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CH2 > Final Exam Module 3 & 4 > Flashcards

Final Exam Module 3 & 4 Flashcards

1
Q

Posterior pituitary releases

A

ADH

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2
Q

Anterior Pituitary releases

A

ACTH, MSH, GH, TSH, Prolactin, LH, and FSH

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3
Q

Deficiency in one or more of the anterior pituitary hormones, resulting in metabolic problems, sexual dysfunction. If it’s selective hypopituitarism only one hormone is deficient and is the most common.

A

Hypopituitarism

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4
Q

Hormone over secretion occurs with pituitary tumors or tissue hyperplasia. Tumors most often in the anterior pituitary cells: produce growth hormone, prolactin, and adrenocorticotropic hormone.

A

Hyperpituitarism

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5
Q

Hyperpituitary Disorders - Growth secreting hormone

Onset of growth hormone hypersecretion BEFORE puberty. Continues into adulthood resulting in abnormal height.

A

Gigantism

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6
Q

Hyperpituitary Disorders - Growth secreting hormone

Hypersecretion AFTER puberty. Occurs in adulthood so changes are seen in face, hands, feet, and ears.

A

Acromegaly

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7
Q

Hyperpituitarism: Assessment

Obtain info about

A

Family hx, change in appearance: change in hat, glove, ring, or shoe size.

Sx: fatigue and lethargy, backache, arthralgias, headaches and change in vision, menstrual changes, changes in sexual functioning.

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8
Q

What is the most common surgical management tx for hyperpituitarism?

A

Hypophysectomy- involves the removal of the pituitary gland along with the tumor. Goal is to decrease abnormal hormone levels, relieve HA, possible reversal of sexual dysfunction.

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9
Q

Concern w/ Hypophysectomy

A

CSF leak

-Postnasal drip - clear
-Increased swallowing
-Halo sign
-Persistent HA often means CSF leak into the sinuses

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10
Q

What is the post-op care for hypophysectomy?

A

-Monitor neuro response hourly x 24hrs, then every 4 hrs and document any changes in vision, mental status, LOC, or decreased strength in the extremities.
-Observe for complications such as DI, CSF leak, infection, & increased ICP.
-Keep HOB elevated, avoid coughing, perform deep breathing exercises hourly, avoid bending forward.
-Perform oral rinses and apply moisturizers over the lips.
-Assess for manifestations of meningitis.
-Teach patient self-administration of prescribed hormones.

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11
Q

What condition?

Patho: H2O metabolism problem caused by ADH DEFICIENCY or inability of kidneys to respond to ADH. Excretion of large amounts of diluted urine.

A

Diabetes Insipidus (DRY INSIDE)

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12
Q

What classification of DI?

Renal tubules do not respond to ADH (severe kidney injury)

A

Nephrogenic

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13
Q

What classification of DI?

Problem in the hypothalamus or pituitary gland > lack of ADH production or release.

A

Primary Neurogenic DI

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14
Q

What classification of DI?

Caused by tumors, head trauma, infections, surgeries

A

Secondary Neurogenic DI

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15
Q

What classification of DI?

Caused by lithium and demeclocycline interfere with the kidney response to ADH

A

Drug-related DI

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16
Q

What are the assessment findings of DI?

A

Large amounts of very dilute urine (greater than 4L per day), causing dehydration and hypovolemia. Increased thirst but often not adequate to compensate for volume loss, which can lead to hypovolemic shock!.

Cardiac sx- hypotension, tachy (signs of hypovolemic shock), weak pulses, hemoconcentration

Skin sx- poor skin turgor, dry mucous membranes

Neuro Sx- decreased cognition, ataxia, increased thirst, irritability, dehydrated

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17
Q

Urine characteristics of DI

A

Dilute urine w/ low specific gravity (less than 1.005)

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18
Q

What is desmopressin?

