Exam 6 Flashcards
1
Q
HTN is determined by average of two or more BP readings
above prehypertension levels on different dates
A
The highest reading obtained determines category of
HTN
2
Q
Having HTN puts the patient at a risk for developing:
A
– Cardiovascular disease
– Stroke
3
Q
Prevalence of HTN is very high
A
– Easy for a healthcare provider to get complacent with
higher BP values because they are seen often
4
Q
Individuals with “normal” BP
18 – 39 years of age
A
Follow up every 3 to 5 years
5
Q
Individuals greater than 39
years of age or at an
increased risk for developing
HTN
A
Follow up annually
6
Q
Individuals at an increased
risk for developing HTN
include
A
• Those with an elevated BP • Systolic: 120 – 129 mmHg • Diastolic: < 80mmHg • Overweight • African American • Increased renin activity, greater sodium and fluid retention • Family history
7
Q
Primary Hypertension (aka Essential Hypertension)
A
• Chronic BP elevation (systolic and/or diastolic)
• Unknown Cause
• Contributing factors may include: Sodium & Water retention, altered RAAS
mechanism, stress, insulin resistance (diabetes)
8
Q
Secondary Hypertension
A
Chronic BP elevation (systolic and/or diastolic)
• Known cause
• Sign of another problem within the body
• Ex: Kidney disease, tumor on the adrenal gland, atherosclerosis, etc.
9
Q
Often no signs and/or symptoms
A
– Referred to as the “Silent Killer” – The only symptom may be an elevated BP reading – HTN is usually diagnosed when seeking healthcare for other reasons
10
Q
Rare signs and symptoms include
A
– Headache
– Bloody nose
– Severe anxiety
– Dyspnea
11
Q
Analyze risk factors for hypertension
A
• Modifiable: Decreased activity level, smoking, poor diet, insufficient sleep, elevated
blood glucose level, elevated weight, poor stress management, diabetes mellitus
type 2
12
Q
Is type 2 diabetes a modifiable risk for hypertension?
A
Yes. Type 2 diabetes can be reversed.
13
Q
Normal”
A
<120 mmHg systolic
<80 mmHg diastolic
14
Q
Elevated
A
120–129 mmHg systolic
< 80 mmHg diastolic
15
Q
Stage 1 Hypertension
A
130–139 mmHg systolic
80–89 mmHg diastolic
16
Q
Stage 2 Hypertension
A
> 140 mmHg systolic
>90 mmHg diastolic
17
Q
If a patient has a SBP and a DBP in two different categories (i.e. 130/95 mmHg)….
A
they should be
placed in the higher BP category
18
Q
Therapeutic Measurements for Hypertension: Lifestyle modifications
A
- Weight reduction
- Incorporate diet changes
- DASH diet
- Dietary Sodium reduction
- Eat more whole foods
- Reduce added sugars
- Increase physical activity
- Tobacco cessation
- Psychosocial risk factors
- Reduce stress
19
Q
Therapeutic Measurements for Hypertension: Antihypertensive Medication Therapy
A
• Medications will be started if lifestyle modifications are unsuccessful or patient doesn’t follow
through with them
• Usually providers will start patient’s on a diuretic or beta blocker with initial therapy
20
Q
Therapeutic Measurements for Hypertension: Patients must be motivated to change their habits
A
• Hypertension will remain present and will return if lifestyle habits regress or medication therapy is
stopped
21
Q
Nursing Response if BP is Above Acceptable
Range (for patient’s baseline)
A
Ensure BP reading is accurate, reassess in 2 minutes on other extremity Observe for related symptoms, although symptoms are sometimes not apparent until BP is extremely elevated. Review orders for antihypertensive treatment • Administer antihypertensive medications as ordered, make this a priority so patient’s blood pressure doesn’t continue to elevate Report and document
22
Q
Complications of Unmanaged
Hypertension
A
■ Atherosclerosis ■ Cardiovascular disease – Coronary Artery Disease ■ Myocardial Infarction ■ Heart Failure ■ Left Ventricular Hypertrophy ■ Stroke ■ Kidney Disease ■ Retina Damage ■ The severity & duration of the increase in the BP determines the extent of vascular changes causing organ damage over time ■ Over time, elevated BP will damage the small vessels of the heart, brain, kidneys, and retina ■ This is known as target organ disease
23
Q
If a patient is having a cardiac infarction, what labs would you run?
A
Troponin and CK_MB
BNP
24
Q
If a patient has had a stroke, what lab would you run?
A
D-Dimer
25
What labs would you run to see if a patient has kidney failure?
Renin
Creatinine
eGFR
26
■ Medications will gradually decrease the blood pressure to an
ideal range
– There are countless medications that can reduce blood
pressure
– When an individual is newly diagnosed with HTN, a
mild/less aggressive anti-hypertensive will be
prescribed
■ Medications will be adjusted/added as necessary
until blood pressure is controlled
27
If the individual is unable to achieve their specific BP goal,
ask questions and follow up!
