) (any error in failing to identify a severe impairment is harmless if that impairment is specifically considered during the subsequent steps).

A "severe impairment" is "any impairment or combination of impairments which significantly limits [a claimant's] physical or mental ability to do basic work activities," including understanding and carrying out simple instructions and responding appropriately to others in usual work situations. 20 C.F.R. § 404.1520(c); § 404.1521. Here, after considering the four broad functional areas of 20 C.F.R. § 404.1520a's special technique for assessing mental impairments, the ALJ found that Plaintiff's depression and anxiety did not cause more than a minimal limitation on her ability to perform basic mental work activities. (R. 15). Specifically, the ALJ stated that Plaintiff had no more than a mild limitation in daily living activities; social functioning; and concentration, persistence and pace; and further found that there were no periods of decompensation of extended duration. (Id.); see 20 C.F.R. § 404.1520a(d)(1) (if the limitations in the first three areas are rated mild or less, and there are no episodes of decompensation, the impairment will not be found severe).

In so concluding, the ALJ gave great weight to the opinions of consultative examiner Gregory Fabiano, Ph.D., who examined Plaintiff November 4, 2010, and non-examining psychologist D. Mangold, who reviewed Plaintiff's records on November 19, 2010. (R. 16, 341, 351). Plaintiff asserts that, because both of these opinions were issued near the beginning of her mental health treatment, neither Dr. Mangold nor Dr. Fabiano had the benefit of treatment notes for the subsequent time period, and were, therefore, unaware of Plaintiff's alleged multiple personality disorder (first divulged on September 20, 2011; R. 531), her Global Assessment of Functioning ("GAF") score of 50 (determined on June 29, 2011; R. 511, 515), and that the last several treatment notes indicated a decline in Plaintiff's mental condition. (R. 488, 553).

Although the ALJ's reconciliation of inconsistencies in the record is owed great deference, it is impossible for the Court to know whether and how the ALJ weighed this potentially notable evidence, as he did not refer to it in his opinion. See Jenkins v. Comm'r of Soc. Sec., 769 F.Supp.2d 157, 162 (W.D.N.Y. 2011) ("the Court is not free to engage in speculation concerning what the ALJ might have concluded" about Plaintiff's impairments had he considered and credited other psychological evidence in the record); but see Greene v. Colvin, 936 F.Supp.2d 216, 226 (W.D.N.Y. 2013) (ALJ is not "required to discuss all the evidence submitted, and [his] failure to cite specific evidence does not indicate that it was not considered"). Generally, when the Court is "unable to fathom the ALJ's rationale in relation to evidence in the record, especially where credibility determinations and inference drawing is required of the ALJ," we will not "hesitate to remand for further findings or a clearer explanation for the decision." Cichocki, 729 F.3d at 177, quoting Berry, 675 F.2d at 469. Thus, this portion of the ALJ's decision is remanded for further examination of the record. Accordingly, Plaintiff's related argument that the ALJ failed to incorporate mental function into Plaintiff's RFC is moot.

15. Finally, Plaintiff argues that the ALJ's credibility analysis was improper because he failed to explain his conclusory findings and appears to have rejected Plaintiff's subjective reports of pain simply because the objective medical evidence did not independently support a finding of disability. (See R. 18). Plaintiff concedes that the ALJ followed the proper two-step framework, but did not consider the appropriate factors listed in SSR 96-7p. Nevertheless, given this case's remand for development of the record, the ALJ is necessarily required to reevaluate Plaintiff's credibility in light of any newly obtained evidence. See Rosa, 168 F.3d at 83.

16. After carefully examining the record, this Court finds cause to remand this case to the ALJ for further administrative proceedings consistent with this decision. Plaintiff's Motion for Judgement on the Pleadings is therefore granted. Defendant's Motion for Judgement on the Pleadings is denied.

IT HEREBY IS ORDERED, that Plaintiff's Motion for Judgment on the Pleadings (Docket No. 8) is GRANTED

FURTHER, that Defendant's Motion for Judgment on the Pleadings (Docket No. 10) is DENIED.

FURTHER, that this case is REMANDED to the Commissioner of Social Security for further proceedings consistent with this Decision and Order.

