HTN Flashcards
What percentage of HTN is PRIMARY
90-95%
What percentage of HTN is SECONDARY?
5-10%
Think secondary HTN if
▪ If sudden onset, esp. if age of onset < 20 or > 50 years
▪ BP > 180/100
▪ Resistance to therapy
▪ Pt with well-controlled HTN has sudden increase in BP
▪ There are symptoms that could cause secondary HTN: headache, daytime
somnolence, fatigue, tachycardia, claudication, cold feet, sweating, thinning of
skin, flank pain, muscle weakness, tremor
HTN Diagnosis
Average of readings taken at 2 or more visits
• Must have 2 separate elevated readings
Describe steps in Renin Angiotensin System (RAS)
Drop in BP to renal arteries stimulates secretion of renin
• Renin activates renin-angiotensin system, yields angiotensin I
• Angiotensin converting enzyme (ACE) converts angiotensin I converted to angiotensin II
• Angiotensin II constricts blood cells, increases secretion of antidiuretic hormone (ADH) and
aldosterone, causes reabsorption of Na+ in kidneys –> water retention, increased blood volume,
increased BP.
Factors that affect BP
Peripheral vascular resistance
• Body position
• Activity
• Blood volume
• Obesity – leads to increased intravascular volume and increased cardiac output
• Lifestyle
• Environmental factors
• Alcohol – increases BP by increasing plasma catecholamines
• Cigarettes – raises BP by increasing plasma norepinephinre
• NSAIDs – cause fluid retention, which can lead to HTN
• Excessive intake of Na+ or low levels of K+ - can contribute to HTN by increasing blood volume
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HTN is a major risk factor for…
Cardiovascular dz o Ischemic heart dz o Heart attack o Heart failure • Stroke • Kidney dz, renal failure • Peripheral vascular dz
Each increase of 20 mm Hg in SBP or 10 mm Hg in DBP
DOUBLES risk of cardiovascular dz
Initial drug therapy for Prehypertension 120-139 or 80-89
none
Initial drug therapy for Stage 1 HTN 140-159 or 90-99
Thiazide diuretic
-may consider ACE,
ARB, BB, CCB, or
combo
Initial drug therapy for Stage 2 HTN ≥160 or ≥100
Two-drug combo
(usually thiazide + ACE,
ARB, BB, or CCB)
Centrally acting α-2 agonists (antiadrenergics) MOA
Stimulate central inhibitory α-adrenergic receptors
• Stimulate sympathetic cardioaccelerator and vasoconstrictor areas
• Results in decreased sympathetic outflow from CNS that causes reduced peripheral resistance,
renal vascular resistance, decreased HR, decreased BP
Clonidine:
• Onset of action: 30-60 min
• Duration of action: 6-10 hr
• Metabolism: extensive hepatic
• Excretion: kidney 65%, feces 22%
• Drug interactions:
▪ Tricyclic antidepressants decease effects of clonidine
▪ Clonidine may enhance CNS effects of alcohol or sedatives
▪ Use cautiously with β-blockers. Clonidine can cause bradycardia. Discontinue gradually.
• Side effects:
▪ Dry mouth, drowsiness, dizziness, sedation, orthostatic hypotension
Methyldopa
Onset of action: 3-6 hr • Duration of action: 12-24 hr • Metabolism: complex liver • Excretion: kidney 70% drug and conjugates • Drug interactions: ▪ Lithium ▪ MAOIs ▪ Iron salts ▪ COMT inhibitors • Pregnancy: preferred HTN drug in pregnancy • Side effects: ▪ Headache, asthenia, dizziness, gynecomastia, GI distress
what are the characteristics of systolic dysfunction?
reduced left ventricular , low ejection fraction
EF usually less than 40%
what are the characteristics of diastolic dysfunction?
Characterized by “stiffening” of the left ventricle
EF is typically preserved,
i.e. normal
What is preload?
Stretch of the ventricle prior to contraction. Preload is
created by blood filling the ventricle in preparation for
contraction
What is afterload?
Resistance the left ventricle has to overcome to empty its
contents into peripheral circulation
What is peripheral vascular resistance?
Pressure (within the periphery) that the left ventricle
must overcome with each contraction
What is the New York Heart Association (NYHA)
HF Classification I-IV?
I –asymptomatic or only symptomatic with activities that
would limit anyone
II– symptomatic with usual exertion
III– symptomatic with minimal exertion
IV—symptomatic at rest
What are Non-Pharmacologic Management of HF?
Sodium restriction
Smoking cessation when applicable
Limited alcohol intake (one drink per day in women or 2 drinks per day in men)
Daily aerobic exercise
Lipid control
Glucose control in diabetics
Tight BP control
Avoid NSAIDS due to potential of increased fluid
retention
Treatment of thyroid conditions when applicable
How do Loop diuretics treat HF?
Work in the ascending loop of Henle to inhibit sodium
and potassium reabsorption
Causes decreased renal blood flow resulting in less fluid
being absorbed back into the bloodstream
How do ACE Inhibitors work to control HF?
Produce vasodilation by inhibiting the conversion of
angiotensin I to angiotensin II
Inhibit the breakdown of bradykinin which is a
powerful vasodilator
Reduce CV preload
Reduce CV afterload
How do ARBs work to treat HF?
Blocks angiotensin II (a powerful vasoconstrictor) on the
surface of target cells
Angiotensin receptors noted as AT1 or AT2
Does not interfere with bradykinin
How do Beta blockers work to treat HF?
Blockade of beta adrenergic receptors resulting in: Decreased heart rate Decreased BP Decreased oxygen demand Promote peripheral vasodilation
How does Spironolactone work to treat HF?
Works in the distal renal tubule
Aldosterone antagonist
Sodium and water are excreted
Potassium is retained
How does Digoxin work to treat HF?
