text:
The William Root House Museum and Garden is one of the oldest surviving houses in Marietta. The museum features a glimpse of life for a typical middle class Georgia family in 1850.
Built in 1845 by early settlers Hannah and William Root, the Root House is one of just a few buildings that survived Sherman’s Atlanta Campaign. The house used as a single-family residence until the 1940’s when it was divided into apartments.
By the late 1980’s, the house was in disrepair and scheduled for demolition. When it was found to be one of the oldest buildings in Marietta, it was purchased by the Cobb Landmarks and Historical Society and restored to it’s 1845 appearance.
Every room in the Root House contains authentic period pieces, allowing visitors to learn the story of the Root family and life in Civil War era Georgia. The tour includes opportunities to touch some of the historic artifacts and play 19th century games, as well as use modern electronic tablets to view historic records, family photos, and more.
Stepping outside, visitors can see the recreated kitchen that includes a working 1850s cook-stove and a garden that features flower beds and vegetables that were available in the area before 1860.
Tours at 11:30, 12:30, 1:30, and 2:30.
For more information, please call (770) 426-4982 or visit RootHouseMuseum.com.

lowercased:
the william root house museum and garden is one of the oldest surviving houses in marietta. the museum features a glimpse of life for a typical middle class georgia family in 1850.
built in 1845 by early settlers hannah and william root, the root house is one of just a few buildings that survived sherman’s atlanta campaign. the house used as a single-family residence until the 1940’s when it was divided into apartments.
by the late 1980’s, the house was in disrepair and scheduled for demolition. when it was found to be one of the oldest buildings in marietta, it was purchased by the cobb landmarks and historical society and restored to it’s 1845 appearance.
every room in the root house contains authentic period pieces, allowing visitors to learn the story of the root family and life in civil war era georgia. the tour includes opportunities to touch some of the historic artifacts and play 19th century games, as well as use modern electronic tablets to view historic records, family photos, and more.
stepping outside, visitors can see the recreated kitchen that includes a working 1850s cook-stove and a garden that features flower beds and vegetables that were available in the area before 1860.
tours at 11:30, 12:30, 1:30, and 2:30.
for more information, please call (770) 426-4982 or visit roothousemuseum.com.


