Need to know Flashcards

1
Q

RA (preload) normal range & definition

A

The pressure in the RA, reflecting the amount of blood returning to the heart and the ability of the heart to pump the blood into the arterial system

Normal range 2-6mmHg

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2
Q

CVP (preload) normal range and definition

A

Reflects the amount of blood returning to the heart and is often a good approximation of RA

Normal range 2-6mmHg

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3
Q

RV pressure normal range and definition

A

a direct measure that indicates RV function and general fluid status. Increased RVP may indicate pulmonary HTN, RV failure, or CHF.

This pressure can be estimated in an echocardiogram

normal range 15-30mmHg (systolic)
2-5mmHg (diastolic)

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4
Q

PA pressure normal range and definition

A

Reflects BP in pulm a. increased pulm a. pressure can indicate: a L–>R cardiac shunt, pulm a. hypertension, COPD, or emphysema, pulmonary embolus, pulmonary edema, and cardiac compression

normal range 20-30mmHg (systolic)
5-10mmHg (diastolic)
Mean 10-20mmHg

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5
Q

Pulmonary capillary wedge pressure (PCWP, PAOP, PAWP) preload normal range and definition

A

Measures the LV pressure when the mitral valve is open. High PCWP can indicate LV failure, mitral valve pathology, cardiac insufficiency, and cardiac compression (preload)

Normal range 8-12mmHg

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6
Q

Systemic vascular resistance (SVR) afterload definition and normal range

A

The measurement of resistance or impediment of the systemic vascular bed to blood flow. An increased SVR can be caused by vasoconstrictor, hypovolemia, or late septic shock. A decreased SVR can be caused by early septic shock, vasodilators, morphine, nitrates, or hypercarbia

Normal range 900-1400(dyne*sec)/cm^5

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7
Q

Cardiac output (CO) definition and normal range (contractility)

A

The volume of blood pumped by the heart in 1min. increased CO indicates high circulating volume. Decreased CO indicates a decrease in circulating volume or a decrease in the strength of ventricular contraction.

Normal range 4.8-6.4L/min

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8
Q

Cardiac index (CI) (contractility) definition and normal range

A

The amount of blood pumped by the heart, per min, per meter square of body surface area

Normal range 2.5-4.2 L/min/m^2

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9
Q

Saturation of mixed venous oxygen (SvO2) definition and normal range

A

The estimate of the amount of oxygen returning to the cardiopulm circulation. reflective of the patient’s ability to balance O2 supply and demand at the tissue level

Norma range 70-75% (60-80%)

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10
Q

ABG Normal pH

A

7.35-7.45
If increased = alkalosis state
if decreased = acidosis state

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11
Q

ABG normal PaCO2

A

35-45 mmHg
If increased = respiratory acidosis
If decreased = respiratory alkalosis

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12
Q

ABG normal HCO3-

A

22-26 mEq/L
If increased = metabolic alkalosis
If decreased = metabolic acidosis

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13
Q

Goal tidal volume (TB)

A

6-8mL/kg

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14
Q

What should you start PEEP at?

A

5

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15
Q

characteristics of hypovolemic shock + treatment

A
  • multiple organ failure d/t inadequate circulating volume
  • All cardiac pressures are less than normal except SVR (increased)
  • treatment - treat underlying cause (usually dehydration), volume replacement, transfuse PRN
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16
Q

characteristics of cardiogenic shock + treatment

A
  • inadequate tissue perfusion secondary to loss of contractile function
  • CVP, PAOP, SVR = increased
  • CO, SvO2 = decreased
  • treatment: treat underlying cause, support CO with inotropic agent, support O2
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17
Q

three types of distributive shock + Characteristics

A
  1. septic shock
  2. anaphylactic shock
  3. neurogenic shock
  • systemic event –> loss of moral smooth muscle vascular response –> direct vasodilating effect
  • all cardiac pressures are below normal values
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18
Q

Anaphylactic shock treatment

A
  • volume replacement
  • epinephrine
  • glucocorticoids
  • antihistamine (prn)
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19
Q

neurogenic shock treatment

A
  • volume replacement + alpha agonists
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20
Q

obstructive shock characteristics + treatment

A
  • obstructed ventricular filling or filling of the great vessels –> inability to produce adequate CO
  • CVP, SVR = increased
  • PAOP, CO, SvO2 = decreased
  • treatment: volume replacement then relieve obstruction
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21
Q

