exam 3 Flashcards
a. BP = BV (blood volume) x PVR (peripheral vascular resistance) x CO (CO is stroke volume X heart rate)
i. Diuretics: work well for BP and fall under BV (if you pee out more fluids you have less blood volume)
1. Thiazide is good for mild hypertension r/t removal of fluid
blood pressure measurement
Detect changes in pressure
Found in:
-arch of the aorta – senses BP and flow out to body/organs/lungs/heart/liver
-carotid arteries – sends info about blood flow to brain
Send information to the brain regarding blood pressure
-vasoconstriction/dilation (PVR peripheral vascular resistance – if big, have high BP, if small have low BP)
-heart rate increase/decrease (CO is SV X HR)
Autonomic nervous system
baroreceptors
process of how it gets BP up
Start at kidneys, it senses decrease in renal perfusion and know BP is low and will secrete renin, and liver makes angiotension and converts to angiotension 1, then the ACE enzyme that comes from the lungs coverts angiotension 1 to 2, the ace inhibitors work at this step, angiotension 2 is a potent vasoconstriction and increases BP and also works on adrenal gland for aldosterone (helps save sodium and water and get rid of potassium and hydrogen – save water to increase volume gets BP up)
RAAS
i. Consistent elevation of systemic arterial blood pressure
1. prehypertension - 120/80 mmHg
2. stage 1 - 140/90 mmHg
3. stage 2 - 160/100 mmHg
ii. 20% of the US population has hypertension
1. most are unaware r/t lack of symptoms
2. African American males have the highest rates
a. Also higher rates of obesity and have gene that makes that more sensitive to salt
3. common complication of pregnancy
hypertension
Essential/primary hypertension
1. no specific cause - multifactorial
2. usually no symptoms
3. accounts for 90% of cases
4. no cure, but can keep it under control
Secondary hypertension
1. known cause such as Cushing’s syndrome, pheochromocytoma, medications
2. correcting the underlying cause will correct the HTN
Four target organs most affected by HTN – most concerned about
a. Box 43.6 in book – set algorithm to treat HTN: lifestyle changes (less salt, lose weight, exercise, then add in medication (thiazide diuretic), then add in another medication (ace inhibitor, calcium channel blocker)
2. heart: increased workload, CAD, HF
3. brain: TIA, CVA
4. kidney: decreased renal function
5. retina: visual impairment, blindness
Types of HTN
Block the formation of angiotensin II
- Ace enzyme converts angiotension 1 to 2 – if you block the ace enzyme the conversion won’t happen
2. reduced vasoconstriction (works with PVR)
3. reduced aldosterone secretion (works with BV)
ii. Blood pressure is reduced with minimal effect on heart rate, stroke volume, or cardiac output
benazepril (Lotensin)
captopril (Capoten) - prototype
enalapril (Vasotec)
lisinopril (Prinivil)
Use
1. hypertension
2. heart failure
3. post-MI – shown to reduce morbidity and mortality after a MI
4. Diabetic nephropathy
- reduced stimulation of angiotensin receptors in the renal arteries slows damage to the kidneys
Most are once a day dosing, which is good for compliance
ACE inhibitors - Prils
I. Usually minor
ii. Result of vasodilation and alterations in blood flow
- orthostatic hypotension, reflex tachycardia (goes with ortho hypotension), chest pain, heart failure, arrhythmias
iii. Dry cough, up to 20% of clients
- Related buildup of bradykinin (this causes inflammation and ace enzyme breaks it down. We block ace enzyme so the bradykinin will build up) – leads to compliance issue
iv. Renal insufficiency, failure
v. Angioedema – swelling of lips, neck; could block airway
- rare and usually occurs after the first dose
- bradykinin?