text:
I. Causes of Heart Failure: What every physician needs to know.
Heart failure (HF) is a clinical syndrome in which the heart is unable to provide sufficient blood flow to meet the metabolic needs of the body, or is only able to do so with significantly increased intracardiac filling pressure. However, this is a somewhat older definition, and many people now define heart failure as a clinical syndrome where there is structural heart disease and impaired function.
Heart failure is often referred to as congestive heart failure (CHF). Many experts believe that the term “congestion” does not uniformly apply to all patients, and the syndrome is often referred to as “heart failure” in more contemporary times.
Heart failure is most often characterized as systolic, if ejection fraction (EF) is decreased, and diastolic, if ejection fraction is preserved. “Diastolic” heart failure is also often called heart failure with preserved ejection fraction (HFPEF) or heart failure with preserved systolic function (HFPSF).
Systolic heart failure is often due to damage to the heart, such as ischemia or alcohol exposure. Diastolic heart failure is often due to longstanding hypertension or intracardiac infiltration such as with amyloid protein, which “stiffens” both ventricles. It is not usually possible to distinguish systolic from diastolic heart failure based on signs and symptoms alone, as both share substantial clinical features.
II. Diagnostic Confirmation: Are you sure your patient has Heart Failure?
Heart failure is diagnosed at the bedside using history and physical findings. There is no absolute laboratory test for the diagnosis of heart failure.
A characteristic history includes exertional dyspnea, fatigue, and edema. Physical exam would be notable for volume overload (jugular venous distention, dependent edema), S3 gallop, and often pulmonary rales.
However, it is important to note that the absence of rales does not exclude heart failure, as the lymphatic system can provide substantial compensation, particularly in patients with chronic heart failure. Pulmonary congestion is typically evident on chest radiography.
Plasma brain natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP) levels are typically elevated, although renal failure and obesity are commonly recognized confounders. The hallmark laboratory exam of heart failure is an echocardiogram.
The presence of a decreased EF is sufficient to give a diagnosis of systolic heart failure; other modalities such as gated nuclear myocardial perfusion imaging, magnetic resonance imaging (MRI), or gated computed tomography (CT) are also able to determine EF.
Diastolic heart failure is diagnosed in the presence of the clinical syndrome of heart failure with preserved EF. Efforts should be made to determine the etiology of heart failure.
Exertional dyspnea and fatigue are virtually universal. Volume overload is usually found, but in the modern era of powerful loop diuretics, some patients do not manifest fluid overload.
Nocturnal symptoms such as orthopnea and/or paroxysmal nocturnal dyspnea (PND) are also highly suggestive of heart failure. Abdominal discomfort or fullness is also a frequently reported symptom. Patients with well-compensated heart failure may have minimal symptoms and no evidence of volume overload. Characteristics of end-stage heart failure may include cachexia and Cheyne-Stokes respirations.
Approximately half of patients with heart failure have systolic failure and the other half have diastolic heart failure. Some have features of both types. Heart failure is perhaps more common in men and in those who identify as black racially.
Risk increases with age. Regardless, the most important risk factors for developing heart failure on a population basis are hypertension, myocardial infarction, and diabetes.
The majority of diastolic heart failure is a result of longstanding hypertension, and this phenotype of heart failure is more common in women. Infiltrative diseases, such as amyloidosis and hemochromatosis, also typically lead to diastolic heart failure, often with restrictive physiology.
Prior chest radiation is another potential cause of diastolic heart failure, and the incidence may increase as prolonged cancer survivorship increases. Once patients are hospitalized with diastolic heart failure, the prognosis is approximately the same as systolic heart failure.
Hypertension and diabetes also increase the risk of systolic heart failure through the increased risk of coronary artery disease and myocardial infarctions. Thus efforts to minimize coronary artery disease would be anticipated to have substantial impact on risk of developing heart failure.
The causes of systolic heart failure are myriad, including coronary artery disease, genetic or familial, viral (including HIV), idiopathic, valvular, inflammatory (myocarditis, sarcoidosis), thyroid disease, tachycardia-mediated (often from previously unrecognized atrial fibrillation), stress-induced (also known as Takotsubo cardiomyopathy), nutritional deficiency (such as thiamine or selenium), systemic myopathies (such as muscular dystrophies), and peripartum cardiomyopathy.
Alcohol, cocaine, methamphetamines, anthracyclines, some antirheumatic medications (such as hydroxychloroquine) and tyrosine kinase inhibitors are common toxic causes of heart failure, which are typically identified through patient history.
Common alternative causes of volume overload include renal failure, liver failure, and hypoalbuminemia. Common alternative causes of exertional breathlessness are chronic obstructive pulmonary disease (COPD), pulmonary embolism (PE), and pneumonia. Coronary artery disease also may present with a dyspnea-predominant phenotype, rather than chest pain, as is classically expected.
Evaluation of the central venous pressure is of the utmost importance.
Profoundly low cardiac output states may be characterized by hypotension and/or narrow pulse pressure along with cool or mottled skin.
Sinus tachycardia is common but may be compensatory.
Chest x-ray (CXR) and EKG are essential in the evaluation of a patient with suspected heart failure. Beyond providing information supporting the diagnosis of heart failure, these diagnostic tests often provide an alternative diagnosis (atrial fibrillation, pneumonia, lung mass, etc.) that implies heart failure may not be the key diagnosis.
Echocardiogram is also essential and will provide substantial information about the size, structure, and function of the heart. MRI, which provides detailed information on the myocardium, should be considered.
MRI can provide strong, noninvasive evidence of etiology in many cases, such as prior infarction, myocarditis, hypertrophic cardiomyopathy, left ventricular noncompaction, stress or “Takotsubo” cardiomyopathy, amyloidosis, sarcoidosis, or hemochromatosis, for example. Positron emission tomography (PET) can also be used to diagnose cardiac sarcoidosis.
Endomyocardial biopsy should be considered in highly select circumstances, such as suspicion of myocarditis. Biopsy also has a role in defining the subtype of amyloid cardiomyopathy (e.g., transthyretin versus amyloid light-chain (AL)). Patients with a family history of cardiomyopathy should be offered the option of referral for genetic counseling and testing.
BNP (or NT-proBNP) should be considered, particularly if other causes of dyspnea such as COPD are being considered if there is doubt about the diagnosis. Very low levels virtually exclude heart failure, but can be confounded by obesity.
Elevated levels can be seen in renal failure without substantial heart failure, but at least suggest volume overload. Elevated BNP in the absence of renal failure is strongly suggestive of heart failure, but BNP levels are increased with age.
Basic metabolic parameters including renal and hepatic function should be measured. Renal dysfunction may be a seen as a result of low cardiac output or elevated venous filling pressure.
Hepatic parameters (ALT, AST, total bilirubin) and international normalized ratio (INR) may be elevated as a consequence of hepatic congestion. Serum albumin is helpful in excluding malnutrition as an alternative explanation for peripheral edema.
Minor elevations in troponin are characteristic of heart failure exacerbation, but typically do not rise and fall as in acute coronary syndrome; myocarditis should be considered if troponin is substantially elevated. Inflammatory markers such as C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) would also be typically elevated in myocarditis, but are not diagnostic if elevated. Anemia (hemoglobin or hematocrit) and gout (uric acid) and are also frequent comorbidities to consider.
Additional testing to establish the etiology of heart failure should be considered and may include: HIV, ferritin (hemochromatosis), thyroid-stimulating hormone, and serum free light chains (amyloid), for example. Testing for specific viruses other than HIV is not routinely performed, but Coxsackie, Epstein-Barr, and varicella zoster could be considered. Exclusion of connective tissue disease with antinuclear antibodies (ANA) is also often performed.
CXR film (Figure 1) may show cardiomegaly, but the absence does not exclude heart failure. Pulmonary edema is an important finding, but can be confused with pneumonitis or other causes of diffuse infiltrates. Accompanying findings such as pleural effusions may be helpful in interpretation.
