Chp 16: Alterations in Blood Pressure

Systolic Blood Pressure (SBP)

The pressure in arteries and other blood vessels when the heart is contracting; the first (top) number recorded.

- stroke volume

Diastolic Blood Pressure (DBP)

The pressure in arteries and other blood vessels when heart is at rest or between beats; the second (bottom) number recorded.

- stroke volume resistance

Pulse Pressure (PP)

a measure of how much pressure your blood vessels experience during a heartbeat and the relaxation period between beats

PP = systolic - diastolic

Mean Arterial Pressure (MAP)

calculated average pressure within the circulatory system throughout the cardiac cycle

MAP = diastolic + 1/3 PP

Direct measurement of BP

catheter commonly placed in the radial artery

Indirect measurement of BP

Sphygmomanometer

Auscultation of Korotkoff sounds

- SBP: onset of Korotkoff sounds

- DBP: disappearance of Korotkoff sounds

Auscultatory gap

a period of diminished or absent Korotkoff sounds during the manual measurement of BP

- common in elderly

Determinants of Systemic Blood Pressure

Cardiac output and the resistance to the ejection of blood from the heart

- CO = SV (stroke volume) x HR (heart rate)

- End-diastolic volume is the preload

- Systemic vascular resistance (afterload) is determined by the radius of arteries and degree of vessel compliance

Cardiac Output (CO)

Volume of blood pumped by heart per minute (5-6L/min)

CO = stroke volume x heart rate

Preload

amount the ventricles stretch at the END of diastole (filling phase of ventricles)

aka EDV: end-diastrolic volume

Afterload

pressure the ventricles must work against to open the semilunar valves to pump blood out the heart

*affected by vascular resistance (pulmonary & systemic)

- systemic vascular resistance: determined by the radius of arteries & degree of vessel compliance

Short-term regulation of systemic blood pressure

changes in BP are mediated through activation of SNS: alpha & beta 1 receptor (epi & norepi)

⬇️ BP ➡️ baroreceptors ➡️ medulla oblongata ➡️ hypothalamus ➡️ increase SNS

- alpha (vasoconstriction) ➡️ increase resistance & blood pressure & decrease blood flow

- beta (SA node & increase conduction in AV node) ➡️ increase HR

- beta (contractility) ➡️ increase stroke volume

*PNS: slows heart

Long-term regulation of systemic blood pressure

Renin-angiotensin-aldosterone system (RAAS) important regulator of BP

⬇️ BP ➡️ decrease blood flow to kidneys ➡️ RAAS

RAAS (renin-angiotensin-aldosterone system)

⬇️ blood volume (renin is released by kidneys) ➡️ angiotensinogen to split & produce angiotensin I ➡️ ACE converts angiotensin I to angiotensin II ➡️

- angiotensin II causes vasoconstriction leading to ⬆️ BP

- angiotensin II releases aldosterone ➡️Na & H2O retention ➡️ increase blood volume & BP

Fluid Volume

- Regulated by neural, hormonal, renal

- Increase in extracellular fluid volume (preload) = increase CO & SVR = ⬆️ BP

SODIUM RETENTION (increased serum sodium level)

⬆️ osmolality & ⬆️ ADH secretion ➡️ kidneys reabsorb H2O (⬆️ preload)

Long-term regulation of systemic blood pressure: Atrial Natriuretic Peptides (ANP)

cause kidneys to increase sodium & water excretion by increasing the glomerular filtration rate (result in decrease of preload)

Normal blood pressure

SBP <120 mmHg

DBP <80 mmHg

Prehypertension

SBP 120-139 mmHg

DBP 80-89 mmHg

Stage 1 Hyperension

SBP 140-159 mmHg

DBP 90-99 mmHg

Stage 2 Hypertension

SBP ≥ 160 mmHg

DBP ≥ 100 mmHg

Isolated systolic HTN

SBP ≥ 140 mmHg

Isolated diastolic HTN

DBP ≥ 90 mmHg

Combined systolic & diastolic HTN

the highest reading determines the degree of HTN

Primary Hypertension

- unknown etiology (95% of all hypertension)

"silent killer"; damage already occurred to organs before diagnosis is made

End organ damage of hypertension

- heart = hypertrophy

- brain = dementia and cognitive impairment, stroke

- peripheral vascular = atherosclerosis (CVD)

- kidney = nephrosclerosis

- retinal complications

Modifiable risk factors of HTN

- dietary factors, sedentary lifestyle, obesity/weight gain, elevated blood glucose levels & total cholesterol, alcohol & smoking

*Lifestyle modification are the first & most important intervention in managing HTN

- weight loss, exercise, DASH diet, decreased sodium intake, moderate intake of alcohol

HTN Medications: Reduce Stroke Volume

Thiazide diuretics

Loop diuretics

Potassium-sparing diuretics

Aldosterone receptor blockers

ACE inhibitors

Angiotensin II receptor blockers

Venodilators

ACE Inhibitors

"-pril's"

- blocks angiotensin I to convert to angiotensin II

- lower BP & reduce workload on the heart & blood vessels

HTN Medications: Reduce Systemic Vascular Resistance

Combination alpha 1 & beta-blockers

ACE inhibitors

Angiotensin II receptor blockers

Calcium channel blockers

Alpha 1 blockers

Central alpha 2 agonists

Direct-acting vasodilators (arterial)

HTN Medication: Decrease Heart Rate

Beta-blockers

Combination alpha1 & beta-blockers

Secondary Hypertension

- known etiology (5% of all hypertension)

- most common form in children (renal disease)

- coarctation of the aorta (aortic narrowing)

- other causes: obstructive sleep apnea

Hypertensive emergency (crisis)

sudden increase in either or both systolic/diastolic blood pressure WITH evidence of end-organ damage

Hypertensive urgency

sudden increase in either or both systolic/diastolic blood pressure WITHOUT evidence of end-organ damage

Orthostatic (postural) Hypotension

An extreme response to the change from supine to upright position; activation of the short-term control mechanisms is slow or inadequate

- causes a decrease in SBP (≥ 10-20 mmHg within 3 min) when moving to an upright position

Complications of Orthostatic Hypotension

- dizziness, blurred vision, confusion & possible syncope

- associated with CVD & is a risk factor for stroke, cognitive impairment & death