Shock

Shock is acute circulatory failure leading to inadequate tissue perfusion and end organ injury

"Acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalized cellular hypoxia."

Shock is caused by a disruption to the cardiovascular system, and inadequate compensation to maintain tissue perfusion.

How do you classify shock?
Shock is hypotension with end organ injury: it classified as being due to malfunction of,
1) the Pump (cardiogenic),
2 ) the Tubing (distributive), or
3) the Fluid (hypovolemic).

Hypotension and Shock are caused by a problem with
Heart Rate, Stroke Volume or Peripheral Resistance.

There are only three types of shock,
problems with the heart, sometimes called cardiogenic shock, problems vascular system, known as distributive shock, and
loss of circulating volume, known as hypovolemic shock.

Although textbooks and examiners often emphasize the classification of shock, in the real world, it is often more effective to use the physiologic approach to shock:

Shock is due to inadequate blood pressure.

Low blood pressure is due to inadequate cardiac output or low peripheral resistance.

Low cardiac output is caused by a problem with heart rate or stroke volume.

Heart rate abnormalities: too fast (tachycardia), too slow (bradycardia).

Stroke Volume abnormalities: failure to receive, failure to eject, inadequate volume

Low peripheral vascular resistance is due to inappropriate vasodilatation.

Cardiac Output

What is the significance of Heart Rate?
The heart rate is a fundamental element of hypotension both in terms of cause (tachyarrhythmias / bradyarrhythmias) and compensation – hypotension should be accompanied by a tachycardia.

The amount of blood pumped from the heart per minute is the cardiac output. It is determined by the volume pumped in each cycle, the stroke volume (end diastolic volume minus the end systolic volume) and the frequency of the cycles, the heart rate.

The ability of the heart to both receive and eject blood is a fundamental function of heart rate. Firstly if the rate is excessive, then the heart is unable to either fill or eject efficiently. If, for any reason the stroke volume falls, the heart is able to compensate by increasing the heart rate. The filling of the left ventricle is not just determined by the venous return, 30% of filling is derived from the “atrial kick”, which is lost in atrial fibrillation. In some circumstances, the stroke volume is fixed, such as in mitral and aortic stenosis and in infancy, the cardiac output is rate dependent.

If baby’s, who normally have a fast heart rate, become bradycardic, then their cardiac output (and thus their blood pressure) falls. Patients who have permanent pacemakers behave in an opposite manner: if their stroke volume falls, they are unable to increase their heart rate to compensate.

Hypotension and bradycardia is characteristic of excessive vagal activity. Cholinergic agents (particularly anticholinesterases such as neostigmine) will mimic vagotonicity. Other drugs may excessively slow nodal conduction - beta blockers, calcium channel blockers, digoxin etc.

Hypotension may be the “egg, not the chicken” - it follow an excessively slow or fast heart rate. Complete heart block may cause hypotension, particularly in the non compliant left ventricle. Tachyarrhythmias will reduce filling time and curtail stroke volume

Arterial Blood Gas Analysis

PESI Score For Pulmonary Embolism

Glasgow Coma Score:

Glasgow Coma Score:
The GCS is scored between 3 and 15, 3 being the worst, and 15 the best. It is composed of three parameters : Best Eye Response, Best Verbal Response, Best Motor Response, as given below :

Best Eye Response. (4)
No eye opening.
Eye opening to pain.
Eye opening to verbal command.
Eyes open spontaneously.

Best Verbal Response. (5)
No verbal response
Incomprehensible sounds.
Inappropriate words.
Confused
Orientated


Best Motor Response. (6)

No motor response.
Extension to pain.
Flexion to pain.
Withdrawal from pain.
Localising pain.
Obeys Commands.

Abbreviated coma scale (AVPU)

Abbreviated coma scale (AVPU)
This sometimes used in the initial assessment ('primary survey') of the critically ill.