FURTHER, that the Clerk of Court is directed to CLOSE this case.

SO ORDERED.

11

Dyspnea, Orthopnea, and Paroxysmal Nocturnal Dyspnea

VASKAR MUKERJI

Definition

Dyspnea refers to the sensation of difficult or uncomfortable breathing. It is a subjective experience perceived and reported by an affected patient. Dyspnea on exertion (DOE) may occur normally, but is considered indicative of disease when it occurs at a level of activity that is usually well tolerated. Dyspnea should be differentiated from tachypnea, hyperventilation, and hyperpnea, which refer to respiratory variations regardless of the patients' subjective sensations. Tachypnea is an increase in the respiratory rate above normal; hyperventilation is increased minute ventilation relative to metabolic need, and hyperpnea is a disproportionate rise in minute ventilation relative to an increase in metabolic level. These conditions may not always be associated with dyspnea.

Orthopnea is the sensation of breathlessness in the recumbent position, relieved by sitting or standing. Paroxysmal nocturnal dyspnea (PND) is a sensation of shortness of breath that awakens the patient, often after 1 or 2 hours of sleep, and is usually relieved in the upright position.

Two uncommon types of breathlessness arc trepopnea and platypnea. Trepopnea is dyspnea that occurs in one lateral decubitus position as opposed to the other. Platypnea refers to breathlessness that occurs in the upright position and is relieved with recumbency.

Technique

A patient with dyspnea may say: "I feel short of breath," "I'm having difficulty breathing," "I can't catch my breath," "I feel like I'm suffocating." Because it is a subjective phenomenon, the perception of dyspnea and its interpretation vary from patient to patient. Begin with a nonleading question: Do you have any difficulty breathing? If the response is affirmative and dyspnea is established as a problem, it should be characterized in detail. When did it begin? Has the onset been sudden or insidious? Inquire about the frequency and duration of attacks. The conditions in which dyspnea occurs should be ascertained. Response to activity, emotional state, and change of body position should be noted. Ask about associated symptoms: chest pain, palpitations, wheezing, or coughing. Sometimes a nonproductive cough may be present as a "dyspnea equivalent." What other significant medical problems does the patient have, and what medications has he been taking? How much has he smoked?

Dyspnea on exertion is by no means always indicative of disease. Normal persons may feel dyspneic with strenuous exercise. The level of activity tolerated by any individual depends on such variables as age, sex, body weight, physical conditioning, attitude, and emotional motivation. Dyspnea on exertion would be abnormal if it occurred with activity that is normally well tolerated by the patient. It is helpful to ask if he has noticed any recent or progressive limitation in his ability to conduct specific tasks that he was able to perform without difficulty in the past (e.g., walking, climbing stairs, performing household chores). The degree of functional impairment can be assessed in this manner.

Additional questions should be aimed at ascertaining whether the patient has orthopnea or paroxysmal nocturnal dyspnea. Inquire about the number of pillows he uses under his head at night and whether he has ever had to sleep sitting up. Does he develop coughing or wheezing in the recumbent position? Did he ever wake up at night with shortness of breath? How long after lying down did the episode occur, and what did he do to relieve his distress? Characteristically, the patient with left ventricular failure sits up at bedside, dangles his feet, and refrains from ambulation or other activity that is likely to worsen his symptoms.

Basic Science

Spontaneous respiration is controlled by neural and chemical mechanisms. At rest, an average 70 kg person breathes 12 to 15 times a minute with a tidal volume of about 600 ml. A normal individual is not aware of his or her respiratory effort until ventilation is doubled, and dyspnea is not experienced until ventilation is tripled. An abnormally increased muscular effort is now needed for the process of inspiration and expiration. Because dyspnea is a subjective experience, it does not always correlate with the degree of physiologic alteration. Some patients may complain of severe breathlessness with relatively minor physiologic change; others may deny breathlessness even with marked cardiopulmonary deterioration.

