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PNUR 151 - Variations in Health > Class 8 - Cardiovascular System > Flashcards

Class 8 - Cardiovascular System Flashcards

1
Q

SA node is

A

the “pacemaker” of the heart (sets the heart rate).
The SA node sends electrical impulses that spread throughout the atria like ripples in a pond,

SA node impulses travel down to the AV node

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2
Q

AV node is

A

The AV node sends electrical impulses to the Bundles of His

  • From the Bundles of His, impulses split and travel to the ventricles.
  • These impulses are divided into 2 branches called the right and left bundle branch which allows the even spread of the electrical signal to both ventricles simultaneously.
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3
Q

information card only

A

The heart is divided by muscle and fibrous tissue into a right and left side. Each side has an upper chamber or atrium that collects blood returning to the heart and a muscular lower chamber or ventricle that pumps that blood away from the heart. The right atrium (RA) receives blood from you body and pumps it into the right ventricle (RV). The right ventricle then pumps it to your lungs. From the lungs, blood returns to your left atrium (LA) and then pumped into the left ventricle (LV). From the left ventricle it is pumped out to your body.

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4
Q

age-related changes to the heart

A
  • valves become stiffer
  • decreased contractility (slower HR)
  • arteries thicken and stiffen
  • baroreceptors become less sensitive
  • heart may fill more slowly
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5
Q

What is an inflammatory disorder of the peripheral blood vessels

A

thrombophlebitis - inflammation of the wall of a vein with associated with a blood clot

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6
Q

Occlusive disorders of peripheral blood vessels are

A 
Peripheral Vascular Disease (PVD)
□ Arterial Occlusive Disease
□ Venous Occlusive Disease
□ Venous Insufficiency
          *Varicose Veins
          *Valvular damage
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7
Q

What is CAD

A

Coronary Artery Disease (CAD)

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8
Q

What are the characteristics of CAD (coronary artery disease)

A
  • atherosclerosis (fatty substances form a deposit of plaque on the inner lining of arterial walls)
  • ateriosclerosis (hardening of the arteries)
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9
Q

What is chronic stable angina

A

Chest pain that occurs intermittently over a long period with same pattern of onset, duration and intensity of symptoms

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10
Q

clinical manifestations of chronic stable angina

A
  • Pain usually lasts 3 to 5 minutes
  • Subsides when the precipitating factor is relieved
  • Pain at rest is unusual
  • May radiate
  • “dull”, “tightness” , “burning sensation”
  • Does not change with position or breathing
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11
Q

What is angina

A

marked by severe pain in the chest, often also spreading to the shoulders, arms, and neck, caused by an inadequate blood supply to the heart.

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12
Q

treatment of angina is aimed at

A
  • decreasing O2 demand or increasing it depending on the situation
  • emphasis on the reduction of risk factors
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13
Q

Collaborative ManagementChronic Stable Angina: drug therapy

What types of drugs can you use

A
  • Short-acting nitrates: Sublingual nitro (first line of therapy for angina)
    *promotes peripheral dilation
    decreasing preload and
    afterload
    • promotes coronary artery
      vasodilation
  • Long-acting nitrates: isosorbide dinitrate (Isordil)
    • used to reduce the incidence
      attacks
  • Transdermal controlled-release Nitrates
    • used to deliver rate
      controlled slow delivery
      of medication over a 24 hour
      period
  • β-adrenergic blockers
    *inhibit SNS stimulation of the
    heart
    *reduce both heart rate and
    contractility
    *decrease after load
  • Calcium channel blockers
    *systemic vasodilation with
    decreased stroke volume
    rate
    *promote coronary
    vasodilation
    *reduce heart muscle
    contractility
  • Angiotensin-converting enzyme inhibitors
    *prevent conversion of
    angiotensin I to angiotensin
    II
    • decrease endothelial
      dysfunction
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14
Q

Strategies for the patient with chronic stable angina should address of these treatment elements in this pneumonic

