Cardiovascular Physiology - Blood Pressure Flashcards
(21 cards)
Key points: MAP, systole, dichrotic notch, diastole
Draw and explain a graph of normal blood pressure over time
IMAGE - Blood pressure
Pressure on the Y axis (mmHg), time on the X axis (s)
MAP drawn on the graph as a horizontal line, and the areas A & B sum to 0.
Area A (systole) followed by the dicrotic notch caused by closure of the AV in diastole), is equal to area B (diastole)
MAP is calculated as MAP = SBP + 2DBP / 3
CPP, CBF, blood flow values for LV and RV
Explain coronary perfusion pressure and flow
IMAGES
Coronary perfusion pressure is what drives flow through the coronary arteries. Predominantly during diastole for the LV, and throughout most of the cardiac cycle for the RV.
Coronary Perfusion Pressure (CPP) = Aortic Pressure - Ventricular Wall Pressure
For the LV, this is therefore Aortic diastolic pressure - LVEDP
Ohm’s law dictates Pressure = Flow x ResistanceCoronary blood flow (CBF) = CPP/Coronary vascular resistance
LV CBF = 100ml/mg/min (Greatest in diastole as CPP is at hits highest, and vessels are least compressed)
RV CBF = 10ml/100g/min
During isovolumetric contraction, Coronary vessels are maximally compressed, leading to a flow of 0.
Categorise by mechanism
What mechanisms underly the body’s response to a rapid change in circulating volume?
A change in circulating volume causes an immediate change in CVP (and thus right sided preload, which transmits to the left side, affecting SV (and thus CO), and therefore blood pressure.
For instance, a sudden drop in circulating volume triggers these compensatory reflexes:
Baroreceptor reflexes to the medulla - pressure sensors have baseline discharge rates which slow when pressure decreases
Vagus from aortic arch, glossopharyngeal from carotid sinus
This inhibits the parasympathetic system, thus causing tachycardia, vasoconstriction and venoconstriction (pulmonary reservoir volume released into circulation)
Humoral responses
Adrenaline/Noradrenaline stimulate both beta and alpha adrenoceptors (inotropy, chronotropy and increased SVR)
ADH (Antidiuretic hormone) is released in response to reduced extracellular volume, acting on the collecting duct to conserve fluid and triggering thirst
Angiotensin II is a powerful vasoconstrictor, triggering ADH release, as well as sodium/fluid retention in the kidney
ANP (Atrial natureitic peptide) - normally secreted by atrial myocytes in response to distension (causing vasodilation and sodium excretion) and reduces as pressure falls, causing the opposite
Trans-capillary refill
Over several hours, fluid moves from cells to the intravascular compartment
Categorise into immediate, rapid and long-term
How does the body resopond if a litre of fluid is rapidly infused?
Immediate
Intravascular expansion raises CVP, and indirectly, preload to the LV. This increases blood pressure, stimulating baroreceptors, increasing parasympathetic tone, and thus causing a reflex bradycardia.
Rapid
If significant increase in plasma volume, Atrial stretch receptors release ANP, causing vasodilation and sodium excretion
Fluid redistributes from intravascular to extravascular spaces - this has no effect on osmoreceptors if the fluid is isotonic.
Angiotensin II and (nor)adrenaline release are suppressed.
Long term
Fluid remaining in the intravascular compartment raises BP until euvolaemia is restored.
There is renal filtration of excess Na and Cl ions.
Categorise into immediate, rapid, and long-term
What happens if the body suddenly loses a litre of blood?
Immediate
Intravascular depletion lowers CVP, and indirectly, preload to the LV. This reduces blood pressure, and therefore baroreceptor stimulation, reducing parasympathetic tone, and thus causing a reflex tachycardia.
Rapid
ANP production from atrial stretch receptors drops, reducing vasodilation and sodium excretion.
(nor)adrenaline release is triggered, activating adrenergic pathways to cause vasoconstriction, positive inotropy, and chronotropy.
Angiotensin II causes vasoconstriction.
