Blood Pressure Flashcards
Sympathetic BP control mechanism
Short term BP control, reacts rapidly to hypotension
Baroreceptors – stretch in vessel wall
-carotids, aortic arch
–>medullary vasomotor center
–>sympathetics, increase vasoconstriction, increased HR
Aortic arch vs carotid sinus baroreceptor signaling
Aortic arch – signal to solitary nucleus via CN X
Carotid arch – signal to solitary nucleus via CN IX
Baroreceptor response to hypotension
Decreased BP = less stretch
- > decreased afferent baroreceptor firing
- solitary nucleus decreases efferent parasympathetic stimulation – Vagus N.
- Increase efferent sympathetic stimulation
- > increased alpha1 vasoconstriction
- increase HR and contractility via beta 1 receptors
Baroreceptor response to hypertension
Elevated BP = increased arterial stretch
- > increased afferent baroreceptor firing
- > solitary nucleus increases parasympathetic stimulation -> decreased HR
Cushing’s reflex
Increased intracranial pressure
Constricts arterioles in brain -> cerebral ischemia
Hypothalamus stimulates SNS -> alpha 1 vasoconstriction
Triad:
Elevated BP
Reflex bradycardia – d/t baroreceptor stretch
Respiratory depression
Carotid massage to dx SVT
Increases stretch in carotid
Tricks body into thinking BP high -> decreased HR
Able to see underlying heart rhythm on EKG
Draw out vasoconstriction physiology
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Cause relaxation:
Via endothelial cell action:
- bradykinin
- ACh
- alpha2 agonists
- Histamine
- Serotonin
- Shear stress
Via sm.m. cell action:
- Nitrates
- LPS
- Ca2+ CCB – dihydropyradines
- Epinephrine (b2)
- Prostaglandin E2
- Sildenafil – PDE5 inhibitors
- BNP and ANP
Peripheral chemoreceptors
Respond to:
Hypoxia
Hypercapnia
Acidosis
Central chemoreceptors
Surface of medulla
Respond to changes in CO2 and pH in CSF not blood
Chemoreceptor primary mechanism
Primarily affect respiratory rate
Atrial natriuretic peptide (ANP)
Hormone produced in atria in response to:
- Increased atrial volume
- Increased atrial pressure
Vasodilator
Natriuretic peptide – diuresis
- act on afferent and efferent arterioles of renal glomeruli
- constrict efferent, dilate afferent -> increased GFR
- promotes diuresis
- decreases BP
Autoregulation – heart
Mediators: CO2, NO, adenosine
Underperfused:
- CO2 -> dilated coronary a.
- NO -> dilated coronary A
In ischemia already max dilated
Nitroglycerine causes systemic venous vasodilation
-reduces preload -> decreased myocardial O2 demand
Adenosine = energy starved state
- potent vasodilator
- > flushing reaction w/ IV push
Autoregulation – lungs
Hypoxia -> vasoconstriction
-delivers pulmonary circulation to well oxygenated areas of lungs
Diagnosing HTN
BP >= 140/90 on 3 or more different occasions
Risk factors of HTN
Age Smoking Excess etOH Excess Na+ intake Physical inactivity Obesity DM FHx Race: AA > whites
Causes of secondary HTN
Renal a. stenosis MC Chronic kidney disease or ESRD Medications: OCP, NSAIDs, antidepressants, glucocorticoids Illicit drugs – cocaine, amphetamines Adrenal diseases: -Hypercortisolism – Cushing syndrome -Hyperaldosteronism – Conn syndrome hypo/hyper thyroidism Hyperparathyroidism Coarctation of aorta OSA
HTN urgency vs emergency
Urgency: >= 180/120
-no end organ damage
Emergency: >= 180/120
-end organ damage: EKG changes, CP, HA, vision abnormalities, kidney, flash pulmonary edema
Tx:
IV nitroprusside – SE cyanide toxicity
IV labetalol
Left ventricular hypertrophy
Increased BP -> increased afterload on LV
-> wall hypertrophy
S4 sound
Increased myocardial O2 demand
- more tissue to oxygenate
- thicker doesn’t mean stronger -> stiffer, less compliant
LV holds less blood during diastole
Precursor for left sided HF and MI
Aortic dissection
Tear of intima of aorta – blood dissects into wall of vessel -> false lumen