– Are they taking the medication as prescribed?
– Medication dosage may be increased and/or additional
of another medication from separate drug class added
in
■ It is not uncommon to see a patient on multiple anti
-hypertensives
28
Patient Education for Hypertension
| Control
Lifelong BP Control
• Self-care Measures
• Decreasing stress
• Lifestyle changes
• Control modifiable risk factors
• Prescribed Medication Regimen
• Stay on medications even if s/s are not present
• Rise slowly & change positions slowly
• If patient becomes dizzy with standing, they may fall & injury themselves
• If medications are abruptly discontinued, dangerous situations may occur
• Rebound HTN: acute elevation of blood pressure
• Angina: chest pain
• Dysrhythmias: Irregularities in cardiac rhythm
29
Hypertension is still present as a patho even if it is well controlled
• If patient does not appropriately manage BP, it will elevate again
30
Know BP and HR before giving
| medications
This is imperative to your nursing care!
Some medications will not affect HR, but BP is
imperative to assess
• Always assess a blood pressure before giving an
antihypertensive
Should take appropriate vitals within 30 minutes to
one hour of administering anti-hypertensives
31
Know if the medication has vital
| sign limits
Ex: Do not administer medication if HR is less than
60 bpm
Ex: Do not administer medication if systolic BP is
less than 100 mmHg
32
Statins
Treat HLD, do not directly treat HTN
33
Diuretics
* Loop Diuretics
* Thiazide Diuretics & Thiazide-Like Diuretics
* Potassium-Sparing Diuretics
34
Medication
Classes for
Hypertension
```
Angiotensin-converting Enzyme Inhibitor (ACE
Inhibitor)
Angiotensin II Receptor Blocker (ARB)
Calcium Channel Blocker (CCB)
Beta Blockers
Combined Alpha & Beta Blockers
```
35
Statins are given to a patient with atherosclerosis and/or coronary artery disease to
reduce LDL levels by reducing cholesterol synthesis
– This will decrease the plaque build up on coronary walls which will improve blood
flow
36
Hypertension may be caused secondary to hyperlipidemia
– You may see the patient may on a statin
■ This is not to treat to the HTN, it is to treat the hyperlipidemia
– The goal here is to reduce the cholesterol levels, reduce plaque build up in the
arteries, which should in turn improve blood pressure
– Statins do not directly treat hypertension
37
Do statins directly affect blood pressure?
No.
38
Does the nurse need to assess the blood pressure before/after administration of a
statin?
No.
39
General Information on Diuretics
■ Diuretics are a common drug class for the
provide to choose as initial treatment to
control hypertension
– This usually occurs after lifestyle
changes and diet changes were
attempted (and not successful)
– If HTN does not improve from diuretics
alone, another drug class will be added
on to medication regimen
■ Diuretics should be given during the morning
so the patient doesn’t experience nocturia
■ Diuretics are given to individuals with
Hypertension, Chronic Heart Failure (CHF),
Edema, and Pulmonary Edema
40
Monitor Lipid Panel Labs while on this medication to see how well it’s working
HDL, LDL, Triglycerides, Total Cholesterol
41
Statins are hepatotoxic, monitor liver function tests:
AST, ALT, ALP
42
Assessments with Diuretics
Prior to giving a diuretic, the blood pressure must be assessed
• Possible side effect of hypotension from decreased fluid volume within the body
Assess blood pressure after diuretic administration
• Urine output will begin to change very soon after diuretic administration
Monitor intake and output
Monitor for signs and symptoms of dehydration
• Weights will slowly decrease each day if patient was fluid overloaded, they will not abruptly change with the first urination
Assess daily weights
• Be sure electrolytes are within normal range prior to administration of a diuretic
• If they are not, do not administer. Notify the provider.
• Monitor for signs and symptoms of electrolyte imbalances
• Hyponatremia and hypochloremia: CNS changes
• Hypokalemia: Muscle cramps, muscle weakness, cardiac dysrhythmias
• Priority concern!
43
Diuretics work on the kidneys to increase
renal secretion of sodium, chloride,
potassium, and fluid
```
– This removes fluid from the body and
increases urine output
– When fluid is removed from the body,
the blood pressure is decreased and
cardiac workload is decreased
```
44
Diuretics can begin working very quickly
| within minutes sometimes
```
– Imperative for the nurse to monitor
urine output right away
– Have room set up for patient to easily
urinate (bedside commode, urinal,
clear path to bathroom)
```
45
Page 21 of the Hypertension power point
Diuretic medication info
46
Be sure electrolytes are within normal range prior to administration of a diuretic
* If they are not, do not administer. Notify the provider.
