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What is normal BP?
systolic <120 mmHg and diastolic <80 mmHg
What is elevated BP?
systolic 120-129 mmHg and diastolic <80 mmHg
What is stage 1 hypertension BP?
systolic 130 to 139 mmHg or diastolic 80 to 89 mmHg
What is stage 2 hypertension BP?
systolic 140+ mmHg or diastolic 90+ mmHg
What is systolic BP?
peak pressure in the arteries near the end of systole (top number)
What is diastolic BP?
resting pressure in the arteries during diastole (bottom number)
What is target SBP / DBP?
130/80
What is blood pressure (BP)?
pressure that occurs when blood pushes against the walls of your arteries
What is cardiac output (CO)?
amount of blood ejected by each ventricle in one minute
What is cardiac output (CO) equal to?
stroke volume (SV) x heart rate (HR)
What is systemic vascular resistance (SVR)?
the resistance to blood flow in the systemic circulation
What is the equation for blood pressure (BP)?
blood pressure (BP) = cardiac output (CO) x systemic vascular resistance (SVR)
What is preload?
the volume of blood in the ventricles resulting in the stretch on the ventricles at the end of diastole
A higher filling volume _____ SV and ____ BP
increases, increases
What is contractility?
the force of the heart muscle contraction
A stronger contraction leads to ____ SV and ____ BP
increased, increased
What is afterload?
the resistance (pressure) the heart must overcome to circulate blood around the body
Higher resistance _____ SV and _____ BP
decreases, increases
How is preload approximated?
by end-diastolic volume (EDV) via:
ventricular filling
force of contraction
fluid/blood volume
What does the Frank Starling Law associate with?
preload
What does the Frank Starling Law say?
increased filling → myocardial stretch → stronger contraction
stretch improves contraction up to an optimal point
overstretching decreases contraction
Analogy associated with preload
rubber band; optimal stretch = most productive snap
What are the major contributors to afterload?
ventricular wall tension
systemic vascular resistance (SVR)
aortic elasticity
arterial pressure
Effect of increased afterload
decreased SV
increased BP
What type of effect does contractility have on the ANS?
inotropic (inc. contractability = (+) inotrope)
What are the pacemakers of the heart?
SA node
AV node
Purkinje fibers
What is the bpm of the SA node?
60-100 bpm
What is the bpm of the AV node?
40-60 bpm
What is the bpm of the Purkinje fibers?
20-40 bpm
What effect does heart rate have on the ANS?
chronotropic (inc. HR = (+) chronotrope)
What is systemic vascular resistance (SVR)?
resistance to blood flow in systemic circulation
Basic rules of systemic vascular resistance (SVR)
vasoconstriction = increased resistance = decreased flow
vasodilation = decreased resistance = increased flow
What are ways that SVR can be regulated in the body?
neural
baroreceptors (pressure/stretch)
chemoreceptors (pH, CO2, O2)
autonomic
sympathetic tone (vasoconstriction/vasodilation)
parasympathetic (vasodilation of select organs)
paracrine
nitric oxide, bradykinin, prostaglandins
smooth muscle relaxation (vasodilation)
How is hypertension diagnosed?
based on average of 2+ readings on 2+ occasions
What are types of out-of-office BP confirmation methods recommended?
home BP monitoring (HBPM)
ambulatory BP monitoring (ABPM)
First and foremost for hypertensive PTs
All PT with hypertension should undergo lifestyle modifications
What are lifestyle modifications associated with hypertension treatment?
