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NSG 533 Exam 3 2025 semester Exam Well
Accredited Questions And Answers Already A
Graded
two organizations for classification of HF
- American Heart Assocation (A,B,C,D) - based on structure
- New York Heart Association (None, I, I, II, III, IV, V) - based on physical activity limitations how to distinguish cardiac dysfunction versus cardiac HF cardiac dysfunction has structural abnormalities w/o symptoms once a patient develops symptoms along with structural abnormalities, they have HF compensatory mechanisms for HF
- Hemodynamics (Frank Starling Law) - can give inotropes as short term use to increase contractility (long-term can cause mortality)
- SNS activation (increase contractility, tachycardia, vasoconstriction)
- RAAS activation (angiotensin II binds to AT 1 Receptor - vasoconstriction)
two types of angiotensin II
- circulating
- tissue-derived effects of circulating angiotensin II on HF
- causes vasoconstriction
- increases secretion of ADH
- increase aldosterone secretion
- increases sodium reabsorption are aldosterone levels high or low in HF? 20x higher than normal effects of aldosterone on HF
- increases sodium and water reabsorption
- decreased potassium and magnesium
- decreased baroreceptor reflex
- sympathetic activation
- bradykinin
- nitric oxide types of ventricular remodeling
- concentric (thickened heart wall, diastolic HF, too stiff, HFpEF)
- eccentric (thin heart wall, systolic HF, contraction dysfunction, HFrEF) blood flow of the heart from right side to left side
- deoxygenated blood from the systemic system enters the superior/inferior vena cava
- right atrium
- tricuspid valve
- right ventricle
- pulmonary valve
- pulmonary artery
- lungs where blood is oxygenated
- pulmonary veins
- left atrium
- mitral/bicuspid valve
- left ventricle
- aortic valve
- aorta
- oxygenated blood to the systemic system
s/s right sided HF
- jugular vein distension
- edema
- ascites
- hepatomegaly s/s left sided HF
- pulmonary congestion
- SOB
- Crackles
- orthopnea Universal stages of Heart Failure (HF)
- At-risk for HF
- Pre HF
- HF
- Advanced HF according to the universal definition, what is "at-risk for HF"?
- do not have HF, but at risk
- no current or prior s/s
synonym for inotropy contraction (HFrEF) synonym for lusitropy relaxation (HFpEF) two types of left sided HF HFrEF (systolic) HFpEF (diastolic) endothelial dysfunction loss of the ability to vasodilate; imbalance of vasoconstrictors (endothelin) and vasodilators (nitric oxide) effect of neprilysin degrades BNP (ARNi can help - LCZ696) HFpEF criteria impairment in:
- filling
- relaxation
- LA pressures myocardial remodeling HFpEF vs HFrEF HFpEF: dysfunction is d/t comorbidities and inflammatory markers coming in contact with the endothelium HFrEF: dysfunction is d/t damage within the actual myocyte what can elevated BNP also be confused with? HF or renal failure endogenous effects of BNP
- lusitropic
- antifibrotic
- anti-remodeling
- balanced vasodilation of veins/arteries
- decreases aldosterone
- decreases endothelin
- decreases norepinephrine
modifiable risk factors associated with CAD
- smoking cessation
- HTN
- Physical inactivity
- Diabetes
- Dyslipidemia
- Obesity non-modifiable risk factors associated with CAD
- family hx
- advanced age (s/s present 10 years earlier in men; even out around menopause)
- gender/sex novel risk factors associated with CAD
- elevated lipoprotein (a)
- elevated high sensitivity C-reactive protein
- elevated fibrinogen
- elevated LDL particle number
- small, dense LDL define atherosclerosis
accumulation of lipid-laden macrophages within the arterial wall, leading to formation of lesions/plaques what is the leading cause of Peripheral Vascular Disease, Coronary Artery Disease, and Cerebrovascular Disease? Atherosclerosis explain the pathophysiology of endothelial cell injury (9 steps)
- endothelial cell injury d/t modifiable risk factors (HTN, smoking, diabetes)
- injured cells become inflamed
- inflamed endothelial cells a) don't make enough antithrombotic and vasodilating cytokines, and b) express adhesion molecules that bind macrophages with inflammatory and immune cells
- inflammatory process creates toxic oxygen free radicals that cause oxidation of LDL in the vessel intima
- oxidized LDL a) creates additional adhesion molecule expression, and b) recruits monocytes that differentiate into macrophages --> infiltrate vessel intima --> engulf oxidized LDL --> form foam cells
- accumulation of foam cells form a lesion called a fatty streak (produce additional toxic oxygen free radicals, inflammatory response/macrophages)
occlusive atherosclerotic plaque plaque rupture and thrombosis unstable angina, MI, coronary death, stroke unstable atheromatous lesions
- Thin, non-uniform cap, clinically silent
- macrophage-rich
- prone to rupture how can unstable plaques rupture?
