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Adult Nursing - 225 > Study Guide ASH > Flashcards

Study Guide ASH Flashcards

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1
Q

Medications to slow the heart down? Non medications that slow down the heart?

A
  • Amiodarone, Lidocaine, digoxin, cardizem

- Vaso maneuver

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2
Q

What speeds up the heart? Medications? Non medications that increase heart rate?

A

Atropine
Epinephrine
Inotropic - Dobutamine

  • Caffeine - stimulants
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3
Q

Manifestations of Cardiac Tamponade?

A

Cardiac tamponade findings:

  • JVD
  • Paradoxical pulse
  • Decreased CO
  • Muffled heart sounds
  • Circulatory collapse
  • Hypotension

-

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4
Q

Disease states that affect Afterload? Drugs used to improve?

A

Disease states that increase resistance makes it harder for the heart to pump blood

  • Hypertension
  • Aortic stenosis
  • Increased blood viscosity

**Antihypertensives - Beta Blockers, Vasodilators

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5
Q

What is ATRIAL FIBRILLATION? Rhythm? P waves?

A

Occurs when the atria beat chaotically and irregularly — out of coordination with the two lower chambers (the ventricles) of the heart

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6
Q

What is the atrial/ ventricular rhythm for a person in Atrial Fibrillation?

A

Irregular

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7
Q

Signs and Symptoms of Atrial Fibrillation?

A
  • irregular rapid heart rate
  • lower blood pressure
  • ortho-hypotension
  • low 02 stat
  • anxious
  • change in level of consciousness
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8
Q

What do the P waves look like in AFIB?

A
  • Wavy with no prominent P wave
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9
Q

Treatment of stable Atrial Fibrillation vs treatment of unstable atrial fibrillation?

A
  • Medications: Antidysrhythmics (Amiodarone, procainamide, lidocaine), beta blockers, calcium channel blockers, procainamide, digoxin)
  • Cardioversion
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10
Q

Manifestations of Atrial Fibrillation?

A
  • No P waves
  • irregular rhythm
  • Decreased cardiac output (loss of 25-30% CO)
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11
Q

What are PREMATURE VENTRICULAR CONTRACTIONS?

A
  • Results from increased irritability of ventricular cells

- lower chambers of the heart contract before they should. When this happens, your heartbeat becomes out of sync.

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12
Q

How does a PVC appear on the EKG? What is the rate?

and Rhythm?

A
  • seen as early ventricular complexes followed by a pause
  • QRS wide (greater than 0.12 sec ), bizarre appearance (uniform or multiform)
Rate = variable; 
Rhythm=  atrial regular, ventricular irregular;
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13
Q

What are the typical causes when PVC is frequent and sustained? Treatment

A
  • ventricular irritability due to hypoxia
  • heart disease
  • drug toxicities
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14
Q

Treatment of PVC ?

A
  • Treatment = antidysrhythmics if symptomatic (amiodarone, lidocaine, procainamide, B-blockers)
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15
Q

Describe VARIANT Angina?

A

Variant - chest pain or discomfort resulting from coronary artery spasm and typically occurs after rest. EKG = ST changes but no changes in troponin or CK levels b/c no tissue has be damaged yet. * begins to block oxygen flow to the tissues

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16
Q

What is the normal EJECTION FRACTION? What does the EF measure?

A
  • 50-70%

- Contractility

17
Q

Who is at high risk for Endocarditis?

A
  • IV drug abusers
    • Valve replacement recipients
    • People who have had systemic infections
    • People with structural cardiac defects
18
Q

Medications for Valvular disease?

A
  • ACE inhibitor - blood pressure
  • Digoxin- decrease contractility
  • Beta Blockers - protects the heart
  • Antibiotics
  • Anticoagulant
  • Diuretics
  • Vasodialators
19
Q

Medications for shock?

A

Insulin
Steroids
Antibiotics
Vasopressors

20
Q

What does Digoxin do?

A
  • increases vagal tone, slowing AV nodal conduction.
21
Q

Treatment of Cardiac Tamponade?

A

-Pericardiocentesis - removes fluid

Pericardial window - involves removing a portion of the pericardium to permit excessive pericardial fluid to drain into the pleural space.

-Pericardiectomy

22
Q

Most common cause of CARDIOGENIC SHOCK?

A

-Myocardial infarction is the most common cause of direct pump failure.

23
Q

what is Hemodynamic monitoring?

A

Invasive system used in critical care areas to provide quantitative information about vascular capacity, blood volume, pump effectiveness, and tissue perfusion

types:
Pulmonary artery catheter
Invasive arterial catheter and monitoring
Pulmonary capillary wedge pressures

24
Q

Interventions for sepsis/septic shock:

A
  • Correct the cause!
  • Use of sepsis resuscitation bundle within 6 hours
  • Oxygen therapy
  • IV therapy: Normal saline (NS) or Lactated Ringers (LR)
  • Drug therapy: Vasoconstrictors: Dopamine, Epinepherine etc.
  • Agents to enhance contractility and perfusion/CO
  • Blood replacement therapy
  • Identify those at risk, early detection!
25
Q

Manifestations of sepsis/septic shock:

A

Early symptoms of sepsis:

  • fever usually higher than 101˚F (38˚C)
  • low body temperature (hypothermia)
  • fast heart rate
  • rapid breathing, or more than 20 breaths per minute