A

Synthetic hormone

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19
Q

Best test to diagnose central diabetes insipidus. In a water deprivation test, urine production, blood electrolyte levels, and weight are measured regularly for a period of 24 hrs, during which the person is NPO. Pt is given ADH (promotes fluid retention ) to determine if neuro or nephrogenic. If osmolarity increases, the kidneys are working so the problem is neurogenic.

A

fluid deprivation test

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20
Q

Urine osmolality
After fluid deprivation <300
After desmopressin >800

A

Neurogenic DI

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21
Q

Urine osmolality
After fluid deprivation <300
After desmopressin <300

A

Nephrogenic DI

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22
Q

DI drug therapy

Teach them to weigh themselves daily

A

-Desmopressin (DDAVP), a synthetic form of vasopressin (or ADH) given intranasally in a metered spray or an oral tablet. May be lifelong with permanent conditions.

-Aqueous vasopressin: for short-term therapy or when the dosage must be changed often; given parenterally

-Chlorpropamide

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23
Q

What condition?

Patho: Too much ADH!! Failure of negative feedback system.

ADH (vasopressin) secretes even when plasma osmolarity is low or normal. Caused by shock, trauma, stress, malignancies.

Water retention> fluid overload. Increase in kidney filtration further inhibits release of renin and aldosterone causing further increase of sodium loss.

A

Syndrome of Inappropriate Antidiuretic Hormone (SOAKED INSIDE)

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24
Q

Assessment finding of SIADH

A

Dilutional Hyponatremia, GI disturbances, N/V, loss of appetite, weight gain, bounding pulses, hypothermia, decreased urine volume and increased urine osmolarity.

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25
Q

Interventions for SIADH

A

-Fluid restriction 500-100 mL/24hrs. ( monitor for fluid overload)
-Drug therapy with vasopressin receptors antagonists (vaptans) and diuretics.
-Treat underlying cause
-Hypertonic saline
-Tube feedings and GI tube med administration consideration? Use saline instead of water.
-Safety: bed alarm, seizure precautions, freq. reorientation

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26
Q

Vaptans (tolvaptan, lixivaptan, satavaptan) treat

A

hyponatremia

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27
Q

Patho: Adrenal cortex production of steroid hormone may decrease as a result of inadequate secretion of adrenocorticotropic hormone (ACTH), dysfunction of the hypothalamic-pituitary control mechanism, or direct problems of adrenal gland tissue

A

Adrenal gland hypofunction

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28
Q

True or False?

Acute adrenocortical insufficiency (adrenal crisis) is life-threatening.

A

True

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29
Q

Common cause of secondary adrenal insufficiency?

A

sudden cessation of glucocorticoid therapy

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30
Q

What condition?

AKA adrenal insufficiency - illness that occurs when the body doesn’t make enough of certain hormones. In this disease, the adrenal glands make too little cortisol and, often too little of another hormone, aldosterone.

A

Addison’s disease

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31
Q

Life threatening event; need for cortisol and aldosterone is greater than available supply. Usually occurs in response to stressful events.

Sx include: profound fatigue, dehydration, Vascular collapse (low BP), renal shutdown, low serum NA+, high Serum K+. hyperpigmentation.

A

Acute adrenal insufficiency/Addisonian crisis

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32
Q

Sx of Addison’s disease

A

bronze pigmentation of skin, changes in distribution of body hair, GI disturbances, weakness, weight loss, postural hypotension, hypoglycemia

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33
Q

What condition?

Hypersecretion of cortisol by adrenal cortex results in this syndrome/disease, hypercortisolism, or excessive androgen production. This can be caused by drug therapy for another health problem. Most common cause is glucocorticoid therapy. Most common non-drug cause is pituitary adenoma. Women are more effected than men.

Pt will have increased appetite & weight gain.

A

Hypercortisolism (Cushing’s disease)

TOO MUCH STEROID

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34
Q

S/sx of Cushing’s disease

A

truncal obesity, moon face, buffalo hump. High fasting glucose. Increased androgen production (acne, more body hair, oligomenorrhea (irregular period) in women. Emotional instability is very common. Poor wound healing.

