Chapter 5 - Water, Electrolyte, Acid-Base, and Hemodynamic Disorders Flashcards
0
Q
What are the major ECF and ICF cations?
A
Na+, K+: major ECF and ICF cations, respectively
1
Q
Describe how water compartment sizes compare to one another.
A
Compartment sizes: ICF > ECF; interstitial > vascular
2
Q
Describe how plasma osmolality differs between isotonic, hypotonic and hypertonic states.
A
Isotonic, hypotonic, hypertonic: normal POsm, ↓POsm, ↑POsm, respectively
3
Q
What is the plasma osmolality equation?
A
POsm = 2 (serum Na+) + serum glucose/18 + serum BUN/2.8 = 275–295 mOsm/kg
4
Q
What is the equation for effective osmolality? How does this equation differ from the plasma osmolality equation?
A
EOsm = 2 (serum Na+) + serum glucose/18; urea diffuses between ECF and ICF
5
Q
Describe two features of osmosis.
A
Osmosis: H2O moves between ECF and ICF; Na+ controlled movement
6
Q
Describe osmosis in hyponatremia.
A
Hyponatremia: H2O moves from ECF to ICF (expanded)
7
Q
Describe osmosis in hypernatremia/hyperglycemia.
A
Hypernatremia/hyperglycemia: H2O moves from ICF (contracted) to ECF
8
Q
What does the serum sodium concentration approximate?
A
Serum Na+ ~ TBNa+/TBW
9
Q
List four clinical findings with decreased total body sodium.
A
↓TBNa+: ↓skin turgor, dry mucous membranes, ↓blood pressure, ↑pulse when sitting/standing up
10
Q
List two clinical findings with increased total body sodium.
A
↑TBNa+: pitting edema, body cavity effusions
11
Q
How does an increase in total body sodium affect Starling forces?
A
↑TBNa+: alteration of Starling forces (↑HP and/or ↓OP)
12
Q
What do Starling forces do?
A
Starling forces: control fluid movements in ECF compartment
13
Q
What is the most common cause of weight gain in a hospitalized person?
A
↑Patient weight in hospital: ↑TBNa+
14
Q
How does an isotonic loss or gain affect serum sodium concentration?
A
Isotonic loss or gain: serum Na+ normal
15
Q
If there is a gain in fluid, how does the ECF respond?
A
Gain in fluid: ECF always expands
16
Q
If there is a loss of fluid, how does the ECF respond?
A
Loss in fluid: ECF always contracts
17
Q
How does an isotonic loss of fluid affect TBNa+ and TBW? Provide an example.
A
Isotonic loss: ↓TBNa+/↓TBW; secretory diarrhea
18
Q
What is the treatment for an isotonic loss of fluid?
A
Rx isotonic loss: normal saline
19
Q
What results from a normal saline infusion?
A
Normal saline: ↑BP; equilibrates between vascular/interstitial space
20
Q
How does an isotonic gain of fluid affect TBNa+ and TBW? Provide an example.
A
Isotonic gain: ↑TBNa+/↑TBW; ↑↑isotonic saline infusion
21
Q
What is the treatment for an isotonic gain of fluid?
A
Rx isotonic gain: restrict water; loop diuretics
22
Q
What is always present in hypotonic disorders? How does the ICF respond?
A
Hypotonic disorders: hyponatremia always present; ICF expansion
23
Q
How does a hypertonic loss of fluid affect TBNa+ and TBW?
A
Hypertonic loss: ↓↓TBNa+/↓TBW
24
List three examples of a hypertonic loss of fluid.
Hypertonic loss: loop diuretics/thiazides (excessive), Addison, ↓21-hydroxylase
25
What is the treatment for a hypertonic loss of fluid?
Rx hypertonic loss: infuse normal saline or equivalent
26
What may result in central pontine myelinolysis?
Central pontine myelinolysis: rapid correction of hyponatremia with saline in alcoholic
27
How does a hypotonic gain of water affect TBNa+ and TBW? Give two examples.