There is no universal theory that explains the mechanism of dyspnea in all clinical situations. Campbell and Howell (1963) have formulated the "length-tension inappropriateness theory," which states that the basic defect in dyspnea is a mismatch between the pressure (tension) generated by respiratory muscles and the tidal volume (change of length) that results. Whenever such disparity occurs, the muscle spindles of the intercostal muscles transmit signals that bring the act of breathing to the conscious level. Additionally, juxtacapillary receptors (1-receptors), located in the alveolar interstitium and supplied by untnyelinated fibers of the vagus nerve, are stimulated by pulmonary congestion. This activates the Hering-Breuer reflex whereby inspiratory effort is terminated before full inspiration is achieved, re-suiting in rapid and shallow breathing. The J-receptors may be responsible for dyspnea in situations where pulmonary congestion occurs, such as with pulmonary edema. Other theories that have been proposed to explain dyspnea include acid—base imbalance, central nervous system mechanisms, decreased breathing reserve, increased work of breathing, increased transpulmonary pressure, fatigue of respiratory muscles, increased oxygen cost of breathing, dyssynergy of intercostal muscles and the diaphragm, and abnormal respiratory drive.

Orthopnea is caused by pulmonary congestion (luring recumbency. In the horizontal position there is redistribution of blood volume from the lower extremities and splanchnic beds to the lungs. In normal individuals this has little effect, but in patients in whom the additional volume cannot be pumped out by the left ventricle because of disease, there is a significant reduction in vital capacity and pulmonary compliance with resultant shortness of breath. Additionally, in patients with congestive heart failure the pulmonary circulation may already be overloaded, and there may be reabsorption of edema fluid from previously dependent parts of the body. Pulmonary congestion decreases when the patient assumes a more erect position, and this is accompanied by an improvement in symptoms.

Paroxysmal nocturnal dyspnea may be caused by mechanisms similar to those for orthopnea. The failing left ventricle is suddenly unable to match the output of a more normally functioning right ventricle; this results in pulmonary congestion. Additional mechanisms may be responsible in patients who experience paroxysmal nocturnal dyspnea only during sleep.'Theories include decreased responsiveness of the respiratory center in the brain and decreased adrenergic activity in the myocardium during sleep.

Dyspnea on exertion is caused by failure of the left ventricular output to rise during exercise with resultant increase in pulmonary venous pressure. In cardiac asthma, bronchospasm is associated with pulmonary congestion and is probably precipitated by the action of edema fluid in the bronchial walls on local receptors. Trepopnea may occur with asymmetric lung disease when the patient lies with the more affected lung down because of gravitational redistribution of blood flow. It has also been reported with heart disease when it is probably caused by distortion of the great vessels in one lateral decubitus position versus the other. Platypnea was originally described in chronic obstructive pulmonary disease and was attributed to an increased wasted ventilation ratio in the upright position. Platypnea in association with orthodeoxia (arterial deoxygenation in the upright position) has been reported in several forms of cyanotic congenital heart disease. It has been proposed that this is precipitated by a slight decrease in systemic blood pressure in the upright position, resulting in increased rightto-left shunting.

Clinical Significance

Dyspnea may be induced in four distinct settings: (1) increased ventilatory demand such as with exertion, febrile illness, hypoxic state, severe anemia, or metabolic acidosis; (2) decreased ventilatory capacity such as with pleural effusion, pneumothorax, intrathoracic mass, rib injury, or muscle weakness; (3) increased airway resistance such as with asthma or chronic obstructive pulmonary disease; and (4) decreased pulmonary compliance such as with interstitial fibrosis or pulmonary edema.

In early left ventricular failure, the cardiac output does not increase sufficiently in response to moderate exercise; tissue and cerebral acidosis occurs, and the patient experiences dyspnea on exertion. The shortness of breath may be accompanied by fatigue or a sensation of smothering or sternal compression. In the later stages of left ventricular failure, the pulmonary circulation remains congested, and dyspnea occurs with mild exertion. Moreover, the patient may develop orthopnea or paroxysmal nocturnal dyspnea. Acute pulmonary edema is the most dramatic manifestation of pulmonary venous overload and may occur in the setting of a recent myocardial infarction or in the last stage of chronic left ventricular failure. Cardiovascular causes of dyspnea include valvular diseases (particularly mitral stenosis and aortic insufficiency), paroxysmal arrhythmia (such as atrial fibrillation), pericardial effusion with tamponade, systemic or pulmonary hypertension, cardiomyopathy, and myocarditis. Unrestricted fluid intake or administration in a patient with oliguric renal failure is also likely to precipitate pulmonary congestion and dyspnea.