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35
Q

What hypermetabolic adrenal disorder?

Nonmalignant catecholamine-producing tumors of the adrenal medulla. Tumors produce, store, and release epinephrine and norepi. Overproduction of catecholamines (epi and norepi/fight or flight).

A

Pheochromocytoma

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36
Q

What potential life-threatening event is a pt w/ pheochromocytoma at risk for?

A

Hypertensive crisis - BP 180/120 or greater

Triggered by stressful event - managing stress is VERY important

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37
Q

Tx for Pheochromocytoma

A

-Alpha-adrenergic blockers (doxazosin, tolazoline)
-Removal of tumor

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38
Q

S/sx of Pheochromoctyoma

A

Classic: hypertension, HA, sweating.

Other: flushing, anxiety/panic, palpitations, abdominal pain, dizziness, blurry vision, sx of diabetes, tachy, heart failure.

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39
Q

What condition?

Thyroid cells fail to produce sufficient levels of thyroid hormones (multiple reasons). Everything SLOWS down.

Etiology/Causes Hashimoto’s, thyroid surgery, radioactive iodine treatment.

A

Hypothyroidism

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40
Q

S/sx of hypothyroidism

A

Sleeping 14-16 hrs a day, constipation, cold intolerance, may have difficulty in psychosocial functioning (similar to depression on a surface level).

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41
Q

Tx for hypothyroidism

A

-Replace thyroid hormone (Synthroid (levothyroxine).

Administer on empty stomach. OTC vitamins or minerals, especially calcium containing preps must be avoided for at least 4 hours. Calcium interferes with the absorption.

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42
Q

Why does the patient need to avoid calcium-containing supplements or preps for 4 hours before & after taking Synthroid?

A

Calcium interferes with the absorption.

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43
Q

Myxedema coma is a medical emergency. It is usually precipitated by trauma or illness. What are the s/sx?

A

profound lethargy, muscle weakness, mental decline, hypothermia, hypotension. Facial swelling of lips, eyelids, and tongue.

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44
Q

How is myxedema coma treated?

A

REPLACE THYROID HORMONE IMMEDIATELY. And give supportive care.

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45
Q

What condition?

Too much thyroid hormone. Everything speeds up.

A

hyperthyroidism

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46
Q

Causes hypermetabolism and increased sympathetic nervous system activity. Can also be caused by adenoma (compresses the pituitary causing increased release of hormone), viral infection, excessive iodine or thyroid hormone intake (including long-term amiodarone use). Affects protein, fat, and glucose metabolism.

A

Thyrotoxicosis (thyroid storm)

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47
Q

1st line tx for hyperthyroidism

A

Propylthiouracil (PTU)-1st line: Inhibits production of thyroid hormone

Other forms of tx for hyperthyroidism:
*Drug therapy: Antithyroid drugs (1st line is methimazole), iodine preparations, beta-adrenergic blocking drugs
*Radioactive iodine: Destroys thyroid tissue upon uptake
*Surgical Management: Total or subtotal thyroidectomy

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48
Q

Post op complications of thyroidectomy

A

Hemorrhage, respiratory distress, hypocalcemia and tetany, laryngeal nerve damage, thyroid storm or thyroid crisis, eye and vision problems of Graves’ disease.

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49
Q

Post op monitoring for thyroidectomy

A

hoarseness or stridor, suture line pressure, hypocalcemia and tetany, thyroid storm (rare) happens during surgery.

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50
Q

What is the priority re: post op monitoring for thyroidectomy?

A

Airway is priority. Hoarseness or stridor means there is a blockage.

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51
Q

Why would a patient experience hypocalcemia and/or tetany with a thyroidectomy?

A

The arterial or venous (or both) blood supply to the parathyroid glands is impaired. As a result, tetany can occur within 12 hours of surgery.

