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NUR 3125 Pathophysiology Exam 2 Newest
2026 - 2026 Questions with 100% Rated Answers
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State College
right heart fxn low pressure system!
- delivers blood through the lungs (pulmonary circulation)
- delivers blood to lungs to be oxygenated left heart fxn high pressure system!
- delivers oxygenated blood through systemic circulation
- delivers metabolic waste products to lungs, kidneys, liver mediastinum where the heart is located
- above the diaphragm, in between the lungs
heart wall layers epicardium (outer, smooth layer) myocardium (thickest layer of cardiac muscle; has its own conduction system) endocardium (innermost layer)
- all layers surrounded by the pericardium (double walled membranous sac:
- parietal (outer layer)
- visceral (inner layer) pericardial cavity space in between the parietal and visceral layers (contains parietal fluid - 20 mL) great vessels: IVC/SVC bring deoxy blood from systemic circulation back into the RA great vessels: right and left pulmonary arteries bring deoxy blood right right side of heart to the right and left lungs
- branch off into pulmonary capillaries
depolarization vs repolarization depolarization = systole = ventricular contraction repolarization = diastole = ventricular resting/filling coronary vessels supply oxygen and nutrients to the myocardium right coronary artery divides into conus artery, right marginal branch, and posterior descending branch left coronary artery divides into the left anterior descending artery and circumflex artery collateral arteries connections (anastomoses) between the branches of coronary circulation
- protects the heart from ischemia
- formed by arteriogenesis (branches from larger vessels) or angiogenesis (growth of new vessels from pre-existing vessels)
- presence of an effective collateral system is protective
diabetes and collateral damage diabetes impedes collateral formation
- increased prod of antiangiogenic factors (endostatin and angiostatin) conduction system pathway order cardiac APs conduction system: SA node through intranodal pathways (main is bachmann bundle), AV node, bundle of HIS (AV bundles), right and left bundle branches, purkinje fibers ECG sum of all cardiac action potentials
- have automaticity and rhythmicity Automaticity property of generating spontaneous depolarization to threshold
- basis for electrical activity
- allows SA and AV nodes to generate cardiac APs without any external stimulus
ECG: ST interval ventricular myocardium depolarization ECG: QT interval "electrical systole" of the ventricles
- varies inversely with the heart rate Propagation of cardiac APs AP fired during depolarization: electrical activation of muscle cells, movement of ions (K+, Ca2+, Cl-) across cardiac membrane
- inflow of (+) ions into the cell causes the inside of the cell to become less negatively charged Membrane potential Mvmt of ions into and out of the cell creates an electrical voltage difference across the cell membrane
- when membrane potential is less negative (during depolarization) and the threshold is reached...an AP is fired Refractory pd No new cardiac APs can be initiated
No muscle contraction; ensures that diastole (relaxation) will occur
- completed the cardiac cycle Autonomic nervous system
- Influence rate of impulse (firing), depolarization and depolarization of myocardium
- influence strength of ventricular and atrial contraction
- produce changes in heart/circulatory system faster than metabolic or humoral agents Cardiac innervation: sympathetic vs parasympathetic Sympathetic NS: increase electrical conduction and strengthen myocardial contractions (induce influx of Ca2+), vasoconstriction Parasympathetic NS: slows conduction of APs through the heart, decreases strength of contractions, vasodilation Adrenergic receptors Alpha or beta Release nori, epi (+) or Ach (-) Adrenergic receptors: beta 1
Stroke volume is dependent on what 3 factors? Pre load, after load, contractility
- all work together to determine SV and CO Normal adult CO 5L/min Factors affecting CO Ejection fraction, pre load, after load Ejection fraction Amt of blood ejected from ventricles with each heart beat
- normal is 66% for women and 58% for men (+- 8%) Calculated by SV divided by EDV
- good indicator of ventricular fxn What is a good indicator for adequate ventricular fxn? Ejection fraction
Pre load (initial muscle stretching prior to contraction - volume/pressure of blood after diastole (ventricular filling)
- aka VEDV; ventricular end-diastolic volume and VEDP; ventricular end-diastolic pressure What 2 factors determine preload?
