Disorders of the heart of blood vessels
Cardiovascular disease
Includes coronary artery disease, heart failure, cerebrovascular disease, hypertension, arrhythmias, peripheral arterial disease, congenital heart disease, heart valve problems, venous thromboembolism
Cardiovascular disease
#1 cause of death globally
1 in every 4 deaths in the US
Cardiovascular disease
Most cardiovascular diseases can be prevented by modifying risk factors (alcohol, tobacco, obesity, diet, inactivity) (T/F)
True
Treatment for HTN is based off of guidelines developed by the JNC- 8 (Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure) (T/F)
True
Elevation in arterial blood pressure is considered
Systolic ? 140 mmHg
Diastolic ? 90 mmHg
Untreated, chronic HTN can lead to: (5)
1. Cerebrovascular accident (stroke)
2. Myocardial infarction (heart attack)
3. Heart failure
4. Renal damage
5. Vision loss
More blood volume _____________ BP
increases
Less blood volume ______________ BP
decreases
Resistance to flow of blood in the arterial vessels
Peripheral vascular resistance
Constriction of smooth muscle in arterial walls ____________ BP
increases
Relaxation of smooth muscles in arterial walls ____________ BP
decreases
Volume of blood pumped per minute
Cardiac output
Increased _____ = Increased BP
CO
Decreased CO = Decreased _____
BP
Cardiac output, peripheral vascular resistance, and blood volume are regulated by _________________ and the ________-_____________-______________ system
baroreflexes; renin-angiotensin-aldosterone system (RAAS)
Baroreceptors located in the aortic arch and carotid sinuses sense a decrease in BP and respond by decreasing parasympathetic nervous system stimulation. The sympathetic nervous system responds by increasing vascular tone and cardiac output.
Baroreflexes
The kidneys sense a decrease in BP or decrease in sodium in the renal tubules and responds by releasing renin. Renin converts angiotensinogen to angiotensin I. Angiotensin-converting enzyme (ACE) then converts angiotensin I to angiotensin II, which is a p
Renin-angiotensin-aldosterone system (RAAS)
Management of HTN through lifestyle modifications include:
- Weight control
- Exercise
- Nutrition
- Tobacco cessation
- Limit salt intake
- Limit alcohol
- Manage stress
Pharmacologic management of HTN is tailored to the individual, taking into account their risk factors, age, comorbidities, degree of HTN, and genetic factors (T/F)
True
In general, treatment for HTN is started with one medication and dose is increased, or another antihypertensive (from a different drug class) is added until the BP goal is met (T/F)
True
First line treatments for HTN:
1. Thiazide Diuretics
2. Calcium Channel Blockers (CCB)
3. Angiotensin Converting Enzyme Inhibitors (ACEI)
4. Angiotensin Receptor Blockers (ARB)
First line HTN treatment for the African American population includes ____________ and _______, as they have a poorer response to ACEIs and ARBs
thiazides; CCBs
Diuretics increase urinary excretion of water and electrolytes (which affects BP by _____________ blood volume)
decreasing
Different classes of diuretics are available, with varying
MOAs
A common concern among most diuretics is effect on serum electrolytes, in particular, _______________
potassium
Other diuretics that can be used for the treatment of HTN: 2
1. Potassium-sparing diuretics (aldosterone antagonists)
2. Loop diuretics
Angiotensin converting enzyme inhibitors (ACEIs) reduce blood pressure by inhibiting the ________ (dilating arteries and decreasing blood volume)
RAAS
Angiotensin converting enzyme inhibitors (ACEIs) are excellent choice for diabetics as ACE inhibitors slow the progression of _________ failure
kidney
Have also been shown to prevent death in clients with heart failure after myocardial infarction
ACE inhibitors
Block the binding of angiotensin II to angiotensin receptors
Angiotensin Receptor Blockers (ARBs)
Similar MOA as ACE inhibitors
Similar adverse effects as ACE inhibitors, but with less incidence of cough and angioedema
Same nursing implications as for ACE inhibitors
Angiotensin Receptor Blockers (ARBs)
Are a good alternative to ACE inhibitors
Angiotensin Receptor Blockers (ARBs)
A client would be prescribed one or the other (ACE inhibitors or ARBs), not both
(T/F)
True
Inhibit the entry of calcium into the cell, inhibiting muscular contraction (which leads to relaxation of arteriolar vasculature and a reduction in blood pressure)
Calcium Channel Blockers
Not typically first drug chosen for HTN or used as monotherapy
Calcium Channel Blockers (CCBs)
__________ ______________ tend to respond more favorably to CCBs
African Americans