vi. Hyperkalemia
- diabetes, renal impairment, potassium supplements, or potassium-sparing diuretics
- -if patient is only on diuretic and is taking potassium supplement for it, then we add in an ACE inhibitor you don’t need that supplement after that r/t aldosterone
adverse effects on ace inhibitors
Monitor closely when combined with diuretics or antihypertensives because you can get hyperkalemia, too low of BP, and ensure they are not being over medicated
Heart failure – category that has least risk for developing HF but still a concern
History of angioedema – especially after first dose
Impaired renal function
Absorption inhibited by food
-take 1 hour before or 2 hours after a meal
Pregnancy category D: blackbox warning
cautions of ace inhibitors
Inhibit the movement of calcium across the membranes of myocardial and arterial muscle cells by blocking calcium channels
-depresses myocardial contractility
-slows cardiac impulse formation – need Ca in SA and AV for a pulse
-relaxes and dilates arteries, so our vessels get bigger and BP goes down
Causes a fall in blood pressure and decrease in venous return
amlodipine (Norvasc)
diltiazem (Cardiazem) – prototype
nicardipine (Cardene)
nifedipine (Procardia XL)
verapamil (Calan SR) – non productive one
Used for:
1. hypertension
2. angina
3. supraventricular dysrhythmias
Usually not used as monotherapy for hypertension
Useful for those who are less responsive to other categories
1. elderly
2. African Americans – are not as responsive to first line treatments like diuretics, so may be put on Ca blocker first
Some are selective for arterioles while others affect both arterioles and cardiac muscle
-at high doses, they all affect cardiac tissue
-Need to assess for bradycardia for all Ca blockers*
calcium channel blockers
Adverse Effects
I. Normally well tolerated
ii. Most are related to effects on cardiac output
-dizziness, headache, fatigue, hypotension, bradycardia, peripheral edema, flushing
-reflex tachycardia
Can worsen heart failure
Cautions
- Caution with heart block due to slowed myocardial conduction because it can effect AV and SA node, especially in high doses
- Increase serum digoxin level by 45%
- Increased risk of heart failure when combined with beta blockers
- Avoid grapefruit juice
– Nurse is preparing to administer first dose of Vasotec. Identify potential adverse effects of this med
–Reflex hypertension, hyperkalemia, persistent cough, angioedema, hypotension, reflex tachycardia
calcium channel blockers
Block beta 1 receptors in the heart
1. reduce heart rate
2. decrease force of myocardial contraction
3. slow conduction velocity through AV node
Inhibit release or renin from kidney which is stimulated by catecholamines
atenolol (Tenormin)
nebivolol (Bystolic)
metoprolol (Lopressor)
propranolol (Inderal)
Use 1. hypertension 2. angina 3. MI 4. dysrhythmias 5. heart failure 6. migraines Can be cardioselective (work beta 1 receptors in heart or beata 2 receptors in lungs) or nonspecific
beta blocker
Adverse Effects
I. Usually well tolerated
ii. Hypotension, bradycardia, arrhythmias*
iii. Bronchospasm, dyspnea especially in patients with COPD or asthma
- Related to blocking of beta2 receptors
iv. Alterations in blood glucose
- mask effects of hypoglycemia
- B2 receptors in the liver control hepatic glucose production
- insulin resistance
v. Decreased libido, impotence
Cautions
I. Withdraw slowly to prevent rebound hypertension, dysrhythmias, and MI
- When you stop fast, the body isn’t used to the citicolines
ii. Bradycardia, heart failure because it can make HF worse, shock
- S/S of HF getting worse: crackles, peripheral edema, fatigue, pink/frothy sputum
iii. COPD, asthma
iv. Diabetes
- insulin dose adjustments
- frequent blood sugar monitoring
beta blockers
I. Monitor VS
- pulse and blood pressure
- Hold if pulse is 60 or systolic BP of 100
ii. Daily weights
iii. Frequent glucose checks
iv. Encourage lifestyle changes* - weight loss, smoking cessation, decreased salt and alcohol, increased exercise
v. Education - change positions slowly, don’t stop abruptly, first dose at bedtime, avoid sudden increase in activity
- report chest pain, weight gain of 1 kg/24 hrs, SOB, frothy sputum
nursing considerations for hypertension medications
beta blockers
calcium channel blockers
ace inhibitors
I. Inability of the ventricles to pump enough blood to meet the body’s metabolic demands
ii. Weakening of the cardiac muscle happens as we age
- contributing factors: MI, hypertension, coronary artery disease, diabetes
-untreated HTN makes vessel much weaker and increases risk
iii. No cure
-prevent or remove the underlying cause
-treat the symptoms
Symptoms
1. dyspnea on exertion – then dyspnea on rest
2. fatigue
3. pulmonary congestion – yucky lung sounds
4. pulmonary edema
5. orthopnea
6. anxiety
7. cough
8. pitting edema
Treatment includes pharmacotherapy and lifestyle modification