* Monitor for signs and symptoms of electrolyte imbalances
* Hyponatremia and hypochloremia: CNS changes
* Hypokalemia: Muscle cramps, muscle weakness, cardiac dysrhythmias
* Priority concern!
47
Hyponatremia and hypochloremia:
CNS changes
48
Hypokalemia:
Muscle cramps, muscle weakness, cardiac dysrhythmias
49
Loop Diuretic
Bumetanide (Bumex)
Furosemide (Lasix)
Potassium wasting diuretic; must monitor potassium levels and replace if necessary
50
Thiazide Diuretic
Hydrochlorothiazide (HCTZ)
Chlorothiazide
Metolazone
51
Potassium Sparing Diuretic
Spironolactone (Aldactone)
How does it work? • Blocks the actions of aldosterone
• Increased sodium & urine output, increased potassium retention
• Produce a modest increase in urine production
• Diuretic effects are limited
• Produce a substantial decrease in potassium excretion
• May be given in combination with a loop or thiazide diuretic to counteract the loss of potassium
52
Potassium Sparing Diuretic
| Common Medications: Spironolactone (Aldactone)
Extra Info:
• Considered a “mild” diuretic
• Used in combination therapy with other drugs/antihypertensives
• Diuresis doesn’t start for 24-48 hours
• Spares (i.e. allows the body to hold on to) potassium
• Assess for hyperkalemia
• Avoid foods rich in potassium
• Oranges, bananas, salt substitutes, avocados, etc.
53
RAAS Refresher
Page 22 of Hypertension power point.
54
Angiotensin-converting-enzyme Inhibitor (ACE Inhibitor)
Common Medications
end in “–pril”
Lisinopril
Enalapril
Captopril
Quinapril
How does it work? • Block synthesis of Angiotensin II, which causes the following actions:
• Prevents vasoconstriction; promotes vasodilation of arteries
• Prevents release of Aldosterone
• Increases renal excretion of sodium and water
• Decreased blood volume (reduces preload & decreases blood pressure)
• Potassium retention (due to excreting sodium)
• Reduces peripheral arterial resistance (i.e. afterload) and blood pressure
• Improves cardiac output
How is it administered? • PO
Why is it given? • Hypertension
• Heart Failure (reduce cardiac afterload, improves cardiac output)
• First line therapy for heart failure, reduces preload and afterload
When is it given? Daily or multiple times a day
Assessments • Assess blood pressure before & after administration and monitor for hypotension
Extra Info • Monitor for new-onset dry, irritating, nonproductive, persistent cough
• Educate and monitor for hyperkalemia
• Educate and monitor for angioedema
• Swollen lips, swollen tongue Blocked airway, emergency!!
55
Angiotensin II Receptor Blocker (ARB)
Common Medications:
end in “–artan”
Candesartan
Losartan
Olmesartan
How does it work? • Block Angiotensin II Receptors and prevents Angiotensin II from binding
• Vasodilation occurs, blood pressure reduced
• Decrease the release of aldosterone
• Increases renal excretion of sodium and water
How is it administered? PO
Can be given intravenously in the acute care setting
Why is it given? • Hypertension
• Heart Failure; reduces preload and afterload
When is it given? Daily or multiple times a day
Assessments • Assess blood pressure before & after administration, monitor for hypotension
Extra Info • Monitor for new-onset dry, irritating, nonproductive, persistent cough
• Not as common as ACE inhibitor, but still possible
• Educate and monitor for hyperkalemia
• Not as common as ACE inhibitor, but still possible
• Educate and monitor for angioedema
• Swollen lips, swollen tongue Blocked airway, emergency!!
56
Drug Class: Calcium Channel Blocker (CCB)
Common Medications
end in “–pine”
Amlodipine
Nicardipine
Nifedipine
Diltiazem (Cardizem)
How does it work? • Calcium is required for electrical excitability of cardiac cells and contraction of both myocardium & vascular smooth muscle
• CCB prevents movement of extracellular calcium into the cell
• CCB’s have the greatest effect on the heart and blood vessels
• Causes vasodilation of peripheral and coronary arteries
• Blood pressure decreases
• Decrease peripheral vascular resistance (afterload)
• Decreases workload of heart
• Blood pressure decreases
• Slow conduction system (calcium slows the firing of the SA node)
• Decreases myocardial contractility, slows heart rate
• Decreases workload of heart
• Decreases myocardial oxygen demand
How is it
administered?
