N352 Cardiovascular Disease

Front 1

When blood pressure drops, what area of the brain senses it? How does it respond?

Back 1

The medulla oblongata in the brain stem receives this information from baroreceptors in the Aorta and Carotid arteries. It then initiates a sympathetic response.

Front 2

What does the response from the Medulla Oblongata affect when BP drops?

Back 2

It sends signals for the Adrenal Medulla to initiate a sympathetic response.

Front 3

List the hormones and receptor sites that are affected when the Adrenal Medulla reacts and list the results.

Back 3

Epinepherine is released and effects the Beta 1 receptors in the heart muscle and conductive tissue. It increases HR and CO. Norepinepherine is also released and effects Alpha 1 receptors. These cause peripheral vasoconstriction, thus elevating BP. (As a side note, Beta 2 receptors are in the lungs).

Front 4

When blood pressure drops, what effect does it have on the kidneys?

Back 4

Low BP causes low blood flow to the kidneys. The kidneys respond by releasing Renin for the renin-angiotensin -aldosterone system.

Front 5

What are the 6 steps of the RAA starting and ending with the kidneys, and what is the result?

Back 5

1. Renin is released from the kidneys
2. Angiotensinogen is released from the liver
3. The two combine and create Angiotensin I
4. ACE is secreted in the lungs and changes Ang 1 to Ang II
5. Ang II acts on the Adrenal Cortex to cause the release of Aldosterone
6. Aldosterone interacts with receptors and causes increased retention of Na+ in the renal tubules and water follows Na+

Front 6

What happens in the Adrenal gland when Ang II is present in the blood? What organ is acted upon next? What is the result regarding BP and plasma osmolarity?

Back 6

The Adrenal Cortex has Ang II Receptors for it. This causes the production of Aldosterone that acts on the kidneys to cause Na+ retention in the distal tubules, which increases water retention. This creates increased plasma osmolarity through the increased Na+.

Front 7

What does the change in blood osmolarity cause in the Hypothalamus? What is the effect?

Back 7

The increased osmolarity causes the Hypothalamus to signal the Posterior Pituitary to release ADH, which acts on the Kidney Collecting Ducts to rebsorb water, thus increasing BV and BP.

Front 8

What two tissues have Angiotensin II receptors?

Back 8

The Adrenal Cortex and blood vessel walls for vasoconstriction.

Front 9

So, when BP drops, what 5 organ systems are affected?

Back 9

1. The nervous system - Baroreceptors signal medulla, and increased plasma osmolarity signals the hypothalamus
2. Adrenal Medulla secretes Epi and Norepi
3. The Kidney secretes Renin and is acted on by Aldosterone and ADH
4. Adrenal Cortex secretes Aldosterone
5. The blood vessels constrict due to Norepi

Front 10

What receptor type is subdivided into alpha and beta receptor sites? What hormones act at the Beta 1 & 2 sites, and what hormone acts on the Alpha 1 receptor site?

Back 10

These receptors are Adrenergic, which means they are acted upon by catecholamines (Epi and Norepi)

Front 11

How does the pharm category Angiotensin II Receptor Blocker act on high BP and name two meds.

Back 11

This medication blocks the production of Aldosterone in the Adrenal Cortex by blocking the receptors for Ang II. This stops water retention caused by Aldosterone. Atacand & Avapro.

Front 12

How does the pharm category of diuretics help reduce HTN and name two classifications of drugs.

Back 12

Diuretics act on the Distal Renal Tubules to decrease water retention through inhibiting Na+ retention -
thiazides & loop diuretics

Front 13

How do CNS Alpha 2 Agonists help fight HTN and give a med name.

Back 13

These medications increase the uptake of Norepi in the presynaptic membrane within the Medulla Oblongotta. This means there is less Norepi available to cause vasoconstriction. Catapress.

Front 14

How does a Beta Blocker act to reduce HTN and give a med name.

Back 14

Beta Blockers act on the heart to decrease the sympathetic response through blocking Beta 1 receptors. This prevents Epi from increasing the HR and CO, which helps lower BP- atenolol.

