Physiology - CVS - Blood Pressure Flashcards
(21 cards)
Key points: MAP, systole, dichrotic notch, diastole
Draw and explain a graph of normal blood pressure over time
X axis: Time (s)
Y axis: Pressure (mmHg)
Graph requires MAP 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 = SBP + 2DBP / 3
CPP, CBF, blood flow values for LV and RV
Explain coronary perfusion pressure and flow
Coronary perfusion pressure 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
~~~
CPP = Aortic diastolic pressure - LVEDP
~~~
Ohm’s law is V = IR, or:
Pressure = Flow x Resistance.
Rearranged to
Flow = Pressure/Resistance
Therefore
CBF = CPP/Coronary vascular resistance
LV CBF = 100ml/100g/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?
CVP immediately drops, reducing right then left sided preload, affecting SV (and thus CO), and therefore blood pressure
Medullary baroreceptor reflexes
Vagus input from aortic arch, Glossopharyngeal input from carotid sinus
Discharge rates slow when pressure decreases, inhibiting parasympathetic tone. thus causing tachycardia, vasoconstriction and venoconstriction (pulmonary reservoir volume released into circulation)
Humoral responses
Adrenaline/Noradrenaline stimulate both α & β adrenoceptors (inotropy, chronotropy and increased SVR)
ADH (Vasopressin) release in response to reduced ECV, acting on the collecting duct to conserve fluid and triggering thirst
Angiotensin II also vasoconstricts, triggering ADH release, as well as sodium/fluid retention in the kidney
ANP (Atrial Natureitic Peptide) is 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 respond if a litre of fluid is rapidly infused?
Immediate
CVP rises, increasing preload to the RV and then LV. A rise in SV increases CO, and therefore BP
Baroreceptors fire more rapidly, increasing parasympathetic tone, and thus causing a reflex bradycardia
Rapid
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
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
CVP drops, decreasing preload to the RV and then LV. A drop in SV reduces CO, and therefore BP
Baroreceptors suppressed, 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 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 (Vasopressin) 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?
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 smaller reduction in 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
An inability to adequately perfuse the vital organs in order to meet metabolic demands.
Cardiogenic shock
Reduction in 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
(SV is Contractility, preload, and afterload)
Chronotropy will compensate to increase CO, but is limited, therefore the SV portion of the equation must be addressed
Cardiogenic shock requires increased contractility, thus inotropes, intra-aortic balloon pump, or LVAD
Obstructive shock requires removal of the obstruction/afterload - for PE (endovascular surgery, ECMO, or thrombolysis), 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?
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
SVR is calculated by taking systemic blood pressure (Mean arterial pressure minus right atrial pressure), dividing it by CO, and multiplying by 80 to convert from mmHg to dynes.s.cm⁻⁵
This is a an application of a rearrangement of Ohm’s law.
R = V/I → R = P/Q
This is not systolic blood pressure
A dyne is the amount of force that will accelerate 1g by 1cm per second squared, 1/100,000 of a newton.
Define and explain how it is calculated
Explain Pulmonary Vascular Resistance
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.
A dyne is the amount of force that will accelerate 1g by 1cm per second squared, 1/100,000 of a newton.
Categorise into four phases
Describe what happens during a Valsalva Manoeuvre in normal physiogy?
Phase 1
From the start of compression and lasting for a few seconds
Increase in intrathoracic pressure, compressing the pulmonary capacitance vessels , causing a rise in BP and reflex bradycardia
Phase 2
End of phase 1 until release of pressure
Sustained rise in intrathoracic pressure reduces systemic 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 refilling of the pulmonary capacitance vessels, dropping blood pressure and sustaining the 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?
Autonomic Neuropathy
Excessive hypotension in phase 2, with a much smaller rise in BP and no bradycardia in phase 4, due to loss of baroreceptor reflexes, and reflex tachycardia/bradycardia.
Cardiac failure
Blood pressure remains elevated thorughout phase two due to pre-existing excessive venous return, via two mechanisms:
- Reduced venous return reduces preload of the failing heart (bringing back to a better area of the Frank-Starling curve)
- 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.
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?
Time (s) along the X axis, and Pressure (0-10 mmHg) on the Y axis.
A wave reflects a sharp rise in CVP due to atrial contraction, from ~4 to 10mmHg
(Absent in AF, 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 at the start of RV systole
The tricuspid valve is dragged progressively downwards throughout RV systole, reducing RA pressure (X descent)
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 (PCWP)
The pressure measured by a pulmonary artery flotation catheter (PAFC, AKA 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.
This allows estimation of LVEDP (LV end-diastolic pressure), and estimation of LVEDV (LV end-diastolic volume)
Together, these can predict the likelihood of pulmonary oedema developing. Normal pressure is 6-12mmHg.
Innacuracies can occur if the PCWP is greater than LVEDP, such as in:
LV failure
MI or Ventricular hypertrophy causing diastolic dysfunction
High PEEP
MV disease
Significant AR
Explain the graph seen when advancing a pulmonary artery flotation catheter (PAFC)
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 (PCWP)
Equal to LA pressure (Between 5-12mmHg)
PCWP only accurate if tip in west-zone 3, with 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