Chest x-ray film demonstrating cardiomegaly and pulmonary edema.
An echocardiogram will provide size; structural detail, including evaluation of valves; and myocardial function, including EF and presence of absence of regional wall motion abnormalities. This is the most important test when considering heart failure as a diagnosis.
Abdominal ultrasound may demonstrate hepatomegaly and/or ascites, although these findings are often evident on exam and thus are not routinely indicated.
The hallmarks of treatment of diastolic heart failure are control of congestion, heart rate in the presence of atrial fibrillation to increase ventricular filling time, and control of systolic blood pressure. The majority of evidence on the treatment of heart failure has been for systolic heart failure, and is thus the focus of the remainder of this section.
There are three “to do’s” in the management of heart failure: (1) control congestion, (2) provide neurohormonal antagonists, and (3) consider sudden cardiac death prevention and cardiac resynchronization therapy (CRT). Since congestion causes most symptoms, this should be prioritized.
Congestion control is achieved with sodium and sometimes (if there is hyponatremia) moderate fluid restriction; most patients need loop diuretics. Congestion is managed the same for systolic and diastolic heart failure.
Second, neurohormonal antagonists (angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB), beta-blockers, aldosterone antagonists, and vasodilators in select populations) are critical for the treatment of systolic heart failure and should be initiated. Although it is critical to use the drugs and doses that were found to be effective in landmark clinical trials, very few patients will tolerate initiation of full doses of these medications, and a period of uptitration over several weeks to months should be anticipated.
There is no consensus regarding whether beta-blockers or ACEI/ARB should be initiated first, and beta-blockers should be avoided in the setting of cardiogenic shock, severe bradycardia, complete heart block, or bronchospasm. Studies of neurohormonal antagonists for diastolic heart failure have been disappointing, but neurohormonal antagonists are still often used for their antihypertensive effect, and their safety in this population is well-established.
Although there is no mortality benefit, digoxin has been noted to improve symptoms and reduce the risk of hospitalization. Finally, consideration should be given to “electrical therapy,” which consists of CRT (if QRS >130 ms) and sudden cardiac death prevention with an implantable cardioverter-defibrillator (ICD).
The risk of sudden cardiac death is much higher with an EF <35%, and in the absence of contraindications such as life expectancy less than 1 year, electrical therapy should be considered. Patients should be receiving optimal medical therapy for at least 3 months before implanting an ICD.
Wearable external defibrillators are sometimes used during the period of medical uptitration to permit reevaluation of EF; a sizable fraction of patients will improve on medical therapy to the point that an implantable ICD is not indicated.
Patients who are unable to tolerate medical therapy or experience progression despite these therapies suggest a very poor prognosis and may be considered for advanced options, such as mechanical circulatory support (MCS, also known as ventricular assist device or VAD) or heart transplant.
ACEI/ARB and beta-blockers are both initiated at minimal dose, but uptitration of ACEI/ARB is typically prioritized, as full dose can typically be achieved more quickly. Beta-blocker dose is then increased every 1 to 2 weeks to the maximally tolerated dose. Timing of the introduction of aldosterone antagonist is individualized based on need for diuretics and potassium supplementation, and often deferred to prioritize ACEI/ARB and beta-blockers.
Administration of diuretics is the hallmark of emergency treatment of heart failure and most patients respond promptly. Inadequate response should precipitate rapid escalation of a diuretic dose.
A common rule of thumb is to double an ineffective dose. Consideration should be given to vasodilators if systemic blood pressure is adequate (e.g., mean arterial pressure greater than 70 to 75 mm Hg). In the event of hypotension or cardiogenic shock, initiation of inotropes, such as dobutamine and/or dopamine, may be necessary. Noninvasive positive pressure ventilation is an option and mechanical support such as an intraaortic balloon pump may also be indicated.
In addition to evaluation of symptomatic response, physical exam findings that should be monitored while providing treatment for heart failure include frequent evaluation of jugular venous pressure and vital signs, with particular attention to blood pressure and heart rate. Sinus tachycardia is often a compensatory response and improvement is thought to represent a favorable response to treatment.
Serial examinations should also focus attention on the presence of absence of S3/S4, liver span, presence or absence of ascites, and degree and distribution of edema. Urine output should also be monitored, as this provides the most direct measure of pace of decongestion and also indicates adequate (or not) renal perfusion.
Basic metabolic panels are typically performed shortly after initiation of therapy (at least daily while hospitalized), to monitor renal function and ensure that diuretics are not causing dangerous perturbations in serum potassium levels. Following initiation of aldosterone antagonists, more frequent monitoring of potassium is indicated.
A commonly used strategy is 1 week after initiation or dose increase, and then again at 1 month. Once a stable medication regimen has been established, routine intermittent testing in heart failure patients is not typically performed. There is some data to suggest that BNP levels may be used to guide therapy.
Maintaining patients with heart failure on maximally tolerated doses of neurohormonal antagonists (ACEI/ARB, beta-blockers, aldosterone antagonists) are critical to minimizing risk of disease progression, symptomatic decompensation, hospitalization, and mortality. Application of CRT when indicated has also been shown to improve outcomes, and should be periodically reconsidered, as patient status or criteria for implant may change over time.
Education on salt avoidance, the role of fluid restriction, and self-care including daily weight monitoring are all important to reduce burden of disease and avoid hospitalization. Over time, it is not uncommon for patients with heart failure to become intolerant to maximal doses of medical therapy.
The need to decrease the doses of medications is a predictor of adverse outcome, and may be an appropriate time to consider evaluation for advanced options. For patients with end-stage disease, palliative care and/or hospice may be appropriate, and deactivation of ICD may be considered.
Digoxin is sometimes used in patients with atrial fibrillation and heart failure with insufficient rate control. Typical dose is 62.5 to 250 mcg daily.
Concurrent anemia: Treatment may improve heart failure symptoms.
Concurrent arrhythmias: Consider the role that uncontrolled arrhythmias may have on heart failure exacerbation. Improved control of atrial fibrillation or premature ventricular contractions (PVCs) may improve symptoms. Many antiarrhythmics are contraindicated in severe heart failure.
Concurrent chronic kidney disease: Continue ACEI/ARB if possible, but if necessary to discontinue, replace with isosorbide/hydralazine combination. May contribute to anemia. Aldosterone antagonists have a substantially increased risk of hyperkalemia.
Concurrent diabetes: Avoid thiazolidinediones (TZDs) in all heart failure patients and metformin if there is significant renal dysfunction.
Concurrent gout: It is likely that diuretic dosing will need to be increased if a gout flareup is treated with steroids.
Concurrent liver disease: Liver congestion is common and may result in the need to alter dose of medications metabolized by the liver.
Concurrent prostatic hypertrophy: Alpha blockers should be avoided, as they have been shown to increase mortality in heart failure patients.
Concurrent sleep apnea: Should be treated aggressively to minimize neurohormonal activation.
Aldosterone antagonists should not be used in patients with underlying chronic kidney disease.
Consider use of the Seattle Heart Failure Model or the Heart Failure Survival Score for estimating a patient’s prognosis.
Consider referral to dietitian to augment teaching on importance of low-salt diet.
Weigh yourself at the same time every day and record the result. Report increases of more than 3 lb in a day or 5 lb in a week to your doctor; however, not all decompensations are preceded by antecedent weight gain.
Avoid sodium intake and strive to keep less than 2,000 mg daily.
Take your medications as prescribed every day.
Report changes in symptoms promptly.
“2009 Focused update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and management of heart failure in adults: A report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines. Developed in collaboration with the International Society for Heart and Lung Transplantation”.