- degradative effects of inflammatory cytokines and enzymes
- wall stress
- neurohumoral changes what are plaques that rupture called? complicated plaques
what happens when a plaque ruptures? platelet adhesion, clotting cascade, rapid thrombus formation --> occlusion of vessel -
ischemia or infarction of vessel list the acute coronary syndromes unstable angina, NSTEMI, STEMI what is an acute coronary syndrome? sudden coronary obstruction caused by thrombus formation over arteriosclerotic plaque manifestations of unstable angina
- emergency
- reversible myocardial ischemia w/ some myocardial damage
- arteriosclerotic plaque has become a complicated lesion
- ECG abnormalities
- treat w/ nitrates, anticoagulants, and antithrombotics ECG abnormalities of Unstable Angina ST Depression
- elevated LDH- 1 ECG abnormalities STEMI
- ST elevation
- T wave inversion ECG abnormalities NSTEMI
- ST depression
- T wave inversion pathophysiology of acute coronary syndromes atherosclerotic plaques with thin fibrous cap and lipid-rich core are prone to rupture force, inflammation, apoptosis, or enzymes cause the plaque to rupture platelet activation and adherence, production of thrombin and vasoconstrictors for a thrombus acute decrease in coronary blood flow resulting in unstable angina or MI
complications of myocardial infarction dysrhythmias, LV failure, RV infarction, cardiogenic shock, pericarditis, LV aneurysm isolated systolic hypertension a condition most commonly seen in the older adult in which the systolic pressure is greater than 140 mm Hg and the diastolic pressure is within normal limits (less than 90 mm Hg) primary/idiopathic hypertension most common of HTN diagnoses, no specific cause known secondary HTN caused by underlying disease or medication that raises PVR or cardiac output what are some medications that may raise PVR or cardiac output? oral contraceptives, antihistamines, corticosteroids risk factors for HTN obesity, diabetes, increased age, black males, family hx
- Renin Angiotensin Aldosterone System dysfunction
- SNS overactivity
- Elevated PVR explain the hypothesis of autoregulation high cardiac output/blood flow to tissues is more than required --> vessles constrict to reduce supply --> increased PVR --> thickening of arterioles target organs affected by chronic HTN
- heart
- eyes
- brain
- kidneys diagnosis for HTN 2 separate readings (averaged, 2 minutes apart)
- person is seated
- arm is supported at heart level
- at rest for at least 5 minutes before reading
- not have smoked or ingested caffeine within the last 30 min
define irreversible dementia abnormal proteins in the CNS that damage neurons three categories of irreversible dementia
- neurodegenerative
- vascular
- infectious three most common forms of dementia
- Alzheimer's Disease
- Lewy Body
- Frontotemporal hallmark clinical manifestations of dementia
- insidious onset (slow, gradual)
- progressive decline of cognition, memory, and ability to care for self define delirium
