Syncope and shock
Dr. Szathmári Miklós
Semmelweis University
First Department of Medicine
14. Nov. 2011.
Syncope
• Definition: Transient loss of consciousness due
to reduced cerebral blood flow
• Symptoms:
– Postural collapse and spontanous recovery
– It may occur suddenly, or may be preceded by
symptoms of faintness (presyncope: dizziness, a
feeling of warmth, nausea, visual blurring)
• Types:
– Benign: Result of inadequate effects of normal
cardiovascular reflexes on heart rate and vascular tone
– Serious: Due to a life-threatening arrythmia
• Recurrent unexplained syncope with structural heart disease is
associated a high risk of death (40% mortality within 2 years)
Pathophysiology of syncope 1.
• Sudden impairment of brain metabolism,
usually brought about by hypotension
with reduction of cerebral blood flow
– Three-fourths of the systemic blood volume is
contained in the venous bed, and any
interference in venous return may lead to a
reduction in cardiac output
– Cerebral blood flow is maintained as long as
systemic arterial vasoconstriction occurs
– When this adjustment fails, the hypotension,
with resultant cerebral underperfusion to less
than half of normal, results in syncope
Syncope-patophysiology 2.
• Normally, the pooling of blood in the lower
parts of the body is prevented by:
– Pressor reflexes that induce contsriction of
peripheral arteriolas and venules
– Reflex acceleration of the heart by means of
aortic and carotid reflexes
– Improvement of venous return to the heart by
activity of the muscles of the limbs
Causes of syncope
• Disorders of vascular
tone or blood volume
– Vasovagal, postural
hypotension
– Carotid sinus
hypersensitivity
– Situational
– Glossopharyngeal
neuralgia
• Cardiovascular
disorders
– Arrhythmias
– Other cardiopulmonary
etiologies
• Verebrovascular
disease
– Vertebrobasilar insuff
• Other disorders that
may resemble syncope
– Metabolic
– Psychogenic
– Seizures
Disorders of vascular tone or blood
volume
• Reflex syncopes
– Disorders of autonomic control of the heart
and circulation
• Common patophysiologic mechanisms:
– a cardioinhibitory component: bradycardia due to
increased vagal activity
– a vasodepressor component:: inappropriate
vasodilatation due to sympathetic withdrawal
• Orthostatic intolerance
Reflex syncopes: Neurocardiogenic (vasavagal
and vasodepressor syncope)
• Common faint that may be experienced by normal
persons. Appr. half of all episodes of syncope
• Frequently recurrent
• Commonly precipitated by hot, alcohol, fatique, severe
pain, hunger, prolonged standing, and emitional situation
• Often preceded by presyncopal syndrome
• Rarely occurs in supine position
• The individual appears pale, the unconscious patient lies
motionless with relaxed muscles. The pulse may be
feeble, the blood pressure is low.
• The duration of unconsciousness is rarely longer than a
few minutes
• The sphinchter control is usually mantained
Neurocardiogenic (vasavagal and
vasodepressor syncope)
• Often occurs in the setting of increased
peripheral sympathetic activity and venous
pooling
• Vigorous myocardial contraction of relatively
empty left ventricle activates myocardial
mechanoreceptors and vagal afferent nerve
fibers that inhibit sympathetic activity and
increase parasympathetic activity
• The resultant vasodilatation and bradycardia
induce hypotension and syncope
• Sudden surge in central serotonin levels may
contribute to the sympathetic witdrawal
Reflex syncopes: Situational
syncope
• These syndromes are caused by abnormal
autonomic control and may involve a
cardioinhibitory response, a vasodepressor
response, or both
– Cough (after prolonged coughing in men with COPD)
– Micturition (in older men with prostatic hypertrophy
and obstruction. Occurs at night during or after
voiding)
– Defecation (secondary to Valsalva’s maneuver in
older individuals with constipation)
Reflex syncopes: Carotid sinus
hypersensitivity
• Precipitated by pressure on the carotid sinus
baroreceptors
• Typically occurs in the setting of shaving, a tight
collar, or turning the head to one side
• This occurs predominantly in men over 50 years
• The afferent impulses (via a branch of
glossopharyngeal nerve) activate cardiac vagal
efferent nerve fibres. The response may cause
sinus arrest or AV block (cardioinhibitory
response) or/and vasodilation (vasodepressor
response)
Postural (orthostatic) hypotension
• This occurs in patients who have hypovolemia or a
chronic defect in vasomotor reflexes
• Systemic arterial blood pressure falls on assumption of
upright position due to loss of vasoconstriction reflexes
• Sudden rising from a recumbent position is precipitating
circumstance
• Orthostatic hypotension may be the cause of syncope in
up to 30% of the elderly
• Causes:
– Drug induced
– Idiopathic postural hypotension (often familial, more common in
men, together with constipation, erectile dyfunction, inability to
sweat, heat intolerance)
– Autonom nervous system disorders (diabetic, nutritional, amyloid
polyneuropathy
– CNS disorders (parkinsonism, progressive cerebellar
degneration)
Syncope because of cardiovascular
disorders 1.