Hypotonic gain water: TBNa+/↑↑TBW; SIADH, compulsive water drinker
28
What is the treatment for a hypotonic gain of water?
Rx hypotonic gain water: restrict water
29
How does a hypotonic gain of Na+ affect TBNa+ and TBW?
Hypotonic gain water + Na+: ↑TBNa+/↑↑TBW
30
List three different pitting edema states. How is cardiac output affected?
Pitting edema states: RHF, cirrhosis, nephrotic syndrome; ↓cardiac output
31
What is the treatment for pitting edema states?
Rx pitting edema states: restrict water/sodium; diuretics
32
Name two hypertonic disorders. How does the ICF respond?
Hypertonic disorder: hypernatremia/hyperglycemia; ICF contraction
33
How does the ICF always respond in hypertonic conditions?
Hypertonic conditions: ICF always contracted
34
How does a hypotonic loss of Na+ affect TBNa+ and TBW?
Hypotonic loss Na+ + water: ↓TBNa+/↓↓TBW
35
List four examples of hypotonic loss of Na+.
Hypotonic loss Na+ + water: osmotic diuresis/diarrhea, sweating, vomiting
36
How does loss of pure water affect TBNa+ and TBW?
Hypotonic loss water: TBNa+/↓↓TBW
37
List two examples of loss of pure water.
Hypotonic loss water: diabetes insipidus; insensible water loss
38
How does hypertonic gain of Na+ affect TBNa+ and TBW?
Hypertonic gain Na+: ↑↑TBNa+/↑TBW
39
Provide two examples of hypertonic gain of Na+.
Hypertonic gain: ↑NaHCO3, Na+-containing antibiotic infused
40
What is DKA and what does it cause?
DKA: hypertonic state with dilutional hyponatremia; osmotic diuresis
41
What occurs in the proximal tubule?
Proximal tubule: reabsorb Na+, reclaim HCO3−
42
How does decreased EABV affect FF, PO and PA?
↓EABV → ↑FF → PO > PH
43
How does increased EABV affect FF, PH and PO?
↑EABV → ↓FF → PH > PO
44
What is reclaiming HCO3-?
Reclaiming HCO3−: retrieving filtered HCO3−
45
What is the effect of decreasing the threshold for reclaiming HCO3-? Provide an example.
↓Threshold for reclaiming HCO3− (carbonic anhydrase inhibitor): lose HCO3− in urine, ↓HCO3− in blood (metabolic acidosis)
46
What is the effect of increasing the threshold for HCO3-? Provide an example.
↑Threshold for reclaiming HCO3− (vomiting): reclaim more HCO3− from urine, ↑HCO3− in blood (metabolic alkalosis)
47
Heavy metal poisoning results in what?
Heavy metal poisoning: Fanconi syndrome
48
What are the functions of Na+-K+- 2Cl− symporter?
Na+-K+- 2Cl− symporter: generates fH2O, reabsorbs Ca2+
49
What type of water does ADH reabsorbs?
ADH: only reabsorbs fH2O not oH2O
50
What do loop diuretics do?
Cl− binding site in Na+-K+-Cl− symporter: inhibited by loop diuretics
51
What electrolyte abnormalities may loop diuretics produce?
Loop diuretic: hyponatremia, hypokalemia, metabolic alkalosis
52
What do thiazides do?
Thiazide: inhibits Cl− site Na+-Cl− symporter; ↑Ca2+ reabsorption
53
How do thiazides affect electrolytes?
Thiazide: ↓serum Na+, ↓K+; ↑HCO3− (metabolic alkalosis), ↑Ca2+ (if ↑PTH)
54
How do thiazides affect Na+ and K+? What is there danger of?
Thiazides: ↑Na+ reabsorption, ↑K+ excretion (danger of hypokalemia)
55
How does hypokalemia affect H+ and HCO3-? What is there risk for?
Hypokalemia: ↑H+ excretion → ↑HCO3− in blood; risk for metabolic alkalosis
56
Name two potassium-sparing diuretics.
