Transcript File - Nutrition and Food Technology-just

Cardiovascular System
Chapter 15
© 2007 Thomson - Wadsworth
Cardiovascular Diseases
• Leading cause of death in U.S.
• 70 million Americans
• $400 billion in direct and indirect
costs
• Rate has dropped 40% in past 30
years
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© 2007 Thomson - Wadsworth
Cardiovascular System
• Anatomy & Physiology
Regulates blood flow to tissues
Retrieves waste products
Thermoregulation
Gas exchange
Closed loop of blood vessels
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Cardiovascular System
• Heart
3 layers
• Epicardium - outer
• Endocardium – inner
• Myocardium – middle: muscle contraction
4 chambers
• Left and right atria
• Left and right ventricles
• See Fig. 15.2 for blood flow
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© 2007 Thomson - Wadsworth
Cardiovascular System
• Heart
Left ventricular hypertrophy (LVH) enlargement of the left ventricle
commonly related to HTN and CHF
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Cardiovascular System
• Electrical activity
Originates at the Sinoatrial (SA) node
(Fig. 15.3)
Measured through the
electrocardiogram (EEG)
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© 2007 Thomson - Wadsworth
Cardiovascular System
• Cardiac cycle
Repeating contraction/relaxation of
the heart
Systole (contraction)
Diastole (relaxation)
Exerted force on the walls of blood
vessels termed “systolic blood
pressure” and “diastolic blood
pressure”
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© 2007 Thomson - Wadsworth
Cardiovascular System
• Cardiac Function
Stroke volume – volume of blood
ejected with each contraction of LV
Regulated by:
•End-diastolic volume (EDV)
– Ejection fraction (EF)
•Mean aortic blood pressure (MAP)
•Strength of ventricular contraction
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Cardiovascular System
• Regulation of MAP
Affects cardiac output and heart rate
•Sympathetic nervous system
•Renin-angiotensin system
•Renal function
See Fig. 15.5 algorithm
Hormones involved
•epinephrine, vasopressin,
angiotensin II
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© 2007 Thomson - Wadsworth
Hypertension
• Chronic elevation in blood pressure
See JNC-7 criteria – Fig. 15.6
> 140/90 mmHg
“Silent killer”
Increases risk for CHF, kidney failure,
MI, stroke, aneurysms, vision
problems
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© 2007 Thomson - Wadsworth
Hypertension
• Etiology
Primary or essential – idiopathic
Secondary – result of another chronic
condition
Lifestyle factors – smoking, exercise,
diet
Sodium intake
Inflammatory response
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Hypertension
• Pathophysiology
Excessive secretion of vasopressin &
angiotensin II
Smoking
Renal disease
Adrenal disorders
Neurological disease
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Hypertension
• Treatment
Reduce risk of CD and renal disease
Lower BP to < 140/90
Through:
• Weight reduction, physical activity,
nutrition therapy, pharmacological
intervention
• See medication classes - Table 15.1
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Hypertension
• Treatment
Medication classes
• “Loop” diuretics
• Thiazides
• Carbonic anhydrase inhibitors
• Potassium sparing diuretics
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Hypertension
• Nutrition Therapy
DASH – Dietary Approaches to Stop
Hypertension
• Decrease sodium, saturated fat, alcohol
• Increase calcium, potassium, fiber
Lifestyle modifications
• See Table 15.3
Weight loss
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© 2007 Thomson - Wadsworth
Hypertension
• Nutrition Therapy
Sodium restriction controversial
• “salt sensitive” or “salt resistance”
Limit processed & cured foods, no
added salt during preparation and
cooking
Limit to 2400 mg/day
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© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
Hypertension
• Nutrition Therapy
Alcohol in moderation
Potassium, calcium, and magnesium
inversely related to BP
• from food intake vs. supplements
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Hypertension
• Nutrition Therapy
DASH
• Comprehensive dietary method
• Variety of foods – high fruit & vegetable
intake
• Complete diet – see Appendix E10
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Hypertension
• Nutrition Therapy
Physical activity
• At least 30 minutes per day
Smoking
• Cessation - single most important factor
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Hypertension
• Nutrition Therapy Prescription
Weight reduction
Assess dietary intake
Meet DASH dietary goals
Tailor exercise goals
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Atherosclerosis
• Thickening of the blood vessel walls
caused by presence of plaque (AS)
 Arteriosclerosis… includes loss of vascular
elasticity
 See Fig. 15.8 stages of plaque
 Results in restriction of blood flow
•
•
•
•
Myocardial infarction (MI)
Cerebrovascular incident (stroke)
Peripheral vascular disease (PVD)
CAD and CHF
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© 2007 Thomson - Wadsworth
Atherosclerosis
• Etiology - risk factors; additive
effect
Family history
Age and sex
Obesity
Dyslipidemia
Hypertension
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© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
Atherosclerosis
• Etiology - risk factors cont.