PO
Why is it given? • Hypertension
• Treat cardiac dysrhythmias (i.e. atrial fibrillation)
When is it given? Daily or multiple times a day
Assessments • Assess pulse and blood pressure before & after administration, monitor for hypotension & bradycardia
• Do not give if HR is less then 60 bpm
57
Beta One Receptor Location &
| Activation
■ Located within:
– Heart
– Kidneys
■ Focus: Heart; Activation of beta one receptors causes
– Increased force of contraction
■ Think: Cardiac muscle is squeezing harder and contracting more forcefully to expel blood
■ Due to this action, cardiac output increases
– The amount of blood the heart is pushing out increases
– Increased impulse conduction
■ Think: electricity passing through the heart has sped up
■ Due to this action, heart rate increases
– Remember, when beta one cells within the heart are activated, the heart is stimulated to work hard to push oxygenated blood out to tissues and muscles
■ Focus: Kidneys; Activation of beta one receptors causes
– Releases renin into the blood
■ Renin causes synthesis of angiotensin, a powerful arterial vasoconstrictor
– Blood pressure increases, which allows blood to be moved more quickly throughout the body (to oxygenate organs and tissues)
58
Drug Class: Beta Blockers
Common Medications:
end in “–olol”
• Cardio-Selective Beta 1 Blockers:
• Metoprolol Tartrate (Lopressor)
• Metoprolol Succinate Extended Release (Toprol
XL)
• Atenolol
• Non-Selective Beta 1 Blockers:
• Propranolol
• These medications will have properties to block Beta
2 receptors avoid in COPD and asthma, will cause
bronchospasms!
How does it work? • Block beta receptors from binding to epinephrine & norepinephrine (Decreased SNS response)
• Decrease heart rate
• Decrease cardiac output
• Decreased workload on heart
• Decreased myocardial oxygen demand
• Prevent release of renin (via kidneys)
• Blood pressure decreases in result of all above actions
How is it administered? PO
Why is it given? • Hypertension
• Tachycardia
When is it given? Daily or multiple times a day
Assessments? • Assess pulse and blood pressure before & after administration, monitor for hypotension & bradycardia
• Do not give if HR is less then 60 bpm
• Do not give is systolic BP < 100 mmHg
59
Alpha One Receptor Location &
| Activation Response
■ Located within:
– Large Peripheral Arteries
■ Focus: Arteries
– Large peripheral arteries within the body vasoconstrict
■ Get smaller
■ This increases the pressure within the arteries, causing blood to
flow more forcefully through them
– This causes a temporary increase in BP
■ Blood pressure will return to baseline after activation of the
SNS is stopped.
■ This increases blood flow to the tissues and muscles
60
Drug Class: Combo Drug: Alpha & Beta Blockers
Common Medications
end in “–lol”
Carvedilol
Labetalol
*Note: these medications are non-selective beta blockers
• These medications will have properties to block Beta 2 receptors avoid in COPD and asthma, will cause
bronchospasms!
How does it work? • Blocks epinephrine and norepinephrine from binding to alpha & beta receptors
• Blocks alpha receptors from binding to epinephrine and norepinephrine
• Blocks effects of SNS on smooth muscle of blood vessels & cardiac muscle
• Promotes vasodilation and decreased blood pressure in arteries
• Block beta receptors from binding to epinephrine & norepinephrine (Decreased SNS response)
• Decrease heart rate
• Decrease cardiac output
• Decreased workload on heart
• Decreased myocardial oxygen demand
• Prevent release of renin (via kidneys)
• Blood pressure decreases in result of all above actions
How is it administered? PO
Why is it given? • Hypertension
• Tachycardia
When is it given? Daily or multiple times a day
Assessments? • Assess pulse and blood pressure before & after administration, monitor for hypotension & bradycardia
• Do not give if HR is less then 60 bpm
• Do not give is systolic BP < 100 mmHg
61
Common cardiac dysrhythmia, classified by:
– Irregular rhythm
| – Irregular or regular rate
62
Abnormal firing of electrical impulses from the atria
– Electrical impulses do not originate from the SA node, they originate from a different part of the atria
– The atria are initiating an impulse faster than the SA node atria take over as the pacemaker
63
Due to the rapidly firing impulses coming from the atria, the atrial are contracting very quickly and chaotically
Atrial rate is so fast it is immeasurable
64
The AV Node blocks most of the chaotic impulses from being sent from the atria, so ventricular rate is much slower
– Heart rate can fluctuate 20 – 30 beats/minute due to irregular rhythm
– Important to assess an apical pulse for a minute to determine an accurate heart rate in these patients!
65
Atrial
Fibrillation
Risk Factors
```
Older Age (65 & above)
Smoking
Heart disease
Heart failure
HTN
Surgery
Excessive amounts of caffeine
Others
```
66
Atrial Fibrillation Signs &
| Symptoms:
■ Can be asymptomatic
– Remember, a lot of individuals don’t realize they
have Afib until they have a stroke because of it!