A = alert
V = responds to vocal stimuli
P = responds to pain
U = unresponsive

Oxygen delivery

Oxygen delivery

Introduction

Indications:

The treatment of documented hypoxemia as determined by SaO2/SpO2 or inadequate blood oxygen tensions (PaO2) Note: Blood gases are not routinely done in children.

The target percentage % of O2 saturation of Hb (SaO2 or SpO2) is:
95 - 97% children/adults
88-92% for all neonates (premature or term less than 28 days of age) nursed in oxygen
>60% Cyanotic heart disease

An acute or emergency situation where hypoxemia or hypoxia is suspected, and if the child is in respiratory distress manifested by:

dyspnoea, tachypnoea, bradypnoea, apnoea
pallor, cyanosis
lethargy or restlessness
use of accessory muscles: nasal flaring, intercostal or sternal recession, tracheal tug

Short term therapy e.g. post anaesthetic or surgical procedure
Palliative care

INDIRECT LARYNGOSCOPES

SOME EXAMPLES OF RIGID

INDIRECT LARYNGOSCOPES
They are according to labels

A - STORZ Video Laryngoscope
B - GLIDESCOPE Video Laryngoscope
C - AIRTRAQ
D - McGRATH Laryngoscope
E - BULLARD Laryngoscope

DIRECT LARYNGOSCOPES:

Types Of Bleeding

Cardiac Arrest vs Heart Attack

Head Injury: part 3

Head Injury: part 3

ANATOMY AND PHYSIOLOGY

E
Cerebral perfusion pressure (CPP) = Mean arterial pressure - ICP.
Maintenance of cerebral perfusion is essential in the management of patients with severe closed head injury. Normal cerebral blood flow (CBF) is approximately 50 mL/100 g brain/minute. CBF <20 mL/100 g brain/minute represents cerebral ischemia, and cell death occurs at approximately 5 mL/100 g brain/minute. In addition to cerebral ischemia in response to injury, the injured brain loses its ability to autoregulate blood flow, increasing susceptibility of the injured brain to further ischemia. The generally acceptable range during active therapy in traumatic brain injury is CPP >60 to 70 mmHg.
II.
TBIs are categorized as mild (80%), moderate (10%), or severe (10%), depending on the level of neurologic dysfunction at the time of initial evaluation. Determination of the Glasgow Coma Scale (GCS) score as early as possible and then serially
P.136
is essential. Loss of consciousness (LOC) is an important indicator of TBI. Classification of TBI is based on the GCS

Head Injury part 2

Head Injury part 2

INITIAL EVALUATION AND TREATMENT OF HEAD INJURY:

C. Secondary management:

1.The avoidance of secondary brain injury is essential. Secondary brain injury is produced by hypoxia and hypotension. A single episode of hypotension (systolic blood pressure <90 mmHg) in the adult will worsen prognosis and can increase mortality up to 50%.

2.The GCS obtained in the emergency department may be a more reliable assessment of the severity of brain injury than the GCS obtained in the field.

3.The GCS cannot be assessed by simple observation and requires stimulation of the patient. In cases of asymmetry in either eye opening or motor scores, the best score is used.

4.If time permits, a lateral cervical spine x-ray study usually can be obtained during secondary survey of the patient, which may detect gross injury or malalignment of the cervical spine ). If available rapid C-spine CT should be used to detect fractures as well

D. Indications for ICP monitoring:

*As a general approach, liberal use of ICP monitoring in patients with severe TBI (GCS ≤8) is recommended. An ICP monitor should be used with a brain oxygen monitor. ICP monitoring is not routinely indicated for patients with moderate or mild closed head injury. An ICP monitor should also be considered in a patient with moderate head injury who is going to the OR for other injuries. ICP monitoring is indicated for:

1.Severe closed head injury (GCS ≤8) and abnormal CT of head,,,

a: Definition of abnormal CT:
*Hematoma
*Contusion
*Edema
*Compressed basal cisterns

