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411 Adult 3 > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

One small box is
One large box is
30 large boxes is
P-R interval is
QRS complex is
Electrical impulses formed in…

A

.04 secs
.20 secs
6 seconds (readable strip)
.12 - .20
.04 - .12
SA node (pacemaker)

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2
Q

Sinus tachycardia boxes
Sinus bradycardia boxes
Supra ventricular tachycardia boxes
What indicates AV block

A

Less than 3
More than 5
Less than 2
PR > .20 secs

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3
Q

Sinus Brady is
Treatment

A

Regular R-R, P for every QRS, rate below 60 bpm
- dose of atroPINE^ 0.5mg

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4
Q

Dysrythmias are caused by
Cardioversion is
Defib vs cardiovert vs pacer (uses)

A

CAD, MI, electrolyte imbalance, drug toxicity
- Synchronized shock for unstable tachydysrythmias, synchronize button must be on
- defib stops heart (v fib & v tach)
- cardiovert slows heart (a fib & a flutter)
- pace speeds up heart (bradycardia or block)

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5
Q

SVT rate
Paroxysmal
Prolonged
If stable what’s the 1st step
Next step (med)
If unstable

A

> 150 to 280
- Doesn’t affect cardiac output
- Decrease in cardiac output
- Vagal patient (ice water, bear down, breath through straw)
- Rapid push ADENOSINE 6mg & flush, repeat 2nd dose 12mg (or cardizem / amiodarone)
- Cardiovert

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6
Q

A fib is
Risk factors
Characterized by
Treatment
If drugs are unsuccessful

A

Most common dysrhythmia
- CHF, HTN, age > 75, diabetes
- no P before QRS
- cardizem to slow AV conduction, amiodarone (don’t shake)
- cardioversion , anticoagulants

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7
Q

Atrial flutter characterized by
Treatments

A

Saw tooth formation , no p waves
- cardioversion, anticoagulants

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8
Q

Premature ventricular contraction
Treatments

A

Premature wide & distorted QRS
- oxygen if hypoxic, potassium (20meq) or mag (1-2g in 50ml D5W) electrolyte imbalance, beta blockers (decrease HR)

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9
Q

Ventricular tachycardia (V tach)
- treatment pulse & stable
- if meds don’t work
Treatment if pulseless

A

No p waves, wide QRS (tombstone)
- first give adenosine 6 & 12mg, vagal patient & give amiodaron
- cardiovert patient
- DEFIBRILLATE

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10
Q

V fib
If no pulse
Treatment
Order of process
When does Defib save a life

A

Squiggly line
- call a code & Defib
- immediate defibrillation 1st (200J), follow with CPR 2 min, Defib (300J), give epi Q3-5min 1mg IV, CPR, amiodaron
- shock, CPR, shock, drug, CPR, shock, drug)
- within 5-10 min of code

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11
Q

Torsades de points characterized
Causes
Treatment

A
  • wide bizarre tornado pattern
  • hypomagnesemia (anorexic, malnourished)
  • mag sulfate
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12
Q

Asystole is
Treatment steps
H’s
T’s

A

Dead rhythm, no complex
- check pt, no pulse = call code & initiate CPR, follow w IV epinephrine 1mg Q3 min, find H & T’s
- Hypovolemia, hypoxia, hydrogen acidosis, hyper or hypokalemia, hypothermia
- Toxins, tension pneumothorax, thrombosis, tamponade, trauma

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13
Q

AV blocks
1st degree & treatment

A
  • P-R > .20s with QRS , give atropine 0.5mg if unstable
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14
Q

2nd degree type 1 name
Characteristics
Usually results from
Treatment if symptomatic

A

Mobitz 1, wenckebach
- progressive increase in PR interval followed by missed beat
- MI
- atropine

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15
Q

2nd degree type 2 name
Characteristics
Results from
Treatment if symptomatic

A

Mobitz II
- PR interval is constant, followed by missed beat
- rheumatic heart disease, CAD, digitalis toxicity
- transcutaneous pacemaker 1st, then atropine, dopamine, epi

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16
Q

3rd degree heart block characteristics
Treatment

A

P waves unassociated with QRS, P moves at its own pace
- Transcutaneous pacing, atropine, dopamine, epi

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17
Q

Transcutaneous pacing
Which 2 heart blocks are always unstable & require pacing

A

2nd degree type 2
3rd degree

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18
Q

Modes of pacing
Synchronous vs
Asynchronous
Pacemaker spike takes place of?
Pacemaker education