Septic shock characteristics + management

A
  • dysreglated response to infection –> severe vasodilation + decreased tissue perfusion –> organ dysfunction
  • w/in 3 hours - measure lactate, blood cultures, broad-spectrum abx, 30mL/kg crystalloid for hypoT or lactate >/= 4
  • w/in 6 hrs - vasopressors (levofed or dopamine) to maintain MAP >/=65, reassess volume status, re-measure lactate if initial lactate was elevated
  • goals of treatment - CVP 8-12, MAP >/= 65, urine output >/= 0.5mL/kg/hr, ScvO2 > 70%
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22
Q

Normal ranges for ABG

A

pH 7.35-7.45
PaCO2 35-45 mmHg
HCO3 22-26 mEq/L

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23
Q

Rule of 9s

A
  • Head and neck 9%
  • upper limbs 9% each
  • trunk 36%
  • genitalia 1%
  • lower limbs 18% each
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24
Q

Mechanical vent settings

A
  • RR 4-20 depending on reason for intubation
  • TV (volume delivered w/ each breath) 5-8
  • FiO2 21-100% maintain PaO2 of at least 60mmHg
  • I:E ration 1:2 or 1-1.5 (incr for COPD pt)
  • PEEP (alveolar pressure) 5
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25
Q

Diagnostic criteria for diabetes

A
  • A1C >/= 6.5 with repeat A1C recommended in asymptomatic adults with glucose </= 200mg/dL. No repeat if >/=200
  • plasma glucose - fasting glucose >/= 126mg/dL on 2 occasions
  • random glucose >/-200 with symptoms
  • oral glucose tolerance test - 2h plasma glucose >/= 200 after 75g glucose load
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26
Q

Treatment for type 1 DM

A
  • insulin replacement - basal insulin supplemented with premeal short or ultra-short acting insulin
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27
Q

Treatment for type 2 DM

A
  • weight loss in obese pts
  • oral therapy - metformin or thiazolidinediones
  • stimulate beta cells with sulfonylureas or non-sulfonylurea insulin secretagogues
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28
Q

Targets for glycemic control

A
  • A1C < 6 or <7 (ADA Goal)
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29
Q

Metformin – why do you use it, MOA, and side effects

A
  • First-line med unless contraindicated for type 2 DM
  • Use - A1C reduction
  • Insulin sensitizer, no hypoglycemic risk when used solo
  • Risk for lactic acidosis, it B12 deficiency
  • stop using 48h before using contrast dye
  • contraindicated in decreased renal blood flow
30
Q

Thiazolidinedione (TZD glitazones) - why do you use it, MOA, side effects

A
  • pioglitazone or rosiglitazone
  • A1C reduction
  • insulin sensitizer, no risk for hypoglycemia
  • risk of edema, hepatic toxicity (monitor ALT periodically)
  • DO NOT USE IN HEART FAILURE (there is not glitz or glam with HF)
31
Q

Sulfonylurea – why do you use it, MOA, side effects

A
  • Glipizide, glyburide, glimepiride
  • A1C reduction (often considered in addition to metformin)
  • increases insulin release, HYPOGLYCEMIA RISK (major cause esp if NPO)
32
Q

Dipeptidyl peptidase-4 (DPP-4) inhibitor – why do you use it, MOA, side effects

A
  • sitagliptin, saxagliptin, linagliptin, alogliptin
  • A1C reduction
  • increases insulin release, largely acts on postprandial blood glucose, minimal hypoglycemia risk
  • risk of pancreatitis, unexplained joint aches
33
Q

GLP-1 agonist

A
  • Exenatide, liraglutide, albiglutide
  • A1C reduction
  • increases insulin release, postprandial, ,minimal hypoglycemia risk
  • slows gastric emptying, can contribute to weight loss
  • risk of pancreatitis, N/V
  • DO NOT USE IN GASTROPARESIS
34
Q

