HTN

baroreceptors and chemoreceptors

• found outside of circulation
• -responses to pain and cold
• -less consistent
• -higher center responses??

• heart rate
• vascular smooth muscle tone

• chemosensitive cells that monitor CO2, O2, and H+ ion content
• -located between two carotid bodies (two common carotids)

regulation ventilation

• vasoconstriction
• -stimulated due to decrease oxygen and increased carbon dioxide/ hydrogen ions

enzyme made, stored, and released by juxtumedullary cells

released in response to increase sympathetic nervous system activity or decrease BP, ECF volume, and sodium concentration

• start with angiotensin----> renin is added---->  this turns into angiotensin I-------> converting enzyme ACE (found in lungs) turns angiotensin I into angiotensin II-----> two things can happen from here
• 1. stimulation of aldosterone secretion----> aldosterone---> increased water and sodium retention----> increased preload
• 2. constriction of vascular smooth muscle----> increased afterload

• strong vasoconstrictor of arterioles (veins to a lesser degree)
• -reduce sodium excretion by increasing sodium reabsorption in the proximal tubules of the kidney.
• -stimulates release of aldosterone (can result in hypokalemia)

• aka ADH -secreted by posterior pituitary
• - secreted in response to decrease in blood volume, bp, and increase in osmolarity.
• -direct vasoconstrictor effect, and anti-diuretic properties.

• high blood pressure not caused by another disease
• -95% of cases

• risk factors
• -family hx
• -age related (diastolic pressure increase until -50 yr old, systolic continues to rise)
• -race (AA have higher incidence and it is more severe)

• -increased sympathetic activity- stress
• -overproduction of sodium retaining hormones (aldosterone) and vasoconstrictors (angiotensin II and vasopressin).
• -high sodium intake
• -increased renin secretion (starts renin-angiotensin-aldosterone system)
• -deficiencies of endogenous vasodilators
• -DM, obesity

• temporary increase in Blood pressure (up to 30 mmHG not uncommon) which is caused from hypoxemia, arousal, and activation of SNS
• - heart is pumping harder to removed excess CO2

pumps harder to remove excess carbon dioxide

increased workload of left ventricle leading to left ventricular hypertrophy (CHF, cardiac dysrhythmias, sudden death)

from 2 am-5 am

• Highest after getting up in morning and decreases through out the day.
• -MIs more common in morning

• **weight reduction
• **reduction of dietary sodium **** no more than 2-6 mg/day
• -limit alcohol intake- male 2 drinks/day female 1
• -quit smoking
• -reduce food high in fat
• -pharm tx based on severity of HTN

• -hemodynamic instability and hypotension
• **maintenance of vascular volume and careful titration of anesthesia is important
• -D/C 24-48 hours prior to surgery

the day before

• HTN
• ** if patient is hypertensive in pre-op they usually go the other way in the OR.

• 110-115 mmHg is most often the criteria for postponement. Can lead to target organ damage.
• *urgency of surgery is a major predictor

• -develop exaggerated responses to direct laryngoscopy (increased bp)
• -more likely to  develop perioperative myocardial ischemia
• -or to require antihypertensive during the perioperative period.
• -evaluate end organ damage ( should be done in preop)
• - If patient has essential HTN presume that they have ischemic heart disease until proven otherwise.

• Beta blockers
• clonidine

• HTN due to another cause
• -tx the cause

kidney disease

• reduced renal blood flow and activation of the renin-angiotensin-aldosterone syndrome .
• * can be in one or both kidneys

• 1. atherosclerosis of proximal artery
• -artherosclerotic stenosis accounts for 70-90%

2. fibromuscular dysplasia ( a non-inflammatory vascular disease affecting the renal arteries)

*genetic factors may be involved

• hyperaldosteronism
• cushing syndrome
• pheochromocytoma

• fatigue, weakness, HA, paresthesia, nocturnal polydipsia, and polyuria
• -hypokalemia and alkalosis
• -high serum, aldosterone, low renin

caused by prolonged exposure to high cortisol levels

clinical findings-truncal obesity, proximal muscle weakness, purple striae, moon faces, hirsutism

HTN caused from increased cortisol levels which enhances the effect of epi as a vasoconstrictor

• tumor of chromaffin tissue
• -mostly common in adrenal cortex
• -causes non continuous sweating and tremors, tx is surgery
• **tumor releases catecholamines- this causes increase in blood pressure

oral contraceptives

• often surgical
• -identifiable causes
• -correction of stenosis, or adrenalectomy (adreanal adenoma or pheochromocytoma)

• Pharmalogical
• -this is for people that revascularization is not possible
• -BP control with ACEI alone or in combination with diuretics

• malignant HTN
• -sudden marked elevations in blood pressure
• -diastolic greater than 120
• -acute or rapidly progressing organ dysfunction
• -cerebral artery vasospasm with encephalopathy, cerebral edema
• -papilledema (swelling around optic nerve)
• -HA, restlessness, confusion, motor deficits, visual disturbances
• -injuries to arterioles
• -intravascular coagulation and fragmentation of RBC
• -renal vessel damaged

elevated BUN, creatinine, low calcium, proteinuria, evidence of renal impairment.

