Showing posts with label Hypertension. Show all posts
Showing posts with label Hypertension. Show all posts

Jul 23, 2015

Nursing Care for Hypertension......

Nursing can be a lot to take into sometimes. You have to study hundreds of diseases and pick out the most appropriate nursing actions to address them. But how do you do that when you have so much to learn? For cases such as hypertension, for example. Here’s a mnemonic trick that would help you remember the interventions needed and things to consider for hypertension.
When hypertensive, remember: DIURETIC
D -daily weight
If the patient is hypertensive or even suspected to be, then his/her weight must be monitored. He/she must be weighed daily. Indicators for risk of hypertension include obesity, abdominal obesity and weight gain.Weight gain was associated with increased risk of developing hypertension.On the other hand, weight-loss can lead to a significant drop in blood pressure.
I-Intake and Output

Intake and output of the patient must also be kept closely monitored. Sodium balance is precisely regulated by intake and output.High salt intake increases extracellular volume (ECV), blood volume, and cardiac output resulting in elevation of blood pressure. Normal blood pressure are attained by increased glomerular filtration and decreased sodium reabsorption. In some individuals, the kidneys have difficulty in excreting sodium, so the equilibrium is achieved at the expense of elevated blood pressure. At times, the sodium balance must be achieved via dialysis and ultrafiltration.
U-Urine Output
When BP is low, renal blood flow drops. This stimulates renin and angiotensin production by the kidney. Angiotensin is converted to angiotensin II in the lung. This is controlled by angiotensin-converting enzyme. Angiotensin II is a vasoconstrictor – which will increase SVR. Angiotensin II also stimulates the adrenal cortex to produce aldosterone. Aldosterone causes sodium and water to be retained by the kidney. This will increase the extra cellular fluid (ECF) volume and therefore the circulating blood volume. This is also supported by antidiuretic hormone (vasopressin) which is produced by the hypothalamus and released by the posterior pituitary in response to angiotensin II. Angiotensin II also stimulates thirst, leading to increased fluid intake.
R-Response of B/P
A person’s blood pressure is not fixed as it rises and falls throughout the day in response to what that person is doing and what is happening around him/her. It’s important that the BP be monitored so as to know whether it is responding appropriately to your interventions, or to modify the treatment regimen.
E-Electrolytes
Dietary choices, even the amount of electrolytes you consume, can influence the blood pressure. These electrolytes such as sodium and potassium play a major role in regulating a person’s blood pressure.One of the functions of electrolytes is the balance of fluid in and around your cells. Electrolytes partially break down in water to form an ion. When this occurs, they influence where the fluids inside your body go. Sodium boosts water retention, leading to excess fluid in blood vessels and higher blood pressure.
TI-Transient Ischemic Episodes (TIA)

A transient ischemic attack (TIA) occurs when blood flow to a part of the brain stops for a brief time.High blood pressure is the main risk for TIAs and stroke.
C-Complications: 4 Cs (CAD, CRF, CHF, CVA)
You also have to remember that if left untreated, hypertension can cause certain complications. Over time this extra pressure can increase your risk of a heart attack, stroke and kidney disease.High blood pressure can cause many different diseases of the heart and blood vessels (medically known as cardiovascular diseases) and can also damage the small blood vessels in your kidneys and stop them from working properly.

Sources:

Jan 9, 2012

Stroke Risk Associated With Diet Quality, Energy Intake Overall.....


 

Clinical Context...

Undernutrition before birth, as well as in infancy, childhood, and adulthood, is associated with an increased risk for stroke in later life. However, the mechanism of increased stroke risk is poorly understood.
In addition, overnutrition also increases stroke risk. The likely mechanism is by hastening the onset of obesity, hypertension, hyperlipidemia, and diabetes. The objective of this review by Hankey was to describe recent evidence regarding the effects of nutrition on stroke risk.

Study Synoposis and Perspective

The overall quality of a person’s diet and the balance between caloric intake and caloric expenditure appear to be more important determinants of stroke risk than the actual foods and nutrients consumed, according to a new review published in the January 2012 special issue of the Lancet Neurology.
In general, the 2 biggest threats to health and risk of stroke are overeating and excess salt, author Graeme J. Hankey, from Royal Perth Hospital, Perth, Western Australia, writes.

"These behaviors are a normal response by people to an abnormal environment," Dr. Hankey notes. "Our living environments have become more conducive to consumption of energy and less conducive to expenditure of energy in developed and increasingly in developing regions."
He writes that between 1970 and 2008, the incidence of stroke in high-income countries fell by 42%, probably as a result of increased public awareness about the dangers of high blood pressure, high cholesterol, and cigarette smoking.