Pulmonary disease constitutes another major category of conditions producing dyspnea and is discussed in Chapter 36. Important pulmonary causes include bronchial asthma, chronic obstructive pulmonary disease, pulmonary embolism, pneumonia, pleural effusion, pneumothorax, allergic pneumonitis, and interstitial fibrosis. In addition, dyspnea may occur in febrile and hypoxic states and in association with some psychiatric conditions such as anxiety and panic disorder. Diabetic ketoacidosis seldom causes dypsnea but commonly induces slow, deep respirations termed Kussmaul breathing. Cerebral lesions or intracranial hemorrhage may be associated with intense hyperventilation and sometimes irregularly periodic breathing called Biot's respiration. Cerebral hypoperfusion from any cause may also result in alternating periods of hyperventilation and apnea called Cheyne-Stokes respiration, although no breathing difficulty may be perceived by the patient.

Diagnosis of the cause of dyspnea can be made relatively easily in the presence of other clinical signs of heart or lung disease. Difficulty is sometimes encountered in determining the precipitating cause of breathlessness in a patient with both cardiac and pulmonary conditions. An additional diagnostic problem may be the presence of anxiety or other emotional disorder. A careful history and physical examination are always helpful, and occasionally cardiac catheterization, pulmonary function studies, or other tests may be necessary.

References

Burki NK. Dyspnea. Clin Chest Med 1980;1:47-55.

Campbell EJM, Howell JBL. The sensation of breathlessness. Br Med Bull 1963;19:36-40,

Carrieri V, Janson-Bjerklie S. The sensation of dyspnea: a review. Heart and Lung 1984:13:436-447.

Fleming PR. Dyspnoea. In: Hart FD, ed. French's index of differential diagnosis. 12th ed. Bristol: Wright, 1985;216-26. Ganong WF. Respiratory adjustments in health and disease. In:

Review of medical physiology, 12th ed. Los Altos: Lange Medical Publications, 1985;558-71.

Rappaport E. Dyspnea: pathophysiology and differential diagnosis. Prog Cardiovasc Dis 1971;13:532-45.

Rees Pi, Clark ITC Paroxysmal nocturnal dyspnea and periodic respiration. Lancet 1979;2:1315-17.

Seward J, IIayes DL, Smith HC, et al. Platypnea—orthodeoxia: clinical profile, diagnostic workup, management, and report of seven cases. Mayo Clin Proc. 1984;59:221-31.

Zack MI3, Pontoppidan H, Kazemi H. The effect of lateral positions on gas exchange in pulmonary disease. Am Rev Respir Dis 1974;110:49-55.

Diseases and Conditions

Myocardial ischemia

By Mayo Clinic Staff

Myocardial ischemia occurs when blood flow to your heart is reduced, preventing it from receiving enough oxygen. The reduced blood flow is usually the result of a partial or complete blockage of your heart's arteries (coronary arteries).

Myocardial ischemia, also called cardiac ischemia, can damage your heart muscle, reducing its ability to pump efficiently. A sudden, severe blockage of a coronary artery can lead to a heart attack. Myocardial ischemia might also cause serious abnormal heart rhythms.

Treatment for myocardial ischemia involves improving blood flow to the heart muscle. Treatment may include medications, a procedure to open blocked arteries or bypass surgery.

Making heart-healthy lifestyle choices is important in treating and preventing myocardial ischemia.

Some people who have ischemia don't experience any signs or symptoms (silent ischemia).

When signs and symptoms occur, the most common is chest pressure or pain, typically on the left side of the body (angina pectoris). Other signs and symptoms — which might be experienced more commonly by women, older people and people with diabetes — include:

When to see a doctor

Seek emergency care if you have prolonged or severe chest pain.

Myocardial ischemia occurs when the blood flow through one or more of your coronary arteries is decreased. The low blood flow decreases the amount of oxygen your heart muscle receives.

Myocardial ischemia can develop slowly as arteries become blocked over time. Or it can occur quickly when an artery becomes blocked suddenly.