A

A = antiplatelet agent, antianginal therapy, ACE inhibitor

B = B-Adrenergic blocker, blood pressure

C = cigarette smoking, cholesterol

D = diet, diabetes

E = education, exercise

F = flu vaccine

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15
Q

What diagnostic tools could you use

A 
Health history/physical exam
Laboratory studies
12-lead ECG
Chest x-ray
Echocardiogram 
Exercise stress test
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16
Q

What acute interventions could be used for an angina attack

A
  • Administer of supplemental O2
  • Vital signs
  • 12-lead ECG
  • Prompt pain relief with a nitrate followed by an opioid analgesic if needed
  • Auscultation of heart sounds
  • Comfortable positioning of the client
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17
Q

What can you teach someone who is ambulatory or at home about their angina

A
  • watch for precipitating factors (ex: what triggers the attacks)
  • risk factor reduction
  • teaching around medications
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18
Q

heart failure means what

A
  • an abnormal condition involving impaired cardiac pumping

- heart is unable to produce an adequate cardiac output (CO) to meet the metabolic needs

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19
Q

heart failure is characterized by what

A
  • ventricular dysfunction
  • reduced exercise intolerance
  • diminished quality of life
  • shortened life expectancy
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20
Q

Heart failure (HF) is not a disease but associated with long-standing what

A

hypertension, coronary artery disease & MI

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21
Q

common causes of HF

A
  • CAD
  • hypertension
  • anemia
  • pulmonary disease
  • congenital heart disease
  • acute MI
  • pulmonary embolus
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22
Q

what leads to HF

A
  • infection
  • anemia
  • pulmonary disease or embolus
  • nutritional deficiencies
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23
Q

What are the 2 ways HF can be described

A

systolic and diastolic

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24
Q

Explain systolic HF

A

this is the most common type of HF which results from an inability of the heart to pump blood.

The hallmark of systolic HF is a decrease in the left ventricular ejection fraction (what is pumped out of the left ventricle with each contraction)

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25
Q

Causes of systolic HF

A
  • Impaired contractile function (e.g., MI)
  • Increased afterload (e.g., hypertension)
  • Cardiomyopathy
  • Mechanical abnormalities (e.g., valve disease)
26
Q

Explain diastolic HF

A

Impaired ability of the ventricles to relax and fill during diastole resulting in decreased stroke volume and CO

27
Q

How is diastolic HF diagnosed

A

based on the presence of pulmonary congestion, pulmonary hypertension, ventricular hypertrophy, normal ejection fraction (EF)

28
Q

what are the 2 types of HF

A

Left-sided HF (most common)

  • Backup of blood into the left atrium and pulmonary veins
  • Manifested as pulmonary congestion and edema

Right-sided HF

  • Causes backward blood flow to the right atrium and venous circulation
    * Results in peripheral edema, hepatomegaly, splenomegaly, GI vascular congestion, jugular vein distension
29
Q

Clinical manifestations of left and right sided HF are

A 
Left-sided failure
-fatigue
-dyspnea
-orthopnea
-dry cough
-pulmonary edema**
-nocturia
-paroxysmal nocturnal dyspnea
     (attacks of severe SOB)

Right-sided failure

  • fatigue
  • dependent edema (legs)
  • right upper quadrant pain
  • anorexia
  • nausea
*Pulmonary edema, often life-threatening 
Early stage
-  Increase in the respiratory rate 
-  Decrease in PaO2 
Later stage
-  Tachypnea 
-  Respiratory acidemia
30
Q

What are some complications of HF

A
  • pleural effusion
  • dysrhytmias (afib being most common)
  • left ventricular thrombus
  • hepatomegaly
  • renal failure
31
Q

what diagnostics tools could be helpful in determining the underlying cause of HF

A 
History and physical exam
CXR
ECG
Lab studies (ex. cardiac enzymes,  BNP)
Hemodynamic assessment
Echocardiogram
Stress testing
Cardiac catheterization
Ejection fraction (EF)
32
Q

