Y93ICD-10-CM Code for Activity codes Y93.
Y93.01ICD-10 code Y93. 01 for Activity, walking, marching and hiking is a medical classification as listed by WHO under the range - External causes of morbidity .
Resistant hypertension has been designated as 997.91 in the ICD‐9 codes.
Z72. 3 is a billable/specific ICD-10-CM code that can be used to indicate a diagnosis for reimbursement purposes. The 2022 edition of ICD-10-CM Z72.
Y93.9ICD-10 code Y93. 9 for Activity, unspecified is a medical classification as listed by WHO under the range - External causes of morbidity .
ICD-10 code X50 for Overexertion and strenuous or repetitive movements is a medical classification as listed by WHO under the range - Other external causes of accidental injury .
Resistant hypertension is defined as a blood pressure that remains above goal despite concurrent use of three antihypertensive agents of different classes taken at maximally tolerated doses, one of which should be a diuretic (the diuretic should be selected based upon kidney function) [1-5].
Resistant hypertension is high blood pressure that does not respond well to aggressive medical treatment. Hypertension is considered resistant when all of the following are true: Someone is taking three* different blood pressure medications at their maximally tolerated doses.
In ICD-10, the diagnosis codes are simplified and the hypertension table is no longer necessary. The concept of controlled and uncontrolled are not a part of the coding choice, although good clinical documentation should include the status of the patient and the type of hypertension being treated.
Z71.82Z71. 82 Exercise counseling - ICD-10-CM Diagnosis Codes.
Exercise intolerance is the reduced ability of the heart to perform activities that involve strenuous movement of your body. It happens when your responses to exercise don't achieve age and gender-appropriate levels. It's associated with heart disease because the heart fails to pump blood properly when exercising.
Other specified counselingICD-10 code Z71. 89 for Other specified counseling is a medical classification as listed by WHO under the range - Factors influencing health status and contact with health services .
Uncontrolled hypertension is not synonymous with resistant hypertension. The former includes patients who lack blood pressure control secondary to poor adherence and/or an inadequate treatment regimen, as well as those with true treatment resistance.
Refractory hypertension is defined as uncontrolled blood pressure despite use of ≥5 antihypertensive agents of different classes, including a long-acting thiazide-like diuretic and an MR (mineralocorticoid receptor) antagonist, at maximal or maximally tolerated doses.
Postoperative hypertension (arbitrarily defined as systolic BP ≥190 mm Hg and/or diastolic BP 100 mm Hg on 2 consecutive readings following surgery) (Plets 1989; Chobanian et al 2003b) may have significant adverse sequelae in both cardiac and noncardiac patients.
ICD-Code I10 is a billable ICD-10 code used for healthcare diagnosis reimbursement of Essential (Primary) Hypertension.
The 2022 edition of ICD-10-CM R03.0 became effective on October 1, 2021.
R03.0 is not usually sufficient justification for admission to an acute care hospital when used a principal diagnosis.
A hypertensive crisis is a severe increase in blood pressure that can lead to stroke, organ damage, heart attack, and more. The Mayo Clinic defines extreme high blood pressure as “a top number (systolic pressure) of 180 millimeters of mercury (mm Hg) or higher or a bottom number (diastolic pressure) of 120 mm Hg or higher.”.
Hypertensive Emergency. If your blood pressure reading is 180/120 or greater and you are experiencing any other associated symptoms of target organ damage such as chest pain, shortness of breath, back pain, numbness/weakness, change in vision, or difficulty speaking then this would be considered a hypertensive emergency.
If your blood pressure is 180/120 or greater, wait about five minutes and try again. If the second reading is just as high and you are not experiencing any other associated symptoms of target organ damage such as chest pain, shortness of breath, back pain, numbness/weakness, change in vision, or difficulty speaking, ...
John Verhovshek, MA, CPC, is a contributing editor at AAPC. He has been covering medical coding and billing, healthcare policy, and the business of medicine since 1999. He is an alumnus of York College of Pennsylvania and Clemson University.
