65468
| Question | Answer |
| What is the problem with the heart over working during failure? | Increased 02 consumption , Hypertrophym, arrhythmias |
| What is the problem with venous compensation during heart failure? | Increased capillary pressure oedema |
| Effects of ANP | Kidney excreted salt and water Relaxes smooth muscle Inhibits RAAS |
| What is the cardiac output equation? | CO=HR x SV |
| What is the ejection fraction? | SV/EDV |
| What is Preload? | Degree of stretch of the ventricular myocardium at the end of diastole |
| What determines preload? | Circulating fluid volume Venous tone Myocardial compliance |
| What can excess of preload cause? | Increased atrial pressure, Increased venous pressure, Signs of congestion |
| What can affect stroke volume? | Mechanical; Neronal; Hormonal |
| What did the Straling heart-lung experiment show? | Intrinsic autoregulation. Allows SV increase without HR and that the higher reservoir the more filling, more stretch and a stronger contraction. Energy of contraction is proportional to the fibre length at rest |
| What happens within the muscle fibres to create a greater contraction? | Increased VEDV/VEDP causing stretch, increase myosin head to actin, increased cross bridges, increased force of contraction |
| What condition can impare the Frank Starling mechanism? | Dilated Cardiomyopathy |
| What determines central venous pressure | Vol. blood, Distribution of blood, Sypathetic nerve activity, Gravity and movement: Pooling decreases CVP and SV. Thoracic pump |
| Arterial baroreceptor reflex | Depressor/Pressor reflex. Medulla oblongata, acts via vagus nerve (heart) or sympathetic to heart, arteries and veins |
| Atrial receptors | Volume receptor. Low pressure stretch. High blood volume= Inhibit sympathetic vasoconstrictor pathways to kidneys, increased diuresis. Inhibition of ADH. |
| Correction from haemorrhage | Baro and atrial receptors Increased ADH from decreased AV receptor firing. Excites sympathetic pathway to kidney. RAAS. Decreased urine |
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