■ Feelings of heart palpitations
■ Chest discomfort
■ Faint radial pulse
– Decreased cardiac output secondary to decreased
stroke volume
■ Generalized fatigue & weakness, lightheaded
– Decreased tissue perfusion due to decreased cardiac
output
■ EKG Changes present
– EKG will show irregular rhythm
■ People can have paroxysmal Afib or persistent Afib
– Treatment will be dependent upon classification
67
Atrial Fibrillation Complication: CVA
■ Atrial Fibrillation puts a patient at an
increased risk for developing a
Cerebrovascular Accident (CVA)
– Most individuals don’t know they have
Atrial Fibrillation until they develop a
CVA
■ The rapid/chaotic impulses that develop in
A Fib cause the atria to quiver/fibrillate
■ Blood cannot completely exit the atria like
it is supposed to, leading to blood stasis
blood then pools in the atria
■ Blood stasis and pooling puts the patient
at increased risk for development of
thrombus (blood clot)
– If a thrombus develops, it then has
the potential to leave the heart travel
to the brain causing a CVA!
68
Atrial Fibrillation
Complication:
CVA
```
■ Signs and symptoms of
a CVA include:
– Facial drooping
– Slurred speech
– One sided
weakness
■ After a stroke, a patient
may have lasting
residual effects
```
69
Atrial Fibrillation Medication Therapy: Goal of treatment
```
• Give medications to
control heart rhythm and
heart rate
• Give medications to
prevent thrombus &
stroke
```
70
Atrial Fibrillation Medication Therapy: Medications to control heart
rhythm and/or heart rate
```
• Beta Blocker
• Regulate rate
• Calcium Channel Blocker
• Regulate rate and
rhythm
• Antidysrhythmic Agents
• Regulate rate and
rhythm
```
71
Atrial Fibrillation Medication Therapy: Medications to prevent
thrombus and CVA
```
• Anticoagulant or
Antiplatelet
• Prevent side effects of
Atrial Fibrillation
prevent clot formation
• Anticoagulant given if
Afib is constant, active
• Antiplatelet given if risks
of bleeding outweigh
risks of afib treatment or
if afib episode only
happened once
```
72
Drug Class: Antidysrhythmic Agent
Common Medications Amiodarone
How does it work? • Used for atrial fibrillation to control heart rhythm & rate
• Decreases cardiac contractility
• Promotes dilation of coronary and peripheral blood vessels
How is it administered? PO
Given intravenously in the acute care setting
Why is it given? • To control heart rhythm and rate
When is it given? Daily
Assessments? • Assess pulse and blood pressure before & after administration, monitor for hypotension
& bradycardia
• Do not give if HR is less then 60 bpm
• Assess heart rhythm before and after administration
Extra Info • Can damage lungs, heart, thyroid, and liver with long term use
73
General Information Regarding
| Anticoagulants
Anticoagulation medications are given to prevent blood clot formation within the vessels or to treat a blood clot after it is already formed
Anticoagulants prolong the clotting time of the blood
There are many different types of anticoagulants that can be administered
• Begins working quickly
• Common anticoagulants via subcutaneous route include:
• Enoxaparin (Lovenox)
• Heparin
For prophylactic treatment of blood clot formation while hospitalized, patients are generally given an anticoagulant in subcutaneous form
• Coagulation studies
Various anticoagulants have specific lab values that should be evaluated while the patient is taking the drug
Some anticoagulants don’t require any lab value monitoring
74
Prior to starting a patient on an anticoagulant, the nurse can
assess the H & H and platelets
• Ensure values are appropriate and there isn’t a bleeding issue before
starting the medication
• This is not routinely monitored while the patient is on the anticoagulant
unless there are signs and symptoms of bleeding
75
All anticoagulants put a patient at increased risk for bleeding
this is an adverse effect of the medication
Increases the risk for GI bleed & hemorrhagic stroke
• Monitor for s/s of bleeding:
• Bleeding gums, petechiae, excessive bruising, blood in the urine, black
tarry stools, coffee ground emesis
• If S/S of bleeding are present, review recent CBC for platelets & H/H
• If there is not a recent CBC, contact the provider
• Educate patients that they may bruise &/or bleed more easily
76
If a patient is experiencing an adverse effect of an
anticoagulant, such as bleeding, an antidote may be given to
reverse effects
These are the common anticoagulants given when a patient has Atrial
Fibrillation to prevent a Cerebrovascular Accident!
– Warfarin (Coumadin)
– Apixaban (Eliquis)
– Rivaroxaban (Xarelto)
77
Drug Class • Anticoagulant
Common
Medications
• Warfarin (Coumadin)
How does it work? • Vitamin K Antagonist
• Warfarin inhibits vitamin K from activating
• Suppresses coagulation of the blood by decreasing production of various clotting factors
• The clotting factors are vitamin-K dependent clotting factors
• i.e. these clotting factors NEED activated vitamin K to allow the blood to clot
How is it
administered?