Inhibits NA+/K+ pump+
Increases myocardial contractility
Decreases heart rate
Very long half-life: 36 hours
5-6 days to reach steady state
Requires loading dose
Narrow therapeutic window
What is some Patient Teaching for HF ?
Medication compliance
Patient participation in treatment plan
Daily weights
Healthy diet
Fluid restriction when applicable
Name the drug classes for HTN - ABCD
ACE Inhibitors (angiotensin-converting enzyme inhibitors)
ARBs (Angiotensin II Receptor Blockers)
Alpha blockers
Beta Blockers
Calcium Channel Blockers
Diuretics
which class of HTN meds end in ‘pril’
ACE inhibitors
which class or HTN meds end in ‘sartan’
ARBs
which class or HTN meds end in ‘osin’ or ‘zosin’?
alpha blockers
which class or HTN meds end in ‘lol’ ?
Beta Blockers
which class or HTN meds end in ‘dipine’?
calcium channel blockers
which class or HTN meds end in ‘ide’?
diuretics
What is the indication for Beta Blockers?
systolic and diastolic failure, but esp. If diastolic HF is caused by increased diastolic filling time
What is the MOA for Beta Blockers?
Blockade of beta adrenergic receptors resulting in:
- Decreased HR
- Decreased BP
- Decreased O2 demand
- Increase diastolic filling time
- Peripheral vasodilation
- Regression of L-ventricular hypertrophy
What are the precautions for Beta blockers and labs to monitor?
Pt has to be dry and in stable HF (minimal fluid retention)
Don’t start or change dose if pt has exacerbation of HF or fluid overload
• Monitoring: CBC, CMP
Why should beta blockers NOT be used as first line for HTN?
high risk of developing DM
Beta Blockers are contraindicated in…
African American pt asthma/COPD severe peripheral vascular dx Raynaud’s depression bradycardia 2nd/3rd defer heart block hypoglycemic prone diabetic patient
Patient education for Beta Blockers
- Reports SOB, nocturnal cough, lower extremity edema
- Don’t stop abruptly
- Monitor pulse, notify MD < 50
- w/ diabetic pts: can mask signs of hypoglycemia
- use caution when performing hazardous task bc of CNS side effects
- exercised induced fatigue may develop
Mechanism of Action for Beta blockers
MOA → competitive blockade of the B adrenergic receptor
• Results in decrease HR, myocardial contractility, BP and myocardial oxygen
demand
• Suppresses renin release
• Relieve the symptoms of angina by competitively inhibiting sympathetic
stimulation of the heart (so reduced HR and contractility)
• Promote peripheral vasodilation
β1 receptor →
mainly in the heart and stimulation from catecholamines causes an
increase in HR, BP, myocardial contractility and AV conduction
β2 receptors →
also in heart but mainly in lungs/ peripheral vascular smooth muscles
Pharmacokinetics of Beta Blockers?
• Either excreted by liver or kidney
Propranolol and metoprolol → lipid soluble; almost completely absorbed by the
small intestine and largely metabolized by the liver(These drugs readily enter CNS; SE: lethargy, confusion, sleep disturbances and depression
• Needs to enter the CNS bc it is used to treat migraines
• Have adverse metabolic effects → limits their usefulness in pts w/
hypercholesterolemia and DM (may blunt s/s of hypoglycemia)
β-Blockers must be used w/ caution in pts w/ certain heart conditions, such as …
heart block,
sinus brady
cardiogenic shock or HF
Βeta blockers can be used to treat:
Angina, arrhythmia, compensated HF, post MI, tremors, glaucoma and vascular
HA
the treatment of choice for CHRONIC STABLE and UNSTABLE angina
Most pts will be on nitrates, but β blockers are used when the pt needs to be nitrate
free
Briefly explain the Renin Angiotensin System (RAS)?
drop in blood flow to the renal arteries results in the release of Renin which subsequently activates RAS
Angiotensin is produced in the liver, separated by renin and then converted to Angiotensin I
Angiotensin Converting Enzyme (ACE) converts angiotensin I to Angiotensin II
Angiotensin II is a powerful vasoCONSTRICTOR.
It also stimulates the release of aldosterone, antidiuretic hormone and causes sodium reabsorption of Na+
This leads to Increased fluid retention, higher blood volume, & higher BP
What is the MOA of alpha 1 receptor blockers?
blocks post synaptic alpha 1 adrenergic receptors resulting in vasodilation and decreased peripheral vascular resistance
tends to affect DIASTOLIC BP more than systolic
also results in relaxation of bladder neck and prostate so often used for the Tx of bladder outlet obstruction such as BPH
examples: doxazosin, prazosin
Describe MOA of centrally acting alpha 2 antagonists
stimulate central inhibitory alpha adrenergic receptors
stimulate sympathetic cardioaccelerator and vasoconstrictor areas
results in decreasedsympathetic outflow from the CNS
-reduced peripheral vascular resistance, reduced pressure in the renal system and decreased heart rate
EXAMPLES: clonidine, methyldopa
nonpharmalogical treatment for HTN?
lifestyle modification is number 1 recommendation dietary modification (low sodium) exercise stress management avoid ETOH smoking cessation
MOA of direct vasodilators?
relaxation of vessel smooth muscle and decreases peripheral vascular resistance
stimulates carotid sinus baroreceptors that can increase HR, renin release and Na+ + H20 retention
EXAMPLE: hydralazine, Minoxidil
MOA of Renin inhibitors
blocks the action of Renin as the RAS cascade begins
EXAMPLE: Tekturna
patient monitoring for Methyldopa?
- CBC at baseline
- LFT’s within 12 weeks of initiating therapy
- periodic LFT’s
- Renal function at baseline and periodically