weight loss
dietary salt restriction
dietary approaches to stop hypertension (DASH) diet
exercise
limited alcohol intake
smoking cessation
stress reduction
Lifestyle modifications: weight loss
goal = at least 5% of body weight reduction
loss of 1 pound = 1 mmHg decreased in BP
Lifestyle modifications: dietary salt restriction
multiple recommendations
<1.5-2 grams daily
Lifestyle modifications: DASH diet
high in:
vegetables
fruits
low-fat dairy products
whole grains
poultry
fish
low in:
sweets
sugar-sweetened beverages
red meats
Lifestyle modifications: exercise
moderate-intensity aerobic exercise approx. 150 min/week
include resistance training >/= 2 days/week
Lifestyle modifications: limited alcohol intake
abstinence
</= 1 drink/day for women
</= 1-2 drinks/day for men
Lifestyle modifications: smoking cessation
temporary increases in BP and HR
long-term causes vessel damage and arterial stiffening
Lifestyle modifications: stress reduction
breathing control
meditation
What type of hypertension can potentially be managed with just lifestyle changes? What does that entail?
stage 1 HTN
no diabetes
no coronary artery disease
no chronic renal disease
age < 65 yrs
re-access every 3-6 months!
When to start medication for a PT with stage 1 HTN
established ASCVD10-year risk >/=10%
chronic kidney disease
diabetes
age >/= 65 yrs
When to start medication for a PT with stage 2 HTN
start BP medications for all PTs
recommend 1-2 first-line agents
potential single-pill combination
What is the goal BP for most adults?
<130/80 mmHg
What does ACC stand for?
American College of Cardiology
What does AHA stand for?
American Heart Association
What does JNC 8 stand for?
Joint National Committee 8th guideline
What does AAFP stand for?
American Academy of Family Physicians
What are the recommended 1st line medications for HTN?
thiazide diuretics
ACEi
ARBs
CCB
Mechanism of thiazide diuretics
inhibits Na+ reabsorption in distal tubules (kidneys) causing increased excretion of Na+, water, K+, and H+
Physiological effects of thiazide diuretics
increased Na+ and water excretion in urine
decreased intravascular volume
decreased preload
*initially: decreased CO
*overtime: decreased SVR due to reduced Na+ in vascular smooth muscle
Why are thiazide diuretics 1st line?
strongest outcome evidence for stroke and HF prevention
effective in most populations
Names of thiazide diuretics and their prefix
hydrochlorothiazide (Microzide)
chlorthalidone (Thalitone)
CHLOR-
What are side effect for all BP meds?
hypotension/orthostatic hypotension
headache, dizziness, fatigue
Side effects of thiazide diuretics
hypokalemia, hyponatremia, hypomagnesemia
hypercalcemia, hyperglycemia
photosensitivity
renal failure
glaucoma
gout
pancreatitis
Contraindications for thiazide diuretics
known hypersensitivity/anaphylaxis
anuria (ex. dialysis PT)
Warnings for thiazide diuretics
PT may require K+ supplementation
should monitor electrolytes
monitor in PT w/ renal disease
What does CCB stand for?
calcium channel blockers
What is the main CCB?
dihydropyridine
non-dihydropyridine not used for HTN specifically
Mechanism of CCBs
inhibits Ca2+ ion from entering certain areas of vascular smooth muscle and myocardium during depolarization, producing a relaxation of vascular smooth muscle causing vasodilation
Physiologic effects of CCBs
decreased calcium entry = smooth muscle relaxation
arteriolar vasodilation
large reduction in SVR
How do CCBs lower BP?
almost entirely through decreased SVR
minimal effect on HR or contractility
Why are CCBs first line?
highly effective across age and race
particularly effective in:
older adults
black PTs
strong strong prevention data
Names of CCBs and their suffix
nifedipine (Procardia)
amlodipine (Norvasc)
nicardipine (Cardene)
-DIPINE
Side effects of CCBs
peripheral edema
reflex tachycardia/palpitations
facial flushing
Contraindications for CCBs
anaphylactic shock
severe heart failure
hypotension
Mechanism of ACEi
prevents conversion of angiotensin 1 to angiotensin 2, blocking vasoconstriction
What cause vasodilation in the body?