1. sodium and fluid restrictions are big ones
Heart failure
Cardiac Output – important for heart function and nourishing the body
BP = BV X PVR X CO (CO = HR X SV)
ii. Cardiac output is the amount of blood pumped by the ventricle per minute CO = HR x SV
iii. A normal healthy heart has a CO of 5 to 6 liters per minute at rest
iv. Two important factors in determining CO are preload and afterload
v. Preload is the degree to which myocardial fibers are stretched just prior to contraction. The more stretch the more forceful the contraction
-Like a rubber band (Frank-Starling law)
-Has to do with how much blood you get in the heart with each beat
-So the more blood the easier it is to stretch
vi. Afterload is the degree of pressure in the aorta that must be overcome for blood to be ejected from the left ventricle
vii. In HF the myocardium becomes weakened & the heart cannot eject all the blood it receives
-Left sided heart failure: cough and shortness of breath (congestive heart failure)
a. Usually starts with left side because of hypertension and pumping to get blood out (TEGRITY)
-Right sided heart failure: peripheral edema
c. Compensation – box 44.2
I. Baroreceptors – when we sense our heart isn’t working right
-sympathetic stimulation: (fight or flight) want an increase in heart failure to get everything back up so we use this
-increases HR, BP, rate and depth of respirations, positive inotropic effect – harder and better with each beat
RAAS
1. Last step is aldosterone which…. Increases blood volume and blood pressure
heart failure 2
Pharmacotherapy
I. Goals of pharmacotherapy
1. Reduction of preload
2. Reduction of systemic vascular resistance (afterload)
3. Inhibition of RAAS and vasoconstriction of SNS
-All of these can decrease work on heart and S/S
Stage A - high risk of developing HF
1. Uncontrolled HTN, diabetes, not taking meds – these are people who are at high risk for developing HF
2. lifestyle modifications, treat associated conditions - ACE inhibitors for hypertension associate with HF
-low sodium diet, low fat, low calorie, low cholesterol diet, exercise
Stage B - structural evidence, no symptoms
1. ACE inhibitor or ARB, beta blocker if previous symptoms, diuretics and salt restriction
2. Cardiac remodeling happens, but compensation is still kicked in so it keeps S/S hidden
Stage C - structural evidence and symptoms
1. Do all the things above and add digoxin and spironolactone, if symptoms don’t improve add loop or thiazide diuretic
Stage D - symptoms at rest – very ill patient/end of life care or transplant
1. IV diuretics, dopamine, dobutamine, nitroglycerine, phosphodiesterase inhibitors
pharm therapy for heart failure
Increases intracellular calcium in our heart cells, which…
1. increased force of contraction
2. increased CO and renal perfusion to rid extra fluid
3. slowed HR
4. decreased conduction velocity through AV node
-does all this to reduce workload on heart
Inhibits/slow it down, not block, the Na-K ATPase pump
1. as sodium accumulates within the cell calcium is released from storage areas in the cell
2. this extra calcium produces a more forceful contraction
Use
I. Heart failure*
ii. Atrial arrhythmias
iii. Was the drug of choice until discovery of ACE inhibitors
- Dig is limited to those with advanced HF r/t narrow safety margin
iv. Very narrow safety margin – can make patient toxic
v. Clients must undergo digitalization when starting therapy – go to doctor and start dose, gradually increases until tissues are saturated and S/S of heart failure is diminished
Digitalization
I. The dose of digoxin is gradually increased until tissues become saturated and symptoms of HF diminish
ii. Oral dosing takes about 7 days
iii. Regular blood work will be needed to determine therapy especially with digitalization
1. normal 0.5 - 2.0 ng/mL
2. toxic >2.0 ng/mL
-2.0 is okay but 2.1 is toxic
3. toxicity is related to symptoms – may show S/S of toxicity at 1.8
iv. Antidote digoxin immune Fab
Cardiac Glycosides
digoxin (Lanoxin)
Adverse Effects
I. Headache, weakness, drowsiness, yellow/green halo with vision, GI upset, anorexia
ii. Arrhythmias*
- sudden death
iii. Toxic*
1. bradycardia, heart block, ventricular tachycardia, N&V, anorexia, malaise
Cautions
I. AV block or ventricular dysrhythmias
ii. Renal failure – can’t rid it like a normal patient can
iii. Elderly
on Beers list, so caution with elderly
iv. Concurrent use of diuretics – concern is hypokalemia; digoxin binds to same place on pump as potassium, the more digoxin binds and takes place of potassium – can be on Lasix and digoxin r/t hypertension
v. Concurrent use of beta blockers – digoxin delays pump so slow it down, but can slow heart rate too – so concern is bradycardia so check heart rate before giving
vi. Lots of drug-drug interactions
1. amiodarone, ACE inhibitors, statins
digoxin (Lanoxin)
Phosphodiesterase is an enzyme that breaks down cAMP