• Cardiac syncope results from a sudden
reduction in cardiac output, caused most
commonly by a cardiac arrhythmia
– As the heart rate decreases, ventricular filling time
and stroke volume increase to maintain normal
cardiac output
– At rates less than 30/min, stroke volume can no
longer increase. At rate more than 180/min ventricular
filling time is inadequate to maintain adequate stroke
volume.
– Upright position, cerebrovascular disease, anemia,
loss of atrioventricular synchrony, coronary,
myocardial, or valvular disease all reduce the
tolerance to alterations in rate.
Syncope because of cardiovascular
disorders 2.
• Bradyarrhythmias if the escape pacemaker rate is
insufficient to maintain cardiac output
– The syncope occurs abruptly without presyncopal symptoms
– It recurs several times daily
• Tachyarrhythmias, mostly ventricular tachycardia with
structural heart disease
– Usually preceded by palpitation or other presyncopal symptoms
• Structural cardiovascular disorders
– When the cardiac output cannot increase to compensate
adequately for peripheral vasodilatation (such as following
exercise)
• Obstruction to forward flow is the most common reason that cardiac
output can not increase (aortic stenosis or HOCM)
Syncope because of
cerebrovascular disease
• Alone rarely causes syncope but may lower the
threshold for syncope in patients with other
causes
• The vertebrobasilar arteries (which supply the
brainstem structures) are usually involved
• Most patients with cerebrovascular syncope also
have symptoms of focal neurological ischemia
(arm or leg weakness, diplopia, ataxia,
dysarthria etc.)
Differential diagnosis of syncope
• Anxiety attacks and hyperventilation syndrome
– The symptoms are not accompanied by facial pallor and are not
relieved by recumbency
– Typical associated symptoms: palpitation, air hunger, tingling of
fingers etc. Attacks can often be reproduced by hyperventilation.
• Seizure
–
–
–
–
May be heralded by an aura
Injury from falling is frequent
Tonic-clonic movements
The period of uncosciousness is longer than in syncope
• Hypoglykaemia
– Most common cause is the excessive administration of insulin
• Acute haemorrhage
– Gastrointestinal bleeding. Black stool.
Approach to the patient with
syncope 1.
• The cause may only be apparent at the
time of the event, leaving few, if any, clues
when the patient is seen later by the
physician.
• The physician should think first of those
causes that constitute at therapeutic
emergency:
– Massive internal hemorrhage
– Myocardial infarction (may be painless)
– Cardiac arrhythmias
Approach to the patient with
syncope 2.
• Careful hystory
– Loss of consciousness in particular situation
– The position of patient at the time of the
syncopal episode:
• Syncope in supine position suggest arrhythmia or
seizure
• Syncope in upright position suggest
neurocardiogenic, postural hypotension
• When the the individual wearing a shirt with a tight
collar, or is turning to look while driving in reverse,
suggest carotid hypersensitivity
Approach to the patient with
syncope 3.
• Physical examination
– Heart rate, blood pressure in the supine, sitting, and
standing position
– An attempt to reproduce an attack (hyperventilation,
or cough syncope induced by Valsalva’s maneuver)
• Laboratory examinations
– Electrolytes, blood glucose and hematocrit are usually
indicated.
– Cardiac enzymes if myocardial ischemia is suspected
– Blood and urine toxicology screens may reveal the
presence of alcohol or other drugs
– In case of suspition of adrenal insufficiency
measurements of the hormone levels
Approach to the patient with
syncope 4.
• ECG should be performed in all patients
• Continuous electrocardiographic monitoring or
Holter monitor for 24 to 48 h.