But in poorer countries, the incidence of stroke increased by more than 100% during this period. This rise coincided with food and lifestyle changes associated with industrialization and urbanization.


Small Number of Trials
In his review, Dr. Hankey examines the evidence linking nutrition and diet to the risk of stroke. He searched PubMed articles published in English from 1970 to October 2011, using a variety of search terms.
The review included a small number of randomized trials and large observational and epidemiological studies.
He found that the findings from these studies were diverse, owing to the fact that most were epidemiological and therefore "prone to substantial methodological challenges of bias, confounding, and measurement error."
For example, one observational study found that a high intake of a healthy diet was associated with an increased risk of stroke, whereas another observational study found just the opposite.
Dr. Hankey's review also revealed the following effects of individual foods and beverages on the risk of stroke:

  • Fish: 3 servings a day associated with a 6% lower risk of stroke
  • Fruits and vegetables: >5 servings a day associated with a 26% lower risk of stroke
  • Meat: Each daily serving associated with a 24% increased risk of stroke
  • Reduced-fat milk: associated with a lower risk of stroke vs full-fat milk
  • Chocolate: High consumption associated with a 29% lower risk of stroke
  • Coffee: 3 to 4 cups per day associated with a 17% lower risk of stroke
  • Tea: ≥3 cups per day associated with a 21% lower risk of stroke
  • Sugar-sweetened beverages: high intake associated with increased obesity, diabetes, metabolic syndrome, and coronary heart disease
  • Whole grains: high intake associated with a 21% lower incidence of cardiovascular events
  • Rice: intake not associated with risk of stroke
  •  
"Further research is needed to improve the quality of evidence relating to the association of many nutrients, foods, and dietary patterns with stroke risk," Dr. Hankey suggests.
This requires adequately powered, large randomized trials with carefully described patient populations and interventions. The outcomes of such trials should also distinguish first-ever and recurrent stroke, as well as ischemic and hemorrhagic stroke, and their different etiologies.
Dr. Hankey also suggests that population-wide salt reduction programs led by governments and with industry cooperation could be highly cost effective.
"In the USA, modest, population-wide reductions in dietary salt of up to 3 g per day…are projected to reduce the annual number of new cases of stroke by 32,000 to 66,000, similar to the benefits of population-wide reductions in tobacco use, obesity, and cholesterol levels," he writes.

Dr. Hankey told Medscape Medical News that he hopes his study will stimulate conclusive studies "by means of large, randomized controlled trials of the effect of dietary nutrients, foods, and patterns on stroke and its pathological and etiological subtypes."
The current evidence associating dietary nutrients, foods, and patterns with stroke is generally suboptimal for providing reliable conclusions about causality, he reiterated.
"The effect of only a few supplements on stroke risk have been studied by means of large, randomized controlled trials, and all of those have shown no benefit of antioxidant vitamins, B-vitamins, and calcium supplements in preventing stroke, despite large, more suboptimal, epidemiological studies claiming they should be beneficial," he said.


Best Diet Still Uncertain
Commenting on this study for Medscape Medical News, Eugene Storozynsky, MD, a cardiologist from the University of Rochester Medical Center, Rochester, New York, said that he agrees with Dr. Hankey's conclusions.

"This is a good review of the literature as to what role diets and their components would have on reducing stroke, and what it tells us is that there still is a lot of uncertainty about the best diet. One study suggests benefit of a certain food or strategy, the other may come to the opposite conclusion," Dr. Storozynsky said.
The take-home message here is as Dr. Hankey notes, Dr. Storozynsky continued. "We need rigorously done randomized controlled trials to really monitor the long-term effects of diets and nutrients, rather than observation studies that look at individual factors, to see whether or not there is any benefit to adopting certain strategies."


Dr. Storozynsky also noted what he considers to be an important omission from Dr. Hankey's review.
"This review did not look at the effect of exercise and how it affects nutrition or stroke results. Does routine daily exercise mitigate the effect of intermittent poor eating? Exercise definitely needs to be part of the equation," he said.


Helmi L. Lutsep, MD, from the Oregon Stroke Center at Oregon Health Science University in Portland, added, "My quick read of the article suggests that it is a very nicely written, comprehensive review of our current knowledge regarding nutrition and stroke."
Dr. Lutsep, who is also a spokesperson for the American Academy of Neurology, added, "While I haven't seen all of these pieces summarized in one place before, I don't think that the article provides novel observations."

Dr. Hankey reports that he was the principal investigator of the VITAmins TO Prevent Stroke (VITATOPS) trial and has financial relationships with Sanofi-Aventis, Johnson & Johnson, Bristol-Myers Squibb, Boehringer Ingelheim, Bayer, and Pfizer Australia. Dr. Storozynsky and Dr. Lutsep have disclosed no relevant financial relationships. 