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52
Q

S/sx of thyroid storm

LIFE THREATENING condition

A

Tachycardia and arrhythmias, hyperthermia, confusion, coma!

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53
Q

Tx for thyroid storm

A

PTU & supportive care

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54
Q

Complications of diabetes

A

-Poor wound healing
-Hearing loss
-Problems with teeth and gums
-Heart disease
-Retinopathy and glaucoma
-Loss of sensation in the foot, skin dryness, cracking, calluses
-Skin infections, itching, dermopathy, blisters

55
Q

Patho of Diabetic Ketoacidosis/DKA

A

-BGL > 600
-Ketones in urine
-Severe dehydration
-Insulin deficiency
-Metabolic acidosis from ketosis and lactic acidosis
-Depletion of electrolytes from osmotic diuresis

56
Q

Precipitating factors of DKA

A

recent infection, stressful event, didn’t know they were diabetic, didn’t take their meds

57
Q

If a patient has a blood glucose level of 650 and a K+ level of 3.2 what is the priority? What do you treat first glucose or K+? Why?

A

Potassium due to life threatening dysrhythmias.

If you treat w/ insulin first, the Potassium will lower even more. Priority must be Potassium before addressing blood sugar

58
Q

Normal Potassium levels

A

3.6 to 5.6

59
Q

S/sx of DKA

A

3P (polyuria, polydipsia, and polyphagia), Kussmaul breathing, decreased LOC, GI upset (n/v & abd pain), fatigue and confusion, fruity breath.

60
Q

If treating DKA and patient becomes lightheaded or sweaty what is going on?

A

hypoglycemic shock

61
Q

DKA Tx

A

insulin, fluid replacement, electrolyte replacement

WATCH FOR HYPOGLYCEMIA, PRIORITY IS TO CHECK BGL

62
Q

LIFE THREATENING complication: serum hyperosmolarity, dehydration, hyperglycemia. Pts who cannot recognize their thirst or express their need for water. Nonketotic. BGL >700-900

A

Hyperosmolar hyperglycemic syndrome (HHS) - AKA HHNKS

63
Q

What is the priority treatment in a patient with HHS/HHNKS?

A

Give fluids to rehydrate

64
Q

Rapid stimulation of atrial tissue occurs at a rate of 100 to 280 beats/min. Often occurs in young people, esp. women. Fast & regular.

EKG looks like spears.

A

Supraventricular Tachycardia (SVT)

65
Q

Paraoxysmal SVT (PSVT) means

A

comes & goes

66
Q

SVT Assessment: signs & sx depend on duration and rate

A

Non-sustained- asymptomatic
Sustained- weakness, fatigue, SOB, nervousness, anxiety, hypotension, and syncope

67
Q

Potential complications of SVT

A

cardiovascular deterioration (angina, heart failure, and cardiogenic shock)

68
Q

SVT treatment

A

As RN, vagal remover is the first priority for SVT to slow heart rate. Ex: Bearing down, coughing/gagging, ice-cold wet towel on face.

Then adenosine which will stop the heart causing pt to flatline then come back.

Keep defibrillator and resuscitative equipment at bedside.

69
Q

Ventricular dysrhythmias are more life-threatening than atrial dysrhythmias. Left ventricle pumps oxygenated blood through the body to perfuse vital organs and other tissues. What are the four types?

A

premature ventricular complexes, ventricular tachycardia, ventricular fibrillation, and ventricular asystole

70
Q

What type of Ventricular dysrhythmia?

Early ventricular complexes followed by a pause - result of increased irritability of ventricular cells. May be caused by electrolyte imbalance (hypokalemia, hypomagnesemia, hypercalcemia, anesthesia, stress, nicotine, alcohol, hormonal fluctuations (esp. postmenopausal pts)

A

Premature ventricular complexes

71
Q

Notify the provider immediately if you see an increase in frequency of PVCs. There is nothing else we can do as a RN besides monitor pt & changes. A run of PVCs can progress to

A

V-Tach

72
Q

PVC tx includes

A

treat underlying causes, remove potential causes, administer beta blockers if causing pt distress

73
Q

What type of Ventricular dysrhythmia?

