Heart Failure/Metabolic Syndrome Flashcards
impairment of the capacity of ventricles to eject blood from the heart or to fill with blood, end stage of all forms of CVD
heart failure
2 most common causes of HF
CHD and hypertension
____ receives blood from tissues around body. ___ pumps through pulmonary artery to lungs, lungs add oxygen and ____ receives oxygenated blood ____ pumps out to rest of body
hight atrium ; right ventricle ; left atrium ; left ventricle
pathophysiology with myocardial infarction:
damage to part of heart and impairs contractility of left ventricle, leading to less cardiac output (L ventricle hypertrophies)
pathophysiology with chronic hypertension
heart must pump against higher pressure chronically, resulting in L ventricle hypertrophy , reduce contractility and less cardiac output
accumulation of blood in venous circulation at expense of arterial volume causes:
decreased CO –> decreased blood flow to kidneys –> release of renin –> ^ adrenal secretion of aldosterone –> ^ Na reabsorption –>^ Na and fluid retention –> ^ BV and worsens situation
how come edema happens?
with blood backing up behind the heart (venous circulation) the organs become congested with blood –> ^ hydrostatic pressure –> interstitial fluid not reabsorbed at venous ends of capillaries –> ^ fluid in ISF –>edema
most common symptoms of HF?
dyspnea, orthopnea, fatigue, weakness, exercise intolerance, poor adaptation to cold temps
treatment goals of HF
removal of underlying cause, control of symptoms, prevent continued damage to heart
examples of med management:
treat hypertension with lifestyle/drug therapy, provide O2 therapy for SOB in advanced states, alter physical activity (decrease later stage, increase earlier stage), reduce negative remodelling of heart with beta blockers and ACE inhibitors, control excessive Na and fluid retention using diet/drugs (diuretics)
treatment of volume overload in acute decompensated heart failure includes:
intravenous diuretics, <2g Na restriction, < 2 L fluid a day
why decrease physical activity late stage and increase early stage?
reduce cardiac workload; improve heart function and prevent progression
most common type of heart failure:
chronic and stable
why wt loss if obese?
decrease the cardiac workload
why na restricted diet?
decrease availability of Na cuz kidney is reabsorbing too much Na and water
1-2 g Na is recommended for ____ HF
refractory
what is refractory HF?
fluid overload that cannot be controlled by diuretics
why is <1g Na hard?
lack of palatable foods (no bread, soup, celery, processed foods)
is fluid restriction indicated for chronic and stable HF?
usually not cuz Na intake decrease = thirst decrease (decreasing fluid intake appropriately), but needed if refractory HF or hyponatremia
this happens in 10-20% of HF patients, usually those with advanced/refractory HF, characterized by negative energy balance, loss of LBM, anorexia, wt loss
cardiac cachexia
summary of mechanisms that cause malnutrition in HF:
Anabolic-catabolic imbalance
- ^ symp nervous system activity
- ^ stress hormones
- some pt have ^ RMR (unless muscle wasting extensive)
Dyspnea
-increases workload of inspiratory muscles
Poor appetite-anorexia
- early satiety from gut/liver edema
- depression
GI malabsorption
- edema of GIT
- poor blood perfusion of GIT -poor blood flow to major arteries supplying GIT due to venous congestion
general supportive treatment strategies for malnutrition:
screen/monitor nutrition status and treat accordingly, high energy high protein diet (1.2-1.5g/kg BW for older adults chronic disease), small frequent feedings, supplements
newer approaches to malnutrition?
appetite stimulants, exercise/rehabilitation when possible (skeletal muscle preservation)
best evidence for micronutrient deficiency existing is for :
thiamin, riboflavin, pyridoxine (roles in energy metabolism, loss in urine)
what is conditionally essential nutrient?
not usually essential (body synthesizes) but under some circumstances (ie. disease) becomes essential
example of conditionally essential nutrient?
taurine (children don’t produce enough, but adults usually can synth enough)
constellation of interrelated risk factors that cluster in an individual and ^ risk for:
CHD and Type 2 Diabetes
major risk factors in metabolic syndrome:
– abdominal obesity
– insulin resistance and ^ plasma glucose
– atherogenic dyslipidemia
– hypertension
– prothrombotic state
– proinflammatory state
What is the difference between insulin resistance and Type 2 diabetes?
If have IR, not necessarily have ^ plasma glucose cuz insulin still may be effective enough to keep glucose range normal (^ insulin production in pancreas, hyperinsulinemia); type 2 have both
A harmonized definition for diagnosis for metabolic syndrome agreed upon by several organizations (including IDF, AHA, and WHO):
1) High blood pressure (≥ 130/85 mm Hg, or receiving medication)
2) High blood glucose levels (≥ 5.6 mmol/L, or receiving medication)
3) High serum triglycerides (≥ 1.7 mmol/L, or receiving medication)
4) Low HDL-Cholesterol (< 1.0 mmol/L in men or < 1.3 mmol/L in women)
5) Large waist circumference (≥ 102 cm in men, 88 cm in women; ranges vary according to ethnicity)
Whether diagnosing MetS predicts increased risk for CHD and diabetes better than adding up the individual risk factors is still debated.
Why diagnose MetS then?
- signal to treat all the risk factors – not just an isolated risk factor
- focuses attention on need for lifestyle therapies that target all metabolic factors concurrently
^ ___ believed to be central in causing metabolic abnormalities
visceral adipose tissue
why visceral adipose tissue?
genetic predisposition, decreased physical activity, adverse diet factors; source of pro-inflammatory molecules (cytokines); insulin-resistant so secretes high concentration of nonesterified fatty acids; inability of subcutaneous fat to act as protective metabolic sink
why NEFAs problematic?
cause metabolic abnormalities, resulting in insulin resistance in skel muscle and liver–>hyperinsulinemia–>endothelial dysfunction and atherogenesis–>drained by portal vein, expose liver to high concentration of these–>rids these by ^ VLDL production, fat accumulation in liver
diet specifically recommended for MetS?
no single diet, choice should target reduction of identified risk factors (smoking, alcohol, Na, kcal restriction, exercise, stress, diabetes, DASH, Mediterranean)
why visceral worse than subcutaneous fat?
deposits fat in undesirable places (liver, heart, muscle)
what is CHANGE program?
- Canadian Health Advanced by Nutrition and Graded Exercise Program
- 12 month personalized diet and exercise program led by family physicians, dietitians, kinesiologists
- Mediterranean diet and exercise
5 keys to success?
- central role of pt’s family doctor
- team approach
- personalization
- gradual intervention
- close and repeated followup over 12 months
additive vs. synergistic?
1+1=2 vs. 1+1=>2