 
Lancet Neurol. 2012;11:66-81. Abstract
The National Stroke Association provides a comprehensive discussion for patients about stroke prevention.

Study Highlights


  • On the basis of a literature review, the reviewer noted the following findings:
    • Vitamin A supplementation increases all-cause mortality risk.
    • β-carotene supplementation increases cardiovascular and all-cause mortality risks and does not prevent stroke.
    • Vitamin C supplementation does not prevent stroke.
    • Vitamin E supplementation increases all-cause mortality risk and does not prevent stroke.
    • Although folic acid supplementation does not prevent stroke in populations with high folate intake, deficiency in regions of low folate intake may be a causal and treatable risk factor for stroke.
    • Vitamin D deficiency is associated with hypertension, cardiovascular disease, and stroke, but to date, supplementation has not been shown to prevent cardiovascular events. Randomized trials are underway.
    • Salt supplementation by 5 g per day is linked to a 23% increase in stroke risk (95% confidence interval [CI], 6 - 43).
    • Although decreasing salt intake has not been shown to reduce stroke risk, lowering consumption by 2 g per day is associated with a 20% decrease in cardiovascular events (95% CI, 1 - 36), and lower salt intake is also linked to blood pressure reduction.
    • Potassium supplementation by 1 g per day is associated with an 11% reduction in the risk for stroke (95% CI, 3 - 17), but supplementation is not proven to prevent stroke.
    • Potassium supplementation by 0.8 g per day is associated with a decrease in blood pressure by 5/3 mm Hg.
    • Calcium supplementation exceeding 0.5 g per day is linked to a 31% increase in the risk for myocardial infarction (95% CI, 2 - 67), does not prevent stroke, and may actually increase stroke risk.
    • High intake of total fat, trans fats, and saturated fats is not associated with an increased risk for stroke, and reduced total fat intake does not lower stroke risk.
    • High intake of plant n-3 polyunsaturated fats is associated with a reduced risk for stroke.
    • Marine n-3 polyunsaturated fat supplementation lowers cardiovascular events and death by 8% (95% CI, 1 - 15), but in a randomized trial, it did not reduce stroke risk.
    • High intake of carbohydrates with high glycemic index and glycemic load is associated with increased blood glucose levels, body weight, and stroke mortality.
    • High fiber intake is linked to lower blood pressure, blood glucose levels, and low-density lipoprotein cholesterol levels.
    • High protein intake is not associated with stroke risk.
    • High intake of a healthy diet was linked to an increased risk for stroke in one observational study and a reduced risk for stroke in another observational study.
    • High intake of an unhealthy diet was linked to an increased risk for stroke and a population-attributable risk for stroke of 19% (99% CI, 11 - 30).
    • In women, a prudent diet or Dietary Approaches to Stop Hypertension (DASH)–style diet is associated with a lower risk for stroke, and a Western diet is linked with a higher risk for stroke.
    • In women, the Mediterranean diet is associated with lower risks for stroke, cardiovascular disease, cardiovascular mortality, and all-cause mortality.
    • The effects of a vegetarian diet and a Japanese diet on stroke risk are unknown.
    •  
    •  

Clinical Implications


  • Reliable evidence from randomized trials suggests that dietary supplementation with antioxidant vitamins, B vitamins, and calcium does not reduce the risk for stroke. However, methodologic limitations of studies to date preclude firm conclusions regarding the effect of many other nutrients on stroke risk.
  • Less reliable evidence suggests that stroke can be prevented by prudent diets; Mediterranean or DASH-type diets; diets that are low in salt and added sugars and high in potassium; and diets that meet, but do not exceed, energy requirements. The overall quality of dietary pattern and the balance between energy intake and expenditure seem to affect stroke risk to a greater extent than individual nutrients and foods.

Borrowed from- Medscape Education Clinical Briefs

Jul 7, 2011

Cardiac Marckers for Acute MI

Cardiac markers are biomarkers measured to evaluate heart function. They are often discussed in the context of myocardial infarction, but other conditions can lead to an elevation in cardiac marker level.

Most of the early markers identified were enzymes, and as a result, the term "cardiac enzymes" is sometimes used. However, not all of the markers currently used are enzymes. For example, in formal usage, troponin would not be listed as a cardiac enzyme.