Physical inactivity
Atherogenic diet
Diabetes mellitus
Impaired fasting glucose/ metabolic
syndrome
Cigarette smoke
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© 2007 Thomson - Wadsworth
Atherosclerosis
• Pathophysiology
Inflammatory response
Injury to endothelial lining
Attracts platelets
Form small clots – thrombi
Continued migration of cells to the
area
Proliferation of the plaque
Rupture of fibrous cap can occur
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Atherosclerosis
• Clinical manifestations
Asymptomatic
May progress to ischemic heart
disease
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Atherosclerosis
• Treatment
NCEP ATP-III guidelines
• Modification of lipids and major risk
factors
• See Table 15.9
Medications
• See Table 15.10
Procedures
• Angioplasty
• CABG
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© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
Atherosclerosis
• Nutrition Therapy
Therapeutic Lifestyle Changes (TLC)
developed as component of ATP-III
• Modifications in fat, cholesterol
• Rich in fruits, vegetables, grains, fiber
• Limit sodium to 2400 mg
• Include stanol esters
• See Table 15.11 for summary, complete
guidelines in Appendix E9
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© 2007 Thomson - Wadsworth
Atherosclerosis
• Nutrition Therapy - Fat Modifications
 Total fat 25-35% of calories
 Very-low-fat diets
 Saturated fat < 7% of calories
 Avoid trans fats
 Increase intake of monounsaturated fats &
 Polyunsaturated omega-6 fatty acids
 Increase intake of omega-3 essential fatty
acids
 Limit dietary cholesterol < 200 mg daily
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
Atherosclerosis
• Nutrition Therapy - Other
Increase sources of soluble fiber
Increase intake of plant sterols
Weight loss – BMI 18.5-24.9
Regular physical activity
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Atherosclerosis
• Nutrition Therapy Prescription
Assessment of dietary fat intake,
saturated fat intake
• MEDFICTS assessment tool
• Dietary CAGE questions – Table 15.12
• REAP –Table 15.13
Target weight calculated
Prioritize nutrition problems
Multiple planned visits with R.D.
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© 2007 Thomson - Wadsworth
Ischemic Heart
Disease
• Inadequate blood supply to the
heart (a.k.a. CAD)
Occlusion caused by AS - may be
asymptomatic
Angina – chest pain
Can precipitate MI causing necrosis of
tissue
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Ischemic Heart
Disease
• Etiology
Acute coronary syndrome – acute MI
or unstable angina
• Plaque erosions, rupture of plaque
forming thrombus, vasoconstriction
Traditional risk factors for AS apply to
IHD
C-reactive protein (CRP) good
predictor
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Ischemic Heart
Disease
• Pathophysiology
MI or angina initiated by:
• Sudden blockage
• Hemorrhage
• Arterial spasm
• Increase in myocardial oxygen demand
All related to occlusion of the lumen
by AS
• Soft lipid more likely to cause MI
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Ischemic Heart
Disease
• Pathophysiology
Angina may be experienced with
increase in cardiac workload
(exertion)
With MI may have no previous
symptoms
Occlusion may initiate ventricular
tachycardia or ventricular fibrillation
Biological markers of MI – see Table
15.14
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Ischemic Heart
Disease
• Complications of MI
Disturbance of cardiac rhythm
Heart failure
Intracardial thrombi
Pericarditis
Cardiac rupture
Papillary muscle dysfunction
Ventricular aneurysm
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Ischemic Heart
Disease
• Clinical manifestations
Stable angina
• Indigestion, nausea, vomiting, sweating,
shortness of breath, weakness, fatigue
Rhythmic abnormalities
• Sudden onset bradychardia, palpitations,
syncope, dizziness
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Ischemic Heart
Disease
• Diagnosis
Non-invasive tests – see Box 15.8
WHO criteria
• Treatment
Oxygen, aspirin, morphine
Other medications – see Table 15.1
Best rest post MI
With slow increase in physical activity
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Ischemic Heart
Disease
• Nutrition Therapy
Post MI
• Decrease oral intake
• Clear liquids, no caffeine
• Progress to soft, more frequent meals
• Individualized – use TLC
recommendations
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Peripheral Arterial
Disease
• Occlusion of blood flow in noncoronary arteries (lower
extremities)
• Pathophysiology similar to AS and
IHD
• Eventually suffer from denervation
of affected muscle
• Can cause ulceration; commonly
foot or toes
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Peripheral Arterial
Disease
• Clinical manifestations/diagnosis
Intermittent claudication – cramp-like
pain with activity
Ankle Brachial Index (ABI)
Treadmill test
Major risk for amputation
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Heart Failure
• Impairment of the ventricles’
capacity to eject or fill with blood
Underlying cause – structural or
functional
End-stage CVD
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Heart Failure
• Etiology/pathophysiology
Stages of heart failure – see Table
15.15
Primary cause – IHD, htn., dilated
cardiomyopathy, valvular disease
Begins with heart injury or LVH
BP changes
Heart becomes weak and dilated
Progressive
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© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
Heart Failure
• Clinical manifestations
Decreased blood flow and oxygen
• Dyspnea, fatigue, weakness, exercise
intolerance, poor adaptation to cold
• Orthopenea - if left-sided failure
• Fluid retention, pulmonary congestion,
edema, hepatomegaly, splenomegaly,
ascites - if right-sided failure
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Heart Failure
• Treatment
Treat underlying cause
Control symptoms
• BP control
Prevent continued damage
Medications
Prevention of respiratory infections
Exercise
Nutrition therapy
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Heart Failure
• Nutrition Therapy Implications
Increased workload/difficulty eating
Cardiac cachexia – malnutrition/
wasting, fatigue, anorexia
• L-carnitine, CoQ10, creatine, thiamin,
taurine
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Heart Failure
• Nutrition Therapy Intervention
Control signs and symptoms
Promote overall nutritional status
rehabilitation – see Table 15.16
Sodium and fluid restriction
• 2000 mg Na
• Fluid 1 mL/kcal or 35 mL/kg
Correction of deficiencies
Increase nutrient density
Enhance oral intake
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
Heart Failure
• Nutrition Therapy
Assess drug-nutrient interactions
• Losses of water-soluble vitamins
Supplementation may be warranted
Consider arginine, carnitine and
taurine in dietary regimen
© 2007 Thomson - Wadsworth