Amiloride, triamterene: K+-sparing diuretics
57
How do proximally-acting diuretics affect distal delivery of Na+? What results from this effect?
↑Distal delivery Na+ (proximally-acting diuretics): ↓K+, metabolic alkalosis
58
Give an example of a titratable acid.
Titratable acid: NaH2PO4
59
What is the most effective way of removing H+?
NH4Cl: most effective way of removing H+
60
What does the H+-K+-ATPase pump excrete and regenerate?
H+-K+-ATPase pump: excretes excess H+; regenerates HCO3−
61
What is spironolactone and what does it do?
Spironolactone: aldosterone inhibitor; spares K+
62
How does an ACE inhibitor affect afterload and preload?
ACE inhibitor: ↓afterload (↓ATII), ↓preload (↓aldosterone)
63
How does Addison disease affect electrolyte levels?
Addison disease: hyponatremia, hyperkalemia, metabolic acidosis
64
What is primary aldosteronism most frequently caused by?
1° Aldosteronism: adenoma in zona glomerulosa
65
What electrolyte abnormalities are present in primary aldosteronism?
1° Aldosteronism: hypernatremia, hypokalemia, metabolic alkalosis
66
How does primary aldosteronism affect renin levels and blood pressure?
1° Aldosteronism: low renin hypertension
67
Why is pitting edema absent in mineralocorticoid excess states?
Absence pitting edema: escape phenomenon (PH > PO; lose Na+ in urine) + ↑ANP/BNP
68
What results from the absence of ADH?
Absence of ADH → dilution → loss of fH2O
69
How does CDI/NDI affect urine concentration?
CDI/NDI: always diluting, never concentrating
70
In CDI/NDI, how do UOsm and POsm compare?
CDI/NDI: UOsm < POsm
71
List one lab finding and two clinical findings in CDI/NDI.
CDI/NDI: hypernatremia, polyuria, polydipsia
72
Describe the results of water deprivation studies in CDI and NDI.
CDI: desmopressin ↑UOsm (concentration); NDI: desmopressin no change in UOsm
73
What is the treatment for CDI?
Rx CDI: desmopressin acetate
74
What is the treatment for NDI? How does the treatment work?
Rx NDI: thiazides; volume depletion decreases polyuria
75
How is the normal concentration of urine affected in CRF?
CRF: loss of concentration and dilution
76
What is a common cause of hyponatremia in a hospitalized patient?
SIADH: common cause of hyponatremia in hospitalized patient
77
What is the most common neoplasm ectopically producing SIADH?
SIADH: MCC small cell carcinoma of lung
78
How does SIADH affect the normal concentration of urine?
SIADH: always concentrating never diluting
79
In SIADH, how do UOsm and POsm compare?
SIADH: UOsm greater than POsm
80
What is diagnostic of SIADH? How are TBNa+ and TBW affected?
SIADH: serum Na+ <120 mEq/L; TBNa+/↑↑TBW
81
How are UOsm and random UNa+ affected in SIADH?
UOsm and random UNa+ increased in SIADH
82
How is mild SIADH treated?
Rx SIADH: restrict water
83
What does demeclocycline do and produce?
Demeclocycline: inhibits ADH; produces NDI
84
How does hypokalemia affect insulin secretion?
Hypokalemia inhibits insulin secretion
85
How does hyperkalemia affect insulin secretion?
Hyperkalemia stimulates insulin secretion
86
What has primary control of potassium?
Aldosterone has primary control of K+
87
How does arterial pH affect potassium levels? What is there the potential for?
Alkalosis causes K+ to move into cells; potential for hypokalemia
88
How does acidosis affect potassium levels? What is there the potential for?
Acidosis causes K+ to move out of cells; potential for hyperkalemia
89
How do insulin and β2-agonists affect potassium levels?
Insulin, β2-agonists enhance Na+/K+-ATPase pump: K+ moves into cell; hypokalemia
90
How do digitalis, β-blockers and succinylcholine affect potassium levels?