A
  • Synchronous is demand pacing based on the clients heartbeat (transvenous)
  • Asynchronous is a fixed rate (used for asystole or profound bradycardia)
  • takes place of P wave
  • no contact sports, don’t get near magnets
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19
Q

Coronary artery disease
Ischemia vs infarction

A

Ischemia leads to insufficient oxygen supply
Infarction is irreversible cell death from prolonged ischemia

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20
Q

Chronic stable angina pectoris (CSA) characterized by
Due to
Treatment

A

Strangling of chest, pain with exertion
- O2 supply & demand imbalance
- MONA , morphine oxygen nitroglycerin aspirin (nitroglycerin 3 tabs every 5 minutes; may cause headaches or hypo)

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21
Q

Unstable angina pectoris characterized by
- treatment

A

New onset, occurs at rest, worsening pattern, no change in CK or troponin
- calcium channel blockers (diltiazem)

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22
Q

NSTEMI due to
STEMI die to
ST during ischemia
ST during infarction

A

Coronary vasospasm, spontaneous dissection, partial occlusion of artery
- rupture of atherosclerotic plaque causing thrombus formation & leading to 100% occlusion of coronary artery
- ST segment depressed
- ST segment elevated

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23
Q

Clinical manifestations of angina

A

Substernal chest pain radiating to left arm
Precipitated by exertion or stress
Relieved by NTG or rest
Lasts less than 15 mins

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24
Q

Clinical manifestations of MI

A

Substernal pain radiating to left arm
Pain in jaw, back, shoulder, abdomen
Occurs without cause (morning)
Relieved only by opioids
Lasts 30 min or more
Other Associated symptoms

25
Q

Treatment of choice for confirmed MI
- pre-op tests
Thrombolytic therapy
Most effective when
Major complication

A

Percutaneous coronary angioplasty
- CBC, chemistry, NPO, glucose

Dissolves thrombi to restore blood flow (TPA)
- within 6 hours of MI
- bleeding, no automatic BP

26
Q

Cardiac catheterization pre-op checks
Indications for cardiac cath

A

Screen renal insufficiency, iodine allergy, diabetes, premed w Benadryl, stop Metformin 24hrs prior
- unstable angina, abnormal perfusion, STEMI, NSTEMI

27
Q

Coronary stent nurse interventions
Pseudoaneurysm
Retroperitoneal bleeding
Treatment
Pt education

A

Best rest with insertion site extremely straight, lay flat no Fowlers
- damage or rupture of vessel leading to hematoma or ecchymosis
- puncture of posterior femoral artery during sheath insertion
- surgical repair, anticoag reverse, fluid/blood rescuscitation
- cannot be in a pool or jacuzzi, don’t carry anything heavier than milk carton

28
Q

Coronary artery bypass graft indicated
Pre-op care
Post-op care
Complications

A

Angina w >50% occlusion of coronary artery, ischemia w HF, valvular disease
- must Medicate for pain, splint incision
- chest tubes for drainage, monitor ECG, urinary catheter to monitor output (30ml/hr)
- chest drainage over 150ml/hr, sudden cessation of previously heavy mediastinal drainage, post pericardial syndrome (blood in sac & leads to infection)

29
Q

Activity teaching for patient w CAD

A

Walk 400ft 3x a day
Carry nitroglycerin with you
Check pulse before, during, after exercise
Stop if pulse increase 20bpm
Gradually increase walking distance
Avoid straining

30
Q

Left sided heart failure known as
Causes
Manifestations

A

Congestive heart failure
- HTN, CAD, valvular disease
- (LUNGS) dyspnea, pulmonary congestion, pink frothy sputum, breathlessness, oliguria, crackles

31
Q

Right sided heart failure causes
Manifestations
Significance of weight gain

A

Left ventricle failure, right ventricular MI, pulmonary HTN (sleep apnea)
- JVD, hepatomegaly, ascites, peripheral edema, abdominal girth, weight gain
- most reliable indicator of fluid status

32
Q

Heart failure risk factors

A

CAD, HTN, valve disease, substance abuse, smoking, diabetes, family Hx, hyperthyroidism, obesity

33
Q

Compensatory mechanisms when cardiac output is insufficient
Normal BNP value
Cardiac Hypertrophy consequences
Best diagnostic test / lab
What happens to PAWP