Repetitive firing of irritable ventricular ectopic focus, usually at 140 to 180 beats/min. May occur in ischemic heart disease, MI, cardiomyopathy, hypokalemia, hypomagnesemia, valvular heart disease, HF, drug toxicity, and hypotension. Commonly the underlying rhythm prior to V-Fib & cardiac arrest.

EKG looks like tombstones.

A

Ventricular tachycardia (AKA V-Tach)

74
Q

Is V-Tach a shockable rhythm?

A

This is not a shockable rhythm. First priority is to check pt’s pulse. If pulseless V-Tach, then shock.

75
Q

Tx for V-Tach based on ACLS guidelines:

A

Stable- elective cardioversion followed by anti-dysrhythmics
Unstable (w/o pulse)- D Fib

76
Q

What type of Ventricular dysrhythmia?

Electrical chaos in the ventricles. There is no ventricular contraction = no cardiac output = no perfusion.

EKG looks like grass.

A

Ventricular fibrillation (AKA V-Fib)

77
Q

Tx for Ventricular fibrillation (AKA V-Fib)

A

D-Fib the V-Fib!

Emergency care is critical for survival. Defibrillate immediately.

78
Q

Drug therapy for sustained, life-threatening dysrhythmias

A

-Epi 1mg every 3-5min
-Amiodarone, 300mg IVP, then repeat 150mg
-Lidocaine 1-1.5mg/kg (Amiodarone is Preferred to Lidocaine)

-Epi is a vasopressor–> increases coronary perfusion pressure
-Amiodarone slows nerve signals in the heart–> Improves return of spontaneous circulation (ROSC)
-Lidocaine used as an antiarrhythmic medication blocks sodium channels

79
Q

What type of Ventricular dysrhythmia?

Complete absence of any ventricular rhythm. Full cardiac arrest = pt has no bp, cardiac output, or perfusion. Results from myocardial hypoxia (advanced HF), severe hyperkalemia, and acidosis.

A

Ventricular asystole (AKA ventricular standstill)

FLATLINE

80
Q

Is asystole a shockable rhythm?

A

No, CPR is the intervention

81
Q

Basic Cardiac Life Support (BCLS): Describe CAB

A

C: Compressions 100-120/minute. Allow full chest recoil.
A: Maintain patent airway.
B: Ventilate w/ mouth to mask device. Breaths at a rate of 10-12/minute or 8-10/minute w/ advanced airway in place.

82
Q

What rhythms are shockable?

A

V-Fib & pulseless V-Tach

83
Q

What condition?

Microbial infection involving the endocardium (most common streptococcus viridans or staphylococcus aureas). Bacterial vegetations develop on valves, which may also attract platelets and fibrin (causing clots!). Large vegetations may obstruct blood flow and may cause stenosis.

Risk factors: Hx of IV drug abuse. Valve replacement recipients. Systemic infections. Structural cardiac defects.

A

Infective endocarditis

84
Q

What diagnostics are used for Infective endocarditis?

Most reliable criteria for diagnosis

A

-Positive blood cultures
-New regurgitant murmur
-Evidence of endocardial involvement by echocardiography/TEE

85
Q

Transesophageal echocardiography (TEE) is an ultrasound technology that provides highly detailed images of the heart and its internal structures. Our heart experts use TEEto detect blood clots, evaluate heart valves, and guide treatment for arrhythmias (abnormal heartbeats) and many other heart conditions.

Why use a TEE?

A

Gives a more clear view of the heart

86
Q

What condition?

Inflammation/alteration of pericardium. Acute versus chronic.
Infective organisms: bacteria, viruses, or fungi.