• PO
When & Why is it
given?
• Given daily to treat current thrombosis and prevent future thrombosis
Assessments? • Assess for signs and symptoms of bleeding!
• Bleeding gums, petechiae, excessive bruising, blood in the urine, black tarry stools, coffee ground emesis
Monitor
Effectiveness of
Therapy
• Prothrombin Time (PT)
• International Normalized Ratio (INR)
• INR should be in therapeutic range (2.0 – 3.0)
• Labs must be checked every 3 – 4 weeks
Extra Info • Warfarin and heparin act similarly in the body
• Both used to prevent thrombosis
• Heparin has a quick/fast onset
• Warfarin has a delayed onset, making it inappropriate for emergencies
• Not suitable for prophylaxis either.
• Well suited for long-term use
• Not given as a prophylactic medication to avoid DVT development while in hospital setting
• If the patient needs medication prophylactically, they will be given heparin only, not in combination with warfarin
• If the patient needs to treat and existing clot, they will start on heparin and warfarin at the same time
• If patient is starting on long-term anticoagulation therapy, they may begin taking both Heparin and Warfarin at the same time
• Heparin begins acting almost immediately
• Warfarin takes a few days
• Once coagulation levels (INR & PT) are within therapeutic range for Warfarin, Heparin will be stopped
• Antidote: Vitamin K
78
Drug Class • Anti-Coagulant
| • Inhibition of factor Xa
Common Medications • Apixaban (Eliquis)
• Rivaroxaban (Xarelto)
How does it work? • Inactivates factor Xa (which is a clotting protein) to prevent blood clots from forming
How is it administered? • PO
When & Why is it given? • Given daily to treat current thrombosis and prevent future thrombosis from forming
Assessments? • Assess for signs and symptoms of bleeding!
• Bleeding gums, petechiae, excessive bruising, blood in the urine, black tarry stools, coffee
ground emesis
Monitor Effectiveness of
Therapy
• No labs to monitor effectiveness
Extra Info • Not given as a prophylactic medication to avoid DVT development while in hospital setting
• Many advantages over Warfarin
• Rapid Onset (doesn’t take days to start working)
• Lower bleeding risk
• No need for INR monitoring
• Antidote: None
79
```
Alternative regimens (instead of anticoagulants) may be used in a patient with
Atrial Fibrillation for various reasons (elderly, low risk for developing stroke, etc.)
```
– Aspirin
| – Clopidogrel (Plavix)
80
Drug Class Anti-Platelet Aggregator *Primary reason ASA is given*
Salicylate
Non-steroid anti inflammatory agent (NSAID)
Common Medications Acetylsalicylic Acid (ASA), trade name is Aspirin
How does it work? • Inhibits platelet aggregation in the arteries
• Unlike anticoagulation therapy which prevents thrombosis in the veins
• Inhibits prostaglandin synthesis within the body, preventing fever and pain
How is it administered? PO
Why is it given? • Commonly given to individuals with Coronary Artery Disease to prevent blood clot formation
• Given to prevent:
• Ischemic stroke or TIA
• Myocardial Infarction
• May be given for pain, fever, inflammation
When is it given? Daily when given as anti-platelet aggregator
Assessments? • Assess for signs and symptoms of bleeding!
• Bleeding gums, petechiae, excessive bruising, blood in the urine, black tarry stools, coffee
ground emesis
Extra Info • Monitor platelets when on this medication
• Increases the risk for GI bleed & hemorrhagic stroke
• If S/S of bleeding are present, review recent CBC for platelets & H/H
• If there is not a recent CBC, contact the provider
• Educate patients that they may bruise &/or bleed more easily
• If the patient takes ASA Daily, it is most likely for anti-platelet properties versus pain control
81
Drug Class Anti-Platelet Aggregator
Common Medications Clopidogrel (Plavix)
How does it work? • Very similar to ASA, inhibits platelet aggregation in the arteries
• Unlike anticoagulation therapy which prevents thrombosis in the veins
How is it administered? PO
Why is it given? • Commonly given to individuals with Coronary Artery Disease to prevent blood clot formation
• Primarily given to prevent:
• Stenosis of coronary stents
• Ischemic stroke or TIA
• Myocardial Infarction
When is it given? Daily
Assessments? • Assess for signs and symptoms of bleeding!
• Bleeding gums, petechiae, excessive bruising, blood in the urine, black tarry stools, coffee
ground emesis
Extra Info • Monitor platelets when on this medication
• Increases the risk for GI bleed & hemorrhagic stroke
• If S/S of bleeding are present, review recent CBC for platelets & H/H
• If there is not a recent CBC, contact the provider
• Educate patients that they may bruise &/or bleed more easily
82
Factors Affecting
Cardiac Output:
Preload
```
■ Amount of pressure stretching the ventricle the
end of ventricular diastole
■ Analogy: Blown up balloon
– More water in the balloon, the more it
stretches
■ What can cause an increased preload?