Front 15

How does a Alpha 1 Blocker act to lower BP and give a med name.

Back 15

Alpha 1 blockers prevent Norepi from acting on Alpha 1 Receptors in the peripheral vascular system, thus lowering vasoconstriction. This works on the postsynaptic membrane. Minipress.

Front 16

How do ACE Inhibitors help combat HTN and give a med name.

Back 16

They block the release of Angiotensin Converting Enzyme in the lungs. These are Beta 2 receptors - lisinopril.

Front 17

How do Angiotensin II Receptor Blockers work to combat HTN and give a name.

Back 17

This blocks the Ang II receptor sites in the Adrenal Cortex and Peripheral Vessels. This blocks Alpha 1 receptors. Atacand, Avapro.

Front 18

Name a Vasodilator and a Calcium Channel Blocker. How does the Ca+ Channel Blocker work?

Back 18

Vasodilator - Apresoline
Ca+ Channel Blocker - Cardizem - It blocks the flow of Ca+ into the Synaptic Knob that creates a Synaptic Transmission.

Front 19

What are 3 Artery problems we are studying? What are 2 Venous problems we are studying?

Back 19

Artery
-HTN
-Acute Occlusion
-Chronic Occlusion
Vein
-DVT
-Chronic Venous Insufficiency

Front 20

When an Artery has Atherosclerosis, what is the name of the area of build up that can block the artery? What else can happen in that area?

Back 20

Athroma - It can rupture and spill out a clot. The clot can stay there, or break off and creat and embolism that can cause damage elsewhere.

Front 21

What is a normal BP and MAP? How do you figure MAP?

Back 21

A normal BP is 135/85
A normal MAP is <100

Figure MAP by adding the systolic pressure and diastolic pressure, then divide by 2.
Ex. 120 + 80 = 200/2 = MAP 100

Front 22

What are three things that cause HTN?

Back 22

1. Artery vasoconstriction
2. Increased blood volume
3. Both vasoconstriction and increased blood volume

Front 23

What are the two types of HTN?

Back 23

Primary (Essential) HTN
Secondary HTN

Front 24

What is the cause of Primary HTN? What diseases can it be associated with and what are the clinical manifestations?

Back 24

Cause - Not usually known
Diseases - Metabolic syndrome, dyslipidemia, and glucose intolerance
Manifestations - Usually none. Later on it causes organ damage due to high pressure

Front 25

What are some of the causes of Secondary HTN? (7)

Back 25

1. Kidney disease
2. Endocrine disorders
3. Narrow or rigid arteries
4. Arteriosclerosis
5. Increased ICP
6. Stress
7. Some drugs

Front 26

What are the 9 risk factors for HTN?

Back 26

1. Cigarette Smoking - Nicotine causes vasoconstriction
2. Obesity
3. Sedentary Lifestyle
4. Hyperlipidemia (damage to vessels leads to atherosclerosis)
5. Metabolic Syndrome (damage to vessels leads to atherosclerosis)
7. Diabetes Type 2 (damage to vessels leads to atherosclerosis)
8. Family Hx/African American **The only factor that can't be prevented!
9. Excess alcohol intake (raises Triglycerides)

Front 27

What are the consequences of Chronic HTN?

Back 27

-Short Life
-Lethal Effects
Increased cardiac workload > CHF > CAD > MI
Stroke
Renal Failure
**MAP >150 is a BP of 200/100 - Means the person will only live a few years!!

Front 28

How does the doctor make a diagnosis of HTN?

Back 28

-Family Hx
- Blood Pressure Pattern - SBP >135, DBP >85
-Elevated serum cholesterol and triglycerides
-Creatinine >1.2 **Very important! It shows kidney function and should be between 0.6-1.2

Front 29

What can the physician order for a patient to do to treat HTN?

Back 29

1. Exercise
2. Weight Loss
3. Lower Dyslipidemia
4. Take Medications:
Diuretics, Beta Blockers, ACE Inhibitors, Ca+ Channel Blockers, Alpha 1 Blockers, Alpha 2 Agonists, Vasodilators

Front 30

What are the 8 things we can do to assess/monitor a patient's HTN treatment/risk factors?