1. cAMP helps to regulate cardiac muscle contraction, increases intracellular calcium
2. more cAMP means increased contractility and decrease in left ventricle afterload
milrinone (Primacor) - prototype
1. preferred medication in this class due to fewer side effects and shorter half-life
2. higher risk of thrombocytopenia
3. must be given IV
4. peak effect in 2 minutes
iii. inamrinone (Inocor)
Use
I. Limited to those who have not responded to other therapies
1. many, serious side effects
2. ventricular dysrhythmias (10% of patients)
ii. Therapy is limited to 2 to 3 days because of this
1. So use on patient in ED, they can’t function anymore and waiting on heart transplant this, use this to bridge for a few days
2. Not first line treatment
iii. Half-life is 3 - 6 hours which makes rapid changes to dose difficult
phosphodiesterase inhibitors
Adverse Effects I. Ventricular dysrhythmias - continuous ECG ii. Angina iii. Hypotension -continuous BP because they can have serious hypotension iv. Headache v. Nausea and vomiting vi. Thrombocytopenia Cautions I. Preexisting dysrhythmias ii. Obstructive valvular heart disease iii. Hypovolemia iv. Electrolyte imbalance v. Other inotropic drugs vi. Other antihypertensives vii. Elderly
phosphodiesterase inhibitors
Milrinone (Primacor)
Inamrinone (Inocor)
Beta Blockers
I. Have a negative inotropic effect
- slows HR and decreases BP
- decreased cardiac workload
ii. Clients with HF have an excessive activation of the sympathetic nervous system
- contributes to cardiac remodeling
iii. If not used properly they can worsen HF
- Gradually increased - dose doubled every 2 weeks until target dose is reached
- may feel worse an initiation of therapy which will make patient not want to take this medication
- good education explaining tiredness, S/S in the beginning of treatment, but it will get better once you reach your target dose
iv. Almost always combined with an ACE inhibitor
v. carvedilol, metoprolol
Vasodilators
I. hydralazine (Apresoline) & isosorbide dinitrate (Isordil)
ii. BiDil
iii. Relax blood vessels, lower BP, reduced workload on the heart
- hydralazine – dilates arteries
- isosorbide dinitrate – dilates veins
iv. Limited role in HF because of side effects
- orthostatic hypotension, reflex tachycardia
v. African Americans population is only case for potential first line drug
vi. nesiritide (Natrecor) – specific patients, only IV, only severe patients
- identical to hBNP, natural hormone secreted by the ventricles in response to HF – constantly trying to fix ourselves and do all these things
- enhances diuresis and renal excretion of sodium
- causes vasodilation which reduces preload and afterload
- So all this reduces workload on heart
vii. Limited use due to severe, rapid hypotension which can persist for hours
viii. Used for acute decompensated HF patients and requires continuous monitoring
ix. Administered IV only
Other meds for heart failure
Beta blockers and vasodialators
ACE Inhibitors
I. Drug of choice for treatment of chronic heart failure
ii. End in “pril”
- lisinopril (Zestril), captopril (Capoten), enalopril (Vasotec), fosinopril (Monopril)
- coughing will cause patient to stop taking
iii. Block the formation of angiotensin II
- reduced vasoconstriction
- reduced aldosterone secretion
- reduced workload on heart
iv. ARBs are used for those who cannot tolerate an ACE inhibitor (like cough)
- Work similar – block use of angiotension 2 in our body (we can’t make it because they’re blocking it) – End in Sartan
Diuretics
I. Reduce fluid volume and lowers blood pressure
- reduces workload of the heart and increases cardiac output
i. Often use in combination with another medication such as an ACE inhibitor
iii. Loop most effective, work quickly - Lasix
iv. Thiazide for mild to moderate HF - Hydrochlorothiazide
v. Potassium sparing has limited role
- spironolactone is an exception due to blocking of aldosterone, which will reduce blood volume
vi. Monitor potassium balance
Diuretics and ace inhibitors
other meds for heart failure
Lumens of the blood vessels become narrowed
Atheromas also damage the intimal lining reducing natural elasticity
Narrowed vessels are not able to respond to increased demand during activity or stress
Heart muscle becomes hypoxic
Angina pectoris
Coronary artery disease
Substance P is released from ischemic myocardial cells
1. pain is felt where ever substance P reacts with pain receptors
2. chest, left arm, jaw, abdomen (wherever substance P receptors react with things in the body)
3. may be described as crushing
Stable angina - predictable, relieved by rest (r/t narrow/hard artery that can’t get blood flow)
Unstable angina - occurs suddenly, occurs at rest (r/t narrow/hard artery that can’t get blood flow)
Vasospastic (Prinzmetal’s) angina - spasm of the vessels, usually at rest, often at the same time each day (vessels constrict and get smaller and spasm)
Angina