lowercased:
i. causes of heart failure: what every physician needs to know.
heart failure (hf) is a clinical syndrome in which the heart is unable to provide sufficient blood flow to meet the metabolic needs of the body, or is only able to do so with significantly increased intracardiac filling pressure. however, this is a somewhat older definition, and many people now define heart failure as a clinical syndrome where there is structural heart disease and impaired function.
heart failure is often referred to as congestive heart failure (chf). many experts believe that the term “congestion” does not uniformly apply to all patients, and the syndrome is often referred to as “heart failure” in more contemporary times.
heart failure is most often characterized as systolic, if ejection fraction (ef) is decreased, and diastolic, if ejection fraction is preserved. “diastolic” heart failure is also often called heart failure with preserved ejection fraction (hfpef) or heart failure with preserved systolic function (hfpsf).
systolic heart failure is often due to damage to the heart, such as ischemia or alcohol exposure. diastolic heart failure is often due to longstanding hypertension or intracardiac infiltration such as with amyloid protein, which “stiffens” both ventricles. it is not usually possible to distinguish systolic from diastolic heart failure based on signs and symptoms alone, as both share substantial clinical features.
ii. diagnostic confirmation: are you sure your patient has heart failure?
heart failure is diagnosed at the bedside using history and physical findings. there is no absolute laboratory test for the diagnosis of heart failure.
a characteristic history includes exertional dyspnea, fatigue, and edema. physical exam would be notable for volume overload (jugular venous distention, dependent edema), s3 gallop, and often pulmonary rales.
however, it is important to note that the absence of rales does not exclude heart failure, as the lymphatic system can provide substantial compensation, particularly in patients with chronic heart failure. pulmonary congestion is typically evident on chest radiography.
plasma brain natriuretic peptide (bnp) or n-terminal pro-bnp (nt-probnp) levels are typically elevated, although renal failure and obesity are commonly recognized confounders. the hallmark laboratory exam of heart failure is an echocardiogram.
the presence of a decreased ef is sufficient to give a diagnosis of systolic heart failure; other modalities such as gated nuclear myocardial perfusion imaging, magnetic resonance imaging (mri), or gated computed tomography (ct) are also able to determine ef.
diastolic heart failure is diagnosed in the presence of the clinical syndrome of heart failure with preserved ef. efforts should be made to determine the etiology of heart failure.
exertional dyspnea and fatigue are virtually universal. volume overload is usually found, but in the modern era of powerful loop diuretics, some patients do not manifest fluid overload.
nocturnal symptoms such as orthopnea and/or paroxysmal nocturnal dyspnea (pnd) are also highly suggestive of heart failure. abdominal discomfort or fullness is also a frequently reported symptom. patients with well-compensated heart failure may have minimal symptoms and no evidence of volume overload. characteristics of end-stage heart failure may include cachexia and cheyne-stokes respirations.
approximately half of patients with heart failure have systolic failure and the other half have diastolic heart failure. some have features of both types. heart failure is perhaps more common in men and in those who identify as black racially.
risk increases with age. regardless, the most important risk factors for developing heart failure on a population basis are hypertension, myocardial infarction, and diabetes.
the majority of diastolic heart failure is a result of longstanding hypertension, and this phenotype of heart failure is more common in women. infiltrative diseases, such as amyloidosis and hemochromatosis, also typically lead to diastolic heart failure, often with restrictive physiology.
prior chest radiation is another potential cause of diastolic heart failure, and the incidence may increase as prolonged cancer survivorship increases. once patients are hospitalized with diastolic heart failure, the prognosis is approximately the same as systolic heart failure.
hypertension and diabetes also increase the risk of systolic heart failure through the increased risk of coronary artery disease and myocardial infarctions. thus efforts to minimize coronary artery disease would be anticipated to have substantial impact on risk of developing heart failure.
the causes of systolic heart failure are myriad, including coronary artery disease, genetic or familial, viral (including hiv), idiopathic, valvular, inflammatory (myocarditis, sarcoidosis), thyroid disease, tachycardia-mediated (often from previously unrecognized atrial fibrillation), stress-induced (also known as takotsubo cardiomyopathy), nutritional deficiency (such as thiamine or selenium), systemic myopathies (such as muscular dystrophies), and peripartum cardiomyopathy.
alcohol, cocaine, methamphetamines, anthracyclines, some antirheumatic medications (such as hydroxychloroquine) and tyrosine kinase inhibitors are common toxic causes of heart failure, which are typically identified through patient history.
common alternative causes of volume overload include renal failure, liver failure, and hypoalbuminemia. common alternative causes of exertional breathlessness are chronic obstructive pulmonary disease (copd), pulmonary embolism (pe), and pneumonia. coronary artery disease also may present with a dyspnea-predominant phenotype, rather than chest pain, as is classically expected.
evaluation of the central venous pressure is of the utmost importance.
profoundly low cardiac output states may be characterized by hypotension and/or narrow pulse pressure along with cool or mottled skin.
sinus tachycardia is common but may be compensatory.
chest x-ray (cxr) and ekg are essential in the evaluation of a patient with suspected heart failure. beyond providing information supporting the diagnosis of heart failure, these diagnostic tests often provide an alternative diagnosis (atrial fibrillation, pneumonia, lung mass, etc.) that implies heart failure may not be the key diagnosis.
echocardiogram is also essential and will provide substantial information about the size, structure, and function of the heart. mri, which provides detailed information on the myocardium, should be considered.
mri can provide strong, noninvasive evidence of etiology in many cases, such as prior infarction, myocarditis, hypertrophic cardiomyopathy, left ventricular noncompaction, stress or “takotsubo” cardiomyopathy, amyloidosis, sarcoidosis, or hemochromatosis, for example. positron emission tomography (pet) can also be used to diagnose cardiac sarcoidosis.
endomyocardial biopsy should be considered in highly select circumstances, such as suspicion of myocarditis. biopsy also has a role in defining the subtype of amyloid cardiomyopathy (e.g., transthyretin versus amyloid light-chain (al)). patients with a family history of cardiomyopathy should be offered the option of referral for genetic counseling and testing.
bnp (or nt-probnp) should be considered, particularly if other causes of dyspnea such as copd are being considered if there is doubt about the diagnosis. very low levels virtually exclude heart failure, but can be confounded by obesity.
elevated levels can be seen in renal failure without substantial heart failure, but at least suggest volume overload. elevated bnp in the absence of renal failure is strongly suggestive of heart failure, but bnp levels are increased with age.
basic metabolic parameters including renal and hepatic function should be measured. renal dysfunction may be a seen as a result of low cardiac output or elevated venous filling pressure.
hepatic parameters (alt, ast, total bilirubin) and international normalized ratio (inr) may be elevated as a consequence of hepatic congestion. serum albumin is helpful in excluding malnutrition as an alternative explanation for peripheral edema.
minor elevations in troponin are characteristic of heart failure exacerbation, but typically do not rise and fall as in acute coronary syndrome; myocarditis should be considered if troponin is substantially elevated. inflammatory markers such as c-reactive protein (crp) or erythrocyte sedimentation rate (esr) would also be typically elevated in myocarditis, but are not diagnostic if elevated. anemia (hemoglobin or hematocrit) and gout (uric acid) and are also frequent comorbidities to consider.
additional testing to establish the etiology of heart failure should be considered and may include: hiv, ferritin (hemochromatosis), thyroid-stimulating hormone, and serum free light chains (amyloid), for example. testing for specific viruses other than hiv is not routinely performed, but coxsackie, epstein-barr, and varicella zoster could be considered. exclusion of connective tissue disease with antinuclear antibodies (ana) is also often performed.
cxr film (figure 1) may show cardiomegaly, but the absence does not exclude heart failure. pulmonary edema is an important finding, but can be confused with pneumonitis or other causes of diffuse infiltrates. accompanying findings such as pleural effusions may be helpful in interpretation.
chest x-ray film demonstrating cardiomegaly and pulmonary edema.
an echocardiogram will provide size; structural detail, including evaluation of valves; and myocardial function, including ef and presence of absence of regional wall motion abnormalities. this is the most important test when considering heart failure as a diagnosis.
abdominal ultrasound may demonstrate hepatomegaly and/or ascites, although these findings are often evident on exam and thus are not routinely indicated.
the hallmarks of treatment of diastolic heart failure are control of congestion, heart rate in the presence of atrial fibrillation to increase ventricular filling time, and control of systolic blood pressure. the majority of evidence on the treatment of heart failure has been for systolic heart failure, and is thus the focus of the remainder of this section.
there are three “to do’s” in the management of heart failure: (1) control congestion, (2) provide neurohormonal antagonists, and (3) consider sudden cardiac death prevention and cardiac resynchronization therapy (crt). since congestion causes most symptoms, this should be prioritized.
congestion control is achieved with sodium and sometimes (if there is hyponatremia) moderate fluid restriction; most patients need loop diuretics. congestion is managed the same for systolic and diastolic heart failure.
second, neurohormonal antagonists (angiotensin-converting enzyme inhibitors (acei) or angiotensin receptor blockers (arb), beta-blockers, aldosterone antagonists, and vasodilators in select populations) are critical for the treatment of systolic heart failure and should be initiated. although it is critical to use the drugs and doses that were found to be effective in landmark clinical trials, very few patients will tolerate initiation of full doses of these medications, and a period of uptitration over several weeks to months should be anticipated.
there is no consensus regarding whether beta-blockers or acei/arb should be initiated first, and beta-blockers should be avoided in the setting of cardiogenic shock, severe bradycardia, complete heart block, or bronchospasm. studies of neurohormonal antagonists for diastolic heart failure have been disappointing, but neurohormonal antagonists are still often used for their antihypertensive effect, and their safety in this population is well-established.
although there is no mortality benefit, digoxin has been noted to improve symptoms and reduce the risk of hospitalization. finally, consideration should be given to “electrical therapy,” which consists of crt (if qrs >130 ms) and sudden cardiac death prevention with an implantable cardioverter-defibrillator (icd).
the risk of sudden cardiac death is much higher with an ef <35%, and in the absence of contraindications such as life expectancy less than 1 year, electrical therapy should be considered. patients should be receiving optimal medical therapy for at least 3 months before implanting an icd.
wearable external defibrillators are sometimes used during the period of medical uptitration to permit reevaluation of ef; a sizable fraction of patients will improve on medical therapy to the point that an implantable icd is not indicated.
patients who are unable to tolerate medical therapy or experience progression despite these therapies suggest a very poor prognosis and may be considered for advanced options, such as mechanical circulatory support (mcs, also known as ventricular assist device or vad) or heart transplant.
acei/arb and beta-blockers are both initiated at minimal dose, but uptitration of acei/arb is typically prioritized, as full dose can typically be achieved more quickly. beta-blocker dose is then increased every 1 to 2 weeks to the maximally tolerated dose. timing of the introduction of aldosterone antagonist is individualized based on need for diuretics and potassium supplementation, and often deferred to prioritize acei/arb and beta-blockers.
administration of diuretics is the hallmark of emergency treatment of heart failure and most patients respond promptly. inadequate response should precipitate rapid escalation of a diuretic dose.
a common rule of thumb is to double an ineffective dose. consideration should be given to vasodilators if systemic blood pressure is adequate (e.g., mean arterial pressure greater than 70 to 75 mm hg). in the event of hypotension or cardiogenic shock, initiation of inotropes, such as dobutamine and/or dopamine, may be necessary. noninvasive positive pressure ventilation is an option and mechanical support such as an intraaortic balloon pump may also be indicated.
in addition to evaluation of symptomatic response, physical exam findings that should be monitored while providing treatment for heart failure include frequent evaluation of jugular venous pressure and vital signs, with particular attention to blood pressure and heart rate. sinus tachycardia is often a compensatory response and improvement is thought to represent a favorable response to treatment.
serial examinations should also focus attention on the presence of absence of s3/s4, liver span, presence or absence of ascites, and degree and distribution of edema. urine output should also be monitored, as this provides the most direct measure of pace of decongestion and also indicates adequate (or not) renal perfusion.
basic metabolic panels are typically performed shortly after initiation of therapy (at least daily while hospitalized), to monitor renal function and ensure that diuretics are not causing dangerous perturbations in serum potassium levels. following initiation of aldosterone antagonists, more frequent monitoring of potassium is indicated.
a commonly used strategy is 1 week after initiation or dose increase, and then again at 1 month. once a stable medication regimen has been established, routine intermittent testing in heart failure patients is not typically performed. there is some data to suggest that bnp levels may be used to guide therapy.
maintaining patients with heart failure on maximally tolerated doses of neurohormonal antagonists (acei/arb, beta-blockers, aldosterone antagonists) are critical to minimizing risk of disease progression, symptomatic decompensation, hospitalization, and mortality. application of crt when indicated has also been shown to improve outcomes, and should be periodically reconsidered, as patient status or criteria for implant may change over time.
education on salt avoidance, the role of fluid restriction, and self-care including daily weight monitoring are all important to reduce burden of disease and avoid hospitalization. over time, it is not uncommon for patients with heart failure to become intolerant to maximal doses of medical therapy.
the need to decrease the doses of medications is a predictor of adverse outcome, and may be an appropriate time to consider evaluation for advanced options. for patients with end-stage disease, palliative care and/or hospice may be appropriate, and deactivation of icd may be considered.
digoxin is sometimes used in patients with atrial fibrillation and heart failure with insufficient rate control. typical dose is 62.5 to 250 mcg daily.
concurrent anemia: treatment may improve heart failure symptoms.
concurrent arrhythmias: consider the role that uncontrolled arrhythmias may have on heart failure exacerbation. improved control of atrial fibrillation or premature ventricular contractions (pvcs) may improve symptoms. many antiarrhythmics are contraindicated in severe heart failure.
concurrent chronic kidney disease: continue acei/arb if possible, but if necessary to discontinue, replace with isosorbide/hydralazine combination. may contribute to anemia. aldosterone antagonists have a substantially increased risk of hyperkalemia.
concurrent diabetes: avoid thiazolidinediones (tzds) in all heart failure patients and metformin if there is significant renal dysfunction.
concurrent gout: it is likely that diuretic dosing will need to be increased if a gout flareup is treated with steroids.
concurrent liver disease: liver congestion is common and may result in the need to alter dose of medications metabolized by the liver.
concurrent prostatic hypertrophy: alpha blockers should be avoided, as they have been shown to increase mortality in heart failure patients.
concurrent sleep apnea: should be treated aggressively to minimize neurohormonal activation.
aldosterone antagonists should not be used in patients with underlying chronic kidney disease.
consider use of the seattle heart failure model or the heart failure survival score for estimating a patient’s prognosis.
consider referral to dietitian to augment teaching on importance of low-salt diet.
weigh yourself at the same time every day and record the result. report increases of more than 3 lb in a day or 5 lb in a week to your doctor; however, not all decompensations are preceded by antecedent weight gain.
avoid sodium intake and strive to keep less than 2,000 mg daily.
take your medications as prescribed every day.
report changes in symptoms promptly.
“2009 focused update incorporated into the acc/aha 2005 guidelines for the diagnosis and management of heart failure in adults: a report of the american college of cardiology foundation/american heart association task force on practice guidelines. developed in collaboration with the international society for heart and lung transplantation”.


