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SHOCK Oliguria

MEDICINE II o Due to decrease of blood volume or perfusion in the kidneys

August 14/19, 2014 o Important to monitor Urine Output
Dr. Helenne Joie M. Brown Hypotension
OUTLINE Narrow pulse pressure (difference between systolic and diastolic pressure)
Forms o Normal pulse pressure
Clinical Presentations 30-40 mmHg
Complications Systolic BP Diastolic BP
Management o Loss of 20 -40 % of blood volume = Moderate hypovolemia
BP at rest is 120/80 mmHg
PATHOGENESIS OF SHOC K Standing BP: 90/60 mmHg
Interplay of many factors Change in mental status
Increased sympathetic activation o Patient with history of volume loss
o Increased in production of catecholamines in response to an Hemoconcentration, hypernatremia, prerenal azotemia
inciting event leading to diffuse vasoconstriction o No exact pathology in the kidneys but only decreased blood flow
o Must have a stress factor for activation therefore resulting to increase of BUN
Resulting to: Hypersthenuria
Vasoconstriction tachycardia o Increase of the specific gravity of the urine
Constriction of arterioles Increase
hydrostatic pressure; and oncotic pressure is Laboratory Test:
the same extravasation of fluid outside CBC: Hct and Hgb (hemoconcentration)
capillaries or outside the vascular bed fluid Serum electrolytes (hypernatremia)
leakage BUN and creatinine (prerenal azotemia)
o Increase in serum creatinine (azotemia)
Neuroendocrine activation Urinalysis
o Pancreas: o Concentrated Urine (hypersthenuria)
Hyperglycemia, increased release of blood sugar
o Activation of RAAS CVP (reflects right atrial pressure): <15mmHg low
o Predominance of anaerobic metabolism Pulmonary Capillary Wedge pressure (reflects left atrial pressure):
o Activation of all systems will result of Organ Injury <15mmHg low
Organ injury o Used on invasive monitoring
o Reduced cardiac output o CVP right atrial pressure
o ALI/ ARDS o PCWP left atrial pressure
o Acute kidney injury o Not enough Blood volume leads to decrease pressures in the heart
o Lactic acidosis
o Diffuse Inflammation Treatment:
o Cellular apoptosis Fluid resuscitation with crystalloids
FORMS o Fluids used which are not high in protein content (water +
Loss of fluid volume in the body 2-3 L over 20-30 mins or 20ml/ kg over 15 min using
Types: large bore needles
o (!) Hemorrhagic shock Example: 100 kg patient presenting with hypovolemic
Loss of RBC mass and plasma volume shock, passing 20 lose stools a day
o (2) Non-hemorrhagic shock Give a bolus of PLRS (indicated for: diarrhea to
Loss of plasma volume alone and due to insensible losses, replenish hypokalemia) 2 liters over 15 min
Restrictive blood transfusion: only replacement the on-going blood loss
GI disturbance such as diarrhea, excessive vomiting,
o Transfusing enough blood to counter blood loss
polyuria or increase in capillary permeability
o If Hgb is > or equal to 7gms/liter: no need to transfuse unless less
Cold clammy extremities
o When you have hypovolemic and when you lose a lot of body fluid
o Increase force of cardiac contraction
Decreased perfusion
Reflex tachycardia o Give only Inotropes when patient is adequately fluid
o In an effort to resupply the body resuscitated but still hypotensive

KarloC/LeahL/DaisyB/LoveM/DianneM Med 2016 <3

o Examples of inotropes: Norepinephrine, Epinephrine, Dopamine, o Treat acidosis
Dobutamine o Treat Hypoxemia
Increase peripheral vasoconstriction o Control arrhythmias
Mechanical ventilation Vasopressors:
o Relieves work of breathing o Increase cardiac contractility
o Allow redistribution of limited CO to other vital organs o Treatment of choice for increasing blood volume
o Dobutamine, Dopamine, Epinephrine, Norepinephrine
Intra-aortic Balloon Counterpulsation
CARDIOGENIC SHOCK o Thrombolytic agents (mainstay treatment for MI)
Depressed cardiac index Revascularization in elevated ST segment MI
o Cardiac Index = Basic cardiac output/ BSA 30-60% success only
Little supply of blood by the body o Send for PCI (percutaneous coronary intervention)
Decreased function of the heart
Sustained arterial hypotension ON INOTROPICS
Elevated PCWP (reflective of the pressure in the left atrium) 1 .Norepinephrine
o Pulmonary congestion, edema is the 1st line therapy due to fewer adverse effects such as arrhythmias in
o Signs and symptoms of heart failure (pump failure) comparisons to Dopamine
Left Ventricular Failure: most common cause of Cardiogenic Shock both a vasoconstrictor and inotropic stimulant
Other Causes: Has not shown definitive survival; based on recent studies
o Acute coronary syndrome 2mcg/kg/min standard dosage for all vasopressors based on ACLS
o Cardiomyopathy
o Severe valvular heart disease (aortic stenosis) 2. Dopamine
o Cardiac tamponade Low dose less than 2mcg/kg/min all vasopressors
o Bradyarrhythmias Dilates the renal vascular bed; controversial still
Moderate doses 2-10 mcg/kg/min
o Positive chronotropic (increase in rate of contraction) and
inotropic effects (increase in force of contraction)
Higher doses >10mcg/kg
o Has a vasoconstrictor effect
Maximum dose of 20-50 mcg/ kg