Causes:
- HTN – MC
- Dz of aorta (e.g. cystic medial necrosis in Marfans)
Ascending aorta
Tearing chest pain, radiates to back
CXR: widening mediastinum
75% mortality if not tx early
Use b-blocker to decrease BP in HTN w/ aortic dissection
Decreases slope of rise in BP
Stanford type A vs B aortic dissection
A:
- Ascending aorta
- tx surgically, emergency
B:
Confined to descending aorta
-“Below the branches”
-tx medically
ACE inhibitors
-pril
inhibit ACE activation of AngII – prevents vasoconstriction
Increases bradykinin -> vasodilation
Decreases pre- and after-load
Use:
HTN, CHF, Post MI – prevent LVH remodeling
Kidney dz – reduce proteinuria, decrease progression of diabetic nephropathy
SE:
Cough, throat clearing d/t bradykinin
Angioedema – anywhere from lips to larynx
-> airway compromise; d/t bradykinin
hyperkalemia
mild renal insuffiency d/t slightly decreased GFR – increased serum Cr
Avoid in renal a. stenosis
Teratogenic
- fetal renal dysfunction
- oligohydramnios
- fetal cardiac malformations
Angiotensin receptor blockers
-sartan
inhibit AngII receptor
Same uses and SE as ACEI except no cough, still causes angioedema
Decreases pre- and after-load
Aliskiren
Renin inhibitor
SE:
Hyperkalemia
Renal insufficiency
Contraindicated in pregnancy
Not indicated for CHF and MI, only HTN
Nitrates
Nitroglycerin
Isosorbide dinitrate
Nitroprusside
Release NO -> venous relaxation, decreases preload
Tx: angina, acute pulmonary edema
SE:
Reflex tachycardia
Flushing
HA
Nitroprusside -> cyanide toxicity
Dihydropyridine CCBs
Amlodipine, felodipine, nicardipine, nifedipine, nisoldipine
MOA: act on vascular sm.m. -> vasodilation
Use: HTN Angina Vasospasm – Prinzmetal’s angina, Raynaud’s Esophageal spasm Migraine prophylaxis
SE: Peripheral edema Flushing Dizziness Constipation Reflex tachycardia
Nondihyropyridine CCBs
Diltiazem, verapamil
Block calcium channels at pacemaker cells
Use:
HTN
Angina
Arrhythmias
SE: Cardiac depression – avoid in CHF AV block Flushing Dizziness constipation
Minoxidil
Opens K+ channels -> hyperpolarize sm.m
-> relaxation of vascular sm.m.
Use:
Severe HTN
Topical application – hair loss
SE: hypertrichosis hypotension reflex tachycardia fluid retention/edema
JNC8 BP goals
Over 60 w/o DM or CKD – less than 150/90
All others less than 140/90
JNC8 initial pharmacotherapy for HTN in CKD pts
ACEI/ARB – renal protective
JNC8 initial pharmacotherapy for HTN in Black pts w/o CKD
Thiazide diuretic
CCB
JNC8 initial pharmacotherapy for HTN in Non-black pts w/o CKD
Thiazide diuretic
CCB
ACEI/ARB
Initial tx option/avoid in HTN plus CHF
ACE/ARBs
b-blocker (carvedilol, metoprolol, bisoprolol)
aldosterone antagonist
Avoid: CCB, b-blocker if acute decompensated CHF or cardiogenic shock
Initial tx option/avoid in HTN plus DM
ACE/ARB
Avoid b-blocker – masks hypoglycemic effects
Initial tx option/avoid in HTN plus Post-MI/CAD
Thiazide, b-blocker, ACE/ARB – decrease mortality
CCB, Nitrates – for angina
Initial tx option/avoid in HTN plus afib
b-blocker, diltiazem/verapamil – slow heart
Initial tx option/avoid in HTN plus bradycardia
Avoid b-blocker, diltiazem/verapamil (slows heart)
Initial tx option/avoid in HTN plus BPH
Alpha-blocker
Initial tx option/avoid in HTN plus pregnancy
Hydralazine
Methyldopa
Labetalol
Dihydropyridine CCB
Avoid: ACE/ARBs
Initial tx option/avoid in HTN plus migraines
CCB
b-blocker
Initial tx option/avoid in HTN plus essential tremor
Propranolol
Hydralazine
Increased cGMP -> stimulation of myosin phosphatase -> arterial relaxation, decrease afterload
Use: HTN urgency/emergency, HTN in pregnancy
SE: Reflex tachycardia Caution in CAD -> increased O2 demand Fluid retention Nausea HA Drug induced lupus
Antihypertensives safe in pregnancy
“Hypertensive Moms Love Nifedipine”
Hydralazine
Methyldopa
Labetalol
Nifedipine or other dihydropyridine CCB