Conditions that can cause myocardial ischemia include:

Chest pain associated with myocardial ischemia can be triggered by:

Factors that can increase your risk of developing myocardial ischemia include:

Myocardial ischemia can lead to serious complications, including:

If you are experiencing chest pain, you likely will be examined and treated in the emergency room.

If you don't have chest pain but are experiencing other symptoms, or are concerned about your risk of myocardial ischemia, you might be referred to a heart specialist (cardiologist).

What you can do

Questions to ask your doctor

In addition to the questions that you've prepared to ask your doctor, don't hesitate to ask other questions during your appointment.

What to expect from your doctor

Your doctor is likely to ask you a number of questions. Being ready to answer them may leave time to go over points you want to spend more time on. You may be asked:

Your doctor will start with a medical history and physical exam. After that, your doctor mighr recommend:

Treatment of myocardial ischemia is directed at improving blood flow to the heart muscle. Depending on the severity of your condition, you may be treated with medications, surgery or both.

Medications

Medications to treat myocardial ischemia include:

Procedures to improve blood flow Sometimes, more-aggressive treatment is needed to improve blood flow. Procedures that may help include:

To follow a heart-healthy lifestyle:

It's important to have regular medical checkups. Some of the main risk factors for myocardial ischemia — high cholesterol, high blood pressure and diabetes — have no symptoms in the early stages. Early detection and treatment can set the stage for a lifetime of better heart health.

The same lifestyle habits that can help treat myocardial ischemia can also help prevent it from developing in the first place. Leading a heart-healthy lifestyle can help keep your arteries strong, elastic and smooth, and allow for maximum blood flow.

References

1. Mann DL, et al. Approach to the patient with chest pain. In: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 10th ed. Philadelphia, Pa.: Saunders Elsevier; —.

2. Podrid PJ. Angina pectoris: Chest pain caused by myocardial ischemia. www.uptodate.com/home. Accessed June 1, 2015.

3. Deedwania PC. Silent myocardial ischemia: Epidemiology and pathogenesis. www.uptodate.com/home. Accessed June 1, 2015.

4. Mann DL, et al. Coronary blood flow and myocardial ischemia. In: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 10th ed. Philadelphia, Pa.: Saunders Elsevier; —.

5. Kannam JP. Stable ischemic heart disease: Overview of care. www.uptodate.com/home. Accessed June 2, 2015.

6. Jhamnani S, et al. Meta-analysis of the effects of lifestyle modifications on coronary and carotid artherosclerotic burden. American Journal of Cardiology. 2015;115:268.

7. Sandesara PB, et al. Cardiac rehabilitation and risk reduction: Time to "rebrand and reinvigorate." Journal of the American College of Cardiology. 2015;65:389.

8. Goldberger AL. Electrocardiogram in the diagnosis of myocardial ischemia and infarction. www.uptodate.com/home. Accessed June 1, 2015.

9. AskMayoExpert. How is chest pain due to coronary artery spasm diagnosed? Rochester, Minn.: Mayo Foundation for Medical Education and Research; 2015.

10. Johnson RJ. Nonpharmacologic prevention and treatment of hypertension. In: Comprehensive Clinical Nephrology. 5th ed. Philadelphia, Pa.: Saunders Elsevier; 2015. https://www.clinicalkey.com. Accessed May 11, 2015.

11. Deedwania PC. Silent myocardial ischemia: Prognosis and therapy. www.uptodate.com/home. Accessed June 1, 2015.

12. Deedwania PC. Silent myocardial ischemia: Diagnosis. www.uptodate.com/home. Accessed June 1, 2015.

13. AskMayoExpert. Which patients with coronary artery disease (CAD) should be considered for angiography and revascularization? Rochester, Minn.: Mayo Foundation for Medical Education and Research; —.

14. Bope ET, et al. The cardiovascular system. In: Conn's Current Therapy 2015. Philadelphia, Pa.: Saunders Elsevier; 2015.

15. Simons M, et al. New therapies for angina pectoris. www.uptodate.com/home. Accessed July 6, 2015.

July 25, 2015

Original article: http://www.mayoclinic.org/diseases-conditions/myocardial-ischemia/basics/definition/con-20035096

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