From a mechanistic point of view, a HRE can be explained by impairment of exercise induced endothelial vasodilation [ 9, 10 ]. Endothelium-dependent vasodilation in conduit arteries occurs in response to systolic wall sheer stress during exercise. Impaired endothelial function may limit vasodilation in response to increased shear stress from exercise, therefore, result in HRE. Indeed, Wilson et al. [ 11] showed significantly higher peripheral resistance at all stages of exercise observed in normotensive individuals with HRE. Consistent with previous studies, Stewart et al. [ 10] demonstrated an independent correlation between flow mediated dilation and exercise BP in normotensive population, suggesting that impaired endothelial vasodilation may contribute to exercise hypertension. Reduced nitric oxide (NO) activity was demonstrated in patients with HRE, even in young subjects without overt cardiovascular risk factors [ 12 ].
During exercise, sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS) play an important role, mediating heart rate and BP increments in normal healthy population [ 11, 14, 15 ]. We have demonstrated that augmented rise of angiotensin II during exercise in individuals with HRE when compared to age and gender matched control group with normal BP reactivity during exercise [ 1 ]. Plasma epinephrine and norepinephrine also increased in both groups of individuals with HRE or normal response during exercise. However, there was no significant difference between two groups. Augmented rise in angiotensin II in HRE group was consistently reproduced in following studies, although extents of increased levels were not the same, possibly due to different magnitude of exercise and sensitivity of measurements [ 12 ]. Importance of angiotensin II in HRE is also evidenced by a significant reduction of peak systolic BP during exercise with angiotensin II receptor blocker [ 16 ].
A HRE is pathologic phenomenon and associated with functional and structural impairment of LV, future development of hypertension and increased cardiovascular event, although conflicting data exist due to diverse reponses to central hemodynamics, various methodologies, and different clinical characteristics of study population. Further consensus on definition and method to measure HRE may provide insightful information to clinicians.
Theoretically, individuals with HRE would be exposed to abnormally high pressure loads to left ventricle (LV), which may result in global subendocardial ischemia due to mismatch between demand and supply from excessive rate-pressure stress. Indeed, a previous study demonstrated a greater likelihood of new or worsening abnormalities of wall motions from echocardiography in individuals with HRE, even in the absence of angiographically significant coronary artery stenosis [ 19 ].
A HRE is generally conceived as a risk for future development of hypertension, evidenced by a substantial number of previous studies with either bicycle or treadmill exercise [ 11, 26 ]. Systolic BP measured during light to moderate exercise is shown to predict masked hypertension with high specificity in individuals with HRE [ 27 ]. However, current guideline does not recommend exercise testing as a screen test for prehypertension given the low predictive value [ 28 ]. A previous meta-analysis revealed that a HRE at moderate exercise workload increased cardiovascular outcomes (fatal or non-fatal myocardial infarction, stroke, or development of coronary artery disease) by 36 % (95 % CI, 1.02-1.38, p = 0.039) after adjustment for other cardiovascular risk factors [ 29 ]. In this study, every 10 mmHg increase in systolic BP during exercise at moderate intensity was accompanied by a 4 % increase in cardiovascular event and mortality independent of mode of exercise. It is interesting that prognostic value of BP during high work load was not as influential as BP during moderate work load. Although future studies are warranted, submaximal workload may better reflect daily ambulatory BP of participants, therefore, clinically more relevant than BP during high work load. Also, difficulties in measuring BP during high work load may have attributed to such results.
As supported by previous studies, a HRE is not a benign phenomenon, however, currently, whether to treat a HRE is controversial with uncertain treatment strategy. Considering underlying mechanisms, angiotensin receptor blockers and beta blockers can be suggested in individuals with HRE, however, evidences for efficacy and outcomes of treatment ...
Many of previous studies demonstrated increased LV mass index and stiffness in HRE, evidenced by higher prevalence of LV hypertrophy and diastolic dysfunction from echocardiography [ 20 – 22 ]. However, it should be noted that some studies reported conflicting data, insisting that a HRE is not accompanied with diastolic dysfunction or LV remodeling compared to those with normal response to exercise [ 1, 23, 24 ].