Back 30

1. Look for risk factors that can be modified (small goals one at a time!)
2. Look for retinal changes (dilated eye exam)
3. Check kidney function levels
4. Take BP at frequent intervals related to the pt's condition
5. Take a daily weight for water gain
6. Monitor I&O and sodium intake
7. Assess Orthostatic HTN
8. Assess for side effects of the meds

Front 31

What are some side effects that blood pressure medications can cause?

Back 31

Dizziness
Syncope
SBP <90
HR <60
Reflex Tachycardia
Fatigue
Weakness

Front 32

What can we do to reduce the risk of a pt falling if they are having problems with orthostatic HTN in the am?

Back 32

They can have a little extra water in the am to compensate for the medication effects.

Front 33

What is Reflexive Tachycardia?

Back 33

It is an automatic compensation the body does when BP is low - the HR will increase

Front 34

How much sodium does the average American get per day? What is the guideline for a sodium restricted diet?

Back 34

Most people have at least 2 tsp of salt a day = 2,000 mg of sodium.
A salt restricted diet should be <2,000 mg
1 hot dog = 500 mg; high sodium foods include lunch meat, soups, etc.

Front 35

What are some Nursing Interventions for taking care of a pt with HTN?

Back 35

*Encourage changing modifiable risk factors
-Weight reduction (BMI <25)
-Decreased sodium intake (<2 gm)
-Moderate alcohol intake (<1-2 oz/day)
-Smoking cessation
-Exercise (20 min 3x/week)
*Encourage taking prescribed medications

Front 36

What is the usual cause/pathology for an Acute Arterial Occlusion?

Back 36

Embolus (clot, rupture of plaque) travels down stream and occludes distal small artery.
Thrombus forms in narrow artery

Front 37

What does Arterial Blockage result in? How long until it happens?

Back 37

Blockage results in necrosis/death of tissue from lack of nutrients, oxygen, etc.
If flow is returned, you can save tissue that has been blocked off for up to 2 hours!

Front 38

What are the clinical manifestations of Acute Arterial Occlusion regarding a limb?

Back 38

Sudden onset of severe pain (the worst they have ever experienced)
Absent distal pulse, even with doppler
Cold and pale skin from no flow of blood
Paresthesia, numbness from nerve damage
Pain increases with movement

Front 39

What are the clinical manifestations of an Acute Arterial Blockage to the heart?

Back 39

Myocardial Infarction
Heaviness in chest
Pain - substernal, epigastric, jaw, radiating to left arm
Sweating and N/V
Rapid Heart Rate, SOB
Or... may have no sx at all

Front 40

What are the clinical manifestations of an Acute Arterial Blockage to the brain?

Back 40

Stroke
Numbness, weakness, paralysis to one side of the body, face, or arm
Dim vision in one eye, burning, double vision
Confusion, trouble speaking or understanding
Severe headache
Confusion or headache may be your only clue!

Front 41

What are some diagnostic tests that can be done to evaluate Acute Arterial Occlusion?

Back 41

CAT Scan - Differentiate between hemorrhagic or ischemic stroke
Arteriogram - Evaluate artery occlusion of a specific artery - May be renal, coronary, cerebral, or lower extremity

Front 42

What are some treatments that can be done for Acute Arterial Occlusion?

Back 42

Embolectomy - Surgical removal of the clot
Anticoagulant - After an arteriogram or embolectomy to prevent further clot extension
Thrombolytics - Dissolve clot

Front 43

What are the typical locations for an Occlusion to form at? Name some specific sites for occlusion.

Back 43

Clots usually grow toward the distal branch and then block flow to a larger area.
At bifurcations:
Messentery
Brain (TIA, Stroke)
Limb (PAD)
Coronary Artery (CAD)

Front 44

What are 5 important parts of Nursing Care after an Arteriogram?

