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Level 4 > Nurs 4000 Final > Flashcards

Nurs 4000 Final Flashcards

1
Q

What are the different layers of the heart tissue?

A
  1. endothelium - line the inside of the chambers
  2. myocardium - cardiac muscles fibers
  3. epicardium - covers the outer surface of heart
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2
Q

What are the different valves?

A
  1. Tricuspid - rt atrium + ventricle
  2. Pulmonary - rt ventricle + lung
  3. Mitral - lt atrium + ventricle
  4. aortic - lt ventricle + aorta
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3
Q

What is atrial fibrillation?

A

COndition which multiple areas of the atria fire simultaneous (up to 300-600 impulses/ min). Atrial cardiac cells are stimulated individually which prevents a unified contraction. Instead, it quivers chaotically

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4
Q

How does afib affect cardiac output?

A

Afib decreases contractility strength & stroke volume = decreased cardiac output by 20-30%

Decreased CO results in decreased O2 and nutriends to body, and increased wastes in the body

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5
Q

What is a heart beat?

A

Combination of electrical impulses which stimulate the mechanical contraction of the heart

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6
Q

What happens with Na+ and K+ during DP & RP?

A
  1. When cells are polarized, K+ is inside cell, Na+ mostly outside
  2. Electrical stimulus causes gates to open, causing K+ to rush out and Na+ in (Depolarization)
  3. Causes muscle to contract
  4. RP - active transport of K inside and Na out to bring the cell to it’s polarized state. Characterized by muscle relaxation
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7
Q

What are the events of the P wave?

A
  1. Atria filled with blood causes the SA node to fire
  2. Impulse travels through the atria
  3. Stimulates the atria muscle to contract (P wave)
  4. Contraction causes blood to fill ventricles
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8
Q

What occurs during the PR interval?

A
  1. Signal from SA node is received by AV node. Signal is delayed to allow ventricles to fill
  2. Atrial repolarize
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9
Q

What occurs during the QRS interval?

A

Q: AV node stimulates the Bundle of HIS and therefore bundle branches in the septum

R: Purkinje fibers stimulate ventricle heart muscles. Reuslts in the depolarization of the ventricle cells. Lt. ventricle contracts

S: Rt ventricle contracts, atria start to fill

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10
Q

What occurs during the T wave?

A
  1. Ventricles relax (repolarize)
  2. Atria fills until it stimulates the SA to start process over again
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11
Q

What does an ECG of someone suffering from afib look like?

A
  • P wave missing
  • QRS compex is present
  • Irregular contractions because of atrial quivering
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12
Q

What are risk factors of developing Afib?

A
  • Older (>60)
  • Male
  • Hx of HTN, CHF, diabetes, coronary heart disease, mitral valves disease, atrial septal defect, alcohol excess, hyperthyriodism
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13
Q

What are S&S of afib?

A
  • asymptomatic
  • palpitations
  • anxiety
  • fatigue/ malaise
  • exercise intolerance
  • nausea
  • dyspnea
  • diziness
  • hypotension
  • chest pain
  • diaphoresis
  • altered mental status
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14
Q

What are the main treatments afib?

A

chemical or electrical cardioversion, anticoaglation, ventricular rate control

If these fails, catheter ablation

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15
Q

What is cardioversion? how is it done?

A

Restore the cardiac conduciton pattern to a normal sinus rhythem/ or maintain a ventricular rate of less than 100bpm

Chemical: K/Ca+ channel blockers. Initially given bolus, then provided with maitenance dose

Electrical: temporarily DP cardiac cells to break the chaotic atrial DP activity

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16
Q

Why is there anticoagulation therapy with afib? What’s used

A

Prevent potential complications in the future (CVA). WO’nt break up clots, but will stop further clot formations

includes Heparin, warfarin, enoxaparin, dalteparin

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17
Q

What happens whien ventricular rate increases?

A

Ventricles have less time to fill, decreases troke volume, which decreases CO and increases workload of heart

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18
Q

What medicaitons are used to control ventricular rate

A
  1. Calcium channel blockers (dilitiazem)
  2. beta blockers (metoprolol)
  3. digoxin
  4. aspirin
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19
Q

What is cather ablation? When is it used?

A

Used when the previous interventions are insucessful

  • catheter is insetered into the femoral vein up to atrium. RFE destroys cardiac tissue which causes the abnormal electrical signals
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20
Q

What is nursing management of someone with Afib?

A

Assess and monitor

  • ECG
  • heart sounds, apical HR
  • SE from medication therapy (hypotension, dizziness, syncope)
  • VS
  • Lab values
  • Signs of bleeding
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21
Q

What lab values do you monitor for heparin, warfarin

A
  • heparin - PTT
  • warfarin - INR
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22
Q

What is CO equation? What is SV?

