Pulse Pressure

Pulse Pressure

Definition: Systolic BP - Diastolic BPExample: 120 - 80 = 40 mmHg

Variations in Pulse Pressure are due to:

• changes in compliance of aorta
• changes in stroke volume

Factors that determine pulse pressure

It is helpful to think of the definition of compliance C = ∆V/∆P and rearrange this to think about factors governing ∆P (stroke volume).

∆P = ∆V/C

Factors affecting systolic pressure

1. Compliance of the aorta
• A highly compliant aorta (i.e., less stiff) has a smaller pulse pressure for a given stroke volume into the aorta.
• A larger stroke volume (not shown in the figure) produces a larger pulse pressure at any given compliance.
• Aortic compliance decreases with age due to structural changes, thereby producing age-dependent increases in pulse pressure.
• For a given stroke volume, compliance determines pulse pressure and not mean aortic pressure.
• However, because vessels display dynamic compliance, increasing the rate of ventricular ejection (as occurs with increased ventricular inotropy) will increase the pulse pressure compared to the same volume ejected at a lower rate.

2. Stroke Volume

Factors affecting diastolic pressure

3. Rate of runoff

3.  Runoff time

References: http://www.cvphysiology.com/Blood%20Pressure/BP002.htm

John Wood, PhD,  KUMC, lecture Power Points

Mitral Stenosis - Pathophysiology

emedicine

Pathophysiology

The normal mitral valve orifice area is approximately 4-6 cm². As the orifice size decreases, the pressure gradient across the mitral valve increases to maintain adequate flow.

Patients will not experience valve-related symptoms until the valve area is 2-2.5 cm² or less, at which point moderate exercise or tachycardia may result in exertional dyspnea from the increased transmitral gradient and left atrial pressure.

Severe mitral stenosis occurs with a valve area of less than 1 cm². As the valve progressively narrows, the resting diastolic mitral valve gradient, and hence left atrial pressure, increases. This leads to transudation of fluid into the lung interstitium and dyspnea at rest or with minimal exertion. Hemoptysis may occur if the bronchial veins rupture and left atrial dilatation increases the risk for atrial fibrillation and subsequent thromboembolism.

Pulmonary hypertension may develop as a result of (1) retrograde transmission of left atrial pressure, (2) pulmonary arteriolar constriction, (3) interstitial edema, or (4) obliterative changes in the pulmonary vascular bed (intimal hyperplasia and medial hypertrophy). As pulmonary arterial pressure increases, right ventricular dilation and tricuspid regurgitation may develop, leading to elevated jugular venous pressure, liver congestion, ascites, and pedal edema.

Left ventricular end-diastolic pressure and cardiac output are usually normal in the person with isolated mitral stenosis. As the severity of stenosis increases, the cardiac output becomes subnormal at rest and fails to increase during exercise. Approximately one third of patients with rheumatic mitral stenosis have depressed left ventricular systolic function as a result of chronic rheumatic myocarditis. The presence of concomitant mitral regurgitation, systemic hypertension, aortic stenosis, or myocardial infarction can also adversely affect left ventricular function and cardiac output.

Buffers

Buffers

The body has a very large buffer capacity.

This can be illustrated by considering an experiment where dilute hydrochloric acid was infused into a dog

(Pitts RF. Mechanisms for stabilizing the alkaline reserves of the body. Harvey Lect 1952-1953; 48 172-209. PubMed.)

In this experiment, dogs received an infusion of 14 mmols H+ per litre of body water. This caused a drop in pH from 7.44 ([H+] = 36 nmoles/l) to a pH of 7.14 ([H+] = 72 nmoles/l) That is, a rise in [H+] of only 36 nmoles/l.

SO: If you just looked at the change in [H+] then you would only notice an increase of 36 nmoles/l and you would have to wonder what had happened to the other 13,999,964 nmoles/l that were infused (14 mmolsH+/L = 14,000,000 nmoles/L.)

Where did the missing H+ go?

They were hidden on buffers and so these 13,999,964 nmoles/L of hydrogen ions were hidden from view.

Buffering hides from view the real change in H+ that occurs.

Because of the large buffering capacity, the actual change in [H+] is so small it can be ignored in any quantitative assessment, and instead, the magnitude of a disorder has to be estimated indirectly from the decrease in the total concentration of the anions involved in the buffering. The buffer anions, represented as A-, decrease because they combine stoichiometrically with H+ to produce HA. A decrease in A- by 1 mmol/l represents a 1,000,000 nano-mol/l amount of H+ that is hidden from view and this is several orders of magnitude higher than the visible few nanomoles/l change in [H+] that is visible.) - As noted above in the comments about the Swan & Pitts experiment, 13,999,994 out of 14,000,000 nano-moles/l of H+ were hidden on buffers and just to count the 36 that were on view would give a false impression of the magnitude of the disorder.

The Major Body Buffer Systems
Site	Buffer System	Comment
ISF	Bicarbonate	For metabolic acids
	Phosphate	Not important because concentration too low
	Protein	Not important because concentration too low
Blood	Bicarbonate	Important for metabolic acids
	Haemoglobin	Important for carbon dioxide
	Plasma protein	Minor buffer
	Phosphate	Concentration too low
ICF	Proteins	Important buffer
	Phosphates	Important buffer
Urine	Phosphate	Responsible for most of 'Titratable Acidity'
	Ammonia	Important - formation of NH4+
Bone	Ca carbonate	In prolonged metabolic acidosis

Henderson-Hasselbalch Calculator

Henderson-Hasselbalch Calculator



calculates pH from values for PCO₂ and HCO₃⁻





Online Acid Base Physiology