There are 3 different sub-classes of CCBs which differ in ability to treat HTN, angina, and arrhythmias (T/F)
True
Second line treatments for HTN: 6
1. Beta adrenergic blockers (antagonists)
2. Alpha1 adrenergic blockers (antagonists)
3. Alpha2 adrenergic agonists
4. Aldosterone antagonists
5. Renin inhibitors
6. Direct vasodilators
Beta adrenergic blockers (antagonists), alpha1 adrenergic blockers (antagonists), and alpha2 adrenergic agonists work on ______________ receptors
adrenergic
Aldosterone antagonists and renin inhibitors work on ________ pathway
RAAS
Directly causes relaxation of arteriolar smooth muscle, lowering blood pressure
Vasodilators
Adverse effects and/or dosing regimen prohibits vasodilators from being used as first line agents (T/F)
True
Adverse effects of vasodilators include: 3
1. Reflex tachycardia (compensation for decrease in BP) which could precipitate angina, MI, or heart failure
2. Sodium and water retention
3. These effects can be minimized by concomitant use of a diuretic and beta blocker
Pharmacologic management of HTN is tailored to the individual, taking into account their risk factors, age, comorbidities, degree of HTN, and genetic factors
Individualized care
The heart is unable to pump enough blood and oxygen to adequately support other organs in the body
Heart failure
Approximately half of people who develop heart failure will die within ___ years of diagnosis
5
Medication and lifestyle changes may help with symptom management and slow progression of the disease
Heart failure
Weakened heart muscle can't squeeze as well --> less blood pumped out of ventricles
Systolic heart failure
Stiff heart muscle can't relax normally --> less blood fills the ventricles
Diastolic heart failure
Common causes of heart failure: 7
1. Coronary Artery Disease
2. Myocardial Infarction (MI)
3. HTN
4. Diabetes
5. Arrhythmias
6. Valvular Heart Disease
7. Congenital Heart Disease
Preload =
stretch
Afterload =
resistance
Degree of ventricular stretch before contraction
Preload
Directly affected by blood volume in ventricles at end-diastole
Preload
Resistance ventricles must overcome during systole
Afterload
Directly affected by aortic tone/pressure
Afterload
These drugs affect contractility
Inotropic drugs
These drugs affect heart rate
Chronotropic drugs
Positive inotropes _____________ force of contraction
increase
Negative inotropes _____________ force of contraction
decrease
Positive chronotropes _____________ heart rate
increase
Negative chronotropes ______________ heart rate
decrease
As blood backs up in the left ventricle, it enlarges and attempts to work harder to compensate for the increased blood volume. This changes the size, shape, and structure of the heart over time as myocytes (cardiac cells) are injured and die. Cardiac tiss
Cardiac (ventricular) remodeling
Treatment of heart failure (lifestyle changes): 8
1. Tobacco cessation
2. Salt restriction
3. Fluid restriction
4. Limit alcohol
5. Aerobic exercise (under medical supervision)
6. Stress management
7. Weight control
8. Limit caffeine
Pharmacologic therapy decreases symptoms of heart failure by: (3)
1. Reducing preload
2. Reducing blood pressure (reducing afterload)
3. Inhibit RAAS and stimulation of sympathetic nervous system
First line drugs for HF (2)
1. ACE inhibitors
2. Diuretics
Decreases afterload by decreasing peripheral resistance and BP
Decreases preload by vasodilation and and inhibition of aldosterone (causing diuresis and decreased blood volume)
ACE inhibitors
ACE inhibitors have a __________________ effect
cardioprotective
Can stop or slow remodeling of the heart
Cardioprotective effect
Increases survival, improves symptoms, and decreases hospitalizations
ACE inhibitors
ARBs can be used in heart failure if client is unable to tolerate adverse effects of ACE Inhibitors (T/F)
True
Decrease preload by lowering blood volume through increased urine output
Diuretics
Commonly used in conjunction with ACE inhibitor
Diuretics
Second-line drugs for HF
Typically a combination of drugs is used
1. Cardiac Glycoside
2. Beta Blockers
3. Vasodilators
4. Phosphodiesterase Inhibitors
Block the effects of the sympathetic nervous system on the heart, decreasing heart rate and BP (decreasing workload of the heart)
Beta blockers
Beta blockers have a ____________ inotropic effect, so it is important to monitor for signs of worsening heart failure
negative
Beta blockers are typically combined with
ACE inhibitors
Shown to decrease numbers of hospitalizations and deaths associated with heart failure
Beta blockers
2 commonly used vasodilators
1. hydralazine