Sodium glucose cotransporter - 2 (SGLT2) inhibitor

A
  • canagliflozin, dapagliflozin, empagliflozin
  • A1C reduction
  • increases amt of glucose excreted in urine, postprandial, hypoglycemia risk
  • risk of genital mycotic infection, UTI, increased urination
  • FDA advisory about DKA and urosepsis risk
35
Q

Short-acting, rapid onset insulin – Lispro (Humalog) – onset, peak, duration

A
  • onset 15-30min (give within 15min or right after meals)
  • peak 30min-2.5hrs
  • duration 3-6.5 hours
36
Q

Short-acting, rapid onset – Aspart (NovoLog) – onset, peak, duration

A
  • onset 10-20min (give 5-10min before meals)
  • peak 1-3 hrs
  • duration 3-5 hrs
37
Q

Short-acting, rapid onset – Insulin glulisine (Apidra) – onset, peak, duration

A
  • onset 10-15min (give w/in 15min or right after meals)
  • peak 1-1.5 hrs
  • duration 3.5 hrs
38
Q

Short-acting regular insulin (Humulin, Novolin) – onset, peak, duration

A
  • onset 30min - 1h (give 30min before meal)
  • peak 2-3 hrs
  • duration 4-6hrs
39
Q

Intermediate-acting (NPH) – onset, peak, duration

A
  • onset 1-2 hrs
  • peak 6-14hrs
  • duration 16-24hrs
40
Q

Long-acting (insulin glargine (Lantus)) – onset, peak, duration

A
  • onset 1h after injection
  • peak none
  • duration >/= 24h
41
Q

Long-acting (insulin detemir (Levemir)) – onset, peak, duration

A
  • onset 1-2 h
  • peak 6-8 h
  • duration is dose-dependent 12h at 0.2 units/kg, 20h at 0.4 units/kg
42
Q

Converting IV to SC Insulin

A
  • wait until the patient can tolerate solid food
  • continue IV insulin for 2-4hrs after the first SC dose is given
  • Do not switch to oral agents from IV insulin in type 2 diabetics
43
Q

DKA patho, symptoms, and treatment (typically type 1 diabetes)

A
  • patho: ketoacidosis
  • symptoms: polyuria, polydipsia, dehydration, N/V, abdominal pain, ileus, Kussmaul’s respirations, changes in mental status
  • treatment: isotonic fluid replacement (10-14mL/kg/hr) after 1L bolus, 10 units regular insulin followed by IV drip (0.1 unit/kg/h) until anion gap is normal. If anion gap is high and glucose is >/=250 add dextrose to fluids. treat precipitating event
44
Q

How to calculate anion gap

A

([Na] + [K]) - ([Cl] + [HCO3])
> 11 = + anion gap

45
Q

Hyperosmolar nonketotic state (HNS) - typically type 2 diabetes symptoms and treatment

A
  • patho: without ketoacidosis –> osmotic diuresis + volume depletion + electrolyte disturbance
    symptoms: dehydration, glucose > 600, increased serum osmolality
  • treatment: isotonic fluid replacement, followed by .45% normal saline, treat electrolyte abnormalities, 10 units regular insulin by IV (0.5-0.1 unit/kg/hr), treat precipitating event
46
Q

General s/s of hypothyroidism

A
  • thick, dry skin
  • hyporeflexia
  • slow thought processing
  • small weight gain, largely fluid
  • constipation
  • menorrhagia
  • easily cold
47
Q

Hashimoto’s thyroiditis

A

autoimmune destruction of the thyroid with lymphatic infiltration. occurs after a period of hyperthyroidism – hypothyroidism

48
Q

Post-radioactive iodine treatment/surgical removal leads to hypothyroidism

A

typically results s/p Grave’s disease treatment, or thyroid cancer treatment

49
Q

Pituitary or hypothalamic dysfunction

A

typically see decrease in T4 and normal/decreased/slightly elevated TSH

50
Q

Myxedema crisis s/s and treatment

A
  • hypothermia, hypotension, hypoventilation, changes in mental status (coma), hyponatremia, hypoglycemia
  • typically results from infection, major cardiopulm disease, or major neuro disease
  • treatment - 5-8mcg/kg T4 IV initially then 50-100 mcg IV daily
51
Q