Digitalis, β-blockers, succinylcholine inhibit Na+/K+-ATPase pump: K+ moves out of cell; hyperkalemia
91
What is the most common cause of hypokalemia?
Loop/thiazide diuretics: MCC hypokalemia
92
List four clinical and laboratory findings of hypokalemia.
Hypokalemia: muscle weakness; ECG shows U wave
Hypokalemia: polyuria; NDI due to vacuolar nephropathy
Hypokalemia: rhabdomyolysis
93
List two clinical findings of hyperkalemia.
Hyperkalemia: ECG shows peaked T waves; heart can stop in diastole
94
What is the benefit of calcium gluconate?
Calcium gluconate cardioprotective in hyperkalemia
95
If there is no compensation, the expected compensation remains where?
No compensation: expected compensation remains in normal range
96
If there is partial compensation, where is the expected compensation and pH?
Partial compensation: expected compensation outside normal range; pH outside normal range
97
If there is full compensation, how is the pH affected? How often does full compensation occur?
Full compensation: compensation brings pH into normal range; rarely occurs
98
What does pH define?
pH defines the primary disorder versus the compensation
99
What do formulas for compensation help with?
Formulas for compensation: help recognize single versus multiple acid-base disorders
100
Respiratory acidosis is due to what?
Respiratory acidosis: alveolar hypoventilation
101
What is the PaCO2 in respiratory acidosis? How are the pH, HCO3-, and PCO2 affected?
Respiratory acidosis: Paco2 >45 mm Hg; ↓pH ~ ↑HCO3−/↑↑PCO2
102
What is the compensation for metabolic alkalosis?
Metabolic alkalosis: compensation for respiratory acidosis
103
What is the most common cause of respiratory acidosis?
Chronic bronchitis: MCC respiratory acidosis
104
What is the PaCO2 in respiratory alkalosis? How are the pH, HCO3, and PCO2V affected?
Respiratory alkalosis: PaCO2 <33 mm Hg; ↑pH ~ ↓HCO3−/↓↓PCO2v
105
What is respiratory alkalosis characterized by?
Respiratory alkalosis: alveolar hyperventilation eliminating CO2
106
What is the compensation for respiratory alkalosis?
Metabolic acidosis: compensation for respiratory alkalosis
107
What is the most common cause of respiratory alkalosis?
Anxiety: MCC respiratory alkalosis
108
Tetany commonly occurs in what acid-base disorder?
Tetany: commonly occurs in acute respiratory alkalosis
109
How is albumin affected in alkalosis?
Alkalosis: ↑COO− groups in acidic amino acids on albumin
110
What is the serum HCO3- in metabolic acidosis? How are the pH, HCO3-, and PCO2 affected?
Metabolic acidosis: serum HCO3− <22 mEq/L; ↓pH ~ ↓↓HCO3−/↓PCO2
111
What is the compensation for metabolic acidosis?
Respiratory alkalosis: compensation for metabolic acidosis
112
What is the formula for calculating anion gap?
AG = serum Na+ − (serum Cl− + serum HCO3−) = 12 mEq/L ± 2
113
What does increased anion gap signify?
↑AG: additional anions are present that should not be there
114
Describe how is HCO3- affected in metabolic acidosis.
Metabolic acidosis: ↓HCO3− due to buffering of excess H+ from an acid
115
In increased AG metabolic acidosis, what replaces buffered HCO3-?
↑AG metabolic acidosis: anions of acid replace buffered HCO3−
116
What is the most common increased AG metabolic acidosis?
Lactic acidosis: most common ↑AG metabolic acidosis
117
What is the osmolal gap useful for?
Osmolal gap: useful in diagnosing methanol or ethylene glycol poisoning
118
In normal AG metabolic acidosis, what replaces HCO3-?
Normal AG metabolic acidosis: Cl− anions replace HCO3−
119
List three clinical findings in metabolic acidosis.
