CVS Theme 3

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  • Created by: Splodge97
  • Created on: 20-05-17 19:40
How can cardiac output be measured?
Via the invasive measurement (intercardiac catheterisation, probes from wrists/pelvis to heart which is now rare) or the non-invasive technique using a doplar ultrasound
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What are the factors affecting heart rate (and therefore CO)?
Autonomic innervation, hormones, fitness and age
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What are the factors affecting stroke voluume (and therefore CO)?
Heart size, fitness, gender, contraction duration, contractile force, preload and afterload. Anything increasing filling increases EDV/preload so SV is increased; also increased when increased contractility decreases ESV.
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What is preload?
The volume of blood acting to stretch one ventricle at the point of maximal filling (EDV). Increased in hypervolaemia, regurgitation into the ventricles and heart failure (maintains CO, but pulmonary oedema occurs as low kidney perfusion)
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What is afterload?
Pressure in the (left) ventricular wall at the point of ejection. Measured as systemic vascular resistance (which it must overcome to open SL valves). Increased by hypertension and vasoconstriction, increasing workload (worsening any heart failure).
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What is stage 1 of the volume pressure loop?
Period of filling - Starts at 50ml (remaining from last contraction) and 2-3mmHg. Volume increase as atria fill the ventricles, producing an EDV of 120ml (at point B, where bicuspid valve closes).
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What is stage 2 of the volume pressure loop?
Isovolumetric contraction - Volume of ventricle doesn't change (as all valves closed, since bicuspid closed after ventricular pressure increase) but early ventricular contraction increases the pressure to 80mmHg so arotic SL valve opens (at point C)
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What is stage three of the volume pressure loop?
Period of ejection - Further rise in pressure due to late ventricular contraction as well as a decrease in ventricular volume as blood leaves via the aortic SL valve. The aortic SL valve closes (point D) as relaxation decreases ventricular pressure.
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What is stage four of the volume pressure loop?
Isovolumetric relaxation - No change in blood volume (as all remaining is left from last contraction) but pressure decrease as walls continue to relax. Returns to point A where ESV occurs and bicuspid valve opens so cycle repeats.
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What is external work output?
The work of the heart, calculated by P x V
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What determines cardiac contraction efficiency?
70-90% due to oxidation of fatty acids, other due to other nutrients (glucose and lactase)
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How is cardiac contraction efficiency determined?
Efficiency = work done (used energy-loss as heat)/used energy. As large loss as heat usually only 20-25% (reduced to 5-10% in heart failure).
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What is abnormal in heart failure?
Preload, afterload, contractility and heart rate
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Describe the stages of heart failure
Inability to pump blood causes hypotension which is counteracted by an increase in vasoconstriction; however this prevents tissue perfusion so ischemia occurs causing angina (death without treatment)
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What is the difference between mild, moderate and severe heart failure?
Mild causes no/slight limitations of physical activity, morderate limits physical activity (may experience fatigue/palpitations/dyspnoea/angina), severe results in an inability to perform any activity without discomfort (may be present at rest)
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What are the generic causes of heart failure?
Coronary artery disease, hypertension, heart valve diseases, inflammation of the heart, congenital defects, lifestyle factors (alcohol/drugs/smoking) lung conditions and past heart attacks/arrythmias
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What is hypertonic cardiomyopathy?
Systolic failure, direct cause of heart disease. Portion of myocardium (between ventricles) enlarged so heart can't fill, reducing CO. More serious in left ventricle, common in athletes/soldiers through intense exercise.
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What is dilated cardiomyopathy?
Diastolic failure, direct cause of heart disease. Heart enlarged so can't pump efficiently as myocardium thickness reduced. EDV increases but SV decreases as walls become rigid so reduced contractility. May cause pulmonary oedema, worse on left.
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What is valve stenosis?
Direct cause of heart failure, when tissue leaflets of SL valves narrrow so become stiff and resist flow
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What is valve incompetence?
Direct cause of heart failure, valves unable to close properly so leak (in case of SL valves into ventricles); means workload must increase, damaging the myocardium
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What is reactive hyperaemia?
Works to counteract hypertension caused by heart failure. Triggered by ischemia/accumulation of waste. Increase in local vasodilators CO2, H+ and K+ acts to increase bloodflow through coronary arteries.
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Why is the left side of the heart impacted more by coronary artery disease?
Left coronary circulation already reduced as flow in it is more pulsatile since the left side of the heart contracts more strongly, squeezing them more tightly
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What substances build up in artery walls during astherosclerosis? What increases the risk of this?
Fats and carbonates. Risk increased in hypercholesterolaemia (through high sat fat intake), smoking and obesity.
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Why can't vasodilation occur to counteract astherosclerosis?
Relaxants from the healthy endothelium opposite cannot breach the plaque to reach the affected endothelium
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What are the risks of heart transplants?
Rejection (as attacked by T cells), graft failure (if pacemaker broken), infection (through immunosupressants, also cause gingival overgrowth), narrowed arteries (as new heart has lower CO) and a lack of extrinsic innervation preventing adapation
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Other cards in this set

Card 2

Front

What are the factors affecting heart rate (and therefore CO)?

Back

Autonomic innervation, hormones, fitness and age

Card 3

Front

What are the factors affecting stroke voluume (and therefore CO)?

Back

Preview of the front of card 3

Card 4

Front

What is preload?

Back

Preview of the front of card 4

Card 5

Front

What is afterload?

Back

Preview of the front of card 5
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