3. Dobutamine
Has positive inotropic effect but minimal chronotropic effect in low doses of
about 2.5 mcg/kg/min
Higher doses:
o Chronotropic activity is moderate
Vasodilating activity at higher doses

Intraaortic Balloon Counterpulsation

Augments both arterial diastolic
pressure and cardiac output
o Suring diastole there is
maximum coronary
Slit on the femoral artery and
put a balloon and placed up in
the Aorta and is monitored by a
Inflates during diastole
Management augmenting coronary blood flow
General Measures should treat the cause Deflates in early systole
o Manage MI reducing afterload
Center piece of treatment of MI: Revascularization or
establish coronary blood flow
KarloC/LeahL/DaisyB/LoveM/DianneM Med 2016 <3
Contraindicated in aortic regurgitation Vasopressors for persistent hypotension
o Access is via femoral artery, insertion of balloon o 1st line: Norepinephrine
o Inserted in the aorta through guided fluoroscopy Balloon is
guided by cari (landmark)
Opens in diastole, closes in systole
Diffuse Vasodilation venous pooling in extremities decreased venous
return and decreased cardiac output
COMPRESSIVE CARDIOGENIC SHOCK o Interruption of sympathetic vasomotor response after a high
Occurs outside the heart cervical spinal cord injury
Results from compression of the heart from an outside source o Severe head injury
Causes: pericardial tamponade (collapse of cardiac chambers), increased o High cervical injury
intrathoracic pressure o Cephalad injury by anesthesia
Treatment: Decompression o Pain
o Pericardiocentesis, pleuropericardial window to reduce volume Treatment
pressure and overload o Fluid resuscitation
o 1st line inotropics: Norepinephrine
BECKs Triad (seen in Compressive Cardiogenic Shock)
1. Neck vein distention
2. Muffle heart sounds (increased in the distance of ant chest wall and heart HYPOADRENAL SHOCK
due to fluid accumulation)
3. Hypotension Critical illness like trauma and sepsis
Normally, adrenal glands produce steroids such as cortisol
Diagnostic: 2d echo cardiogram Secondary to chronic glucocorticoid use or critical illness
o Chronic pain, arthritis, skin diseases
Others Causes of Increased thoracic pressure Body perceives the exogenous/ synthetic steroids as steroids produced by
Tension Pneumothorax the body therefore the body suppresses its natural production
o Needling/Chest tube thoracotomy o Yields hypotension and electrolyte imbalance; decreased
Herniation of abdominal viscera by diaphragmatic hernia Treatment:
o Hydrocortisone until weaning off
Excessive positive pressure ventilation in mechanical ventilation o volume resuscitation,
o Vasopressors

Hallmark: Decreased peripheral vascular resistance
Overwhelming infection resulting to a decrease in PVR

Surviving Sepsis Campaign Bundle includes

Early detection means early diagnosis
o Lactate levels
Sepsis leads to septic acidosis
o Culture sample specimen if there is an abscess
o C&S of sputum if with pneumonia
Early goal- directed therapy. Give..
o Broad spectrum antibiotics
Cover gram + and - , anaerobes as well
Best given within 1 hr of presentation
o Control source of infection
Catheters (remove), abscess (Drain), wounds (debride),
foreign body (remove foreign body)
Fluid resuscitation of sepsis
o Give 30 ml/kg of crystalloids containing Protein
Increase plasma oncotic pressure Someone has to share the weight of the world with you, someday, soon <3

KarloC/LeahL/DaisyB/LoveM/DianneM Med 2016 <3

20 years old female
Voluminous diarrhea
No UO for 24 hours
BP: 100/60, 40 palpatory, CR 120 120/min, conscious
Clear breath sounds
Cool extremities, weak pulses

Diagnosis: Non-hemorrhagic Hypovolemic shock

Electrolytes: Sodium and Potassium
Stool exam
Fluid resuscitation: 50 x 20: 1000ml or 1L of PLNSS or PLRS

42 year old male, diabetic hypertensive
Severe chest pains
Anterior Wall MI on ECG
BP:80mmHg palpatory, weak pulse
Neck vein distention, crackles both lung filed
Cold extremities, weak pulses

Diagnosis: Cardiogenic shock

o Fibrinolysis: if we catch the patient at the 1st hour after the onset
of symptoms and
o PCI: if after an hour of the onset of the symptoms,
Inotropics (epinephrine then dopamine then dobutamine up to 20 mcg
Ultimately (?) intra-aortic balloon and counter pulsation.

75 year old male
Fever for 2 days
With IFC for 2 weeks
BP: 90/60, 99/min, RR 30/min, hypoxemic, drowsy
Crackles all over the lungs

Diagnosis: Septic Shock

Blood culture of the tip of the IFC
Lactic acid levels or ABGs for blood gas
Treatment: Fluid and broad spectrum antibiotics

KarloC/LeahL/DaisyB/LoveM/DianneM Med 2016 <3