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If im the ra and unoxygenated blood is coming in

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If im the RA and unoxygenated blood is coming in- fatiguedBlood is still in the blood vessel- blood pressure increases.The blood never went into the heartAscites: area of back of fluid- in the abdomenEnlarged spleen- if it’s going to back up it might back upinto the organ- close to the atrium. Organs will be engorged.Distended jugular viensThe proximity between the congestion and the stomach-everything is backed up? HepacticWeight gain- the kidney are not peeing any fluid; organs are not getting any oxygenated blood- no fluid andorgans can’t work properlyEdema everywhereLeft Sided Heart FailureLV is very sickThe oxygen was last in pulmonary bed- mostsymptoms are pulmonaryNocturnal dysnpnea- cant lay down in bed-oxygenated blood is sitting in pulmonary bedElevated artery pressure- stuck in pulmonaryarteryPulmonary congestion-Restlessness- hold breath no oxygen = restlessConfusion- not enough blood bc LV is depriving itOrthopenia- short of breath when changingpositions; sitting to lyingTachycardia- body doesn’t have enough oxygen soits trying to increase heart rate to increase oxygeneven if it is not thereExertional dyspnea – SOB, does not have O2FatigueCyanosis- blood not pumped into the fingernailsCompensatory Mechanisms
When cardiac output is insufficient to meet body’s demands, these mechanisms operate to increase cardiacoutput:oSympathetic nervous system stimulationas a result of tissue hypoxia represents the most immediate compensatory mechanism.Stimulation of the adrenergic receptors causes an increase in heart rate (beta adrenergic) andblood pressure from vasoconstriction (alpha adrenergic).Because cardiac output (CO) is the product of heart rate (HR) and stroke volume (SV), anincrease in HR results in an immediate increase in CO.The HR is limited, though, in its ability to compensate for decreased CO.If it becomes too rapid, diastolic filling time is limited, and CO may start to decline.An increase in HR also significantly increases oxygen demand by the myocardium. Ifthe heart is poorly perfused because of arteriosclerosis, HF may worsen.Stroke volume (SV) is also improved by sympathetic stimulation.Sympathetic stimulation increases venous return to the heart, which further stretchesthe myocardial fibers causing dilation.According to Starling's law, increased myocardial stretch results in more forcefulcontraction.More forceful contractions increase SV and CO.After a critical point is reached within the cardiac muscle, further volume and stretchreduce the force of contraction and cardiac output.Sympathetic stimulation also results in arterial vasoconstriction.Vasoconstriction has the benefit of maintaining blood pressure and improving tissuePERFUSION in low-output states.However, constriction of the arteries increases afterload, the resistance against whichthe heart must pump.Afterload is the major determinant of myocardial oxygen requirements.As it increases, the left ventricle requires more energy to eject its contents, and SVmay decline.oOther renin-angiotensin system activation

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