Clinical findings: hyperventilation, warm shock, osteoporosis
120
Metabolic alkalosis is due to what?
Metabolic alkalosis: lose H+ or gain HCO3−
121
What is the serum HCO3- in metabolic alkalosis? How are the pH, HCO3-, and PCO2 affected?
Metabolic alkalosis: serum HCO3− >28 mEq/L; ↑pH ~ ↑↑HCO3−/↑PCO2
122
What is the compensation for metabolic alkalosis?
Respiratory acidosis compensation for metabolic alkalosis
123
What are the characteristic findings of chloride responsive metabolic alkalosis?
Cl− responsive: volume depletion, ↓serum/urine Cl−, ↑reclaiming HCO3−, corrects with normal saline
124
List two examples of chloride responsive metabolic alkalosis.
Cl− responsive: vomiting, loop/thiazide diuretics
125
Describe the characteristic findings of chloride resistant metabolic alkalosis.
Cl− resistant: volume overload, ↑serum/urine Cl−, no correction with normal saline
126
What is the cause of chloride resistant metabolic alkalosis?
Cl− resistant: mineralocorticoid excess (e.g., 1° aldosteronism)
127
What is a clinical findings of metabolic alkalosis?
Clinical findings: ↑risk ventricular arrhythmias
128
What is a mixed acid-base disorder?
Mixed acid-base disorder: two or more primary acid-base disorders
129
Describe salicylate intoxication as an example of a mixed acid-base disorder.
Salicylate intoxication: mixture 1° metabolic acidosis and 1° respiratory alkalosis; normal pH
130
Describe chronic bronchitis and loop diuretic use as a mixed acid-base disorder.
Chronic bronchitis + loop diuretic = 1° chronic respiratory acidosis + 1° metabolic alkalosis and normal pH
131
Describe cardiorespiratory arrest as a mixed acid-base disorder.
Cardiorespiratory arrest = 1° respiratory acidosis + 1° metabolic acidosis = extreme acidemia
132
What are the clues for a mixed disorder?
Clues for mixed disorder: normal pH; extreme acidemia or alkalemia
133
What is edema?
Edema: excess fluid in interstitial space
134
What is a transudate?
Transudate: protein-poor and cell-poor fluid
135
Transudates are associated with what?
Transudate: pitting edema, body cavity effusions; alteration in Starling forces
136
What is an exudate?
Exudate: protein-rich and cell-rich fluid
137
What does hydrostatic pressure do?
HP: move transudate out of capillaries/venules
138
What does the oncotic pressure equate with and what does it do?
OP (albumin): opposes filtration out of capillaries/venules
139
What are three clinical examples of increased HP?
↑HP: pulmonary edema, pitting edema RHF, ascites due to PH
140
What are four clinical examples of decreased OP?
↓OP: nephrotic syndrome, malnutrition, cirrhosis, malabsorption
141
Give an example of increased HP and decreased OP.
Ascites in cirrhosis: ↑HP (portal vein hypertension), ↓OP (hypoalbuminemia)
142
How does renal retention of sodium and water affect HP? Give two examples.
Renal retention sodium and water: ↑hydrostatic pressure; renal failure, glomerulonephritis
143
When is vascular permeability increased?
↑Vascular permeability: acute inflammation
144
What does lymphatic obstruction produce?
Lymphedema: lymphatic obstruction
145
List three examples of lymphedema.
Lymphedema: modified radical mastectomy and radiation; inflammatory carcinoma breast; filariasis
146
What is the pathogenesis of thrombi?
Thrombi: endothelial injury, stasis of blood flow, hypercoagulability
147
What is the pathogenesis of venous thrombi?
Pathogenesis venous thrombi: stasis blood flow, hypercoagulable state
148
What is the most common site for venous thrombosis?
MC site for venous thrombosis: deep veins, lower extremity below the knee
149
Where do thrombi in the lower extremity deep veins propagate toward?
Deep veins lower extremity: thrombi propagate toward the heart
150
What is the composition of a venous thrombus?