Overall goal for acute HF and pulmonary edema is to improve what and how

A 
Left ventricular function by
- Decrease intravascular volume 
       *loop diuretics                 
             (ex: furosemide) 
- Decrease venous return   
        (preload)
       - reduce volume returned to 
           the left ventricle during  
           diastole
       - high-Fowler’s position 
       - IV nitroglycerin
  • Improve cardiac function
    - for clients who do not
    respond to conventional
    pharmacotherapy
    (ex: diuretics, vasodilators,
    morphine sulphate), inotropic
    therapy is used:
    digitalis
    hemodynamic monitoring
    (in CCU or ICU)
  • Reduce anxiety
    - distraction, imagery,
    sedative medications
33
Q

What are the main treatment goals

A
  • Treat the underlying cause and contributing factors
  • Provide treatment to alleviate symptoms
  • Preserve target organ function
  • Improve mortality and morbidity - - Oxygen administration
  • Physical and emotional rest
  • Non pharmacological therapies
34
Q

What are the different types of drug therapy that can be used

A
  • diuretics
    * thiazides (hydrochlorothiazide)
    * furosemide (Lasix)
    * K+ sparing (spironolactone)
  • Angiotensin-converting enzyme (ACE) inhibitors {“prils’}
    *Angiotensin II receptor
    blockers in clients who can
    not tolerate ACE inhibitors
    {“sartans”}
  • B-Adrenergic blockers {“lols”}
  • Inotropic drugs
    *Sympathomimetic agents
    (ex: dopamine)
    *Phosphodiesterase inhibitors
    (ex: milrinone)
    *Digitalis preparations
    (ex: digoxin)
    *Vasodilator drugs
    (ex: nitrates, nitroprusside)
35
Q

In terms of nutritional therapy what are you going to do for the patient with HF

A
  • Diet and weight reduction
  • Dietary Approaches to Stop
    Hypertension (DASH) diet is
    recommended
  • Sodium is usually restricted to
    2g per day; usually no fluid
    restriction
  • Daily weights are important
  • Weight gain of 2 kg over a 2 to 5
    day period should be reported
    to the physician
36
Q

What ypes of health promotion should be provided

A 
- treatment or control of  
     underlying disease
     (ex: hypertension)
- antidysrhythmic agents or 
    pacemakers for more serious 
    situations
- vaccinations
- stop smoking
37
Q

What is Peripheral Vascular Disease

What is Peripheral Arterial Disease

A

PVD -
Term for disorders that affect blood vessels distant from the large central blood vessels supplying the myocardium or that circulate blood directly in and out of the heart

PAD - this is the thickening of artery walls, which results in a progressive narrowing of the arteries of the upper and lower extremities

38
Q

what arteries are affected with PVD

A

Affects aortoiliac, femoral, popliteal, tibial or peroneal artery

39
Q

what are the clinical manifestations of PVD

A
  • severity depends upon the site - extent of obstruction
  • amount of collateral circulation

Classic symptom is:
intermittent claudication.
This means when a muscle pain (ache, cramp, numbness or sense of fatigue), classically in the calf muscle, which occurs during exercise, such as walking, and is relieved by a short period of rest.

40
Q

Nursing Dx for PAD would be

A 
Ineffective tissue perfusion
Impaired skin integrity
Acute pain
Activity intolerance
Ineffective therapeutic regimen
41
Q

Nursing implementation for PAD would be

A

Health promotion:
*Teach clients about risk factors, screening clinics, smoking cessation, diet modification

Acute Intervention:
*After surgical intervention, usual postop care with particular attention given to the affected extremity; avoid knee-flexed positions

Ambulatory & home care: * *Management of risk factors, meticulous foot care

42
Q

Nursing planning for PAD would be (goals)

A
  • Adequate tissue perfusion
  • Relief of pain
  • Increased exercise tolerance
  • Intact, healthy skin on
    extremities
43
Q

What is acute arterial ischemic disorders

A

Acute arterial ischemia occurs suddenly, without warning
Can be caused by embolism, thrombosis or trauma
Clinical manifestations include the

44
Q

What are the clinical manifestations of acute arterial ischemic disorders

A 
They are the six Ps: 
pain
pallor
pulselessness
paresthesia (pins and needles)
paralysis
poikilothermia (the inability to  
                  regulate core body  
                  temperature)
45
Q