A

CO = SV x HR

SV = EDV - ESV

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23
Q

What is preload, contractility, afterload?

A
  • Preload: amount of stretch in ventricular muscles before it contracts
  • Contractility: force of muscle contractions
  • Afterload: Pressure in arteries above semilunar valves
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24
Q

What is congestive heart failure?

A

heart cannot pump enough blood to meet the metabolic needs of the body.

Heart cannot handle normal blood volume

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25
Q

What is CHF characterized by?

A
  • Volume overload
  • inadequate perfusion to brain and heart
  • exercise intolerance
  • venous congestion
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26
Q

What are intrinsic risk factors? Intrinsic RF of developing CHF?

A

Intrinsic RF- related to the structure and function of the heart

  • CAD (decreases preload)
  • MI (scar tissue decreases contractility)
  • Valve disease (backflow causes heart to overwork)
  • Congenital defects
  • Dysrhythmias
  • Infection
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27
Q

What are extrinsic risk factors of CHF?

A
  • HTN (increases afterload)
  • Hypervolemia (increases afterload)
  • Chronic ETOH used
  • Tobacco use
  • obesity
  • diabetes
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28
Q

WHat is left sided failure? Maintestations

A

Inability for left side to pump blood to the rest of the body. Blood builds up in the lungs

  • pulmonary edema
  • dyspnea/ orthopnea/ tachypnea
  • tachycardia
  • confusion, weakness
  • nocturia
  • cough
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29
Q

What is right sided heart failure? Manifestations?

A

Inability for heart to pump blood to lungs. Blood pools in rest of body

  • Peripheral edema
  • hepatomegaly (venous congestion of liver)
  • Acites
  • Jugular vein distension
  • sudden weight loss
  • cyanosis
  • muscle wasting
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30
Q

What is BNP?

A
  • Hormone stored in the ventricular myocardium, released in quantities in proportional to heart stress
  • Normal heart function will not have elevated levels
  • Measures worsening as well. Higher the level, worst the prognosis
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31
Q

What is LVEF?

A

Left ventricle ejection fraction.

Amount of blood ejected by the ventricles each contraction. Normal = 55-70%

Ef = (SV / EDV) x100%

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32
Q

How is CHF diagnosed?

A

Combination of

  • hx taking
  • physical exam
  • ECG
  • BNP
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33
Q

What are some nursing management for CHF?

A
  • High fowlers with legs down
  • Na/H2O restriction
  • Supplemental O2
  • Bedrest
  • Decrease anxiety (Loxapine)
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34
Q

What medications are used with CHF? How do they affect CHF?

A
  • diuretics (furosemide). Symptom management. Decreases blood volume, decreases preload
  • beta blockers (metoprolol). Reduces risk of death. Blocks SNS stimulation (decreases workload). Causes vasodilation (decrease afterload)
  • Vasodilator (Nitroglycerin)
  • Ionotropes (digoxin). Increases contractility therefore SV
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35
Q

What should nurses assess with CHF patients?

A
  1. VS
  2. daily weights
  3. I &O
  4. Peripheral Edema
  5. Listen for crackles
  6. LOC & CWMS
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36
Q

What is an MI?

A

Myocardial infarction

WHen the heart doesn’t receive enough blood to continue contracting. Can result in insult or injury. Usually dt arterial occlusion or blood clot

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37
Q

What is the continuum of chest pain? What causes it?

A
  • Stable angina Stable plaque
  • Silent ischemia Plaque rupture
  • Unstable angina PLaque rupture
  • NSTEMI Incomplete occlusion
  • STEMI Complete occlusion
  • Sudden death Complete occlusion
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38
Q

What are S&S of an MI?

A

Symptoms

  • chest pain radiating from jaw or lt arm, sweating, SOB, N&V, anxiety

Signs

  • Pallor
  • Diaphoresis
  • Circulatory shock (hypoTN, cap refil >2s)
  • Hypoxia
  • Oliguria
  • Weak pulse
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39
Q

How long do professioals have to tx an MI?

A

20 - 30 minutes before tissue starts to die

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40
Q

How is an MI diagnosed?

A
  • 12 lead ECG
  • Triponin - hormone specific to myocytes released when dead
  • CK, AST, LDH - found in skeletal muscle death
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41
Q

How is a heart attack managed?

A
  • early perfusion
  • anti-plateley therapy
  • anticoagulants
  • controlling risk factors
  • secondary prevention
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42
Q

What’s the difference between STEMI and NSTEMI?