2.Severe closed head injury (GCS ≤8) and normal CT of head, particularly if two or more of the following exist,,,

a .Age >40 years
b. unilateral or bilateral flexor or extensor posturing
c. Systolic blood pressure <90 mmHg (rapid correction of hypotension is essential)

Head Injury part 1

Head Injury
INITIAL EVALUATION AND TREATMENT OF HEAD INJURY

A. General:

1.Patients suspected of having suffered a head injury, particularly if confused or unresponsive, require emergency evaluation and treatment at a center with capabilities for immediate neurosurgical intervention. General objectives are rapid diagnosis and evacuation of intracranial mass lesions, expedient treatment of extracranial injuries, and avoidance of secondary brain injury due to hypoxia and hypotension. Other secondary insults such as hyperglycemia, hypothermia, and anemia may also exacerbate outcome during the hospital course.

2,Severe brain injury is associated with cerebral ischemia. Therefore, a principal therapeutic goal is to enhance cerebral perfusion and oxygenation and avoid further ischemic injury to the brain.

B. Initial management of the unresponsive patient with head injury:

1.Intubation with controlled ventilation (avoid routine hyperventilation). If possible, a focused neurologic examination, including assessment of GCS, pupillary response, and all four extremity movement, is critical before intubation and pharmacologic paralysis.

2.Venous access,,

* Restore intravascular volume, blood pressure, and perfusion.
*Avoid hypotonic or dextrose-containing solutions.

3.Immobilize the patient with rigid backboard and cervical spine (C-spine) collar. Assume that all patients with TBI have a spine injury until proved otherwise.

4.Pharmacologic paralysis and sedation, if agitated or combative,,

a.Short-acting agents are recommended.
*Vecuronium bromide, cisatracurium, or succinylcholine
*Opioid sedation: fentanyl or morphine
*Avoid benzodiazepines

5.Monitor blood pressure and O2 saturation continuously.

6.Check arterial blood gases (ABG), blood glucose, electrolytes, prothrombin time (PT), partial thromboplastin time (PTT), hematocrit, and platelet count. With active therapy, serum sodium levels and osmolality should be tracked.

7.Initiate medical management of the head injury. Proceed with rapid acquisition of a computed tomographic (CT) scan of the head and complete cervical spine (if time permits). Based on time, distance, and local capabilities, transfer may be necessary Rapid referral to a center capable of immediate neurosurgical intervention may be required. Do not delay transport to definitive care to obtain a CT scan of the head. Early diagnosis and evacuation of cranial mass lesions are critical.

8.Repeated neurologic examination and assessment of GCS. Documentation of the GCS in patients who are intubated, or “tubed,” should be noted by a T (i.e., 11[T]) patients who are intubated and pharmacologically paralyzed are noted by a TP (i.e., 3[TP]). This is needed for meaningful interpretation of the GCS values. # showing GCS #

9.Hyperventilation causes cerebral vasoconstriction and can worsen cerebral ischemia. Routine hyperventilation should no longer be used. Hyperventilation is indicated only in the setting of abrupt neurologic deterioration with suspected herniation.

Penetrating Trauma

                                                         Penetrating Trauma

D= Documented with their , P= Possible Associated Injuries

1.
D=Cervical (platysma penetration) injuries
P= Jugular vein/carotid artery injury, tracheal/ esophageal injury

2.
D=Transmediastinal injury
P= Cardiac/tracheobronchial and pulmonary/vascular/ diaphragmatic/gastrointestinal injury

3.
D=Thoracoabdominal injury P=Pulmonary/diaphragmatic/cardiac/gastrointestinal injury

4.
D=Transabdominal injury
P= Gastrointestinal/hepatic/vascular injury

5.
D=Transpelvic injury
p= Bladder/intestinal/uterine/vascular injury

6.
D=Flank injury
P= Genitourinary/intestinal injury