Back 44

They have punctured an artery!
-Use a sandbag to apply pressure over the artery for up to 8 hours to stop the bleeding
-Assess peripheral pulses in that extremity for possible blockage by sand bag
-Observe puncture for bleeding or hematoma
-Pt will need bed rest for 8 hours to allow the soft clot harden to a firm clot and decrease pt's oxygen demands
-Increase fluids to help hydrate pt and dilute contrast used

Front 45

What are the names of 3 arteries that pts usually get Chronic Arterial Occlusions at regarding the heart?

Back 45

1. Proximal right coronary artery
2. Left anterior descending artery
3. Circumflex artery

Front 46

What are the locations in the lower limbs that most often form Arterial Occlusions?

Back 46

-Bifurcation of common iliac arteries
-Bifurcation of anterior tibial arteries
-Popliteal arteries

Front 47

What is the general pathology regarding Atherosclerosis?

Back 47

-Plaque forms a fissure and a clot forms there
-The clot can become incorporated in the plaque and be a 'buried thrombus' after the fissure heals
-The plaque can rupture and the clot leaks out forming a partial obstruction or breaking off and becoming an embolism
-The plaque ruptures and the clot completely blocks the artery

Front 48

What is the pathology behind Peripheral Artery Disease (PAD)?

Back 48

It is a gradual artery blockage in the extremity.
The blockage is gradual - partial blockage can cause pain and ischemia as the arterial lumen size decreases
As the blockage progresses, they can get vasodilation that causes a red color to the skin, collateral circulation is trying to develop at this time
When the obstruction becomes complete, there is no blood supply and tissue necrosis

Front 49

What are the Clinical Manifestations of PAD?

Back 49

-An artery has to be 70% occluded before you will notice any sx
-Intermittent claudication
Aching, gramping leg calf with walking (sedentary may not notice it) due to decreased blood flow
Pain at rest eventually develops
Elevation of limb increases the pain and limb becomes pale (no flow against gravity)
Eventually they have to hang their leg over the side of the bed
-Hair loss, shiny, tight skin
-Pulses not palpable, only noticed on doppler

Front 50

What are the Clinical Manifestations of Chronic Arterial Occlusion?

Back 50

-Leg and foot ulcers
Have a punched out effect
Minimal drainage
Pale wound bed - decreased circulation
Won't heal unless revascularized
Pulses may not be palpable, only heard with doppler

Front 51

How is PAD diagnosed and treated?

Back 51

Diagnosis - Angiogram
Treatment - Medications - Antiplatelet meds inhibit platelet aggregation
*Plavix (clopidogrel)
Percutaneous Transluminal Angioplasty (PTA) - Guide wire is inserted into blocked area and balloon is inflated to push the blockage open - Can restenosis
Stent - Inserted to keep artery open - need Plavix for 12 months - Can restenosis
Arthrectomy - Atheroa (plaque) removed surgically with a rotating shaver or laser
Bypass graft - Synthetic or autologous graft diverts circulation around blockage

Front 52

What is the 1st thing that can be used for treatment of PAD??

Back 52

-Diet - Eat a heart-healthy, low fat, low cholesterol diet
-Exercise to improve collateral circulation development (walk to the point of pain, rest, walk again)
-Exercise 30-60 min 3x/week - 5x/week is better!

Front 53

What is Claudication?

Back 53

Muscle discomfort in lower limb reproducibly reproduced with exercise and relieved by rest within 10 minutes
Usually located in calf, can be in buttocks
Muscle fatigue develops first, then aching, then cramping
Pain causes activity to slowly disappear, eventually, there is pain with rest

Front 54

What should the nurse Assess with a pt who has PAD?

Back 54

-Severity - How long can they walk? How long do they need to rest?
-Hx - HTN, DM, CAD, etc.
-Smoking
-Diet
-Impact of PAD on their life
-Peripheral pulses and an Ankle-Brachial Index (ABI)
-Skin - Is there hair on their legs or toes? Are their nails healthy?
-Any skin breaks? Poor Healing?
-Color changes with position changes of leg?
-Muscle wasting from little use?
-Decreased skin temp?
-Cholesterol and Triglycerides

Front 55

How do you calculate an Ankle-Brachial Index?