A

Pericarditis

87
Q

What is the classic sign of pericarditis?

A

When pt is supine pain is increased, sitting up pt finds some relief

Different from MI in that the pain is constant & feels like elephant is standing on chest

88
Q

Interventions & main focus for pericarditis?

A

Interventions: If pt is experiencing chest pain, seat them up and lean forward for comfort.

Main focus: promote comfort and pain relief and treat the underlying cause before severe complications occur.

89
Q

Pts w/ pericarditis must be monitored for pericardial effusion (excessive fluid in the pericardial cavity). Can lead to

A

Cardiac tamponade

This is an extreme emergency!

90
Q

What are cardiac tamponade findings?

A

-JVD
-Paradoxical pulse (pulsus paradoxus)- SBP at least 10 mmHg higher on expiration than on inspiration
-Decreased cardiac output
-Muffled heart sounds
-Circulatory collapse

91
Q

What is Beck’s Triad?

-Requires hemodynamic monitoring-

A

hypotension, elevated systemic pressure (JVD), muffled heart sounds

92
Q

Permanent localized dilation of artery, enlarging artery to twice its normal diameter.

Types: fusiform vs saccular? Dissecting (aortic dissection), abdominal aortic, thoracic aortic .

Atherosclerosis is the most common cause. Also HTN, HLD, and smoking.

A

Aneurysm of the central arteries

93
Q

S/sx of Abdominal Aortic Aneurysm (AAA)

A

*Commonly asymptomatic
*Pain related to AAA is usually steady with a gnawing quality, unaffected by movement, may last for hours or days.
*Gnawing pain in abdomen, flank, or back
*Abdominal mass is pulsatile- auscultate for bruit but avoid palpating, if suspicious!

94
Q

What would be an indication in vital signs that your patient has a ruptured AAA?

A

-hypotension & tachycardia

95
Q

Aneurysm rupture is most frequent complication and is life threatening. Sx are severe and sudden pain in back. Pts are at risk for

A

hypovolemic shock caused by hemorrhage

(Hypovolemic shock! → RAAS system kicks in; increasing BP due to massive vasoconstriction)

96
Q

Signs/symptoms of AAA rupture

A

Hypotension, diaphoresis, decreased LOC, oliguria, decreased or absent pulses distal to the aneurysm, and dysrhythmias

97
Q

Signs/symptoms of TAA rupture

A

sudden excruciating back or chest pain

98
Q

Aortic Dissection is a sudden tear in aortic intima; blood enters aortic wall. Highly lethal, emergent situation. Can occur anywhere, but the ascending and descending thoracic aorta are most common.

S/sx include:

A

*Pain depends on location: Common pain in the anterior chest, back, neck, throat, jaw, or teeth. Pain described as tearing, ripping, stabbing.
*Diaphoresis, nausea, apprehension, pallor, and rapid/weak pulse, neurological changes.

99
Q

Emergency care goals for Aortic Dissection

A

-Pain management (IV morphine).
-Insert 2 large IV. Patient will require fluid administration and medications for BP control.
-Manage HR and BP. SBP goal 100-120. Administer IV beta blockers (esmolol), Nitroprusside, and/or nicardipine.

100
Q

Shock is the inadequate perfusion of tissues.

What are the types of shock?

A

Hypovolemic
Cardiogenic
Distributive
Obstructive

101
Q

What type of shock?

Loss of circulating volume: Causes mean arterial pressure (MAP) to decrease and inadequate total body oxygenation. Results in ineffective tissue perfusion.

Commonly caused by hemorrhage and dehydration.

A

Hypovolemic shock

102
Q

What type of shock?

Blood volume is not lost, fluid is distributed to the interstitial tissues.

A

Distributive shock

103
Q

What type of shock?

Hypersensitive reaction to an antigen resulting in inadequate perfusion to the tissues. Pt presents w/ acute onset, hypotension, tachycardia, respiratory distress, and skin can have erythema and lesions.