2. isosorbide dinitrate
Is secreted by ventricles in response to fluid overload
Human B-Type Natriuretic Peptides (BNP)
Causes natriuretic effect (increases sodium excretion) and inhibits the RAAS system (vasodilation)
Human B-Type Natriuretic Peptides (BNP)
_____________ (Natrecor) is a vasodilator identical to BNP and is used for acute decompensated heart failure
nesiritide
Hypotension is a common adverse effect. Do not administer if SBP < 90 mm Hg
Human B-Type Natriuretic Peptides (BNP)
The partial blockage of the coronary arteries
Angina pectoris
More physical activity or stress --> chest pain
Stable angina
Buildup of a blocked artery --> can experience chest pain at rest
Unstable angina
Vasospasm of the coronary artery (not a blockage) --> chest pain
Prinz metals
Lifestyle changes that help to manage angina: 9
1. Limit alcohol
2. Low fat/cholesterol/sodium diet
3. Manage cholesterol levels
4. Tobacco cessation
5. Maintain normal BP
6. Regular exercise
7. Weight management
8. Maintain normal glucose levels
9. Reduce stress
The pharmacologic goals of angina are to: (4)
1. Reduce intensity and frequency of episodes
2. Improve exercise tolerance
3. Increase tolerance for ADLs
4. Prevent consequences of ischemic heart disease
Medications for __________ are used to terminate an episode or decrease the frequency of episodes
angina
Medications for angina decrease myocardial oxygen demand by: (4)
1. Slowing HR
2. Dilating veins (decrease preload)
3. Decreasing contractility
4. Decreasing BP (decrease afterload)
3 drug categories used for angina
1. Organic nitrates
2. Beta-adrenergic antagonists (beta blockers)
3. Calcium channel blockers
2 types of organic nitrates:
1. Rapid acting: terminate episode
2. Long acting: reduce frequency
Beta-adrenergic antagonists (beta blockers) are first-line drugs and reduce _____________
frequency
Used when beta blockers are not tolerated and work to reduce frequency
Calcium channel blockers
Relax both arterial and venous smooth muscle, reducing workload of the heart; dilate coronary arteries
Nitrates
Given sublingually to stop acute angina attack
Short acting nitrates
Given via oral or transdermal route to decrease frequency and severity of attacks
Long acting nitrates
Isosorbide and nitroglycerin are both __________ and are available in short and long acting formulations
nitrates
Adverse effects of nitrates
Hypotension, dizziness, headache, flushing of face, reflex tachycardia, development of tolerance
Administration of Nitroglycerin for angina
- Administer 1 tablet sublingual
- If no relief after 5 minutes, give a 2nd dose
- If no relief after 5 minutes, give a 3rd dose
- If no relief after 3 doses, call EMS
Reduce the cardiac workload by slowing heart rate and reducing contractility
Used for angina prophylaxis
Adverse effects: Bradycardia, hypotension, dizziness, fatigue/lethargy, decreased sexual ability, depression, worsening heart failure symptoms, bronch
Beta Adrenergic Antagonists (Beta Blockers)
Beta blockers patient teaching: (5)
1. Rise slowly
2. Do not suddenly stop taking
3. Check pulse daily & report < 60
4. Check BP daily & report < 90/60
5. Report depression/fatigue
Inhibit the transport of calcium into myocardial cells, relax arteriolar smooth muscle (decreasing workload on the heart), dilate coronary arteries
Calcium channel blockers
Reduce myocardial oxygen demand by lowering BP and HR (the different classes of CCBs vary in their ability to affect HR)
Calcium channel blockers
Adverse effects of calcium channel blockers
Hypotension, bradycardia (for some classes), heart failure symptoms, headache, fatigue, arrhythmias
The goals of treating ______________ ______________ is early diagnosis and treatment to reduce myocardial ischemia & damage, relieve pain, reduce mortality & long term disability
myocardial infarction
For MI, restoring blood supply (reperfusion) is done by (3)
1. PTCA
2. Thrombolytics
3. CABG
For MI, reducing myocardial oxygen demand is done by (3)
1. Organic nitrates
2. BB
3. CCB
For MI, controlling/preventing dysrhythmias is done by (2)
1. Beta-blockers
2. Other antidysrhythmics
To reduce post MI mortality one uses (3)
1. Aspirin (ASA)
2. BB
3. ACE inhibitors
For MI, pain/anxiety is managed by (1)
1. Narcotic analgesia (morphine)
For MI, to prevent enlargement of clots one uses (2)
1. Anticoagulants
2. Antiplatelets
Dissolve clots obstructing coronary arteries to restore perfusion to myocardium; followed by anticoagulant therapy (heparin, warfarin, enoxaparin) to prevent additional clots
Thrombolytics
Should be administer within 12 hours after onset of symptoms (the sooner the better!)