What is the collaborative care for acute ischemic disorders

A 
- Early treatment is essential to
        keep limb viable
- Anticoagulant therapy- 
        ie: Heparin to prevent  
        development of further clots 
        or the extension of those 
        already present
- Thrombolytics
- Bedrest to monitor dissolution of 
        the clot
- Surgery
46
Q

What is Venous Thrombosis (DVT)

A

is a disorder involving a thrombus in a deep vein, most commonly the iliac and femoral veins

47
Q

What are the 3 factors that cause venous thrombosis to occur (Virchow’s triad)

A
  1. venous stasis (blood pooling in the veins)
  2. endothelial damage (inner lining of the veins)
  3. hypercoaguability of the blood
48
Q

Factors that contribute to venous thrombosis are

A
  • inactivity
  • compromised circulation
  • compression of veins in the pelvis or leg
  • smoking
49
Q

What are some of the sing and symptoms of venous thrombosis

A
  • discomfort of affected extremity
    • heat
    • redness
    • edema
    • cap refill (less than 2 secs)
  • fever
  • malaise
  • fatigue
  • anorexia
50
Q

What are some of the nursing Dx you could use for venous thrombosis

A 
Acute pain
Ineffective health maintenance
Risk for impaired skin integrity
Potential complication: Bleeding
Potential complication: Pulmonary embolism
51
Q

What are some of the planning goals that could be used for venous thrombosis

A 
relieve pain
decrease edema
no skin ulcerations
no complications from drug  
      therapy
no pulmonary emboli
52
Q

What collaborative care measures would you put in place

A 
- Complete bed rest (prevent 
          embolus)
- Anticoagulant therapy
      - heparin/coumadin  
        /LMWH/Platelet inhibitors
- Fibrinolytic agents (emergent 
        situations)
  • Surgery (if large vein involved or
    danger of PE)
    *thrombectomy
53
Q

What is venous insufficiency

A

-flow of blodd is impaired through deep or superficial veins. this is a chronic condition that ususally affects the lower extremities (normally around the ankle)

54
Q

What are some of the signs and symptoms of venous insufficiency

A
  • non pitting edema
  • superficial veins are dilated and
    obvious
  • non uniform skin color
  • shiny appearance to feet and
    ankles
  • delicate, easily damaged skin
  • possible weeping dermatitis
  • moderate pain
  • pedal and tibial pulses difficult
    to palpate
55
Q

What is the goal for venous insufficiency and how can we achieve this goal

A 
to promote venous circulation
by:
- using elastic compression 
      stockings
- mild analgesics
- elevate legs periodically (raise
      foot of bed)
- walk or isometric calf exercises
- avoid hot showers (dilates 
      vessels = congestion)
- avoid constricting clothing
56
Q

What is superficial thrombophlebitis

A

the formation of a thrombus in a superficial vein

57
Q

Clinical manifestations of superficial throwbophlebitis include what

A

palpable, firm, subcutaneous cordlike vein with the surrounding area tender, reddened and warm

58
Q

What can be done to help with superficial thrombophlebitis

A
  • elevation of the affected limb
  • warm, moist heat
  • analgesics
  • NSAIDs
59
Q

What are varicose veins

A

dilated, tortuous subcutaneous veins most commonly found in the saphenous leg veins

60
Q

What causes varicose veins

A 
Familial tendency
DVT
Congenital venous malformations
Multiple pregnancies
Prolong standing
Increased intraabdominal pressure
obesity
61
Q

What are some of the clinical manifestations for varicose veins

A 
Legs heavy and tired
Activity or elevation of legs relieves discomfort
Feet, ankles and legs may appear swollen
Leg veins appear distended and tortuous,
    -Dark blue or purple, snakelike  
     elevations
    -Abnormal capillary refill
62
Q

What can be done to manage varicose veins

A 
Focus on ↑ venous flow
        *walking, swimming  
             /isometric exercises
        *compression stockings
        *occupational modifications
Preventing tissue injury
        *avoid restrictive clothing
Sclerotherapy
Vein ligation /Vein stripping

PNUR 151 - Variations in Health (5 decks)

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