Fluid redistributes from extravascular to intravascular spaces - this has no effect on osmoreceptors if the fluid is isotonic.
Long term
Compensatory mechanisms will largely maintain blood pressure until the volume is restored.
The renal system will retain Na and Cl ions, and therefore water.
ADH induces thirst and promotes retention of water in the collecting duct.
Describe the Starling equation and the forces that affect it
The forces that determine fluid flow across the capillary wall.
Hydrostatic
Push fluid out of a given space
Oncotic
Draw fluid into a given space (higher solute concentration generate more oncotic pressure)
Starling equation:Net fluid flux = K[(Pc - Pi) - σ(πc - πi)]
K is the filtration coefficient (how much fluid crosses the membrane per unit of pressure)
Pc is capillary hydrostatic pressure
Pi is interstitial hydrostatic pressure
σ is the reflection coefficient (how permeable the membrane is to solutes and proteins)
πc is capillary oncotic pressure
πi is interstitial oncotic pressure
How is flow across capillaries affected by Starling Forces?
IMAGE
At the arterial end of the capillary, hydrostatic pressure is higher, with a net outward driving pressure into the interstitium.
At the venous end, the hydrostatic pressure is lower, so the the oncotic pressure draws fluid back into the capillary.
Poor venous drainage results in a higher hydrostatic pressure, causing oedema.
Dehydration increases capillary oncotic pressure, increasing reabsorption of fluid back into the plasma.
Consider hydrostatic/oncotic pressures at the start/end of capillaries
How would Starling forces be affected by a sudden loss of a litre of blood?
There would be significantly reduced hydrostatic pressure at the arterial end of the capillary.
The net driving pressure would thus favour inward flow of fluid into the vasculature.
This can restore up to 1000ml/hour into the circulating volume
Define and categorise, with examples
Describe shock
Shock describes an inability to adequately perfuse the vital organs in order to meet metabolic demands.
Cardiogenic shock - factors affecting contractility
(ACS/Arrhythmias)
Obstructive shock - Extreme afterload
(Tamponade/PE)
Distributive shock - Adequate CO but lack of SVR causing a lack of preload
(Sepsis/Anaphylaxis/Neurogenic)
Hypovolaemic shock - Lack of preload
(Haemorrhage/Dehydration/Burns)
How does categorising shock affect managment?
Knowing the cause is crucial to management
CO = HR x SV (Contractility, preload, afterload)
Chronotropy will compensate to increase CO, but is limited.
Cardiogenic shock requires increased contractility, thus inotropes, intra-aortic balloon pump, or LVAD
Obstructive shock requires removal of the obstruction - for PE (endovascular surgery, ECMO, or thrombolyis), and for tamponade, pericardiocentesis.
Distributive shock requires vasopressors to restore SVR
Hypovolaemic shock requires volume replacement (IV fluids or blood products)
How can the severity of shock be categorised?
TABLE
Add image of table
Define Systemic Vascular Resistance
SVR is the opposition or resistance to blood flow in the systemic circulation, against which the left ventricle must push blood, in dynes.s.cm^-5
It is usually between 1,000 and 1,500 dynes.s.cm^-5
A dyne is the amount of force that will accelerate 1g by 1cm per second squared, 1/100,000 of a newton.
How is SVR affected by blood pressure
IMAGE
Starting with systemic blood pressure (Mean arterial pressure minus right atrial pressure)
The relationship is as follows
Systemic blood pressure = CO x systemic vascular resistance
After dividing systemic blood pressure by cardiac output, it is multiplied by 80 to convert from mmHg to dynes.s.cm^-5
This is not systolic blood pressure
Define and explain how it is calculated
Explain Pulmonary Vascular Resistance
IMAGE
SVR is the opposition or resistance to blood flow in the pulmonary circulation, against which the right ventricle must push blood, in dynes.s.cm^-5
It is usually between 100 and 150 dynes.s.cm^-5
The calculation is similar as for SVR, but instead uses mean pulmonary arterial pressure and left atrial pressure.