Thrombolytics
Narrow margin of safety
Side effects - hemorrhage, hypotension
Short half life
Thrombolytics
Be aware that there are contraindications for administration of thrombolytics (T/F)
True
________________ are administered IV through dedicated line
Thrombolytics
Frequent vital signs (every 15-30 min during infusion) should be taken for
Thrombolytics
Hourly (or more frequent) neurological checks (monitoring for intracranial bleeding) and monitoring for bleeding are nursing considerations for
Thrombolytics
Client is on bed rest when taking _________________
thrombolytics
Requires ECG monitoring
Avoid invasive procedures
Monitor for arrhythmias which may occur with reperfusion
Thrombolytics
Other medications used with MI (6)
1. Beta blockers
2. Antiplatelet/anticoagulants
3. ACE inhibitors
4. Pain medication
5. Statins
6. Nitrates
Reduce cardiac oxygen demand by slowing HR, decreasing contractility, and reducing BP. Helps suppress reperfusion dysrhythmias. Decreased mortality if given within 8 hours of MI
Beta blockers
Aspirin (325 mg) given ASAP when MI suspected and then daily (81 mg). Other drugs that may be used in addition to aspirin include clopidogrel (Plavix), eptifibatide (Integrilin), or heparin
Antiplatelets/anticoagulants
Started within first 24 hours (after client has been stabilized). Shown to reduce mortality post-MI
ACE Inhibitors
Typically morphine or fentanyl are given for pain control and relaxation
Pain medication
Considered a cholesterol medicine
Statins
Is the stopping of blood flow; it is a complex process that attempts to maintain a balance between blood fluidity and coagulation
Hemostasis
Drugs can be used to alter processes along the clotting cascade (T/F)
True
Clots stop excessive bleeding but restrict blood flow to the affected area (T/F)
True
To restore circulation to the tissues, clots are removed by
fibrinolysis
Abnormal impulse formation or conduction in the myocardium
Dysrhythmias (Arrhythmias)
Starts 24-48 hours after clot formation and continues until clot is dissolved
Fibrinolysis
Drugs to modify coagulation (4)
1. Anticoagulants
2. Antiplatelet agents
3. Thrombolytics
4. Hemostatics
Are used to prevent formation of clots; increase normal clotting time; used primarily to prevent clot formation in VEINS
Anticoagulants
Inhibit platelet aggregation; primarily used to prevent clot formation in ARTERIES
Antiplatelet agents
Are used to dissolve life-threatening clots
Thrombolytics
Promote formation of clots; inhibit normal removal of fibrin; speed clot formation
Hemostatics
Usually started IV or SQ (for rapid onset), and then switched to PO
Anticoagulants
Most frequent adverse effect for anticoagulants is =
bleeding
Reversal agents are available for some anticoagulants (2)
Protamine sulfate reverses heparin
Vitamin K or Fresh Frozen Plasma (FFP) reverses warfarin (Coumadin)
2 Low Molecular Weight Heparins (LMWH):
1. enoxaparin (Lovenox)
2. dalteparin
Anticoagulants do not have direct effect on a clot that has already formed. (Do not dissolve existing clots). Anticoagulants are used to prevent clot formation, or prevent extension of an already existing clot. (T/F)
True
Interfere with platelet aggregation; used to prevent clot formation in arteries
Monitor for signs and symptoms of bleeding
Antiplatelet drugs
Classes of antiplatelet drugs: 3
1. aspirin (ASA)
2. adenosine diphosphate (ADP) receptor blockers (clopidogrel/Plavix, ticlodipine/Ticlid)
3. glycoprotein (GP) IIb/IIIa receptor blockers (abciximab/ReoPro)
Active bleeding is a contraindication to using anticoagulants and antiplatelet medications (T/F)
True
Goal is to quickly restore blood flow to tissues
Thrombolytics
Used in acute MI, pulmonary embolism, acute ischemic CVA (stroke), deep vein thrombosis (DVT), arterial thrombosis, blocked IV catheter
Life or limb threatening situations
Thrombolytics
Promote clot destruction by converting plasminogen to plasmin which initiates fibrinolysis
Narrow margin of safety; continuously monitor vital signs and for evidence of bleeding
Cerebral hemorrhage is the greatest risk
Followed by anticoagulants or antipl