• Invasive cardiac electrophysiologic testing provides
information regarding sinus node function, AV
conduction, and supraventricular and ventricular
arrhythmias
• Upright tilt table testing is indicated for recurrent
syncope, or a single syncopal event in a high-risk setting
(pilot, commercial vehicle driver etc)
• To determine the presence of structural heart disease:
echocardiogram with Doppler examination
Treatment of syncope 1.
• The patient should avoid situation in which sudden loss
of consciousness might result in injury (operating heavy
machinery, driving, swimming alone etc.)
• Patients with vasovagal syncope should be instructed to
avoid situations that have caused them to lose
consciousness and to assume a recumbent position
when premonitory symptoms occur
• Patients with orthostatic hypotension should be
intstructed to rise slowly and systematically (supine to
seated, seated to standing) from the bed or a chair
• Family members should be educated, this will ensure
appropriate therapy and may prevent delivery of
inappropriate therapy
In patients who are resistant to the preventive
measures and in cases of recurrent episodes
of syncope
• In patients with vasovagal syncope:
•
•
•
•
•
•
β-adrenergic receptor antagonists
Serotonin reuptake inhibitors
Fludrocortisone (also in patients with postural hypotension)
α-receptor agonist (proamatine)
Disopyramid is a vagolytic antiarrhythmic drug
Permanent dual chamber cardiac pacing
• In patients with orthostatic hypotension:
• Whenever possible, medications that aggravate the problem
(vasodilatators, diuretics etc) should be discontinued
• Use of compression stocking may help
Shock
• Definition: Shock is a clinical syndrome that results from
inadequate tissue perfusion.
• The hypoperfusion-induced imbalance between the
delivery of and requirements for oxygen and substrate
leads to cellular dysfunction. The inadequate oxygen
supply induces the production and release of
inflammatory mediators that further compromise
perfusion through functional and structural changes
within the microvasculature. The cellular hypoperfusion
causes multiple organ failure.
• If the process is not interrupted, leads to death of the
patient
• Clinical manifestation: result of sympathetic
neuroendocrine responses to hypoperfusion and the
breakdown in organ function
Classification of shock
• Hypovolemic
• Traumatic
• Cardiogenic
– Intrinsic
– Compressive
• Septic
– Hyperdynamic
– Hypodynamic
• Neurogenic
• Hypoadrenal
Pathogenesis and organ response 1.
• Microcirculation
– Systemic vascular resistance rises to maintain a
level of systemic pressure that is adequate for
perfusion of the heart and brain at the expense of
other tissue. Arteriolar vascular smooth cells has both
α- and β–adrenergic receptors. Norepinephrine
release - acting on α1-receptors as vasocontsrictor - is
the fundamental compensatory response in shock.
– Reduced filtration because of decreased capillary
surface area across which filtration occurs.
Consequence: increased interstitial and intravascular
volume at the expense of intracellular volume.
Pathogenesis and organ response 2.
• Cellular response
– Decline of intracellular high energy phosphate
stores (decreased amount of ATP) because of
the mitochondrial dysfuction.
– Consequences:
• Accumulation of hydrogen ions, lactate (products
of anaerobic metabolism)
• As shock progresses, these vasodilatator
metabolits cause further hypotension and
hypoperfusion
Pathogenesis and organ response 3.
• Neuroendocrine response
– Hypovolemia are sensed by baro- and
chemoreceptors
• Increased adrenergic output – release of norepinephrine –
vasocontriction and metabolic effects : increased glycolysis
and gluconeogenesis
• Reduced vagal activity – increased heart rate and cardiac
output
• Severe stress causes ACTH release – this stimulates
cortisol secretion
• Increased renin release because of the hypoperfusion of
JGA. Renin induces the formation of angiotensin II, an
extremely potent vasoconstrictor and stimulator of
aldosterone release. Aldosterone enhances renal tubular
reabsorption of sodium, resulting in low-volume,
concentrated, sodium-free urine
Pathogenesis and organ response 4.
• Cardiovascular response
– Decreased ventricular filling (decreased
preload). The increased heart rate is a useful
but limited compensatory mechanism to
maintain the adequate stroke volume
– Impaired myocardial contractility which
reduces the stroke volume
– Elevated sytemic vascular resistance (except
of hyperdynamic stage of septic shock)
increases the afterload
Pathogenesis and organ response 5.
• Pulmonary response
– Increased pulmonary vascular resistance
(particularly in septic shock)
– Tachypnoe, but restricted ventilation,
reduced functional residual capacity –
atelectasis.
– Acute respiratory distress syndrome
characterized by noncardiogenic pulmonary
edema secondary to pulmonary capillary
endothelial and alveolar epithelial injury
Pathogenesis and organ response 6.