A

NSTEMI - damage to the heart because of a partial occlusion but damage isn’t enough to affect ECG. No ST elevation

STEMI - sufficient cardiac damage decreases ability to contract, causing changes on ECG (elevatoin of ST peak)

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43
Q

What do you do if you suspect your patient is having a heart attack?

A
  1. Thorough assessment of pain to ensure isn’t muscle pain? Have they had pain before? Radiating?
  2. Set of VS
  3. Pg doctor
  4. Dr to order stat cardiac panel
  5. Administer nitro c Drs order
  6. Stat ECG
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44
Q

How are symptoms of an MI controlled?

A
  1. Nitroglycerin - vasodilation, antiinflammatory, antithrobotic
  2. Metocloperamide - minimize nausea. Met acts on dopamine receptors
  3. Morphine - pain + lessens autonomic features of MI
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45
Q

What medications are used to increase mortality after an MI?

A
  1. Reperfusion therapies
  2. B blockers - beta receptor antagonist, decreases work load of the heart
  3. ACE - prevents the conversion of angiotensin 1 to angiotension II (potent vasoconstrictor)
  4. Antiplatelets - clopidogrel, ASA. Decreases blood viscosity, decreases workload of the jeart
  5. Glycemic control- decrease blood viscosity
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46
Q

What are some secondary lifestyle changes which can prevent MI?

A
  • diet
  • alcohol
  • weight
  • smoking
  • smoking cessation
  • cardiac rehabilitation
  • stress management
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47
Q

What drugs are use to prevent future MI?

A
  • ASA - anti platelet
  • B Blocker - decreases workload of heart
  • ACE inhibitor - vasodilation
  • Statin - prevents plaque build up
  • Control HTN
  • Control diabetes
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48
Q

What is a nursing care management acronym?

A

MOVE

  1. Monitor - nature, severity, duration, intensity of pain. Monitor ECG q15min. BP & urine output
  2. Oxygen - up to 15L hi flow
  3. Venous Access -
  4. Expert advice
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49
Q

What’s a good assessment of chest pain?

A
  • Palliative/ provocative factors
  • Quality of pain
  • Region of body affected/ radiation
  • Severity
  • Timing
  • Treatments tried
  • Associated symptoms
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50
Q

What is angina?

A

Chest pain dt coronary artery insufficiency (heart being unable to meet O2 supply and demand

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51
Q

What are the typical S&S of angina?

A
  • Pressure
  • burning
  • heaviness
  • constriction
  • gradual onset
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52
Q

What is CKD defined as?

A

Having an eGFR <60ml for >3mos

or

structural/ functional kidney damage w/o changes to eGFR

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53
Q

What is the patient more likely to die drom? CHF or CKD?

A

CHF!

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54
Q

What are normal kidney functions?

A
  1. Removes metabolic wastes
  2. Filters blood; removes drugs/ hormones
  3. Regulates H2O, E7 and PH
  4. Secretes erythropoieten
  5. Activates Vit D
  6. Regulates BP
  7. Regulares Ph & Ca
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55
Q

What hormones affect the kidneys release to maintain fluid balance? What do they do?

A
  1. Anti diuretic hormone - secreted from post pituitary. Controls Distal tubule permeability. When released, retains H2O to maintain fluid volume
  2. Aldosterone - secreted by adrenal cortex. Retains Na, expels K. Retains volume, increases fluid volume
  3. Atrial Natriuretic hormone - secreted from the heart. Causes Na secretion. Expels H2O
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56
Q

What is BUN? Normal Value?

A

Blood urea nitrogen - normal waste produce formed from breakdown of protein

Normal: 1.8 - 8.2

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57
Q

What is creatinine? Normal value?

A

Normal waste product from muscle activity.

60 - 115 umol/L

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58
Q

WHat is GFR? Normal range

A

Rate which the kidneys filter blood therefore a reflection of how well the kidneys are working

>90 ml/min

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59
Q

What are normal HbG rates?

A

120 - 160 g/L

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60
Q

What is acute kidney failure?

A

Rapid onset/ short duration of reversible damage to both kidneys

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61
Q

What causes acute kidney failure (3)

A

1. Decreased blood flow - decreased end organ perfusion from show or chronic heart failure

2. Inflammation/ necrosis of the tubules - causes obstruction and increased pressure on the renal artery. Causes activation of SNS & RAAS. Results in vasoconstriction and therefore decreased GFR

3. Burns-. Breaks down RBC. Free floating Hgb accumulates and blocks & destroystubules

4. Trauma - blunt force. Release of creatinine kinase which is lethal to kidneys

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62
Q

What are the different types of acute renal failure? What causes them?

