43 year old lady is recovering on the intensive care unit following a Whipples procedure. She has a central venous line in situ. Which of the following will lead to the "y" descent on the waveform trace?
B.Emptying of the right atrium
C.Emptying of the right ventricle
D.Opening of the pulmonary valve
3 Upward deflections and 2 downward deflections
- a wave = atrial contraction
- c wave = ventricular contraction
- v wave = atrial venous filling
- x wave = atrium relaxes and tricuspid valve moves down
- y wave = ventricular filling
The 'y' descent represents the emptying of the atrium and the filling of the right ventricle.
- The heart has four chambers ejecting blood into both low pressure and high pressure systems.
- The pumps generate pressures of between 0-25mmHg on the right side and 0-120 mmHg on the left.
- At rest diastole comprises 2/3 of the cardiac cycle.
- The product of the frequency of heart rate and stroke volume combine to give the cardiac output which is typically 5-6L per minute.
Detailed descriptions of the various waveforms are often not a feature of MRCS A (although they are on the syllabus). However, they are a very popular topic for surgical physiology vivas in the oral examination.
- Intrinsic myogenic rhythm within cardiac myocytes means that even the denervated heart is capable of contraction.
- In the normal situation the cardiac impulse is generated in the sino atrial node in the right atrium and conveyed to the ventricles via the atrioventricular node.
- The sino atrial node is also capable of spontaneous discharge and in the absence of background vagal tone will typically discharge around 100x per minute. Hence the higher resting heart rate found in cardiac transplant cases. In the SA and AV nodes the resting membrane potential is lower than in surrounding cardiac cells and will slowly depolarise from -70mV to around -50mV at which point an action potential is generated.
- Differences in the depolarisation slopes between SA and AV nodes help to explain why the SA node will depolarise first. The cells have a refractory period during which they cannot be re-stimulated and this period allows for adequate ventricular filling. In pathological tachycardic states this time period is overridden and inadequate ventricular filling may then occur, cardiac output falls and syncope may ensue.
Parasympathetic fibres project to the heart via the vagus and will release acetylcholine. Sympathetic fibres release nor adrenaline and circulating adrenaline comes from the adrenal medulla. Noradrenaline binds to β 1 receptors in the SA node and increases the rate of pacemaker potential depolarisation.
Image sourced from Wikipedia
Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow valves shut. Aortic pressure is high.
Late diastole: Atria contract. Ventricles receive 20% to complete filling. Typical end diastolic volume 130-160ml.
Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric ventricular contraction. AV Valves bulge into atria (c-wave). Aortic and pulmonary pressure exceeded- blood is ejected. Shortening of ventricles pulls atria downwards and drops intra atrial pressure (x-descent).
Late systole: Ventricular muscles relax and ventricular pressures drop. Although ventricular pressure drops the aortic pressure remains constant owing to peripheral vascular resistance and elastic property of the aorta. Brief period of retrograde flow that occurs in aortic recoil shuts the aortic valve. Ventricles will contain 60ml end systolic volume. The average stroke volume is 70ml (i.e. Volume ejected).
- Early diastole: All valves are closed. Isovolumetric ventricular relaxation occurs. Pressure wave associated with closure of the aortic valve increases aortic pressure. The pressure dip before this rise can be seen on arterial waveforms and is called the incisura. During systole the atrial pressure increases such that it is now above zero (v- wave). Eventually atrial pressure exceed ventricular pressure and AV valves open - atria empty passively into ventricles and atrial pressure falls (y -descent )
The negative atrial pressures are of clinical importance as they can allow air embolization to occur if the neck veins are exposed to air. This patient positioning is important in head and neck surgery to avoid this occurrence if veins are inadvertently cut, or during CVP line insertion.
- Preload = end diastolic volume
- Afterload = aortic pressure
It is important to understand the principles of Laplace's law in surgery.
- It states that for hollow organs with a circular cross section, the total circumferential wall tension depends upon the circumference of the wall, multiplied by the thickness of the wall and on the wall tension.
- The total luminal pressure depends upon the cross sectional area of the lumen and the transmural pressure. Transmural pressure is the internal pressure minus external pressure and at equilibrium the total pressure must counterbalance each other.
- In terms of cardiac physiology the law explains that the rise in ventricular pressure that occurs during the ejection phase is due to physical change in heart size. It also explains why a dilated diseased heart will have impaired systolic function.
- Increase in end diastolic volume will produce larger stroke volume.
- This occurs up to a point beyond which cardiac fibres are excessively stretched and stroke volume will fall once more. It is important for the regulation of cardiac output in cardiac transplant patients who need to increase their cardiac output.
- Baroreceptors located in aortic arch and carotid sinus.
- Aortic baroreceptor impulses travel via the vagus and from the carotid via the glossopharyngeal nerve.
- They are stimulated by arterial stretch.
- Even at normal blood pressures they are tonically active.
- Increase in baroreceptor discharge causes:
*Increased parasympathetic discharge to the SA node.
*Decreased sympathetic discharge to ventricular muscle causing decreased contractility and fall in stroke volume.
*Decreased sympathetic discharge to venous system causing increased compliance.
*Decreased peripheral arterial vascular resistance
Atrial stretch receptors
- Located in atria at junction between pulmonary veins and vena cava.
- Stimulated by atrial stretch and are thus low pressure sensors.
- Increased blood volume will cause increased parasympathetic activity.
- Very rapid infusion of blood will result in increase in heart rate mediated via atrial receptors: the Bainbridge reflex.
- Decreases in receptor stimulation results in increased sympathetic activity this will decrease renal blood flow-decreases GFR-decreases urinary sodium excretion-renin secretion by juxtaglomerular apparatus-Increase in angiotensin II.
- Increased atrial stretch will also result in increased release of atrial natriuretic peptide.