• arterial monitoring
• -rigorous medical tx
• chronic HTN is associated with auto regulatory changes, care should be taken to avoid a rapid decrease (do not bring bp down to quickly this can lead to ischemia. 20% in first hour then gradually over next 2-6 hours)
• -goal is to reduce the blood pressure to a safer level.

blood pressure is severly elevated but the patient is not exhibiting signs evidence of target organ damage.

Pt presents with HA, epitaxis, or anxiety.

• systolic 18-25
• diastolic 6-10

the mean pulmonary artery pressure is higher than 25mmHg at rest or greater than 30 mmHg during exercise.

• occurs in absence of left sided heart disease, myocardial disease, congenital heart disease, or clinically significant respiratory, connective tissue, or chronic thromboembolic disease.
• (no familial context, and no identifiable risk factors- patients just get it)

no more than 15 mmHg and greater than 3 woods units (mmHg/L/min)

• a simplified measurement of pulmonary vascular resistance that uses pressures instead of more complicated units measured by subtracting pulmonary capillary wedge pressure from the mean pulmonary arterial pressure and dividing by the cardiac output.
• normal=0.3-1.6 mmHg/L/min

• vague sx
• -breathlessness, weakness, fatigue
• -abdominal distention
• -*angina and syncope (chest pain usually reflects reduced coronary blood flow to a hypertrophic right ventricle)
• -*limited CO are indicative and possible of severe cardiac ischemia
• -murmurs
• -tricuspid regurg
• -JVD
• -peripheral edema, hepatomegaly, ascites
• -pronounced pulmonic component of S2
• *uncommon- Left laryngeal nerve can become paralyzed

• Right heart cath is definitive means of determining severity of disease and which patients will respond to vasodilator therapy
• -given vasodilator considered positive f PVR and mean pulmonary artery pressure decrease acutely by 20% or more.

• -develops as a result of vasoconstriction, vascular wall remodeling, and thrombosis in situ
• -RV wall stress increases in response to increase in afterload produced by pulmonary HTN
• ----RV stroke volume and volume available for left ventricular filling decrease
• ----decreased CO, hypotension
• ---Rv dilated leading to tricuspid regurg

pulmonary HTN can be caused by a number of factors all of which force the hearts right side to work harder to pump blood to the lungs. The right chambers enlarge as they struggle to function, and blood is often forced backward through the tricuspid valve.

• right sided pressure increases, right to left shunting (if patent foramen ovale)
• -relatively fixed CO, increase in oxygen extraction with exertion
• -V/Q mismatch
• ** this can worsen overall pulmonary HTN

• right sided heart failiure
• due to:
• -RV afterload increase
• -hypoxemia
• -hypotension
• -inadequate RV preload

• oxygen, anticoagulation, and diuretics
• O2- reduces magnitude of hypoxic pulmonary vasoconstriction
• -anticoag- recommended because of sluggish pulmonary blood flow
• diuretics- decrease preload in patients with right side failure (especially useful in patients with hepatic congestions, ascites, and severe peripheral edema)

• long term benifits
• -give if patient exhibits response to vasodilator therapy
• -first class of drugs to provide long term benifit

• -inhibit the hydrolysis of cyclic GMP, reducing intracellular calcium concentration, leading to smooth muscle relaxation
• -produce pulmonary vasodilation and improve CO
• -associated with improved exercise capacity and reduction in RV mass
• -long term mortality benefits have not yet been proven

• activates guanylate cyclase, increasing cyclic GMP (leads to smooth muscle relaxation)
• -all NO is rendered inactive in pulmonary circulation which eliminates systemic effects
• -improves V/Q mismatch
• -improve oxygenation and lowers pul artery pressure in conditions associated with severe pulmonary HTN

• systemic and pulmonary vasodilators that also have antiplatelet effects
• -reduce PVR, improves CO and exercise tolerance

**complications- worsened intrapulmonary shunting, rebound PAH, systemic hypotension, infection, and bronchospasm

• -endothelin reacts with two receptors A and B
• -Endothelin A causes vasoconstriction and smooth muscle proliferation
• -endothelin B produce vasodilation via enhanced endothelin clearance and increased production of NO and prostacyclin
• *** (know) receptor antagonists have been shown to lower PA pressure and PVR and improve RV function, exercise tolerance, quality of life and mortality.

• RV assist devices in severe pulmonary htn and right heart failure
• -lung transplant in the only curative tx for many types of PAH
• --long term survival is similar with one or both lung transplant.