text: A copy of the agenda will be available 72 hours before a meeting. If you need a reader, amplifier, qualified sign language interpreter, or any other form of auxiliary aid or service to attend or participate in the meeting, please contact Jane Tabor at least 48 hours prior to the hearing. Public documents can be provided in various accessible formats. Please email jane.tabor@state.nm.us or call (505) 476-3400 if a summary or other type of format is needed.

lowercased: a copy of the agenda will be available 72 hours before a meeting. if you need a reader, amplifier, qualified sign language interpreter, or any other form of auxiliary aid or service to attend or participate in the meeting, please contact jane tabor at least 48 hours prior to the hearing. public documents can be provided in various accessible formats. please email jane.tabor@state.nm.us or call (505) 476-3400 if a summary or other type of format is needed.


text:
Albino hairs are AKA grey Haha!
I have these too! What IS this? :confused: My 'le hairs' are short and new, and on top of my head just like Martyna's…they're not noticeable until you look closely, but this bothers me a bit.
I have a few, and I found one on my husband recently. I think its normal to have different hair textures mixed in. I have a mix of fine and medium mostly, with some super coarse and super fine mixed in. Occationally I find those type 4 hairs mixed in but they don't worry me :P its these "albino" hairs I keep finding that bother me...... they seem to be growing in numbers lol!
When I was a teen I had a weird "le hair" on the middle of my head, right at my forehead, it was thicker than dog hair and had a massive root with a diameter of a few mm. To this day I don't know what caused that to grow there. After pulling it out (it was too thick even for a fine toothed comb to pass over), it never grew back. I had a gaping little hole for a few weeks, though.
I giggled at barbed wire fence.
I'm 45 now with a section trying to be a cool stripe and some sparklies scattered about.
You have to be very close to notice the silvers.
So early invasion can be slow colonization as far as grey is concerned.
Texture? I think that's so random. I joke that it's proof I should have been curly.
At 45, there's an age related texture shift possibility.
I'm so relieved to hear that I'm not the only one. I started finding these in 2008, and they're super coarse, black and crinkly. 2-3x the width of the other hairs. I fried and dyed my hair for a few years straight, so I've never noticed how many there are, but now that I'm growing it out, I have at least 30% coverage of them. I'm brunette, at least, so it's harder to tell, but they're all JET BLACK and crinkly. They stand up in weird ways, too.

lowercased:
albino hairs are aka grey haha!
i have these too! what is this? :confused: my 'le hairs' are short and new, and on top of my head just like martyna's…they're not noticeable until you look closely, but this bothers me a bit.
i have a few, and i found one on my husband recently. i think its normal to have different hair textures mixed in. i have a mix of fine and medium mostly, with some super coarse and super fine mixed in. occationally i find those type 4 hairs mixed in but they don't worry me :p its these "albino" hairs i keep finding that bother me...... they seem to be growing in numbers lol!
when i was a teen i had a weird "le hair" on the middle of my head, right at my forehead, it was thicker than dog hair and had a massive root with a diameter of a few mm. to this day i don't know what caused that to grow there. after pulling it out (it was too thick even for a fine toothed comb to pass over), it never grew back. i had a gaping little hole for a few weeks, though.
i giggled at barbed wire fence.
i'm 45 now with a section trying to be a cool stripe and some sparklies scattered about.
you have to be very close to notice the silvers.
so early invasion can be slow colonization as far as grey is concerned.
texture? i think that's so random. i joke that it's proof i should have been curly.
at 45, there's an age related texture shift possibility.
i'm so relieved to hear that i'm not the only one. i started finding these in 2008, and they're super coarse, black and crinkly. 2-3x the width of the other hairs. i fried and dyed my hair for a few years straight, so i've never noticed how many there are, but now that i'm growing it out, i have at least 30% coverage of them. i'm brunette, at least, so it's harder to tell, but they're all jet black and crinkly. they stand up in weird ways, too.