Back 55

**60% of pts with PAD have CAD!!
ABI:
-Measure systolic BP in both arms using a doppler to assess highest pressure
-Measure systolic BP in both legs - Cuff on calf, use doppler to assess pressures on the Dorsalis Pedis artery AND the Posterior Tibial, use the highest for calculation
-Calculate the ratio by dividing each side's arm pressure by leg pressure - Will give a %, .95-1.0 is normal.

Front 56

What are some Nursing Interventions for PAD?

Back 56

1. Promote tissue perfusion
-Keep environment warm, socks on feet
-No heating pads or hot water bottles!
-Avoid cold - vasoconstriction
-Avoid tight clothing on the legs, crossing legs, or long sitting periods - decreases circulation
-Keep legs slightly dependent - use aid of gravity
-Stop smoking - Nicotine vasoconstricts and causes vasospasms
2. Prevent injury to the skin
-Inspect feet daily for dryness, redness, and injury
-Use moisturizing cream to prevent dryness (lotion contains alcohol that dries)
-Wear well-fitting shoes
-Use a Podiatrist to get nails trimmed
-When in bed, KEEP HEELS OFF OF MATTRESS
3. Increase exercise
-Exercise to the point of pain, rest, exercise again, etc
-Increase exercise daily

Front 57

What the cause/pathology of Deep Vein Thrombosis (DVT)?

Back 57

1. Clot forms with no accompanying sx, then inflammation starts and produces paid, redness, and edema
-Comes from Low BP at the site, venous stasis, and dehydration
-Obstruction causes clotting
-Coagulation disorders
2. Inflammation from an injury can cause clots
3. Being inactive causes clots to form
-Prolonged immobility slows blood flow! (Sitting in a car or airplane, bed rest, cast, etc.)
-Venus pressure is low, so if a person is inactive, clots form
-A thrombus may occlude the vessel
-A thrombus may dislodge and become an embolus

Front 58

What are the Clinical Manifestations of DVT?

Back 58

-If there is no inflammation, there may be none
-Can get redness and tenderness over the site due to inflammation
-Swelling of the foot, ankle, calf, thigh r/t decreased blood flow and edema
-Can dx through a doppler ultrasound

Front 59

What is the Nurse's role in preventing DVT?

Back 59

-Perform leg exercises to tighten calf muscles
-Increase venous return with TED hose or SCDs
-Heparin/Lovenox to prevent clot extension or development
-Coumadin for long-term anticoagulation
-Walk the pt
-Keep hydrated
-No tight clothing around the legs

Front 60

What causes Veins to move out of the dependent limbs?

Back 60

-Gravity goes against venous return
-Foot/calf muscles squeeze the blood out of deep veins
-Walking compresses the veins as we move
-Blood moves when the veins are compressed
-One-way valves prevent backflow

Front 61

What causes Varicose Veins?

Back 61

-Valve leaflets usually keep the blood flowing upwards
-Dilation of the veins from standing a log time causes the leaflets to not meet and close tight
-Results in a reflux of venous blood
-Retrograde flow creates venous hypertenesion

Front 62

What things are used to treat Varicose Veins?

Back 62

-Rx for compression stockings (not TED hose) that are graded in pressure as they move up the leg and thigh
-Exercise moves the blood and reduces sx and ulcer formation
-Sclerotherapy - Using laser therapy or injected solution to damage the endothelium and cause fibrosis of the vein. A Radiofrequency Closure Technique can also be used (heats and collapses the vein, it is then reabsorbed by the body)

Front 63

What is Chronic Venous Insufficiency and what are its clinical manifestations?

Back 63

Inadequate venous return r/t valvular incompetence
-Clinical manifestations:
-Hyperpigmentation of skin over feet and ankles
-Edema, marked ulcers on the ankles with any trauma
-Drainage is excessive!
-Borders are irregular!
-Creates a tight 'band' of skin around the limb

Front 64

How is Chronic Venous Insufficiency treated?