Thrombolytics
Contraindications to administration of Thrombolytics
- Previous intracranial hemorrhage
- Recent ischemic stroke (within 3 months)
- Recent internal bleeding
- Recent intracranial or spinal surgery
- Recent major surgery, trauma, prolonged CPR
- Intracranial neoplasm
- Arteriovenous malformation or aneurysm
Action is opposite of anticoagulants (shorten bleeding time)
Antifibrinolytics
Prevent fibrin from dissolving, enhancing the stability of clots
Antifibrinolytics
Most often used to prevent excessive bleeding after surgery or in clients with systemic clotting disorders
Antifibrinolytics
Is an enzyme secreted by blood vessels located near the clot. TPA converts plasminogen to plasmin which digests fibrin strands, dissolving the clot
Tissue Plasminogen Activator (tPA)
Vary in severity from being completely asymptomatic to life-threatening
Dysrhythmias
________________________ is required to diagnose a dysrhythmia
Electrocardiogram (ECG/EKG)
Symptoms experienced from a dysrhythmia are typically related to decrease in
cardiac output
Some dysrhythmias can lead to stroke or heart failure (T/F)
True
Goal of therapy is to prevent or terminate dysrhythmias
Antidysrhythmic drugs
Since these drugs affect the electrical conduction system of the heart, they carry the potential to worsen or create new dysrhythmias
Antidysrhythmic drugs
Are typically reserved for symptomatic dysrhythmias, or those dysrhythmias that cannot be controlled by other means (due to serious adverse effects)
Antidysrhythmics
Understanding action potential seems complicated,
but blocking sodium, calcium, or potassium ion
channels is one of the primary ways cardiac drugs work (slowing conduction velocity)
Another way is to prolong the _______________ _________
refractory period
Drugs classes for dysrhythmias: 4
Drugs can have characteristics of more than one class
Class I Sodium channel blockers
Class II Beta-adrenergic blockers
Class III Potassium channel blockers
Class IV Calcium channel blockers
Miscellaneous drugs (digoxin, adenosine)
Largest group of antidysrhythmics
Sodium Channel Blockers
Subgroups (A, B, C) are differentiated by speed of binding and dissociation from receptor sites
Sodium Channel Blockers
Chemical structure and action similar to local anesthetics
Sodium Channel Blockers
Frequent ECGs should be obtained due to potential to worsen or cause new dysrhythmias
Sodium Channel Blockers
Slowing of heart rate and decreased conduction velocity through AV node can suppress several types of dysrhythmias
Beta-adrenergic blockers
Typically used to treat atrial dysrhythmias
Beta-adrenergic blockers
Prolongs the refractory period, which stabilizes dysrhythmias
Potassium channel blockers
Is a resting period occurring after depolarization, in which the cell cannot initiate another action potential
Refractory period
Produces a slowing of the heart rate
Can worsen dysrhythmias
Potassium channel blockers
Stabilize dysrhythmias by decreasing automaticity at SA node, slowing conduction velocity through the AV node, and prolonging the refractory period
Calcium Channel Blockers
Calcium channel blockers are generally well tolerated (T/F)
True
Decreases automaticity of SA node and slows conduction through AV node. Used for atrial dysrhythmias. Narrow therapeutic window and many interactions with other medications
Digoxin
Is given IV (rapid IV push) to decrease automaticity of SA node and slow conduction through AV node. Used to terminate atrial dysrhythmias or slow conduction (to determine underlying rhythm). Duration of action is 15 seconds
Adenosine
2 sodium channel blockers
procainamide, lidocaine
2 beta-adrenergic blockers
propranolol, metoprolol (off-label)
2 potassium channel blockers
amiodarone, sotalol
2 calcium channel blockers
verapamil, diltiazem
Nursing implications for antidysrhythmic drugs:
- Educate client about side effects of medication, monitoring of pulse, and not to discontinue medication (even if feeling well)
- ECG monitoring while in hospital for changes in heart rate or rhythm
- Monitor BP
- Be aware of factors which may increase r