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Science
Medicine
Cardiology
3107 Exam 1: Heart Conditions
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Coronary Artery Disease, Heart Failure, Valvular Disorders
Terms in this set (49)
coronary atherosclerosis
abnormal accumulation of plaque (fatty substances) and fibrous tissue in the lining of arterial vessels causing blockages and narrowing which reduces blood flow to the myocardium
collateral circulation
network of tiny blood vessels which are essentially idle under normal conditions; when CAD limits blood flow to the myocardium, these vessels enlarge and become active to compensate for the narrow/blocked coronary arteries
-this is how people don't immediately die from narrowed/clogged arteries
CAD risk factors: modifiable
-smoking, alcohol
-diet; unhealthy diets raise LDL
-exercise; physical activity raises HDL and reduces triglycerides
-stress, medications
-hypertension; increases vessel stiffness & contributes to inflammation of the arteries
-diabetes
CAD risk factors: non-modifiable
-family history
-age: coronary arteries naturally lose elasticity and narrow with age
-gender: males have higher propensity and develop CAD earlier than females
-race: African-Americans have higher incidence of heart disease
diet: what foods should people with heart conditions eat?
-oats
-berries, citrus fruits
-low in saturated fat (limited amounts of healthy monounsaturated fats, like olive oil)
-low sodium
-high fiber
-white fish/salmon, lean protein
-limit red meat & alcohol (minimal red wine is fine b/c it has beneficial antioxidants)
pathophysiology of CAD
-plaque
-clot formation
-inflammatory response
-vasospasms
clinical manifestations of CAD
-myocardial ischemia
-angina pectoris
myocardial ischemia
inadequate blood supply which deprives cardiac muscles of oxygen
angina pectoris
chest pain brought about by myocardial ischemia
-results in damage but CAN occur w/o ACUTE MI
labs: evidence of CAD (CTHC mnemonic)
-cholesterol: HDL, LDL, total
-triglycerides
-homocysteine
-c-reactive protein
labs: evidence of myocardial damage (cant make this work)
-creatine kinase (CKMB)
-myoglobin
-troponin
-WBCs
clinical manifestations of MI (ppttsndc)
-pressure
-pain: caused by ischemia and may radiate (left arm &neck/jaw for men; epigastric region for women)
-tachycardia
-tachypnea
-shortness of breath
-nausea/vomiting
-diaphoresis
-cyanosis
what is heart failure? what is it characterized by?
clinical syndrome resulting from structural or functional cardiac disorders that impair the ability of the ventricles to fill or eject blood
-characterized by pump insufficiency, inadequate tissue perfusion, fluid overload
two types of left-sided HF: systolic HF and diastolic HF
-systolic HF: alteration in ventricular contraction from weakened heart muscles (left ventricle is unable to contract vigorously so pumping is insufficient)
-diastolic HF: stiff/noncompliant heart muscle impairs filling; left ventricle cannot fully relax/fill. diastolic HF is HF w/ preserved EF because ejection fraction is normal
HF predisposing/risk factors (hcrmv)
-hypertension: increases afterload/cardiac workload leading to hypertrophy; long-term hypertension impairs filling
-CAD
-renal dysfunction (fluid build-up)
-MI
-valvular dysfunction
pathophysiology of HF
-contractility/inotropic effect:
strength of contraction (positive inotropic meds increase contractility)
-preload:
amount of stretch of the myocardium prior to systole; HF compromises this
-afterload:
amount of resistance heart must overcome to open aortic valve and eject blood into systemic circulation; HF increases afterload, making it harder to eject blood
-cardiac output: low SV decreases total CO
cardiac output
volume of blood the heart ejects per MINUTE
CO = SV x HR
what is stroke volume (SV)? how is it measured?