A
  1. Prerenal - dt decreased bloodflow to kidneys. Most common cause. Dt CHF, sepsis, athrosclerosis
  2. Intrarenal - Dt damage to the tubules by disease (kidney stones) or nephotoxins (beta lactams, contrast media)
  3. Post renal - urinary obstruction causing a build up of pressure in the kidneys. Least common cause
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63
Q

What are S&S of ARF?

A
  • Rapid change of lab values - BUN, Cr, GFR, PH
  • Hyperkalemia
  • Metabolic acidosis
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64
Q

What are risk factors of CRF?

A
  • Diabetes
  • untreated HTN
  • smoking
  • poverty
  • obesity
  • >65 yo
  • Diseases such as SLE, pyelonephritis, hep B/C
  • exposure to nephrotoxic substances
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65
Q

What is the relationship between CRF and heart disease

A

Heart diease can advance the progression of CRF

heart disease decreases CO, decrease in renal perfusion causing renal ischemia

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66
Q

What ethnicities are at greater incidence of CRF leading to kidney failure?

A
  • Hispanic and african americans
  • pacific islanders
  • american indians
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67
Q

What can trigger chronic renal failure?

A
  1. HTN - nephrosclerosis*
  2. diabetic nephropathy - nephrosclerosis*
  3. glomerulonephritis - locally activates cellular, immunologic and biochemical mediators of inflam cause damage
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68
Q

What are the stages of CKD? What is the associated GFR? What action is taken

A
  1. Kidney damage. Normal of increased GFR. Tx comorbid conditions, slow progression. Reduce risk of cardiovascular disease. >90
  2. Kidney damage, mild decrease GFR - same. 60 - 89
  3. Moderately decreased GFR - evaluate and tx complications. 30 - 59
  4. Severely decreased GFR. Prepare for renal replacement therapy. 15 - 29
  5. Kidney failure. Hemodialysis, peritoneal dialysis, transplant or hospice <15
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69
Q

What are common tests used to diagnose CRF?

A
  1. Urine dipstick for protein - persistent proteinuria
  2. Urinalysis - presence of casts (RBC/tubules) Decreased specific gravity (can’t concentrate urine)
  3. Albumin to Cr ratio: estimate of albumin excretion. >300A:1Cr (w/o diabetes) or >30 (w diabetes)
  4. eGFR
  5. Blood chemistty - liver profile, PTH
  6. CBC
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70
Q

What lifestyle changes can slow the progression of CRF?

A
  1. Maintain BP <130/80
  2. Regulate blood glucose levels
  3. Manage dyslipidemia
  4. Encourage weight loss
  5. Smoking cessation
  6. Restrict dietary protein
  7. Limit Na, K, Ph and H2)
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71
Q

What medications should CRF patients avoid?

A
  1. NSAIDs
  2. metformin
  3. contrast agents
  4. biphospinates
  5. beta lactams
72
Q

Why are ACE/ ARBs prescribed in CRF?

A

Can protect kidney from further damage, manage HTN

73
Q

How can a nurse care for a CKD pt?

A
  1. Review medications to ascertain appropriateness for CKD pt
  2. Monitor I&O. Ensure adherance to CRF diet
  3. Monitor BP
  4. Assess for fluid overload
  5. Educate pt
74
Q

What are ECGs?

A

A grpahic tracing of the electrical forces produced by the heart

75
Q

What do the vertical and horizontal axis represent on an ECG?

A
  1. Vertical - amplitude of the impulse in mvolts
  2. Horizontal - time in seconds
76
Q

What is the effect of adding more ECG leads?

A

Helps narrow down what type of MI/ how severe

77
Q

What is a lead?

A

an electrical view of the heart

78
Q

What leads are placed on the front chest?

A

V1 - 6. Obtains a view of heart horizontally

79
Q

What are deflections? What are common ones?

A

Shift up (towards electrode) or down (away from electrode) from baseline on the ECG

Normal: P, QRS, T, U

80
Q

How should ECGs be interpreted?

A
  1. Rhythem
  2. Rate
  3. P Wave
  4. PR interval
  5. QRS complex
81
Q

What are you assessing with rhythem?

A
  • P waves (atrial) or R waves (ventricular) equal distance apart

Caliper method/ paper method (3 P/R waves)

82
Q

How is rate assessed?

A
  1. Small box method - Count # of boxes between 2 different waves. Divide small boxes into 1500 to get bpm
  2. Quick and dirty method - irregular method. Number of P/R waves in a 6 second strip. Multiply by 10. Gives average HR
83
Q

How is the P wave assessed?

A
  • Positive deflection?
  • Do all the P waves look the same
  • What is the shap of the P waves (round?)
  • Is the ratio P to QRS (should be 1:1)
84
Q

How is the PR interval assessed?