A

Anaphylactic shock

104
Q

What type of shock?

Pump is not effective, decrease in cardiac output = decreased MAP. Pt presents w/ hypotension, tachycardia, and follows a cardiac event/injury.

A

Cardiogenic shock

105
Q

Hypovolemic shock tx

A

Fluid bolus, blood unit. (do not put fluids on a pump, just open it up all the way and maybe put a bp cuff on it so its faster)

106
Q

Stages of Hypovolemic shock

A

Initial
Nonprogressive/Compensatory
Progressive
Refractory

Shock syndromes will continue to progress throughout these stages if the aggravator remains uncorrected

107
Q

What stage of Hypovolemic Shock?

*Baseline MAP decreased by <10 mm Hg
*Heart and respiratory rate increased from baseline, or slight increase in diastolic blood pressure
*Adaptive responses (compensatory mechanisms) of vascular constriction, increased heart rate

Compensatory mechanisms are still effective in this stage: Cardiac output and MAP remain “normal.” Vital organ function not disrupted, however may start to see presence of lactic acid

A

Initial stage

108
Q

What stage of Hypovolemic Shock?

*MAP decreases by 10 to 15 mm Hg
*Kidney and hormonal adaptive mechanisms activated: Renin, ADH, aldosterone, epinephrine and norepinephrine = ?
*Tissue hypoxia begins in non-vital organs (skin, GI tract)
*Acidosis and hyperkalemia
*Stopping conditions that started shock and supportive interventions can prevent shock from progressing: Reversible damage at this stage

A

Nonprogressive/compensatory Stage

109
Q

S/sx of nonprogressive/compensatory stage of Hypovolemic Shock

A

-Thirst and anxiety are subjective changes
-Urine output decreases
-Blood vessel constriction increases

110
Q

What stage of Hypovolemic Shock?

*Sustained decrease in MAP of >20 mm Hg from baseline
*Compensatory mechanisms are functioning, but not able to deliver sufficient oxygen to VITAL organs
*Vital organs develop hypoxia
*Less vital organs may become ischemic
*Life-threatening emergency

A

Progressive stage

111
Q

S/sx of progressive stage of Hypovolemic Shock

A

*Signs and symptoms of worsening decreased tissue perfusion
*Rapid, low pulse; low BP; pallor; cool, moist skin; anuria, decrease in oxygen saturation
*Patient may feel sense of impending doom
*Low serum pH, rising lactic acid and potassium levels

112
Q

How quickly do the conditions causing shock need to be corrected?

A

within 1 hr of the progressive stage onset

113
Q

What stage of Hypovolemic Shock?

*Too little oxygen reaches tissues; cell death and tissue damage result
*Vital organs have extensive damage = **cannot respond properly to interventions: Rapid loss of consciousness, nonpalpable pulse, cold, dusky extremities; slow, shallow respirations; unmeasurable oxygen saturation
*MODS will result, as metabolites and enzymes damage vital organs

A

Refractory stage

TOO LATE

114
Q

What condition?

A systemic response to an infection that causes tissue damage, organ failure, and death if not treated properly

A

Sepsis

115
Q

A subset of sepsis. Associated with SIRS (Systemic Inflammatory Response Syndrome) & MODS. It is the most common form of distributive shock!

A

Septic shock

116
Q

What is the most common form of distributive shock?

A

septic shock

117
Q

What is the earliest stage of sepsis?