text:
Experimental design and architectural firm, D*Haus Company, takes their inspiration for the creation of structures, furniture, and lighting from mathematics, most specifically from Henry Ernest Dudeney, the mathemetician who figured out how to evolve a perfect square into an equilateral triangle.
Their D*Haus modular homes demonstrate their belief that ideas “can help improve and inspire our daily lives… through flexibility, adaptability and originality.” Available in four different versions, the D*Haus can be delivered in a single kit from which a minimum of eight configurations can be constructed.
From a single D*Static kit of identical parts, eight different houses can be affordably constructed. Dubbed as “one of the most economic and sustainable ways of building prefabricated homes,” the D*Static can be built into as many as five bedrooms in one- or two-story configurations. Each kit is constructed off-site from cross-laminated timber, so that on-site construction can happen in a matter of days. Facade panels are made of highly available and sustainable arctic spruce. Window glazing allows for passive gain of incoming solar energy and outstanding U-values are achieved from super insulation.
The upscale D*Lux version for luxury homes will also permit eight different versions of a home to be built from a single kit. Made from high-quality materials while utilizing the same process as in the D*Static model, the D*Lux home is eco-friendly and sustainable while featuring larger living areas, balconies, porches, and standard swimming pools in hot climates.
From the D*Modular kit, an infinite number of houses can be built. With a focus on sustainability, efficiency, and flexibility, the D*Modular home can grow as you grow.
The centerpiece of the D*Haus collection is the D*Dynamic, billed as “a house for all seasons.” The D*Dynamic is capable of dynamic response to the environment by “controlled adaptation to seasonal, meteorological and astronomical conditions.” Moving inside itself, the D*Dynamic transforms into eight different configurations in response to changes in seasons and time of day. Heavy external walls can unfold into internal walls, permitting glass internal walls to transform into facades, changing the shape and perspective of the building to take advantage of environmental energy sources.

lowercased:
experimental design and architectural firm, d*haus company, takes their inspiration for the creation of structures, furniture, and lighting from mathematics, most specifically from henry ernest dudeney, the mathemetician who figured out how to evolve a perfect square into an equilateral triangle.
their d*haus modular homes demonstrate their belief that ideas “can help improve and inspire our daily lives… through flexibility, adaptability and originality.” available in four different versions, the d*haus can be delivered in a single kit from which a minimum of eight configurations can be constructed.
from a single d*static kit of identical parts, eight different houses can be affordably constructed. dubbed as “one of the most economic and sustainable ways of building prefabricated homes,” the d*static can be built into as many as five bedrooms in one- or two-story configurations. each kit is constructed off-site from cross-laminated timber, so that on-site construction can happen in a matter of days. facade panels are made of highly available and sustainable arctic spruce. window glazing allows for passive gain of incoming solar energy and outstanding u-values are achieved from super insulation.
the upscale d*lux version for luxury homes will also permit eight different versions of a home to be built from a single kit. made from high-quality materials while utilizing the same process as in the d*static model, the d*lux home is eco-friendly and sustainable while featuring larger living areas, balconies, porches, and standard swimming pools in hot climates.
from the d*modular kit, an infinite number of houses can be built. with a focus on sustainability, efficiency, and flexibility, the d*modular home can grow as you grow.
the centerpiece of the d*haus collection is the d*dynamic, billed as “a house for all seasons.” the d*dynamic is capable of dynamic response to the environment by “controlled adaptation to seasonal, meteorological and astronomical conditions.” moving inside itself, the d*dynamic transforms into eight different configurations in response to changes in seasons and time of day. heavy external walls can unfold into internal walls, permitting glass internal walls to transform into facades, changing the shape and perspective of the building to take advantage of environmental energy sources.


text:
Hi everyone. Firstly I must apologise for the lack of blog posts in the last few weeks; in fact since 5 March when I posted the last one. I've had a manically busy few weeks having taken on a number of new clients. Also, I am preparing for a photo shoot of my flat in mid April which has been stressing me out somewhat. So I've been furiously upcycling some of my furniture with Annie Sloan paint (separate blog post shortly) and changing lampshades on all my table lamps.
Table lamps can be so boring and serve no other purpose than to provide a lighting source. Gone are the days when you only had a limited choice of shades, mainly 50 shades of beige or cream!! Now you can buy the most divine shades and make a real statement, a wow factor, even if the lamp base is a bit "meh". The reverse is a statement lamp base with a plain shade that doesn't compete. However, beware as you can spend hundreds of pounds on a lamp shade and even thousands of pounds on a lamp base. It's a matter of finding something affordable and you really love.
There is a great shop in London called Pooky Lighting which sells affordable and fun lamp bases and shades so I popped in and bought three pairs of lampshades for the bedrooms and kitchen. What a difference they have made to the rooms; the lighting has transformed the spaces from "meh" to "tah-dah" !!!
In the kitchen I changed the shades from plain taupe coloured silk to these gorgeous silk Ikat pleated shades by Pooky Lights. In the sitting room I replaced a pair of beige linen shades in the alcoves with black & white Ikat ones which really draw the eye in.
And finally, I bought a rather expensive but absolutely divine lamp base from Nicholas Haslam designed by Paolo Moschino. It is my piece de resistance but one of those items that you see and just have to have!! It is solid handcarved brass and it was the way it opened up like a flower and had such beautiful flowing lines that made me fall in love with it. The jury is out on whether any of my friends like it !!
I would love to hear what sort of table lamps you have and would be happy to offer some advice if you are thinking of changing them so do contact me.

lowercased:
hi everyone. firstly i must apologise for the lack of blog posts in the last few weeks; in fact since 5 march when i posted the last one. i've had a manically busy few weeks having taken on a number of new clients. also, i am preparing for a photo shoot of my flat in mid april which has been stressing me out somewhat. so i've been furiously upcycling some of my furniture with annie sloan paint (separate blog post shortly) and changing lampshades on all my table lamps.
table lamps can be so boring and serve no other purpose than to provide a lighting source. gone are the days when you only had a limited choice of shades, mainly 50 shades of beige or cream!! now you can buy the most divine shades and make a real statement, a wow factor, even if the lamp base is a bit "meh". the reverse is a statement lamp base with a plain shade that doesn't compete. however, beware as you can spend hundreds of pounds on a lamp shade and even thousands of pounds on a lamp base. it's a matter of finding something affordable and you really love.
there is a great shop in london called pooky lighting which sells affordable and fun lamp bases and shades so i popped in and bought three pairs of lampshades for the bedrooms and kitchen. what a difference they have made to the rooms; the lighting has transformed the spaces from "meh" to "tah-dah" !!!
in the kitchen i changed the shades from plain taupe coloured silk to these gorgeous silk ikat pleated shades by pooky lights. in the sitting room i replaced a pair of beige linen shades in the alcoves with black & white ikat ones which really draw the eye in.
and finally, i bought a rather expensive but absolutely divine lamp base from nicholas haslam designed by paolo moschino. it is my piece de resistance but one of those items that you see and just have to have!! it is solid handcarved brass and it was the way it opened up like a flower and had such beautiful flowing lines that made me fall in love with it. the jury is out on whether any of my friends like it !!
i would love to hear what sort of table lamps you have and would be happy to offer some advice if you are thinking of changing them so do contact me.