A
  • How long is the PR interval (3-5 small boxes)
85
Q

How is the QRS complex assessed?

A
  • How tall is the complex (should be tallest)
  • How long is it? (should be 3 small squares)
86
Q

How is the T wave assessed?

A
  • Is the T wave positive?
  • Is it taller than the P wave
  • What is the shape (should be round and slightly asymmetrical)
87
Q

What does afib look like on ECG? How are these pts cared for?

A

Small irrefular baseline wabes which vary in shape and size

Anticoagulation therapy

88
Q

What does A flutter look like on ECG?

A
  • Saw tooth atrial wave
  • P waves are inverted

anticoagulant therapy

89
Q

What does ventricular fibrillation look like? Nursing implications?

A

Extreme rapid, erratic impluse. Impossible to distinguish P, QRS or T waves

Initiate CPR/ defibrillation

90
Q

Which pathway does heparin work on? Warfarin?

A

Heparin works on prothrombin and fibrinogen factor on the common pathway. Therefore, monitored wth PTT value.

Warfarin prevents synthesis of factors dependant of vit K on the extrinsic pathway (oral)

91
Q

Why is heparin given?

A
  • prophylaxis and tx of VTE
  • Prevention clotting after cardiac surgery
  • Dx & tx of consumptive coagulopathies
  • Tx unstable angina/ acute MI
  • Pvt in atrial fib
92
Q

What medications increase risk of bleeding when administered with heparin?

A
  • ASA, NSAIDs
  • some antidepressants
  • Ginseng, garlic, ginger
93
Q

What is heparin induced thrombocytopenia?

A

Formation of abnormal antibodies which target platelets. if found, stop heparin

94
Q

What are the clinical features of delerium?

A
  1. Acute onset (hours - days)
  2. Fluctuates (worse at night)
  3. Resless/agitation vs lethargic/inactive
  4. Changes in conciousness
  5. inattention
  6. disruption of sleep
  7. emotional disturbances
  8. Disordered thoughts, language, memory & orientation,
  9. Preception changes (MSE)
95
Q

What tools can be used to assess for delerium?

A
  • Confusion assessment method
  • Montreal cognitive assessment
96
Q

If you can’t get a pt to pay attention long enough for a CAM, what else can be done?

A
  • ask family baseline
  • previous medical listory
97
Q

What tests should be performed to investigate the cause of delerium?

A
  • CBC
  • E7
  • BUN/ Cr
  • Albumin
  • Liver function tests
  • TSH
  • Urinalysis
  • Blood gases
  • blood culture
  • Xray
  • ECG
98
Q

If you suspect delerium, what things need to be assessed for immediately?

A
  1. Neurological examination
  2. Hydration and nutritional status
  3. Evidence of sepsis
  4. ETOH abuse/ withdrawal
    5.
99
Q

What are common potential causes of delerium?

A
  • Drug induced
  • ETOH / drug withdrawal
  • Surgical procedures
  • Infection
  • fluid/ E7 imbalance
  • Severe pain
  • Metabolic endocrine
  • cardiopulmonary hypoperfusion
  • intracranial
  • sensonry/ environment
100
Q

What is the difference between stroke volume and ejection fraction?

A

Stroke volume: te volume of blood leaving the heart each beat

Ejection fraction: compares te stroke volume to the end diastolic fraction to express te percentage of blood which leaves te heart eac beat

101
Q

What is a normal ejection fraction? What is an EF of CHF? of heart hypertropy?

A

Normal 50 - 70%

CHF

Hypertrophy >70%

102
Q

How is ejection fraction measured?

A

Use of echocardiography (US)

103
Q

Wat is echocardiography?

A

A A sonogram of te heart. Can be transthoracic or transesopageal

104
Q

What is the difference between transthoracic and tranesophageal ECG

A

Tranthoracic - US placed against te chest wall. Non evasive but has less clear images

Transesophageal - Placed through pts esopagus. Clearer picture. Can evaluate aorta. Requires prep, medical team, risk of esophageal damage, risk of aspiration

105
Q

What can cause a low ejection fraction?

A

Dilated myocardium

Damaged myocardium

Valve dysfunction

Chronic HTN

106
Q

How can low EF be managed?

A

Ionotropes elp increase myocardial contractility

ARBs to reduce heart stress

B blockers - slow and regulate heart rate

restrict salt and fluid

moderate daily activity

107
Q

What are the differences between linear, depressed and basilar fractures?

A
  1. Linear: Usually just a crack. No treatment nexessary
  2. Depressed: blunt force trauma, bone is pushed in. Can cause bleeding or pressure on brain
  3. Basilar: fracture to the base of skull. Severe force needed
108
Q

What is the difference between concusion, contusion and diffuse axonal injury?