A

Sympathetic nervous system stimulation, RAAS system, BNP chemical rises, myocardial hypertrophy
- BNP <100 ; increased lab value indicates Heart failure
- poor contractility, high oxygen demand, displaced point of maximum impulse to the left
- echocardiogram / BNP lvl
- increases with left sided HF

34
Q

What is Afterload
Drugs to reduce afterload
Acute results

A

Pressure required to move blood from left ventricle to body
- ACE inhibitors (-pril) , ARBs (-artan)
- improves cardiac output & decreases pulmonary congestion

35
Q

What is preload
Interventions to reduce preload

A

Blood volume that enters the right atrium
- Na restriction (2-3g D), diuretics (loop furosemide - acute acting) (thiazides - long acting) & vasodilators (nitrates)

36
Q

Drugs to enhance contractility
Which drugs only given in high stages of CHF
Digoxin education

A

Inotropic drugs - digoxin, dobutamine
Beta blockers - carvedilol
- primacor & natrecor
- therapeutic range 0.5-2.0 , digibind is antidote, can cause digitalis toxicity

37
Q

Indications for worsening HF

A

Rapid weight gain 3lbs a week or 1-2lbs a day
Decrease exercise tolerance
Excessive nocturia
Dyspnea/angina at rest
Increased edema to feet/ankles

38
Q

Valvular heart disease
Which murmur is most lethal
Systolic murmurs
Diastolic murmurs
Valve replacement education

A

Diastolic murmur
- mitral regurgitation & Aortic stenosis (MRASS)
- mitral stenosis & aortic regurgitation (MSARD)
- must be on anticoagulants for life due to production of clots , INR value should be 3-3.5

39
Q

Mitral regurgitation manifestations
Aortic stenosis manifestations
Aortic regurgitation

A

Fatigue & weakness, dyspnea on exertion
- early pulmonary congestion, late right sided CHF
- volume overload, LV compensated by hypertrophy (advanced disease causes dyspnea)

40
Q

Acute cardiac tamponade is
Emergency care measures

A

Cardiac tamponade is an extreme emergency due to increased fluid volume
- pericardiocentesis (uses a needle to remove fluids)
- pericardiectomy (removes entire pericardium)

41
Q

What is MAP
What factors influence MAP
What is a normal MAP
What lvl indicates shock
Cardiac output normal range
Central venous pressure normal

A

Most important factor relating to shock, indicates perfusion of oxygen
- total blood volume, cardiac output
- normal value around 90
- 60-70
- 4-6 L/min
- 2-4 mmHg

42
Q

Cardiovascular manifestations of shock
Respiratory manifestations
GI manifestations
Neuromuscular
Kidney

A
  • decreased BP, thready pulse, narrow pulse pressure (normal 40)
  • increased RR, cyanosis
  • diminished or absent bowel sounds, N/V, constipation
  • early anxiety, thirst, changes in LOC
  • decreased urine output, increased specific gravity due to protein
43
Q

Stages of shock
Initial
Non-progressive
Progressive
Refractory

A
  • MAP drops less than 10, HR & RR increase, lactic acid production
  • MAP drops 10-15, kidney compensates by releasing hormones, hyperkalemia, thirst, tachy (REVERSIBLE)
  • MAP drops 20+, vital organs hypoxic, life threatening (treated within 1Hr), Anuria <40ml/24hr, 5-20% decrease in O2
  • irreversible tissue damage, Rapid loss of consciousness, no palpable pulse, unmeasurable O2
44
Q

Hypovolemia shock common cause
Manifestations
Management

A

Hemorrhage, dehydration, trauma
- CV collapse, BP changes, increased RR, decreased urinary output, decreased capillary refill & DTRs
- must replace fluids, give albumin or blood, vasoconstrictors & inotropics, nitropress

45
Q

Cardiogenic shock causes
Manifestations
Management

A

Pump failure, typically MI
- systolic <90, narrow pulse pressure, weak thready pulse, S3 & S4, oliguria
- nitrates, epinephrine, CABG

46
Q

Distributive shock characterized by
Typical causes

A

Blood is distributed to tissues & cannot circulate to perfuse properly
- anaphylaxis & sepsis

47
Q

Septic shock etiology
Progression
Multiple organ dysfunction syndrome
Gold standard to indicate sepsis
Interventions