- amt of blood returning to ventricle during diastole (amt of blood during filling)
- blood left in ventricle after systole - ESV (blood left in ventricle after contraction) What happens when preload exceeds physiologic range? Further muscle stretching, causing a decline in CO what does fluid retention do to preload? increases preload Frank-Starling Law the greater the stretch, the stronger the heart contracts...more volume, increases length of muscle fibers (direct relationship)
- can lead to myocardial hypertrophy
- decrease in CO Force of myocardial contractility depends on:
- Strength of ventricular myocardium in response to preload ex. Increase in venous return stretches muscle, increase in preload, increase in SV, increase in CO (however if preload exceeds normal range will decrease SV and CO)
- Alterations in inotropic agents (affect sympathetic innervation of ventricle)
- inotropic agents are hormones, neurotransmitters, meds that affect contractility
- Myocardial O2 supply (decrease in O2, decrease in contractility) do arteries or veins have valves? only veins; low pressure so need to prevent back flow when traveling back to heart cardiovascular vasomotor control centers in the brain control HR; mainly pons and medulla
- cardioexcitatory and inhibitory centers neural reflex effect on HR
- baroreceptor reflexes: regulate BP
ex. decrease in BP; will speed up HR, increase stretch and myocardial/smooth muscle contractions
- bainbridge reflexes: mechanoreceptors that change HR in response to atrial pressure
- atrial receptors
- hormones and biochemicals activation of sympathetic and parasympathetic system on HR sympathetic: speeds up HR parasympathetic: decreases HR; controls resting HR avg HR in healthy adults 70 bpm arteriogenesis vs angiogenesis formation of new blood vessels
- arteriogenesis: branching from larger vessels (arterioles)
- angiogenesis: growth of new vessels from existing ones (capillaries) roles of the endothelium (vasculature, lining of BVs)
effects of TPR on BF neural control
- changes in vessel diameter (arterioles)
- baroreceptors (change stretch of vessels to reg BP)
- arterial chemoreceptors (paO2, PaCO2, pH; reg BP) regulation of BP depends on
- MAP
- effects of CO
- effects of TPR
- effects of hyperemia (increased BF to one part of body) - vasodilation...decrease in BP
- effects of hormones (epi, norepi, antidiuretic, renin-angiotensin system, natriuretic peptides) MAP vs PP MAP: average pressure in arteries throughout the cardiac cycle - calculated by using systolic and diastolic values in a formula PP: difference in systolic and diastolic how are vessels arranged?
in series (greater resistance) or parallel (lesser resistance) adrenomedullin regulates BP vasodilator released by adrenal medulla and endothelial cells
- antagonizes aldosterone and angiotensin- 2 insulin protective mechanism on BV
- increase NO from endothelial and increase Ach (increases vasodilation)
- reduce platelet aggregation (clotting)
- anti-inflammatory NO - vasodilate decreases inflammatory reaction
- decreases monocyte-macrophage binding to vessel wall
- released by bradykinin
- potent vasodilator coronary perfusion pressure
arterial BP is controlled by? SNS, renal system, endocrine system, baroreceptors, chemoreceptors arterial BP ABP = CO x SVR (physiological factors + physical factors)
- physiological factors: CO, preload, afterload, contractility, HR
- physical factors: arterial blood volume and arterial compliance short term and long term control of BP short term: baroreceptors long term: kidneys (fluid regulation) causes of changes in BP baroreceptors, ANS, humoral factors, renal fxn, metabolic changes where are baroreceptors located?
carotid sinus, aortic arch, peripheral chemoreceptors, vagal and sympathetic efferent and afferent pathways what happens when baroreceptors increase stretch? an increase in stretch, increases firing of receptors
- causes vasodilation baroreceptors in HTN constantly overstretched, increases the settings of baroreceptors
- causes inadequate vasodilation...leads to vasoconstriction what are peripheral chemoreceptors sensitive to? PaO2, PaCO2, pH humoral factors autonomic response to stress: epi and norepi humoral factors: decrease in epi vasodilation in peripheral skeletal muscles