– Increased central venous pressure
■ Fluid volume overload
– Heart Failure
```
83
Factors Affecting
Cardiac Output:
Afterload
■ Systemic vascular resistance
■ Amount of resistance the heart/left ventricle must overcome to
open the aortic valve and push blood out into systemic
circulation
■ Analogy: Knot at the end of the balloon
– Balloon must push, squeeze, and work against the knot
to get the fluid out of the balloon
■ What can cause an increased afterload?
– Hypertension
■ Increased pressure in the vessels, harder to push
fluid into vessels with increased pressure
– Vasoconstriction
■ Narrow vessels, harder to push fluid into them
■ The cardiac workload must increase if afterload is increased
– Heart needs to work harder to push blood out against the
resistance
84
Heart Failure: Pathophysiology
Syndrome occurs from progressive inability of heart to pump enough blood throughout the body to meet body’s oxygen/nutrient needs
Pump (heart) is failing, not working correctly weaker then normal
•Tissues aren’t receiving ample amount of nutrients and oxygen
•If blood returned to the heart is more than either ventricle can handle, heart is no longer an effective pump
Each ventricle should pump equal amount of blood
•The fluid will back up in different locations depending on the side of the pump that has failed
Due to the pump being inefficient, blood begins to back up through the system
•Left ventricle typically weakens first
•Greatest workload to eject blood against resistance in aorta
•Failure of one usually leads to failure of other
Can have either left-sided HF or right-sided HF
•Left ventricle typically weakens first
•Greatest workload to eject blood against resistance in aorta
•Failure of one usually leads to failure of other
•In early stages, HF is asymptomatic
85
Causes of Heart Failure
Various diseases can cause heart failure; these are only a
few
■ Coronary Artery Disease
– Decreased oxygen delivery to cardiac muscle, heart is
not an efficient pump
■ Chronic Hypertension
– Increased resistance, heart must work harder to
maintain cardiac output
■ Myocardial Infarction
– Area of the heart died due to lack of oxygen, heart is
no longer an efficient pump
■ Dysrhythmias (Atrial Fibrillation)
– Decreased cardiac output from dysrhythmia causes
heart to work harder to attempt to maintain cardiac
output
86
Left ventricle has to work harder to pump
| blood into the aorta/to the body due to:
```
Increased afterload from increased peripheral
vascular resistance (usually due to hypertension)
```
87
Overtime, the increased workload causes
strain on the left ventricle and it becomes
an inefficient pump
Thus causing Left Sided Heart Failure
88
As the left side of the heart fails, it cannot
pump out as much blood into the aorta/body
decreased cardiac output
The muscles & tissues experience decreased
| perfusion & oxygen delivery
89
What Happens with Left-Sided Heart
| Failure
■ As the left side of the heart fails, it cannot keep
up with the demands of the blood entering the
left ventricle
– Blood backs up into the lungs
– Left ventricle Mitral Valve Left
Atrium Pulmonary Vein Lungs
(alveoli)
■ Blood in the alveoli causes pulmonary edema
– Pulmonary edema can range from mild to
severe
– Many signs and symptoms of left sided
heart failure are due to fluid accumulation
within the lungs
90
```
Left Sided
Heart
Failure
Signs &
Symptoms: Pulmonary S/S:
```
* Crackles &/or wheezing
* Dry hacking cough
* Pink Frothy Sputum
* Tachypnea
* Dyspnea on Exertion
* Orthopnea
* Paroxysmal Nocturnal Dyspnea
91
```
Left Sided
Heart
Failure
Signs &
Symptoms: Mental Status S/S:
```
* Restlessness
| * Confusion
92
```
Left Sided
Heart
Failure
Signs &
Symptoms: Systemic S/S:
```
Fatigue
• Cyanosis
• Nocturia
• Tachycardia
93
Right-Sided
| Heart Failure
A major cause of Right-sided Heart Failure is Left-sided Heart Failure
•Right side of heart must continually pump blood against increased fluid/pressure in pulmonary artery and
lungs
•Right side of the heart eventually weakens
As the right side of the heart works harder, the muscle (epicardium) gets larger
•This is called Cor Pulmonale
94
As the right side of the heart fails, it cannot
keep up with the demands of the blood
entering the right ventricle
– Blood backs up into the body
– Right ventricle tricuspid valve
right atrium inferior & superior vena
cava body
■ Many signs and symptoms of right sided
heart failure are due to fluid overload/blood
backing up into the body
95
```
Right Sided
Heart
Failure
Signs &
Symptoms
```
```
Systemic S/S:
• Fatigue
• Weakness
• Nocturia
• Tachycardia
Fluid Overload S/S:
• Weight Gain
• Dependent peripheral edema
• Ascites
• Hepatomegaly
• Splenomegaly
• GI Upset
• Anorexia, Nausea, Pain
• Jugular Venous Distension
```
96
Diagnostic Tests for HF (Review!)