bradykinins
Physiologic effects of ACEi
vasodilation leads to decreased SVR
decreased aldosterone leads to decreased Na+ and water retention, decreasing the preload
improved endothelial function
reduced maladaptive cardiac and vascular remodeling
How do ACEi lower BP?
decreasing SVR
minor effect: decrease CO through volume reduction (decreased preload)
Why are ACEi first line?
proven reduction in AMI, stroke, heart failure, and CKD progression
disease-modifying, not just BP-lowering
Names of ACEis and their suffix
benazepril (Lotensin)
enalapril (Vasotec)
lisinopril (Prinivil, Zestril) → most common
quinapril (Accupril)
ramipril (Altace)
-PRIL
Side effects of ACEi
angioedema
dry cough
hyperkalemia
increased creatinine
Contraindications for ACEi
anaphylazis/hypersensitivity
angioedema
renal failure/renal artery stenosis
hyperkalemia
hypotension
PREGNANCY!!!
Mechanism of ARBs
interfere with the RAAS by inhibiting the action of angiotensin 2 (vasconstriction)
Physiological effects of ARBs
vasodilation leads to decreased SVR
decreased aldosterone leads to decreaed volume/preload
Why are ARBs first line?
same BP and CV outcome benefits as ACEi
better tolerated vs ACEi
less cough
less angioedema
Names of ARBs and their suffix
azilsartan (Edarbi)
candesartan (Atacand)
irbesartan (avapro)
losartan (Cozaar) → most common
olmesartan (Benicar)
telmisartan (Micardis)
valsartan (Diovan)
-SARTAN
Side effects of ARBs
angioedema/dry cough (less than ACEi)
hyperkalemia
increased creatinine
Contraindications of ARBs
anaphylaxis/hypersensitivity
angioedema (from previous ACEi use)
renal failure/renal artery stenosis
hyperkalemia
hypotension
PREGNANCY
When should BBs be given?
after an acute MI
CAD
to stable PT with HF (HFrEF only)
What do BBs do following an AMI and in HF?
reduce mortality
What are BBs usually combined with?
ACEi
Mechanism of beta-blockers
inhibits beta-adrenergic receptors
blocks the harmful effects of chronic SNS activation to protect the heart from excessive adrenaline
decreases inotrophy (contractility) & chronotrophy (HR)
What do cardio-selective BBs block and effect?
Beta 1
heart
What do non-slective BBs block and effect?
Beta 1 and 2
heart, lungs, kidneys, GI tract, liver, uterus, and vascular smooth muscle
What BB is newer/second generation?
cardio-selective BB
Physiological effects of BBs
decreased HR
decreased myocardial O2 demand
improved diastolic function
prevents arrhythmias
promotes reverse remodeling of left ventricle over time
Names of non-selective 1st gen BB and their suffix
nadolol (Corgard)
propranolol (Inderal)
timolol maleate (Blocadren)
sotalol hydrochloride (Betapace)
-OLOL
*No Point To Select
Names of cardio-selective 2nd gen BB and their suffix
atenolol (Tenormin)
bisoprolol fumarate (Zebata)
esmolol hydrochloride (Brevibloc)
metorpolol (tartrate = Lopressor, succinate = Toprol XL)
nebivolol (Bystolic)
-OLOL
*select MEN with ABs
Side effects of BBs
bradycardia
fatigue
bronchospasm/respiratory distress
masks hypoglycemia in PT w/ diabetes!!!
Contraindications for BBs
hypersensitivity/anaphylaxis
bradycardia
2nd/3rd degree AV blood
hypotension
What are some compelling indications for use of BBs in HTN?
CAD
post-MI
HFrEF
tachyarrhythmias (a-fib)
What is the mechanism of alpha & beta blockers?
blocks both alpha 1 and beta 1 & 2 receptors
Names of alpha & beta blockers and their suffix
labetalol (Normodyne)
safer in pregnancy
carvedilol (Coreg)
-LOL
Physiological effect of alpha & beta blockers
vasodilation (alpha) in addition to decreased HR (beta)