A
  1. Concussion - jarring of entire brain. can result in LOC
  2. Contusion - bruising in the brain. Areas of hemorrhage
  3. DAI: injury to entire brain, results in coma
109
Q

What are intracerebral bleeds? How do they present?

A

Bleeding directly into brain.

Presents with hemiparesis/ hemiplegia. Symptoms depend on location. Often rapid progression of symptoms

High mortality rate

110
Q

WHere does an epidural hematoma occur. Special feature? Presentation

A

Occurs between skull and dura mater

Often arterial and associated with a skull fracture. Requires immediate intervention

Present with immediate change in LOC, lucidity then LOC pupil dilation

111
Q

WHere does an subdural hematoma occur. Special feature? Presentation

A

Occurs between dura mater and arachnoid mater

Often venous

Presents similar to epidural, but with slower onset

112
Q

What is considered elevated ICP?

A

>20 mmHg

113
Q

What is cushings triad?

A

Widening systolic gap, increased BP, brady cardia, irregular resp rate

114
Q

What is sepsis?

A

Presence of infection and activation of the inflammatory cascade (SIRS present with known infection)

115
Q

What is systemic inflammatory response syndrome?

A

aka sepsis - the infection is no longer localized. Systemic response to circulating cytokines results in vasodilation causing increased HR & RR

116
Q

What is severe sepsis?

A

Sepsis with evidence of end organ dysfunction dy hypoperfusion.

  • coagulation cascade is systemic
  • Decrease in CO results in shunting of blood away from organs other than heart and blood
  • Compensatory mechanisms are overwhelmed
117
Q

What is septic shock?

A

Persistent hypoTN despite fluid rescusitation. Causes end organ failure

118
Q

What are the parameters of SIRS?

A

Two of the following 4 are present

  • Temp 38
  • HR >90
  • RR >20
  • Elevated WBC
119
Q

What are some nursing interventions of SIRs?

A
  1. Supplemental O2
  2. Initiate IV
  3. Fluid replacement (NS or Ringers lactate)
  4. Prepare to initiate Abx
120
Q

What are clinical manifestations of severe sepsis?

A
  • HypoTN
  • Hyperglyceia
  • Altered mental state
  • acute oliguria
  • Increased INR/ PTT
121
Q

Nursing interventions for severe sepsis?

A
  • Initiate O2
  • IV bolus
  • Abx
  • Monitor urine output
  • Norepinephrine/ dopamine after fluid replacement
  • Insert foley catheter
122
Q

What are systemic complications of septic shock?

A
  1. Acute renal failure
  2. Acute Resp distress syndrome
  3. GI complications
  4. DIC
  5. Multiple organ dysfunction syndrome
123
Q

What is shock?

A

Inability of cardiovascular system to maintain adequate perfusion to vital organs. Failure of heart, vascular tone or blood volume

124
Q

What are the three classifications of shock?

A
  1. Hypovolemia
  2. Cardiogenic/ obstructive
  3. Distributive/ Vasogenic (anaphylactic, neurogenic, septic)
125
Q

What is the pathophysiology of hypovolemic shock?

A
  • compensatory mechanisms are unable to to maintain organ and tissue perfusion dt loss of fluid or 3rd shift or dehydratoin
126
Q

What’s the pathophysiology of cardiogenic shock?

A
  • failure of the lt ventricle to pump adequate blood. Body vasoconstricts to compensate, as well as raises HR
  • spiral of decreased CO, poor tissue perfusion and increased work of heart
  • Caused by MI, CHF, valve disorders, emboli
127
Q

What is the pathophys of vasogenic shock?

A
  • loss of vasomotor tone dt histamie, spimal damage or inflammatory factors
  • Vasodilation decreases organ perfusion
128
Q

What are the 3 stages of shock? Duration?

A
  1. Compensated Nonprogressive - body can compensate to maintain CO. Lasts 30s - 48hts
    * Decrease in BP causes sympathetic NS responses (vasoconstriction, release n/epinephrine, Ald + ADH release, hypoxia)
  2. Decompensated Progressive Shock - body is losing ability to compensate. Loss of 15-20% of circulating volume. (Decreased BP = heart and kidney failure, hypoxia, cellular destruction, increased lactate)
  3. Irreversible shock - loss >25%. Cell and organ damage beyond point of return. No recovery. (Nausea, acidosis, reduced urine output, altered mental status, tachycardia)
129
Q

What is the golden hour?

A

Time from when the patient starts to decline to receive treatment to prevent irreversible shock.

130
Q

What are the interventions for hypovolemic shock?