Back 64

-Elevation to increase venous return
-Compression boots ordered by Dr.
-Avoid injury
-Wound care - Vitamin A, C, and Zinc help, may need to use a Wound Vac (pulls fluid out of the wound and aids in closure of the wound - works well)

Front 65

What are the characteristics/causes of Heart Failure?

Back 65

It is inadequate arterial perfusion of the cardiac tissues
-Results from pump failure
-Decreased CO can't meet the needs
-Systolic Failure - Left ventricle CAN'T PUMP and ejection fraction is reduced to <40% (should be 80-90%)
-Diastolic Failure - Stiff ventricle CAN'T STRETCH and fill during diastole
-Heart failure on one side leads to heart failure on the other side!

Front 66

What are some common causes of Systolic Heart Failure?

Back 66

Coronary Artery Disease
HTN
Metabolic Disorders
Myocarditis
Alcohol
Cocaine
Cardiac Valve Disease
End-Stage Dilated Cardiomyopathy

Front 67

What are some common causes of Diastolic Heart Failure?

Back 67

CAD
Hypertrophy
Fibrosis due to advanced age
Constrictive Pericarditis
Myocarditis
HTN
Aortic Stenosis
Ventricular Remodeling
Collagen Diseases
Cardiomyopathy

Front 68

What are normal Sympathetic Responses that occur due to decreased CO, that actually exacerbate HF?

Back 68

*Epinephrine effects Beta receptors
-Increases HR to Tachycardia (>100), which increases the workload
-Increases Contractility, which increases CO
-Increases HR, workload, myocardial oxygen demand, and then myocardial ischemia due to poor blood supply
-Increased HR causes decreased filling, and after time, decreased CO
*Norepinephrine - Alpha receptors
-Causes Vasoconstriction that increases BP and workload
-Increases Preload because of increased peripheral venous return, which increases left ventricular end diastolic volume (LVEDV)
-Left ventricle stretches and dilates, leading to to decreased contractility
-Increased Afterload causes increased workload that results in hypertrophy
-Afterload is the resistance the Left Ventricle pumps against. Causes:
-increased peripheral vascular resistance (PVR)
-decreased renal perfusion
-Baroreceptors develop decreased responsiveness
-Hypothalamus secretes ADH that causes increased work load

Front 69

What are the other normal responses that occur to try to compensate for decreased cardiac output, but make HF worse?

Back 69

*Decreased kidney perfusion causes
-Activated renin-angiotensin-aldosterone system
-Vasoconstriction, which increases workload
-Angiotensin increases mycyte hypertrophy (need Ang II Blockers!)
Aldosterone increases water retention > increased BV > increased CO > increased work load
*Hypertrophy - Results from an increased workload, but the muscle outgrows the blood supply, creates angina
*Ventricular Dilation - Increased fluid retention causes increased ventricular stretching, myocardial fibers overstretch, and ventricle dilates - Reduces ejection fraction and the heart can't contract

Front 70

What are the Pulmonary Clinical manifestations of Left Heart Failure?

Back 70

-Pulmonary vascular congestion
-Dyspnea - Oxygen can't cross alveolar wall due to fluid
-Orthopnea - When supine, fluid re-enters the vascular system and increases pulmonary edema
-Paroxysmal Nocturnal Dyspnea - Like orthopnea, but person doesn't feel it right away and wakes up gasping for air
-Rales from fluid in the alveoli
-Wheezes from fluid in the larger airways
-Frothy Sputum - Lots of fluid!

Front 71

What are the Systemic Clinical Manifestations of Left Heart Failure?

Back 71

-Fatigue and activity intolerance due to decreased CO; heart rate goes up, but doesn't come back down after rest
-Decreased urine output r/t decreased renal perfusion
-Peripheral dependent edema from high venous pressure
-Weight gain from fluid retention
-Liver congestion and ascites from fluid leaking out of the intestine into the abdomen
-Anorexia and weight loss from decreased peristalsis from edema creates decreased desire to eat (may be shadowed by water weight)
-Fat and muscle wasting from disuse

Front 72

What causes Right Heart Failure and what does it lead to ?