Composition venous thrombus: entrapped RBCs, platelets, white blood cells
151
What are heparin and warfarin?
Heparin/warfarin: anticoagulants that prevent venous thrombosis
152
What is the pathogenesis of arterial thrombi?
Arterial thrombi: endothelial cell injury points of bifurcation/overlying atherosclerotic plaques
153
What is the most common arterial thrombus?
MC arterial thrombus: coronary artery thrombus overlying an atherosclerotic plaque
154
What is the composition of an arterial thrombus?
Composition arterial thrombus: fibrin clot composed of platelets
155
What prevents arterial thrombi?
Prevention arterial thrombi: aspirin, other agents that prevent platelet aggregation
156
Where are mixed thrombi located?
Mixed thrombus: heart chambers and aneurysms in aorta
157
What is the composition of mixed thrombi?
Mixed thrombus: laminated; pale areas platelets, red areas predominantly RBCs
158
Give two examples of thrombi that develop in heart chambers.
Heart chamber thrombi: left ventricle (post acute myocardial infarction), left atrium (mitral stenosis)
159
What are the complications of arterial thrombi?
Arterial thrombi complications: infarction, embolization
160
Describe the composition of postmortem clots.
Postmortem clot: nonadherent fibrin clot of plasma without cells
161
Describe the site of origin of PE,
PE: majority originate in deep veins of lower extremities and pelvis
162
What are the clinical findings of PE?
PE clinical: sudden death, pulmonary infarction
163
Why is pulmonary infarction uncommon?
Pulmonary infarction uncommon: dual blood supply—pulmonary arteries, bronchial arteries
164
What is a paradoxical embolus?
Paradoxical embolus: venous embolus passing thru ASD/VSD into systemic circulation
165
Where do systemic emboli originate?
Systemic embolism: majority originate in left side of heart
166
What are two sources for noncardiogenic embolization?
Noncardiogenic embolization: aortic aneurysms, ulcerated atherosclerotic plaques
167
What are the target sites of systemic emboli?
Target sites: upper/lower extremities, spleen, kidneys, small bowel
168
What are the clinical findings of systemic embolism?
Clinical findings systemic embolism: pale and hemorrhagic infarctions
169
What is the most common cause of fat embolism?
Fat embolism: fracture of long bones most common (e.g., femur), pelvis
170
Describe the pathogenesis of fat embolism.
Marrow fat enters ruptured marrow sinusoids and venules
| Fat emboli initially trapped in pulmonary capillaries: enter arteriovenous shunts to disperse to distant sites
171
When do symptoms/signs of fat embolism occur?
Symptoms/signs of fat embolism occur in 1−3 days
172
What are the clinical findings of fat embolism?
Fat embolism: dyspnea, tachypnea, petechiae over chest/upper extremities
173
What are the lab findings of fat embolism?
Fat embolism: hypoxemia, ↑A-a gradient, thrombocytopenia
174
Describe the epidemiology of AF embolism.
AF embolism: occurs during labor or immediately postpartum
| Maternal mortality 80%
175
What is the pathogenesis of AF embolism?
Pathogenesis: tear placental membrane, rupture uterine veins
176
What are the clinical findings of AF embolism?
Clinical: abrupt onset dyspnea, hypotension, bleeding
Clinical: ARDS, DIC
177
What are the autopsy findings in AF embolism?
Autopsy: pulmonary vessels—fetal squames, lanugo hair, vernix
178
What is the prognosis in AF embolism?
Prognosis: permanent neurologic impairment 85%
179
What are the lab findings in AF embolism?
Laboratory: hypoxemia, respiratory acidosis, ↑PT
180
Describe the epidemiology of DCS.
DCS: form of gas embolism; scuba diving, deep sea diving
181
What is the pathogenesis of DCS?
DCS: nitrogen gas goes into solution in blood and tissue with descent
DCS: rapid ascent causes nitrogen gas bubbles in vessel lumens and tissue (e.g., joints)
182
What are the clinical findings in DCS?
