CardioVascular Flashcards
Arteries
carry blood away from heart
Veins
Carry blood towards the heart
Capillaries
Where nutrients and gases exchange occur
Functions of the cardio system?
Regulates blood flow to tissues Retrieves waste products Thermoregulation Gas exchange Closed loop of blood vessels
Blood flow pattern??
- 02 poor blood returns via inferior and superior vena
- R atrium
- R ventricle
- LR Pulmonary
- Lungs
- Co2 removed and O2 added
- Blood returns
- Heart via LR pulmonary vein
- L atrium
- L ventricle
- Pumped to the systemic circulation through aorta
SA node?
Sinoatrial node (Pacemaker) Initiates heartbeat and causes atria to contract on average 0.85 seconds
Systole?
Contraction of the heart chambers
Diastole?
Relaxation of the heart chambers
Stroke volume?
Volume of blood ejected with each contraction of the L ventricle with each systolic phase
Ejection Fraction (EF):
Fraction of blood that is ejected from heart by contraction of left ventricle.
Mean arterial BP(MAP):
determined by a combo of cardiac output and total peripheral resistance
Normal range BP:
70-110 mm Hg to perfuse all organs, tissues
Regulation of MAP:
Sympathetic nervous system
Renin-angiotensin system
The role of kidney in BP regulation
Kidneys role in RAAS
Kidneys secrete peptide hormone renin in response to reduced NaCl, ECF volume, and arterial BP.
Renin activates angiotensinogen
What is angiotensinogen?
plasma protein produced by the liver
Conversation of angiotensinogen
Angio 1 to angio 2 by ACE (angiotensin-converting enzyme) produced by lungs.
Ang 2 stimulates the adrenal cortex to secrete hormone aldosterone which stimulates Na reabsorption by kidneys. Resulting retention of Na exerts osmotic effect that holds more h20 in ECF.
Vasopressin?
Antidiuretic hormone
known as Arginin Vasopressim (AVP)
Secreted from posterior pituitary gland in response to increased plasma osmolality. Results in concentration of urine and reduced urine volume
Hypertension
Defined as chronic elevation in BP > 140/90 mmHg
Silent killer damages heart and arteries
Etiology of HTN
Primary or essential idiopathic- no known causes 90% of all cases
Age, ethnicity, family history. high BW
Secondary- results of another chronic condition: Renal, cvd, endocrine disorders, or neurogenic disorders.
Lifestyle factors- smoking, exercise, diet, sodium intake
Pathophysiology of HTN?
Excessive secretion of Vasopressin and angio2-increase BP
Smoking
Renal disease: interferes with action of nitric oxide, impairs endothelial relation and vasodilation
Adrenal disorders: excessive secretion of epinpherine and norepinephrine
Neurological disease: affecting medulla oblangata
Treatment of HTN?
Reduce risk of CVD and renal disease
Lower BP < 140/90
Weigh reduction, physical activity, nutrition therapy, pharmocological intervention
Medical treatment for HTN?
- Loop diuretics: Acted by inhibiting Na, Cl, K reabsorption in loop of henle of kidney
- Thiazides: same action as loop but in distal tubule and ascending loop of henle
- Carbonic anhydrase inhibitors: block enzyme involved with exchange of H+ with Na and H20.
- Potassium sparing diuretics: acts within the collecting and convoluted tubes- prevent sodium-potassium exchange and reduce aldosterone stimulation
Lasix
Lasix (furosemide) is a loop diuretic (water pill) that prevents your body from absorbing too much salt. This allows the salt to instead be passed in your urine.
DASH diet?
Dietary Approaches to Stop Hypertension 4-5 servings of Fruit 4-5 servings of vegetables 2-3 servings of nonfat, low fat dairy 6-8 servings of whole grains 2 or less servings of meat, poultry, or fish Nuts, seeds, and dry beans- 4/5 week Decrease total and sat fat Decrease sodium: 1500-2400mg/d Increase Ca, K, and Mg
Core of Lipoprotein
TG and Cholesterol esters
Lipoprotein surface?
Phospholipids
Proteins
Cholesterol
LDL is made up of what?
Mostly free cholesterol
Atheroscelrosis
Thickening of blood vessel walls caused by presence of plaque (AS) “hardening”
Arterioscelerosis
more general term includes loss of vascular elasticity- results in restriction of blood flow
Plaque development?
Renin-angiotensin system plays a role, tobacco, oxidized LDL, glycated substances from DM, and homocysteine.
What does nitric oxide have to do with atheroscelrosis?
An imbalance of NO is caused by oxidative stress, and NO contributes towards endothelial control like normal relaxation of smooth muscle in arteries, regulates leukocyte adhesion, platelet adhesion, and thrombosis.
Foam cells?
filled with cholesterol and are released into EX spaces where they form fatty streaks. This streak can occur as early as age 5
Thrombus
blood clot that stays
Embolus
blood clot that breaks from cellular surface and freely moves through the circulation.
Pathophysiology of Athersclerosis
Inflammatory response Injury to endothelial lining Attracts platelets Forms small clots Continued migration of cells to area Proliferation of the plaque Rupture of fibrous cap can occur
Gynoid obesity?
Fat around the hips
Android?
Fat around abdominal fat and insulin resistance, have a higher waist circumference which is assoc with risk of CVD
Diagnosing criteria for Metabolic Syndrome
Any 3 of the 5 constitutes MS Waist circumference TG HDL BP and Fasting Glucose
Desirable Lab Values
Total Cholesterol: <200 mg/dL
HDL >60mg/dL
LDL: <100mg/dL
TG: <150mg/dL
TLC Diet
Sat fat: <7% PUFA: up to 10% MUFA: Up to 20% Total F: 25-35% of kcal Chol: <200 mg/day Carb: 50-60% kcal Fiber: 20-30g/day Pro: Approx 15% of kcal Na: 2400 mg/day Stanol esters: 3.4g
Plant sterols?