```
Blood Tests:
Brain Natriuretic
Peptide
• Monitor to see
progression of CHF
Troponins
• Monitored during
acute exacerbation
of heart failure
```
97
Diagnostic Tests for HF (Review!)
| Chest X-Ray
Shows size of heart
Shows lungs,
determine extent of
pulmonary edema
98
Diagnostic Tests for HF (Review!)
| Echocardiography
Determine ejection
fraction
<40% may indicate
heart failure
99
Diagnostic Tests for HF (Review!)
| EKG
View heart rate,
rhythm, heart chamber
enlargement, etc.
100
Goals of Therapeutic
| Interventions
■ Improve heart’s pumping ability and decrease
heart’s oxygen demands
– Identify and correct underlying cause
– Increase strength of heart’s contraction
– Maintain optimum water and sodium balance
– Decrease heart’s workload
101
Nursing Actions
```
Daily weights
• Especially when in acute exacerbation
• More then 2 lbs in 24 hours, notify physician
Supplemental Oxygen
• If necessary
Balance Rest and Activity
• Conserve oxygen but keep independence
Positioning
• High Fowlers
Fluid Restrictions
Medications/Teaching
Low-sodium Diet
Education
Coping with disease
```
102
Medication
| Management
May see a patient on multiple medications to
control the disease & s/s of disease
Various drug classes to manage heart failure:
• ACE Inhibitors
• First-line therapy for HF
• Help to decrease the heart’s workload, improve
cardiac function and improve symptoms of CHF
• ARBs
• Can be used if ACE Inhibitor is contraindicated
• Diuretics
• Reduce fluid volume
• Beta Blockers
• Decrease SNS response, decrease cardiac workload
• Cardiac Glycosides
• Improve efficiency of cardiac contractions
103
Drug Class: Angiotensin-converting-enzyme Inhibitor (ACE Inhibitor)
Common Medications
end in “–pril”
Lisinopril
Enalapril
Captopril
Quinapril
How does it work? • Block synthesis of Angiotensin II, which causes the following actions:
• Prevents vasoconstriction; promotes vasodilation of arteries
• Prevents release of Aldosterone
• Increases renal excretion of sodium and water
• Decreased blood volume (reduces preload & decreases blood pressure)
• Potassium retention (due to excreting sodium)
• Reduces peripheral arterial resistance (i.e. afterload) and blood pressure
• Improves cardiac output
How is it administered? • PO
Why is it given? • Hypertension
• Heart Failure (reduce cardiac afterload, improves cardiac output)
• First line therapy for heart failure, reduces preload and afterload
When is it given? Daily or multiple times a day
Assessments • Assess blood pressure before & after administration and monitor for hypotension
Extra Info • Monitor for new-onset dry, irritating, nonproductive, persistent cough
• Educate and monitor for hyperkalemia
• Educate and monitor for angioedema
• Swollen lips, swollen tongue Blocked airway, emergency!!
104
Drug Class: Cardiac Glycoside, Inotrope
Common Medications Digoxin
• How does it work? • Exerts a positive inotropic action on the heart, which means:
• Increases the strength/force of heart’s contraction
• This increases stroke volume (amount of blood pushed out of left ventricle in each beat)
• Increased stroke volume leads to increased cardiac output (this is important for heart
failure!)
• Slows heart rate so that the heart doesn’t work as hard (decreases workload)
• Summary: Heart is working more efficiently but not as hard!
How is it administered? PO
Why is it given? • To control heart failure
When is it given? Daily
Assessments? • Assess pulse before & after administration, monitor for bradycardia
• Do not give if HR is less then 60 bpm
Extra Info • While taking this medication, Serum Digoxin Levels should be between 0.8 – 2.0 ng/mL
• Educate the patient to take the medication at the same time every day
• Educate the patient on s/s of digitalis toxicity & to report them immediately (discussed on next
slide!)
105
While taking this medication, Serum Digoxin Levels should be:
between 0.8 – 2.0 ng/mL
106
Digoxin: Digitalis Toxicity
```
■ Caused by high levels of digoxin in body
■ Signs & Symptoms
– Bradycardia
– GI Disturbances
■ Loss of appetite / Anorexia
■ Nausea, vomiting, diarrhea
■ Abdominal discomfort
– CNS Disturbances
■ Vision changes: blurred vision, yellow-green vision changes, may see yellow/green
halos
■ Fatigue
■ Confusion, Decreased LOC
```