Severe sepsis:

  • noticeably lower amounts of urine
  • acute confusion
  • dizziness
  • severe problems breathing
  • bluish discoloration of the digits or lips (cyanosis)
26
Q

Pathophysiology of SHOCK:

A 
-Cells forced to produce energy with anaerobic (w/o 02) metabolism
This causes:
Low yield of energy and ATP
Produces lactic acid (why we draw lactic acids)
Acidotic cell environment
Membrane more permeable
Electrolytes and fluid seep in and out
Na-K pump fails
Cell structures damaged
Cell death

3 major components:

  • Volume
  • Pump
  • Vasculature

Must respond to feedback systems: (3 compensatory responses)

  • Neural (sympathetic vs parasympathetic, baroreceptors/epi/norepi)
  • Chemical( RAAS and kidneys that are trying to make adjustments in order to maintain adequate blood volume and flow )
  • Hormonal (aldosterone NA/water retention in order to maintain blood volume and increase blood volume to increase CO)

When one fails, the others compensate

Eventually no longer able to compensate

Tissues are then not perfused adequately

Shock occurs

27
Q

Initial (early) stage of SHOCK?

A
  • Difficult to detect!
  • Baseline MAP decreased by less than 10 mm Hg
  • Heart and respiratory rate increased from the baseline or a slight increase in diastolic blood pressure
  • Adaptive responses of vascular constriction and increased heart rate
  • Compensatory mechanisms effective
  • Overall metabolism still aerobic
28
Q

Nonprogressive (compensatory) Stage of SHOCK?

A
  • BP stays WDL
  • MAP falls 10 t0 15 mm/hg below baseline
  • Kidney, baroreceptors, and hormonal adaptive mechanisms activated.
  • Stimulates sympathetic NS
  • Kidneys sense decreased MAP
  • Renin/angiotensin system activated
  • Pituitary kicks in with ADH
  • Tissue hypoxia in nonvital organs.
  • Acidosis and hyperkalemia.
  • Stopping conditions that started shock and supportive interventions can prevent shock from progressing
  • Can have no permanent damage
  • Best time to intervene

Still have some clinical signs that indicate poor organ perfusion:

Anxiety, restlessness, thirst
Resp: increased resp rate, decrease in O2 sat
Cardiac: tachycardia, falling systolic pressure, rising diastolic pressure, narrow pulse pressure, cool extremities, decreased UO

29
Q

Nonprogressive (compensatory) interventions:

A
  • ID cause: Correct underlying disorder
  • Compare changes to baseline
  • Support by: Help maintain BP and adequate perfusion
  • Vasoconstrictors, inotropic, enhance CO
  • Fluid replacement: Crystalloids, colloids, blood products
  • Medication
  • Oxygen
  • Monitor tissue perfusion, vitals
  • Patient safety
  • Reduce anxiety for pt and family
30
Q

Progressive Stage (intermediate) of SHOCK:

A

MAP falls more than 20 mm Hg from baseline

Compensation functioning, no longer adequate
Vital organs develop hypoxia
Less vital ischemia
Life-threatening emergency-critical rescue!
Immediate interventions are needed.
Vital organs can only tolerate so long
Survival depends on age and overall health

31
Q

Progressive stage manifestations:

A
  • Laboratory data: Low blood pH, rising lactic acid, hyperkalemia
  • Cardiac: Rapid, weak pulse, Hypotension, Pallor, cool, moist skin, anuria
  • Pulmonary: Cyanosis, Hypoxemia
  • Neuro: Decreased cerebral perfusion, Mental status deteriorates, Feeling of doom
32
Q

Progressive Stage Medical Management:

A

-Depends on type of shock and cause
-Based on degree of decompensation
-Some interventions are common to all:
Appropriate IV fluids
Prevent complications
Close, continuous monitoring

-Medications to restore perfusion:
Support pumping action of heart (inotropics-dobutamine)
Vasoconstrictors (dopamine, norepi)
Perfusion through dialation (Sodium nitroprusside)
Support resp system-ABGs
Hemodynamic monitoring-CVP, Art line, PCW

33
Q

Refractory (Irreversible) Stage of SHOCK:

A

Rapid loss of consciousness, nonpalpable pulse, cold, dusky extremities; slow, shallow respirations; unmeasurable oxygen saturation

MODS can occur here or as separate syndrome

Therapy ineffective, death imminent

34
Q

What is the primary factor in the development of Coronary Artery Disease ?

A

Atherosclerosis

35
Q

What are the modifiable risk factors for Coronary Artery Disease?

A
  • Elevated serum cholesterol
  • Smoking/ tobacco use
  • Limited physical activity
  • Hypertension
  • Diabetes mellitus
  • Obesity
  • Excessive alcohol
  • Excessive stress/ decreased coping skills
36
Q

Right sided heart failure

A
  • Characterized by insufficient force of cardiac contraction and/or inadequate filling of the heart with blood.

Symptoms:
Peripheral edema, JVD, weight gain, ascites, hepatomegaly, S3 gallop on auscultation

37
Q

Contributing factors to vessel damage

A 
Elevated BP
Elevated lipid levels
Turbulent blood flow (hypertension)
Increased amounts of catecholemines
Irritants from cigarette smoke
Impaired glucose tolerance, DM

Adult Nursing - 225 (9 decks)

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