Acute care focused diagnosis and treatment for hypothyroidism

A
  • Diagnosis - decreased T4, increased TSH
  • Treatment - Levothyroxine 1.5-1.7mcg/kg/day. Need to increase dose in pregnancy
    Follow up TSH in 4-6 weeks and titrate to euthyroidism
52
Q

General s/s for hyperthyroidism

A

skin - smooth, silky
reflexes - hyperreflexia
mentation - mind racing
weight loss
frequent, low volume, loose stool
oligomenorrhea
heat intolerance (always warm)

53
Q

Common etiologies for hyperthyroidism

A

Grave’s disease
thyroiditis
toxic adenomas
TSH secreting pituitary tumor
select meds - amiodarone, interferon

54
Q

Grave’s Disease s/s and treatment

A

autoimmune, multisystem presentation including exophthalmos, tachycardia, proximal muscle weakness, and goiter
Treatment - antithyroid drugs (methimazole or radioactive iodine) or surgical removal

55
Q

Thyroid storm s/s and treatment

A

delirium, systolic hypertension (wide pulse pressure and decreased MAP), hyperthermia
treatment - beta blocker, PTU or methimazole, iopanoic or iodine, consider steroids

56
Q

How do you calculate pulse pressure? what does the number tell you

A

systolic - diastolic = pulse pressure
>40-60 = widend pulse pressure

57
Q

Treatment for hyperthyroidism

A

beta-blocker (propranolol preferred)

58
Q

Adrenal cortex hormones

A

cortisol
aldosterone
androgens

59
Q

Adrenal medulla hormones

A

Epinephrine
Norepinephine
Dopamine

60
Q

Adrenal cortex disorders

A

Cushing’s syndrome
Addison’s disease

61
Q

Cushing’s syndrome

A

Excess cortisol
typically caused by pituitary adenoma
s/s - central obesity, round faces, purple striae, hypertension, hirsutism, poor wound healing
Diagnostic eval - dexamethasone suppression test (give 1mg of dexa at 11pm, measure serum cortisol at 8am)
Treatment - remove source of excess, manage consequence (hypoT, hypokalemia, hyperglycemia)

62
Q

Addison’s disease

A

Decreased cortisol production
Primary - damage to the adrenal cortex
Secondary - pituitary failure to release ACTH (sudden withdrawal of corticosteroids)
s/s - weakness, orthostatic hypoT
Diagnostic eval - Cosyntropin (ACTH) stimulation test

63
Q

Treatment for acute adrenal insufficiency

A

Volume resuscitation with NSS
Dexamethasone 2-4mg IV Q6H + fludrocortisone 50mcg IV daily prior to ACTH stimulation test, then hydrocortisone 50-100 mg IV q 6-8hrs

64
Q

Treatment for chronic adrenal insufficiency

A

hydrocortisone 20-30mg PO daily
prednisone 15mg AM, 10mg PM
dexamethasone 4mg IM prefilled for emergencies

65
Q

Adrenal medulla disorders

A

pheochromocytoma

66
Q

Pheochromocytoma

A

benign hormone-producing tumor of the adrenal medulla causing excess release of catecholamines

67
Q

Signs and symptoms of pheochromocytoma

A

5Ps
pressure (persistent hypertension)
pain (headache)
palpitations (tachy + tremors)
perspiration (profuse with flushing)
pallor (secondary to vasoconstriction)

68
Q

Lab abnormalities for pheochromocytoma

A

increased urinary metanephrines increased urinary vanillylmandelic acid

69
Q

Treatment for pheochromocytoma

A

control CV status w/ alpha blockers followed by beta blockers until tumor removal
preoperative volume expansion to prevent post op hypotension

70
Q

Disorders of ADH

A

Diabetes insipidus
syndrome of inappropriate AHD (SIADH)

71
Q

Diabetes insipidus

A

insufficient ADH or decreased sensitivity to ADH
Central - c/b damage to pit gland
Nephrogenic - kidney doesn’t respond to ADH
Plasma free water depletion –> serum hypernatremia + serum hyperosmolality. Opposite for urine
treatment - fluid replacement, maybe replace ADH