Back 72

Cor Pulmonale causes it - Heart failure from pulmonary disease
-COPD
-Cystic Fibrosis
-ARDS
These create increased pressure due to decreased capillary beds in the lungs and increased pressure
-Right HF leads to Left HF!

Front 73

What kind of an Output Failure is Heart Failure?

Back 73

It is a High Output Failure - Inability to supply blood to meet metabolic needs. Can be from:
-Anemia - Decreased oxygen causes tachycardia, increased pressure, and HF
-Septemia - Bacteria in the blood causes massive vasodilation, which causes decreased CO and HF in the elderly or weak
-Hyperthyroidism - Causes increased HR of >100 at rest, if prolonged, it causes increased workload and HF
*Have to treat the disorder

Front 74

What are the Diagnostic Tests that are performed for HF?

Back 74

-Chest X-Ray for pulmonary congestion, and enlarged hypertrophied heart
-Liver congestion through palpation
-Cardiac Nuclear Scan to determine perfusion to muscle, ventricular function, and ejection fraction
-Echocardiogram that detects valve and muscle wall pathology and measures ejection fraction (<40% = HF)

Front 75

What is the Treatment for HF?

Back 75

-Oxygen to keep O2 sats up
-Beta Blockers to decrease the sympathetic response
-Decrease the Preload through:
Diuretics - Excrete water
Decreased salt intake - Lower water retention
HOB up - Fluid stays in the extremities
ACE Inhibitors - Decrease water retention
-Decrease Afterload through:
Rest
ACE Inhibitors - Decrease vasoconstriction
Alpha Agonists -Decrease vasoconstriction
-Increase Cardiac Contractility through Cardiac Glycosides

Front 76

What steps should a nurse go through to assess HF?

Back 76

** Know the baseline first!
Assess for:
Decreased HR
Clear breath sounds
Decreased RR, less dyspnea
Less distended neck veins
Decreased daily weight, increased urine output
Decreased S3 from rapid ventricular filling (increased preload)
Assess effectiveness of meds
*If pt is getting IV fluids, check breath sounds regularly
*Record assessment and notify physician of changes

Front 77

What are Interventions for HF?

Back 77

-Oxygen via NC at a standard 2-6 L/min to keep O2 sat >90%
-HOB up to decrease venous return (preload)
-Encourage activity to tolerance r/t dyspnea, HR, etc.
-Prevent foot injuries
-Teach about low sodium diet, if ordered
-Teach about medications

Front 78

What are some potential patient problems and the NsDx for them?

Back 78

-Impaired gas exchange r/t fluid retention in respiratory membrane AEB O2 sat <90% on RA, cough/wheezing/crackles, RR >26, difficulty lying flat
-Fluid volume excess r/t fluid-retaining mechanisms of renin-angiotensin-aldosterone syste, ADH, and decreased CO AEB feet swelling, weight gain, anorexia, confusion (from low Na+)
-Activity intolerance r/t decreased CO AEB RR >26, palpitations, HR that doesn't return to baseline w/in 10 min of activity

Front 79

What are the different normal and abn sounds of the heart?

Back 79

S1 - Mitral/Tricuspid valves
S2 - Aortic/Pulmonic valves
S3 - Increased rate of ventricular filling
S4 - Premature closing of

Front 80

What 7 nutrients are needed for effective healing?

Back 80

1. Calories - Fuel for cell energy
2. Protein - Collagen formation, wound remodeling, immune function
3. Vitamin C (absorbic acid) - Collagen synthesis, capillary wall integrity, fibroblast function, immunologic function, antioxidant
4. Vitamin A - Epithelialization, wound closure, inflammatory response, angiogenesis, collagen formation
5. Vitamin E - Antioxidant
6. Zinc - Collagen formation, protein synthesis, cell membrane and host defense
7. Fluid - Needed for a viable environment of cells