A
  1. fluid resuscitation (NS/rigners lactate)
  2. O2
  3. Control hemmorhage
  4. Colloids
  5. blood transfusion
  6. Catheter
131
Q

What are interventions for hypovolemic shock?

A
  • Fluid bolus
  • O2
  • Diuretics for fluid overload
  • Ca channel blockers
  • Dopamine/ norepinephrine
  • morphine
  • thrombolytic therapy
  • angioplasty?
132
Q

Interventions for neurogenic shock?

A
  • fluid replacement if hypoTN. Crystalloids or colloids
  • norepinephrine, vasopressin
  • dopamine for heart
  • steroids
  • surgery
133
Q

Interventions for anaphylactic shock?

A
  • Epinephrine
  • IV bolus/ flud repleacement
  • O2
  • Dimahydramine
  • Corticosteroids
  • Bronchodilators
  • H2 blockers
134
Q

What is liver failure? What are the 3 main types?

A

Unable to perform functions (80-90% has been destroyed)

Cirrhosis, hepatitis and liver cancer

135
Q

What are the three types of liver disease

A

Hepatitis

Cirrhosis

Cancer

136
Q

What causes hepatitis?

A

inflammation of liver which can lead to necrosis.

Caused by viruses (hep a/b etc), toxins (metals/tylenol) or chimical (ETOH/rifamprin, ibuprofen)

137
Q

What is cirrhosis?

A

progressive, widespread chronic fibrosis and nodule formation in the liver. It interferes with hepatic blood flow and bile clearance

138
Q

What are complications of cirrhosis?

A
  1. portal HTN
  2. decreased liver fxn
139
Q

What are normal liver functions?

A
  1. Bile, urea, plasma proteins and antibody production
  2. Metabolism of fats, aminio acids, sugars and toxins
  3. Storage for fats, Vit A,D,E,K, B12, iron and glycogen
  4. Activation vit d
140
Q

What are Kupffer cells?

A

Cells in liver that break down RBCs and excretes bilirubin into the bile

141
Q

What are sinusoids?

A

Functional component of the liver. Contains bile duct, hepatic arteriole/ portal venule. Exchange of bile and nutrients and O2

142
Q

How much blood does the hepatic portal vein contribute to the liver.

A

75%

143
Q

What is the patho of portal HTN? S&S?

A

Scarring of the liver tissue impedes blood flow from the portal vein into the sinusoids. Blood backs up into the low pressure veins and capillaries.

Results in varices, edema, ascites, hepatic encephalopathy

144
Q

What are varices? WHere are the formed? What is the issues with varices?

A
  • dilated veins that occur from pressure build up. Can rupture easilty.
  • Can form in esophagus/GI/lower abdomen
  • They are easily ruptured = bleeding
145
Q

How are varices managed?

A
  1. Beta blockers - decreases BP
  2. Anti-ulcer agents - prevents reflux
  3. Balloon tamponade procedure
  4. transjugular intrahepatic portosytemic shunt
146
Q

What is the balloon tamponade procedure?

A
  • a tube is inserted into the nares and a balloon is inflated to apply pressure to bleeding area.
  • can only be inflated for 24 hours. otherwise tissue necrosis
147
Q

What is TIPS?

A
  • transjugular intrahepatic portosystemic shunt
  • Stent between jugular vein and liver creating a connection between portal and hepatic vein
148
Q

Why do liver failure patients have edema and ascites?

A
  • decreased osmotic pressure dt decrease in albumin production
  • Increased hydrostatic pressure dt portal HTN
  • Kidneys detect low BP - aldosterone secreted. H2O and Na retained. Liver can’t metabolize aldosterone
149
Q

How is liver failure ascites management?

A
  • Albumin then diuretics
  • Restrict Na/ fluid
  • Monitor I&O
  • Monitor E7
  • Daily weight
  • Paracentesis
150
Q

Whats a risk of paracentesis in a liver failure patient?

A

Patients can lose up ot 2-4L of fluid. Risk of hypovolemia

151
Q

What is hepatic encephalopathy?

A

Altered mental state dt NH3 toxicity (Liver is unable to convert NH3 to urea)

152
Q

What are the 4 stages of hepatic encephalopathy?

A
  1. Abnormal sleep pattern, decrease attention span, depression, irritability
  2. Lethargy, amnesia, slurred speech, ataxia, hyporeactive reflexes
  3. paranoria, bizarre behviour, hyperreactive refleces, nystagmus
  4. Coma, unconciousness, dilated pupil
153
Q

What are precipitating factors of hepatic encephalopathy?

A
  1. excess dietary protein
  2. GI bleed
  3. Dehydration and ocnstipation
154
Q

How is hepatic encephalopathy managed?