A

Sepsis/Systemic Inflammatory Response Syndrome (SIRS)

118
Q

SIRS Criteria: (≥2 meets SIRS definition)

A

*Temp >38°C (100.4°F) or <36°C (96.8°F)
*Heart rate >90
*Respiratory rate >20 or PaCO₂ <32 mm Hg
*WBC >12,000/mm³, <4,000/mm³, or >10% bands

119
Q

SIRS + suspects/present source of infection =

A

SEPSIS

120
Q

The big difference between severe sepsis and septic shock is

A

refractory hypotension

121
Q

Sepsis & septic shock assessment: Pt will appear

A

decreased patience, restless & fidgety

122
Q

Sepsis treatment bundle includes

A
  1. Measure lactate level:
    -Remeasure lactate if initial lactate level is >2mmol/L
    -A lactate ≥4 mmol/L is considered the cutoff value for the diagnosis of severe sepsis
  2. Obtain blood cultures before administering antibiotics
  3. Administer broad-spectrum antibiotics
  4. Begin rapid administration of 30 mL/kg crystalloid for hypotension or lactate 4 mmol/L and greater
  5. Apply vasopressors if hypotensive during or after fluid resuscitation to maintain a MAP of at least 65
123
Q

Why does a foley need to be placed?

A

To measure I&Os. Kidneys are princesses. They are the first organs to go.

124
Q

Acute Coronary Syndrome/ACS includes

A

unstable angina & acute myocardial infarction (heart attack)

125
Q

Nitro administration steps

A

Place 1 tablet placed under the tongue or between the cheek and gum at the first sign of an angina attack. 1 tablet may be used every 5 minutes as needed, for up to 15 minutes. Do not take more than 3 tablets in 15 minutes.

CALL EMS after administration of 2nd tablet. Notify the provider/EMS after the first dose if no symptom improvement after 5 min. Continue giving the next two doses of Nitro.

126
Q

Myocardial tissue abruptly and severely deprived of oxygen. Most serious ACS.

A

Myocardial infarction (heart attack)

127
Q

What is MONA?

A

Morphine, O2, Nitro, Aspirin

Morphine alleviates pain, while decreasing the oxygen demand of the myocardium

Have pt chew the aspirin -325mg

128
Q

NSTEMI= Non ST elevation MI
Some ischemia may be present, troponin will be elevated. Initially troponin may be normal, then elevates 3-12 hours later.

STEMI= ST elevation MI
Ischemic changes leading to necrosis. Occlusion of arteries.

In order to know if there is ST elevation, you need a

A

12 lead EKG

Obtain within 10 minutes of the patient’s presentation of chest pain

129
Q

What labs will be elevated (ACS)?

A

Troponin & BNP

130
Q

A patient who presented with chest pain and ST elevation on their 12-lead EKG. The provider tells you that they were not able to achieve reperfusion in the occluded vessels with percutaneous coronary intervention (PCI). What do you think the next step is?

A

OR for CABG

131
Q

After CABG, What do you do if the chest tube fills with excessive blood?

A

Immediately contact the provider

132
Q

CABG Pre-op Care

A

*Elective versus emergency surgery may impact planning.
*Sternal wound infection is a potential complication
*Shower with 4% chlorhexidine gluconate (CHG)
*Surgical prep – clipping hair and topical CHG
*Prophylactic antibiotics administered 1 hour before the procedure
*Assess anxiety, fears, and coping

133
Q

CABG Post-op Care

A

*Pt will be transferred to an open-heart surgery unit
*Assess for dysrhythmias (bradycardia, atrial fibrillation, and heart block)
*Manage Fluid & Electrolyte balance
*Report any of the following complications: Fluid and electrolyte imbalance, hypotension, hypothermia, hypertension, bleeding, cardiac tamponade, decreased/change in level of consciousness, anginal pain.
*Hypotension: large concern – may lead to collapse of the graft.
*Hypothermia: common problem after surgery. Initiate rewarming if temp is below (96.8F or 36C). Use warming blankets, lights, etc.
*Avoid shivering! Results in metabolic acidosis > increased myocardial O2 demand, and hypoxia. Also promotes vasoconstriction and hypertension. Rewarm no faster than 1C per hour.
*Hypertension (SBP >140-150). May cause suture bleeding. Nitroprusside commonly used to manage.
*Maintain patency of pleural and mediastinal chest tubes

CH2 (8 decks)

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