Categorise into four phases
Describe what happens during a Valsalva Manoeuvre in normal physiogy?
IMAGE
Phase 1
From the start of compression and lasting for a few seconds
Increase in intrathoracic pressure, increasing venous return, causing a rise in BP and reflex bradycardia
Phase 2
End of phase 1 until release of pressure
Sustained rise in intrathoracic pressure reduces venous return, lowering BP and causing a compensatory reflex tachycardia
Phase 3
From the release of pressure for a few seconds
Sudden pressure release enables a large empty pool of venous capacitance vessels, dropping blood pressure and causing a sustained tachycardia
Phase 4
End of phase 3 until normal parameters return
Restoration of venous return results in the tachycardia causing a rise in BP above baseline. This self-corrects through a reflex bradycardia, and gradually returns to normal
What abnormal responses to a Valsalva manoeuvre are seen in neuropathy and heart failure?
IMAGE (for context)
In autonomic neuropathy there is an excessive drop in blood pressure in phase two. In phase 4, there is a much smaller rise in BP and no bradycardia, due to loss of baroreceptor reflexes.
In cardiac failure, the blood pressure remains elevated thorughout phase two due to pre-existing excessive venous return, via two mechanisms:
1. Reduced venous return reduces preload of the failing heart (bringing back to a better area of the Frank-Starling curve)
2. Increased intrathoracic pressure reduces transmural pressure in the LV, aiding contractility and improving SV.
Explain Central Venous Pressure (CVP)
The hydrostatic pressure exerted on the walls of the great veins by venous blood, and can be measured in the IVC or SVC using a pressure transducer on a CVC.
It is used as an approximation of RA pressure, which in turn reflects the filling status of the RV and therefore the heart as a whole.
Draw and explain the waveform seen when transducing CVP?
IMAGE
Time (s) along the X axis, and Pressure (0-10) mmHg) on the Y axis.
The A wave is seen first, as atrial contraction produces a sharp upstroke in CVP, from ~4 to 10mmHg, which is the A wave.
(Absent in AF, and cannon A waves seen in tricuspid stenosis and CHB)
This peak drops off as the RA empties, to a trough at end-diastole. The next upstroke is the C wave, where the tricuspid valve bulges back into the RA during RV systole.
The X descent is seen next, as the tricuspid valve is dragged downwards throughout RV systole, reducing RA pressure
The V wave reflects ongoing atrial filling against a closed tricuspid valve. (Giant V wave in tricuspid regurg)
The Y descent reflects opening of the tricuspid valve and passive emptying of the RA into the RV.
The principle at play here is that there are no valves between the RA and the vena cava, so therefore there is a continuous column of fluid, and pressures will be very similar.
Explain pulmonary capillary wedge pressure
IMAGE
The pressure measured by a pulmonary artery flotation catheter (PAFC, also known as swan-ganz), wedged into a branch of the pulmonary artery, where there is a continuous column of blood between the catheter tip and the LA
It is therefore a measure of left atrial pressure, and thus, left atrial filling.
Explain the graph seen when advancing a pulmonary artery flotation catheter
IMAGE
RA - CVP (Between 0-8 mmHg)
RV - Systolic pressures of 25mmHg, but Diastolic pressures similar to CVP
PA - Systolic pressure similar to RV, but Diastolic held up by closure of PV (Windkessel effect)
Wedge pressure - LA (Between 5-12mmHg) (should be in West zone 3, where there is constant perfusion)
What factors affect pulmonary vascular resistance?
Increase PVR
Reduced CO
Increased blood viscosity
Lung volume much higher or lower than FRC
Vasoconstrictors
Histamine/Serotonin
Hypoxia
Hypercapnoea/Acidosis
Sympathetic stimulation
Decrease PVR
Increased CO
Reduced blood viscosity
Lung volume at FRC
Vasodilators
Acetylcholine
Hyperoxia
Hypocapnoea/Normal pH
Parasympathetic stimulation