Naturally occuring component of plant membranes just as cholesterol (animal).
Most abundant:
Beta-sitosterol
Campesterol
Stigmasterol
Structurally resemble cholesterol, not synthesized by humans.
Lowers serum cholesterol by inhibiting absorp of dietary and biliary cholesterol
Foods bearing claim must contain:
- 65g of plant sterols per serving
1. 7g of stanol esters per serving
Ischemia:
local temporary reduced blood supply d/t obstruction of heart “restriction”
Soft lipid?
more likely to cause MI
less likely to occlude large areas within the lumen
More prone to rupture
have a fibrous cap covering lipid rich core with macrophages
Inflammation from within the plaque will weaken the cap
Macrophages secrete substances that weaken cap
Large hardended plaques
Have more smooth muscle cells Less likely to rupture May occlude up to 70% of artery May cause angina Collateral circulation may develop over time will occlude the artery without infarct
Occlusion
Narrowing of the coronary artery from the buildup of cholesterol. This buildup is known as plaque in arteries throughout the body is called atheroscelrosis
Angina
Condition when a pt complains of chest pain due to lack of blood supply
Happens slowly with warning signs
Sudden blockage of vessel d/t acute plaque rupture and closure of artery w/ clot buildup
Stable angina
sub sternal pain when workload is increased, physical or emotional stress
Unstable angina
rapidly worsening chest pain on minimal exertion or at rest
MI and angina initiated by:
Sudden blockage Hemorrhage Arterial spasm Increase in myocardial oxygen demand One common factor: occlusion of lumen by AS plaque
Infarction:
area of dead tissue d/t loss of blood supply- resulting in development of necrotic tissue
What are the biomarkers for dx in MI?
Levels increase in blood then return to normal
CK-MB: more specific for cardiac tissue
CK: Creatine kinase
M and B: 2 polypeptides and form an isoenzyme of creatine kinase
Lactate dehydrogenase isoenzyme (LD-I)
cTnT and cTnI: Cardiac troponin T and I
What are cardiac biomarkers?
protein molecules released into blood stream from damaged heart muscle
Characteristic rise and fall pattern
Creatine kinase:
Increased in over 90% of MI, can also be increased in muscle trauma, physical exertion, post-op, convulsions
LDH-I
Predominates in heart and red cells Increases later than CK Normal levels; 313-618U/L Reaches max level in 48-72h Remains elevated for 7-10 days after MI
Troponin T and I
protein complex located on thin filament of striated muscles and are used as biomarkers for MI dx
Cardiac troponins different than skeletal muscle.
Isoforms very specific to cardiac injury
Preferred markers
Normal levels: 0.5ng/dL
Rise 4-6 hours, peak 12 hours, and return to normal 3-10 days
Post-MI Nutrition Therapy?
Reduce oral intake d/t pain, anxiety, fatigue, SOB
Limit intake to clear liquids
No caffeine to prevent arrhythmias, and decrease risk of vomiting and aspiration
Progress to soft, easily chewable foods
Small freq meals
Reduce exertion
Follow ATP III guidelines
The primary target of therapy
LDL Cholesterol
Stroke?
Sudden brain damage b/c lack of blood flow to the brain caused by a clot or rupture of a blood vessel Embolic: travels to the brain Thrombotic: Clot develops in artery Hemorrhagic= bleed Bleeindg around brain and into blain
Peripheral artery disease (PAD)
Occlusion of blood flow in non-coronary arteries (lower extremities)
Similar to AS and IHD
Eventually suffer from denervation of affected muscle
Can cause ulceration; commonly foot or toes.
Claudication
fatigue- heaviness, tiredness, cramping in the leg,
Pain or discomfort goes away once the activity is stopped or during rest.
Heart failure-
Impairement of ventricles capacity to eject or fill with blood
underlying cause- structural or functional
End stage CVD
Stages of Heat Disease
A: at risk but no structural abnormalities
B: Have structural disease but demonstrate no symptoms of HF
C: Patients w/ past or current symptoms of HF who have underlying structural HD
D: Patients with end-stage disease req specialized treatment, mech circulatory support, procedures to facilitate fluid removal.
Dyspnea
shortness of breath (SOB)
Orthopnea
SOB of breath associated with lying in supine position
Cardiac cachexia
Unintended weight loss due to cardiac complications
Left-sided failure
includes dyspnea and orthopnea
Right-sided failure
fluid retention
pulmonary congestion, edema, hepatomegaly, splenomegaly, ascites.
Nutrition therapy for CHF
50% of HF failure patients are malnourished Increased workload/difficulty eating Goal decrease work of heart 2g sodium is standard fluid restriction 1mL/kcal or 35mL/kg Alcohol non to mod Caffeine can cause MI or cardiac arrhythmia Fluid restricting EN formula if needed
Arginine
for increased production of NO
Carnitine:
ships FA into mitochondria for oxidation
Taurine:
reduced BP and combined with carnitine alleviates muscle fatigue in strenous workouts and raises exercise capacity
Factors assoc with development of cardiac cachex
Generalized cellular hypoxia Decreased energy intake Anorexia secondary to ascites with drug therapy Unpalatable diet and fluid restriction Breathlessness and exhaustion from eating Altered taste and smell Depression N/V
Heart transplant phases
Pre-transplant: control kcal, pro, Na, K, Fat, Chol
Avoid fluid overload
Immediate post: increase diet as tolerated
Follow DASH diet plan, Omega-3 FA, Vit Supp
Long-term post: Continue with education/monitoring