text:
Amber Associates Recruitment Solutions is a traditional recruitment agency & business. The co-Directors have over 45 years combined experience recruiting the right staff for clients of all sizes, in Media, IT, Construction, Medical, HealthTech, Finance and Public Sector. From BBC- to- Sky, JLL, HFEA, AWIN & UKGOV.
From office support staff, including GDPR savvy administrators, PA's and Office Managers, to Data Protection Officers, IT Managers, Data Science Executives, Analysts and Security and Compliance Managers, Project Managers and Regulatory Officers.
We spend time with our clients assessing and listening to your needs and conduct face to face interviews with all our candidates. We pride ourselves on ‘getting it right’, saving you time and saving you money. Use our expertise, call us and experience the difference.
Amber Associates was originally founded in 2001 by Joanne James. After working for the leading High Street agencies, Joanne sensed that many clients and candidates had become disillusioned with the recruitment industry and in particular recruitment agency reliance on sheer weight of numbers to fill a single vacancy.
We are a UK limited company, we are GDPR compliant and we adhere to the REC Guides and Codes of Conduct. We are fully insured and regsitered with the Crown Commercial Service.
Contact Mark James through his Urbano Profile for more details on how we can help.

lowercased:
amber associates recruitment solutions is a traditional recruitment agency & business. the co-directors have over 45 years combined experience recruiting the right staff for clients of all sizes, in media, it, construction, medical, healthtech, finance and public sector. from bbc- to- sky, jll, hfea, awin & ukgov.
from office support staff, including gdpr savvy administrators, pa's and office managers, to data protection officers, it managers, data science executives, analysts and security and compliance managers, project managers and regulatory officers.
we spend time with our clients assessing and listening to your needs and conduct face to face interviews with all our candidates. we pride ourselves on ‘getting it right’, saving you time and saving you money. use our expertise, call us and experience the difference.
amber associates was originally founded in 2001 by joanne james. after working for the leading high street agencies, joanne sensed that many clients and candidates had become disillusioned with the recruitment industry and in particular recruitment agency reliance on sheer weight of numbers to fill a single vacancy.
we are a uk limited company, we are gdpr compliant and we adhere to the rec guides and codes of conduct. we are fully insured and regsitered with the crown commercial service.
contact mark james through his urbano profile for more details on how we can help.


text:
Seven years ago, I was in Syria and I had a vision. It was like a dream, but I wasn’t sleeping. I saw myself in a war. People were fighting in all kinds of ways, and babies were crying. But in the dream, I was safe.
When I woke up, I wondered if I was crazy! I didn’t believe those in my dream who said that Jesus is the real way and we should believe him. I didn’t know what to believe.
Before I had this vision, I had asked God to show me the real truth. It was then I had this dream. After that, I believed in Him, and I know that this way is the truth.
– Let’s take a moment to remember that there are people from different faiths and background seeking the truth. Pray that they will see visions and dreams. Pray that the Lord will send them believers to help them be established in the word and to grow in the knowledge of Christ.

lowercased:
seven years ago, i was in syria and i had a vision. it was like a dream, but i wasn’t sleeping. i saw myself in a war. people were fighting in all kinds of ways, and babies were crying. but in the dream, i was safe.
when i woke up, i wondered if i was crazy! i didn’t believe those in my dream who said that jesus is the real way and we should believe him. i didn’t know what to believe.
before i had this vision, i had asked god to show me the real truth. it was then i had this dream. after that, i believed in him, and i know that this way is the truth.
– let’s take a moment to remember that there are people from different faiths and background seeking the truth. pray that they will see visions and dreams. pray that the lord will send them believers to help them be established in the word and to grow in the knowledge of christ.


text:
Check out our recipe for a Southern classic, BBQ Shrimp & Grits.
**To coarse-grind the peppercorns, use a blender or peppermill. The grind is important to the taste of the finished dish.
Place the shrimp, Worcestershire, pepper, Creole seasoning, garlic, and 1 tablespoon water in a heavy 10-inch, stainless-steel sauté pan. Squeeze the juice from the lemon half over the shrimp and add the rind and pulp to the pan.
Over high heat, cook the shrimp while gently stirring and occasionally turning the shrimp.
If the shrimp are the colossal size, add 2 tablespoons water to the pan. Otherwise, don’t add water.
Reduce the heat to medium-high and continue cooking as you gradually add the cold pieces of butter to the pan. While turning the shrimp occasionally, swirl the butter pieces until they are incorporated into the pan juices, the sauce turns light brown and creamy as it simmers, and the shrimp are just cooked through. This will take about two minutes total if the shrimp are extra-large, and about three minutes total if they’re colossal. Do not overcook the shrimp.
Combine the grits, chicken stock, heavy cream, a pinch of salt and a pinch of pepper in a pot. Bring to a boil and reduce to a slow simmer.
Stir the grits frequently to prevent sticking and burning.
Continue to cook on a slow simmer making sure to constantly stir the grits if they get to thick before they are tender.

lowercased:
check out our recipe for a southern classic, bbq shrimp & grits.
**to coarse-grind the peppercorns, use a blender or peppermill. the grind is important to the taste of the finished dish.
place the shrimp, worcestershire, pepper, creole seasoning, garlic, and 1 tablespoon water in a heavy 10-inch, stainless-steel sauté pan. squeeze the juice from the lemon half over the shrimp and add the rind and pulp to the pan.
over high heat, cook the shrimp while gently stirring and occasionally turning the shrimp.
if the shrimp are the colossal size, add 2 tablespoons water to the pan. otherwise, don’t add water.
reduce the heat to medium-high and continue cooking as you gradually add the cold pieces of butter to the pan. while turning the shrimp occasionally, swirl the butter pieces until they are incorporated into the pan juices, the sauce turns light brown and creamy as it simmers, and the shrimp are just cooked through. this will take about two minutes total if the shrimp are extra-large, and about three minutes total if they’re colossal. do not overcook the shrimp.
combine the grits, chicken stock, heavy cream, a pinch of salt and a pinch of pepper in a pot. bring to a boil and reduce to a slow simmer.
stir the grits frequently to prevent sticking and burning.
continue to cook on a slow simmer making sure to constantly stir the grits if they get to thick before they are tender.