A

Mostly caused by gram negative bacteria (E. Coli) (urosepsis - check urine)
- sepsis leads to systemic inflammatory response syndrome (SIRS), all tissues hypoxic
- MODS results from SIRS leading to uncontrolled bleeding & death
- lab values ; LACTIC ACID >4mmol (gold standard), hyperglycemia w/o diabetes, C reactive protein
- Give O2, Broad spectrum antibiotic therapy, glycemic control (keep below 150 with insulin)

48
Q

Neurogenic shock causes
Manifestations
If injury below C5 vertebrae
If above C3
Neurogenic shock treatment

A

Damage to CNS leading to low BP & HR (spinal cord, brain, cervical injury)
- instant hypotension, warm flushed skin, priapism, bradycardia
- diaphragmatic breathing
- immediate respiratory arrest
- dopamine, vasopressin, atropine

49
Q

Anaphylactic shock onset
Anaphylactic shock management

A

Swollen lips & tongue, respiratory distress, loss of consciousness, N/V, hypotension <90 systolic
- immediately asses respiratory status, apply O2, change IV tubing & run NS, Give epinephrine, Benadryl, Albuterol

50
Q

Obstructive shock causes
How does pericarditis look on EKG

A

Impairment of heart to pump, like pericarditis or cardiac tamponade
- there is ST elevation on every lead

51
Q

Basic kidney functions

A

Produce renin to regulate BP, GFR & release aldosterone that promotes reabsorption of water & sodium to restore BP & blood volume
Also secretes erythropoietin for RBC production

52
Q

Types of acute renal failure
Pre-renal - perfusion reduction causes
Intrarenal - kidney damage
Postrenal - urine flow obstruction

A
  • fluid loss, hypotensive drugs, MI or CHF, infection, NSAIDs, anaphylaxis
  • glomerulonephritis, thrombi in kidney, sepsis, ingested toxins
  • bladder cancer, cervical cancer, prostate cancer, kidney stones, neurogenic bladder
53
Q

Normal kidney lab ranges
BUN
Cr
Specific gravity
Treatment of acute renal failure

A

10-20
0.6-1.2
1.00-1.30
- diuretics to remove fluid, calcium channel blockers if AKI from nephrotoxins, reduce protein intake 40g/day (no dialysis) or 1.5g/kg (dialysis)

54
Q

End stage renal disease involves
Defined as presence of
What is normal GFR & GFR during last stage
Oliguria vs Anuria

A

Progressive, irreversible loss of kidney function
- kidney damage or GFR <60 ml/min for 3+ months
- normal GFR 90-125ml/min ; last stage when GFR is <15ml/min
- oliguria (<400ml/24hr). Anuria (<40ml/24hr)

55
Q

Chronic kidney disease manifestations
Uremic syndrome
Metabolic disturbances
Electrolyte imbalances
Hematologic system
Respiratory system

A
  • metallic taste in mouth, anorexia N/V, muscle cramps, uremic frost on skin (shiny skin), fatigue, dyspnea, hiccups, edema
  • increased BUN & Cr , lethargy or fatigue, can lead to uremic encephalopathy (seizure/coma)
  • hyperkalemia (most serious electrolyte disorder - can cause cardiac arrest)
  • anemia (decreased erythropoietin) , bleeding tendencies (no platelets) , bruising, Petechiae
  • dyspnea , kussmaul respirations (ketosis), pulmonary edema, urine breath
56
Q

Chronic kidney disease management
Hyperkalemia
HTN
Nutritional therapy

A
  • give insulin or D50
  • diuretics, Beta blockers, CCBs, ACE inhibitors, ARBs
  • LOW PROTEIN DIET
57
Q

Dialysis fistula vs graft
Fistula
Graft

A
  • made of own body, 1st choice (better), lasts 5-10yrs, small chance of infection or clotting, must wait a couple months before use
  • made of synthetic material, 2nd choice, lasts 2-3yrs, moderate chance of infection or clotting, can be used immediately
58
Q

Caring for vascular access site of dialysis pt
Call MD immediately if

A
  • palpate for thrills & listen for bruits, no carrying heavy objects, no sleeping on fistula side, assess distal pulses, assess for bleeding & infection at needle sites
  • swelling of arm, infiltration of site, absent thrill, prolonged bleeding, cyanotic fingers

411 Adult 3 (3 decks)

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