Types include:
Test Sensitivity and specificity Approximate peak Description



Troponin test The most sensitive and specific test for myocardial damage. Because it has increased specificity compared with CK-MB, troponin is a superior marker for myocardial injury. 12 hours Troponin is released during MI from the cytosolic pool of the myocytes. Its subsequent release is prolonged with degradation of actin and myosin filaments.
Differential diagnosis of troponin elevation includes acute infarction, severe pulmonary embolism causing acute right heart overload, heart failure, myocarditis. Troponins can also calculate infarct size but the peak must be measured in the 3rd day. released in 2–4 hours and persists for up to 7 days.



Creatine Kinase (CK-MB) test It is relatively specific when skeletal muscle damage is not present. 10–24 hours CK-MB resides in the cytosol and facilitates high energy phosphates into and out of mitochondria. It is distributed in a large number of tissues even in the skeletal muscle. Since it has a short duration, it cannot be used for late diagnosis of acute MI but can be used to suggest infarct extension if levels rise again. This is usually back to normal within 2–3 days.



Lactate dehydrogenase (LDH) LH is not as specific as troponin. 72 hours Lactate dehydrogenase catalyses the conversion of pyruvate to lactate. LDH-1 isozyme is normally found in the heart muscle and LDH-2 is found predominately in blood serum. A high LDH-1 level to LDH-2 suggest MI. LDH levels are also high in tissue breakdown or hemolysis. It can mean cancer, meningitis, encephalitis, or HIV. this usually back to normal 10–14 days.



Aspartate transaminase (AST) This was the first used.is not specific for heart damage, and it is also one of the liver function tests.


Myoglobin (Mb) low specificity for myocardial infarction 2 hours Myoglobin is used less than the other markers. Myoglobin is the primary oxygen-carrying pigment of muscle tissue. It is high when muscle tissue is damaged but it lacks specificity. It has the advantage of responding very rapidly, rising and falling earlier than CK-MB or troponin. It also has been used in assessing reperfusion after thrombolysis.



Ischemia-modified albumin (IMA) low specificity IMA can be detected via the albumin cobalt binding (ACB) test, a limited available FDA approved assay. Myocardial ischemia alters the N-terminus of albumin reducing the ability of cobalt to bind to albumin. IMA measures ischemia in the blood vessels and thus returns results in minutes rather than traditional markers of necrosis that take hours. ACB test has low specificity therefore generating high number of false positives and must be used in conjunction with typical acute approaches such as ECG and physical exam. Additional studies are required.



Pro-brain natriuretic peptide This is increased in patients with heart failure. It has been approved as a marker for acute congestive heart failure. Pt with < 80 have a much higher rate of symptom free survival within a year. Generally, pt with CHF will have > 100.


Glycogen phosphorylase isoenzyme BB high sensitivity and specificity early after chest pain 7 hours


Glycogen phosphorylase isoenzyme BB (abbreviation: GPBB) is an isoenzyme of glycogen phosphorylase. Glycogen phosphorylase exists in 3 isoforms. One of these Isoforms is GP-BB. This isoform exists in heart and brain tissue. Because of the blood-brain barrier GP-BB can be seen as heart muscle specific. During the process of ischemia, GP-BB is converted into a soluble form and is released into the blood. This isoform of the enzyme exists in cardiac (heart) and brain tissue. GP-BB is one of the "new cardiac markers" which are discussed to improve early diagnosis in acute coronary syndrome. A rapid rise in blood levels can be seen in myocardial infarction and unstable angina. GP-BB elevated 1–3 hours after process of ischemia.




Recently, the intentional destruction of myocardium by alcohol septal ablation has led to the identification of additional potential markers.



Limitations

Depending on the marker, it can take between 2 to 24 hours for the level to increase in the blood. Additionally, determining the levels of cardiac markers in the laboratory - like many other lab measurements - takes substantial time. Cardiac markers are therefore not useful in diagnosing a myocardial infarction in the acute phase. The clinical presentation and results from an ECG are more appropriate in the acute situation.


However, in 2010, research at the Baylor College of Medicine revealed that, using diagnostic nanochips and a swab of the cheek, cardiac biomarker readings from saliva can, with the ECG readings, determine within minutes whether someone is likely to have had a heart attack.


Further reading

Cardiac Intensive Care: Expert Consult: Online and Print (Expert Consult Title: Online + Print)Cardiovascular Critical Care


 Davis's Comprehensive Handbook of Laboratory and Diagnostic Tests With Nursing Implications (Davis's Comprehensive Handbook of Laboratory & Diagnostic Tests With Nursing Implications)Nursing Implications of Lab Tests (A Wiley medical publication)


Ross G, Bever F, Uddin Z, Devireddy L, Gardin J (2004). "Common scenarios to clarify the interpretation of cardiac markers". J Am Osteopath Assoc 104

www.magnabiosciences.com/cardiacMarkers.html

https://www.aarphealthcare.com/galecontent/cardiac-marker-tests