The bends: nitrogen gas in skeletal muscle vessels and joints
Nervous system: mimics spinal cord trauma
Pneumothorax: rapid ascent; rupture preexisting subpleural/intrapleural bleb; dyspnea pleuritic chest pain
PE: ↑pressure on lower extremity veins → stasis → thrombosis → embolism; dyspnea, pleuritic chest pain
183
What is caisson disease?
Caisson: persistent nitrogen gas bubbles in bone; aseptic necrosis femur, tibia, humerus
184
What is the treatment from DCS?
Rx DCS: recompression in high pressure chamber followed by slow decompression
185
What is hypovolemic shock due to?
Hypovolemic shock: excessive fluid loss (blood/sweat/sodium in urine)
186
What loss of blood volume produces shock?
Loss of >20% of blood volume produces shock
187
What are two causes of external bleeding?
External bleeding: penetrating trauma, gastrointestinal bleeding
188
What are causes of internal bleeding?
Internal bleeding: trauma to solid organs (liver/spleen), ruptured abdominal aortic aneurysm
189
How are Hb and Hct affected in blood loss?
Blood loss: no initial drop in Hb and Hct
190
What uncovers RBC deficit immediately in blood loss?
Normal saline uncovers RBC deficit immediately
191
When does reticulocyte response to RBC deficit begin?
Reticulocyte response to RBC deficit begins in 5-7 days
192
What is the best indicator of tissue hypoxia?
MVO2: best indicator of tissue hypoxia
193
How are CO, LVEDP, PVR, and MVO2 affected in hypovolemic shock?
Hypovolemic shock ↓CO, ↓LVEDP, ↑PVR, ↓MVO2
194
What are the clinical findings in hypovolemic shock?
Clinical: cold/clammy skin, hypotension, tachycardia,↓urine output
195
What are the lab findings in hypovolemic shock?
Laboratory:↑AG metabolic acidosis due to lactic acidosis
196
What is the most common cause of cardiogenic shock?
Cardiogenic shock: MCC AMI
197
How are CO, LVEDP, PVR, and MVO2 affected in cardiogenic shock?
Cardiogenic shock: ↓CO, ↑LVEDP, ↑PVR, ↓MVO2
198
What are the lab findings in AMI?
Laboratory findings in AMI: ↑CK-MB, ↑troponin I and T
199
What is the most common site for infection leading to sepsis?
MC site for infection leading to sepsis is the lungs
200
What is the most common cause of death in intensive care units?
MCC of death in intensive care units is septic shock
201
What is the most common cause of septic shock?
Septic shock: MCC sepsis due to gram-positive organisms (coagulase-negative Staphylococci)
202
What is the most common cause of gram-negative septic shock?
Escherichia coli: MCC of gram-negative septic shock
203
What is the most common fungal cause of septic shock?
Candida species: MC fungal cause septic shock
204
What is the most important factor producing septic shock in gram-positive pathogens?
Lipoteichoic acid: most important factor producing septic shock in gram-positive pathogens
205
What does IL-1 do?
IL-1: fever, activate neutrophil adhesion molecules (neutropenia)
206
What does TNF do?
TNF: damages endothelial cells (releases vasodilators; NO, PGI2)
207
What do endotoxins do?
Endotoxins: activate macrophages, complement system, tissue thromboplastin (DIC)
208
How are CO, LVEDP, PVR, and MVO2 affected in the initial phase of septic shock?
Septic shock (initial phase): ↑CO, ↓LVEDP, ↓PVR, ↑MVO2
209
What are the clinical findings in early septic shock?
Clinical: warm skin, strong peripheral pulses, hypotension, DIC
210
What is there increased risk for developing in septic shock?
Septic shock: ↑risk for ARDS
211
What are the hematologic findings in early septic shock?
Hematologic findings: anemia, thrombocytopenia, neutropenia
212
What is the most common cause of death in shock?
MODS: MCC of death in shock