A
  • restrict dietary protein
  • Lactulose (prevents diffusion of ammonia into colon). Want 2-3 BM xday
  • Liver transplantation
155
Q

What does AST test for?

A

Elevated in serum when hepatic, myocardial or skeletal muscle injury occurs

156
Q

Whats the difference between AST and ALT?

A

AST is found in higher concerntrations in the liver and ALT is found in higher concertrations in cardiac muscles

157
Q

What is the AST/ALT ratio?

A

Important diagnostic in identifying liver damage. Ration >1 means liver damage, >2 alcoholic hepatitis

158
Q

What is ALP?

A

Elevated in hepatitis and liver disease

159
Q

What is LDH?

A

Lactate dehydrogenase: elevated when hepatic, myocardial or skeletal muscle death occurs

160
Q

WHat is hepatorenal syndrome?

A

Kidney failure found in those with liver cirrhosis. Dilation of vessels causes decreased cardiac output. Kidneys detect drop in BP which activates RAAS and sympathetic SNS

Causes vasoconstripction which decreases renal perfusion

161
Q

When does ETOH consumption become severe? Life threatening?

A

Severe - 0.16 - 0.3

Life threatening - 0.31 - 0.45

162
Q

How is ETOH metabolized?

A
  • abosrbed by intestine/ met by liver and stomach
  • Acetaldehyde binds to dopamine and decreases albumin secretion
  • Converted to acetate, then metabolized into CO2 in heart, braincells and muscles

In chronic use, brain may use acetate rather than glucose for energy

163
Q

What are asterixes?

A

Hand flopping around when raised

164
Q

What is alcohol abuse?

A

a pattern of drinking resulting in harm to one’s health, interpersonal relationships or the ability to work. Can lead to dependence

165
Q

What is alcohol dependence?

A

a pathological dependency on ethanol characterized by physical dependence, tolerance and or physiological changes

166
Q

What happens to the brain during alcohol abuse?

A
  • ETOH increases levels of dopamine (reward and pleasure) GABA (inhibitory NT regulates excitability, muscle tone and fear), glutamate (mediated excitatory signals and involves fxns such as memory, learning and cognition) and endogenous opiods (analgesia and feelings of well being).
  • Neural adaptation - chronic activation of reward system causes sensitization and tolerance
167
Q

What is ETOH withdrawal syndrome?

A

S&S following an abrupt cessation or reduction of ETOH use after the brain has been exposed to high dose of ETOH for a prolonged period of time

168
Q

Why does ETOH withdrawal syndrome occur?

A
  • There is decreased dopamine and serotonin through the nucleus accumbens
  • Increases opiod receptor activity (more sensitive to GABA)
  • Decreased GABA, increased glutamate (toxic)
169
Q

When does ETOH withdrawal syndrome occur

A

5-10 hrs after last drink. Peaks in intensity after 2-3 days

170
Q

What effects the severity of ETOH withdrawal?

A
  • daily amount and duration of ETOH abuse
  • Age and medical hx
  • # prior withdrawal
  • age, genetics
171
Q

What are the three stages of withdrawal? S&S of each?

A
  1. Minor - 6 - 24 hrs after last drink. Peaks 24 - 26 hrs. Resolves 2-3 days. anxiety, irritability, N&V, tremor, tachycardia, HTN, insomnia, diaphoresis
  2. Intermediate - hallucinations, seizures (after 2 days)
  3. Major - 2-3 days after last drink, peaks @ 4 days, resolves in 5. Global confusion, disorientation, severe agitation, tremor, psychomotor and autonomic hyperactivity.
172
Q

When should CIWA be initiated?

A
  1. Men - consumes >30 drinks a week. Women >20 drinks a week
  2. Hx of ETOH withdrawal sx, seizures or DT
  3. CAGE score of 2 or more
173
Q

What does a CIWA score <10 require for interventions?

A
  1. No medications required
  2. Monitor q1-2hrs x3, increase q8h x3, q24hx3 then DC
174
Q

What do you do for a CIWA score >10?

A

Requires MD dx confirmation, lab work and

Initiate treatment protocol

175
Q

When do you call an MD with CIWA?

A
  • pulse >120
  • BP >180/120
  • O2 sat < 90
  • Seizures / hallucinations / unresponsive to medications
176
Q

What medicatoins are given for ETOH withdrawal?

A
  • Benzodiazipine unless BP <90 or RR <8
  • Thiamine 100 mg PO/ IV then glucose if necessary
  • Multivit daily
  • Mg Sulphate (IV)
177
Q

What is WErnicke’s encephalopathy

A

A neurological disorder caused by thiamine deficiency

characterized by acute confusion, ataxia, nystagmus,. Amnesic syndrome

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