text:
May is a busy month, with various key dates of celebration and recognition. Over the course of the month, i am going to share with you some tools and suggestions. First up, in honour of Maternal Mental Health Week, here is a tool that i put together. After studying both Dialectical Behaviour Therapy as well as more body-based self-compassion modalities, i find this tool can be helpful to help you take control of your emotions. I love acronyms as it makes it so much easy to remember the suggestions. Plus it’s a helpful reminder that we can be in control of our feelings.
It can be hard to take time for yourself, especially when we are told to take care of others and that it’s selfish to do kind things for ourselves. This tool can be a great way for you to steal some moments to yourself, in an intentional way. It also can manifest some good feelings that linger. Rainbows are incredible symbols of everyday magic or woo woo, and taking time to notice the joy and beauty in the everyday helps us with our emotional well-being. We deserve to notice these moments, and deserve to take time to pause.
It’s important to slow down and catch your breath. We can only see rainbows when we are able to be aware of what’s in front of us. This is also a great way to notice what we need an a given moment. What can you do in this moment to rest and relax? Can you put your feet up and just take in the sights and sounds around you? Linger a bit longer in the shower, add some luxurious hand lotion to your sensory self-care. Have a cat-nap. Maybe treat yourself to a nice mala bracelet with your favourite crystal – this can be a calming tool and a way to practice some mindful meditation.
Radical Acceptance is a helpful tool to be able to acknowledge something for what it is. That doesn’t mean we have to truly agree with it, but the acceptance can be a first step to let things go. This stops the pain from turning into suffering, and it allows us to be more present with ourselves in the present. When we don’t accept something, it keeps us stuck. So, try working with this idea and practice saying “it is what it is.” See how that starts to feel in your body. Maybe some parts feel less stuck or tight.
Setting intentions for a day, a week, or a year can be a guide that sets you with following where your want your life to go. The intention can be a simple word that carries meaning for you, or a mantra/affirmation that holds significance for you. If you don’t already have one, take some time to journal and brainstorm the words and phrases that are meaningful for you. It is a good way of giving ourselves permission to focus on what we really want, and to take ownership of our moods and behaviour. Then work on ways to implement it into your everyday life. Maybe there is a symbol that speaks to you as a guide – be it a rainbow of hope and luck, a butterfly of resilience, or a lavender flower that helps you feel calm. When you have a symbol that acts as Recalled Anchor (i wrote about it more here) or resource, seeing it in your everyday life is a great way to boost your mood.
Self-Compassion is not the same as self-esteem and yet they work well together. To have self-compassion, it implies that we need to treat ourselves with the loving kindness we give others when they need our support. Think of some ways to give yourself self-compassion – it can be a permission slip to eat some chocolate after a hard day, and to enjoy it without judgement. It can be to not do the dishes and instead watch some marathon TV. It can be a yoga stretch or dance to your favourite music. The compassion comes from reminding yourself that your matter and deserve this break.
Reading is a great way for your brain to take a break from the monkey mind or inner critic. It is especially helpful when we are able to distract ourselves from the everyday worries and thoughts. You can get your dog-eared favourite book, or a new book that you have never read; it can be a fiction novel, self-help book, or a how-to book for something you want to learn. Take time to write in your own journal, free writing or following a guide. If reading is not your thing, no worries. Listen to an audio book or a podcast. This podcast that talks more about everyday magic and woo woo is a great listen! Watch a movie that you have never seen before – the idea is to let your brain relax and absorb what it is taking in, instead of the constant chatter it typically takes you to.
Research has shown links to fresh air, being outdoors and mental health. Our brains are elastic and benefit from the change in scenery as well as air changes. Sensorimotor Psychotherapy and Polyvagal theory also show us that a quick walk outdoors can do a lot to change our mood. Everything is better outside. Think of some simple things you can do – a walk, sitting on your porch our balcony, a picnic snack during your lunch break for instance. Another benefit to getting outside is that there may be other people that you can connect with – it helps us feel less alone or isolated after being indoors when feeling down. You don’t need to have a long chat with someone, but a quick hello can be a great break your mind and body needs too.
In keeping with Maslow’s Hierarchy of Needs, it’s imperative to take care of your basic needs. Research shows that we need to nurture our physical body in order to heal our mental health. Do a quick checklist – when was the last time you drank some water, had a healthy snack, slept enough, did some exercise for your body? If it’s been 2 hours since your last water break, have a glass right now. And then find ways to allow time for the other ways to take care of your body.

lowercased:
may is a busy month, with various key dates of celebration and recognition. over the course of the month, i am going to share with you some tools and suggestions. first up, in honour of maternal mental health week, here is a tool that i put together. after studying both dialectical behaviour therapy as well as more body-based self-compassion modalities, i find this tool can be helpful to help you take control of your emotions. i love acronyms as it makes it so much easy to remember the suggestions. plus it’s a helpful reminder that we can be in control of our feelings.
it can be hard to take time for yourself, especially when we are told to take care of others and that it’s selfish to do kind things for ourselves. this tool can be a great way for you to steal some moments to yourself, in an intentional way. it also can manifest some good feelings that linger. rainbows are incredible symbols of everyday magic or woo woo, and taking time to notice the joy and beauty in the everyday helps us with our emotional well-being. we deserve to notice these moments, and deserve to take time to pause.
it’s important to slow down and catch your breath. we can only see rainbows when we are able to be aware of what’s in front of us. this is also a great way to notice what we need an a given moment. what can you do in this moment to rest and relax? can you put your feet up and just take in the sights and sounds around you? linger a bit longer in the shower, add some luxurious hand lotion to your sensory self-care. have a cat-nap. maybe treat yourself to a nice mala bracelet with your favourite crystal – this can be a calming tool and a way to practice some mindful meditation.
radical acceptance is a helpful tool to be able to acknowledge something for what it is. that doesn’t mean we have to truly agree with it, but the acceptance can be a first step to let things go. this stops the pain from turning into suffering, and it allows us to be more present with ourselves in the present. when we don’t accept something, it keeps us stuck. so, try working with this idea and practice saying “it is what it is.” see how that starts to feel in your body. maybe some parts feel less stuck or tight.
setting intentions for a day, a week, or a year can be a guide that sets you with following where your want your life to go. the intention can be a simple word that carries meaning for you, or a mantra/affirmation that holds significance for you. if you don’t already have one, take some time to journal and brainstorm the words and phrases that are meaningful for you. it is a good way of giving ourselves permission to focus on what we really want, and to take ownership of our moods and behaviour. then work on ways to implement it into your everyday life. maybe there is a symbol that speaks to you as a guide – be it a rainbow of hope and luck, a butterfly of resilience, or a lavender flower that helps you feel calm. when you have a symbol that acts as recalled anchor (i wrote about it more here) or resource, seeing it in your everyday life is a great way to boost your mood.
self-compassion is not the same as self-esteem and yet they work well together. to have self-compassion, it implies that we need to treat ourselves with the loving kindness we give others when they need our support. think of some ways to give yourself self-compassion – it can be a permission slip to eat some chocolate after a hard day, and to enjoy it without judgement. it can be to not do the dishes and instead watch some marathon tv. it can be a yoga stretch or dance to your favourite music. the compassion comes from reminding yourself that your matter and deserve this break.
reading is a great way for your brain to take a break from the monkey mind or inner critic. it is especially helpful when we are able to distract ourselves from the everyday worries and thoughts. you can get your dog-eared favourite book, or a new book that you have never read; it can be a fiction novel, self-help book, or a how-to book for something you want to learn. take time to write in your own journal, free writing or following a guide. if reading is not your thing, no worries. listen to an audio book or a podcast. this podcast that talks more about everyday magic and woo woo is a great listen! watch a movie that you have never seen before – the idea is to let your brain relax and absorb what it is taking in, instead of the constant chatter it typically takes you to.
research has shown links to fresh air, being outdoors and mental health. our brains are elastic and benefit from the change in scenery as well as air changes. sensorimotor psychotherapy and polyvagal theory also show us that a quick walk outdoors can do a lot to change our mood. everything is better outside. think of some simple things you can do – a walk, sitting on your porch our balcony, a picnic snack during your lunch break for instance. another benefit to getting outside is that there may be other people that you can connect with – it helps us feel less alone or isolated after being indoors when feeling down. you don’t need to have a long chat with someone, but a quick hello can be a great break your mind and body needs too.
in keeping with maslow’s hierarchy of needs, it’s imperative to take care of your basic needs. research shows that we need to nurture our physical body in order to heal our mental health. do a quick checklist – when was the last time you drank some water, had a healthy snack, slept enough, did some exercise for your body? if it’s been 2 hours since your last water break, have a glass right now. and then find ways to allow time for the other ways to take care of your body.