volume of blood pumped from left ventricle per BEAT/CONTRACTION
-normal SV is 70 ccs/mL
-measured by testing ejection fraction
ejection fraction
measurement of the volume percentage of left ventricular contents ejected with each contraction
-SHOULD BE 55% (55-65%)
chemoreceptors
receptors in the carotid sinus which detect low blood O2/high CO2 (inadequate perfusion)
baroreceptors
receptors in the carotid sinus which measure blood volume; when CO drops, they will detect the low stroke volume
compensatory cycle
-SNS:
chemoreceptors trigger SNS (with the help of epinephrine from adrenal medulla) to initiate vasoconstriction to increase HR & BP
-RAA Cascade:
chemoreceptors stimulate Renin & Angiotensin which also increase HR & BP through vasoconstriction; baroreceptors trigger aldosterone (adrenal cortex) which causes sodium and water retention to increase blood volume & BP
-BNP: protein in the atria which is stimulated by baroreceptors tp trigger release of antidiuretic hormone (ADH, posterior pituitary)
-ADH signals kidneys to decrease urine output to conserve water to maintain blood volume
left-sided HF: causes and clinical manifestations
causes: compromised left coronary artery, mitral valve, aortic valve; damage in the left side of the heart
-blood will back up into the lungs (pressure builds up in vessels and pushes fluid into the alveoli)
-dyspnea/orthopnea
-low oxygen saturation
-crackles
-cough (productive or non-productive)
-high respiratory rate
-cyanosis
-dizziness/lightheadedness (decreased perfusion to brain)
-fatigue
-oliguria (low urine output [below 30ml per hour])
right-sided HF: causes and clinical manifestations
causes: compromised right coronary artery/tricuspid valve
-blood/fluid will back up into systemic circulation
-hepatomegaly: liver enlarges as blood flows back from inferior vena cava into the liver
-periorbital edema
-dependent edema
-jugular venous distention (JVD)
-weight gain
-nocturia
labs: evidence of HF
BNP blood test
-normal: less than 100, over 100 indicative of HF
Echocardiogram
-measures ejection fraction
-normal EF is 55%, under 55% indicates HF
fluid restriction
often ordered for patients with heart conditions; maximum fluid intake is determined by adding 500mL to the patient's urine output in the last 24 hours
predisposing factors & causes: valvular disorders
-aging (degeneration, wear & tear, lose elasticity)
-congenital defects
-infectious diseases of the heart: rheumatic fever, endocarditis
-smoking
mitral stenosis
narrowing/obstruction to blood flowing from the left atrium into the left ventricle
pathophysiology & manifestations: mitral stenosis
-snap murmur; click upon listening to auscultation of apical pulse
-enlarged left atrium (dilation & hypertrophy) & embolus & thrombus
-left-sided HF (followed by right sided)
mitral regurgitation
inability of the mitral valve to close completely causing blood to flow back into the left atrium from the left ventricle during systole
pathophysiology & manifestations: mitral regurgitation
-weak, floppy valves
-blood trickles back into atrium (but blood is still moving, so it won't pool and clot as it does with stenosis)
-Left sided HF, then right
aortic stenosis
narrowing of the aortic valve (between the left ventricle and aorta)
pathophysiology & manifestations: aortic stenosis
-loud, rough, harsh systolic murmur over aortic area (right 2nd intercostal space)
-syncope (inadequate brain perfusion > dizziness > loss of consciousness)
aortic regurgitation
flow of blood backward from the aorta into the left ventricle during diastole
pathophysiology and manifestations: aortic regurgiation
-increased pulsations in head/neck (thrills/heaves)
-high pitched murmur
-widened pulse pressure (normal is approx. 40)
aneurysm
ballooning of a weakened portion of an arterial wall
pathophysiology & manifestations: aortic abdominal aneurysm
-abdominal bruit (loud, audible rush of blood)
-usually occurs in men over 50
-ballooning and possible rupture
-hematuria (microscopic, requires urinalysis; can be first indication of aneurysm)
raynaud's disease
condition which causes "attacks" that limit blood supply to fingers and toes in response to cold temps/stress
pathophysiology & manifestations: raynaud's
-smoking, autoimmune disease, extreme anxiety are predisposing factors
-intermittent vasoconstriction in hands/feet
-more common in females
-may be autoimmune
-pallor > cyanosis > rubor
-paresthesia (prickling, tingling) and burning
labs & diagnostics: aortic/mitral stenosis, regurgitation
BNP and echocardiogram (to measure myocardial hypertrophy
labs & diagnostics: aortic abdominal aneurysm
CAT/CT scan to see and determine size of the aneurysm
path of blood flow through the heart
superior/inferior vena cava > right atrium > tricuspid valve > right ventricle > pulmonary valve > pulmonary trunk > pulmonary arteries > lungs (receives oxygen) > pulmonary veins > left atrium > bicuspid/mitral valve > left ventricle > aortic valve> aorta > systemic circulation
which heart chamber generates highest pressure?
left ventricle
primary cardiovascular control center is located in the:
medulla oblongata
ischemia (general)
an inadequate blood supply to provide adequate oxygenation
hypoxia
deficiency in the amount of oxygen reaching the tissues (ischemia will lead to THIS)
atrioventricular valves
between atria and ventricles (mitral/bicuspid & tricuspid)
semilunar valves
pulmonary valve and aortic valve
the ___ is known as the pacemaker of the heart.
sinoatrial (SA) node; located in the right atrium
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