• Renal response
– Consequences of hypoperfusion: reduced
renal blood flow, increased afferent arteriolar
resistance – reduced glomerular filtration rate
together with the increased aldosterone and
vasopressin production will cause reduced
urine volume
– Acute tubular necrosis as a result of
interaction of shock, sepsis and administration
of nephrotoxic agents
Pathogenesis and organ response 7.
• Inflammatory responses
– Activation of an extensive network of proinflammatory
mediator systems plays a significant role in the
progression of shock and contributes to the
development of organ injury
• Activation of classic and alternative pathways of
complement cascade causing cell damage
• Activation of coagulation cascade causes microvascular
thrombosis
• Tumor necroris factor-α, produced by activated
macrophages contributes to hypotension, lactic acidosis, and
respiratory failure
• IL-8 upregulate adhesion molecules on the neutrophil to
enhance aggregation, and damage to the vascular
endothelium
• Increased Thromboxan A2 levels is potent vasoconstrictor
that contributes to the pulmonary hypertension
Specific forms of shock
• Hypovolemic shock: Most common form of shock
results either from the loss of red blood cell mass and
plasma
Mild (<20% blood
volume)
Moderate (20-40% blood
volume
Severe (>40% blood
volume)
Cool extremities
Diaphoresis
Collapsed veins
Anxiety
Same plus:
Tachycardia
Tachypnoe
Oliguria
Postural change
Same plus:
Hemodynamic instability
Marked tachycardia
Hypotension
Mental status deterioration
(coma)
The transition from mild to severe hypovolemic shock can be insidious or
extremly rapid
Diagnosis and treatment of the
hypovolemic shock
• Diagnosis is more difficult when the source of blood loss
is occult, or when plasma volume alone is depleted.
• After acut hemorrhage, Hb and Ht values do not change
until compensatory fluid shifts have occured or
exogenous fluid is administered. Plasma loss causes
hemoconcentration, and free water loss leads to
hypernatremia
• Essential to distinquish between hypovolemic and
cardiogenic shock. Both form associated with reduced
stroke volume, elevated systemic vascular resistance
and tachycardia. However, the findings in cardiogen
shock of jugular vein distension and S3 galopp
distinquish it from the hypovolemic shock.
• Therapy: fluid repletion, blood transfusion, dopamin, or
dobutamin may be required. Norepinephrine is
inappropriate. Support of respiratory functions.
Specific forms of shock
• Traumatic shock
– Hypovolemia (fluid loss into the interstitum of injured
tissues), and blood loss. These fluid losses are
compounded by injury-induced inflammatory
responses, leading to multiple organ failure.
• Neurogenic shock
– Interruption of sympatetic vasomotor input after high
cervical spinal cord injury, severe head injury
– Arteriolar dilatation and venodilatation, which
decreases venous return and cardiac output. Warm
extremities. Correction of the hypovolemia and
norepinephrine may be necessery to augment
vascular resistance
Specific forms of shock
• Intrinsic cardiogenic shock
– Caused by sudden failure of the heart as an effective pump. It
occurs most commonly as a complication of acute myocardial
infarction, but it may also be seen in patients with severe bradyor tachyarrhythmias, valvular heart disease, or in terminal stage
of chronic heart failure (ischemic heart disease, or dilated
cardiomyopathy)
– Low cardiac output, reduced systemic perfusion, elevation of
systemic vascular resistance and pulmonary vascular pressure.
Absolute or relative hypovolemia is usually not present.
Pulmonary edema, reduction in lung compliance
– Treatment: The goal is to increase contractility without significant
increases in heart rate (dopamine, dobutamine). Pulmonary
congestion may be responsive to intravenous furosemid. In case
of inadequate response intraaortic balloon-pump.
Revascularization in patients with AMI, correction of anatomic
defects such as rupture of the papillary muscles.
Specific forms of shock
• Septic shock
– Caused by the systemic response to a severe
infection. Most frequently in elderly or
immuncompromised patients and in those who
have undergone an invasive procedure in which
bacterial contamination has occured.
– Clinical findings in septic shock are a consequence of
metabolic and circulatory derangements driven by
the systemic infection and the release of toxic
components of the infectious organisms.
– Organism toxins lead to the release of cytokines
– Tissue factor expression and fibrin deposition are
increased, and DIC may develop
– NO-synthase is stimulated, and NO, a powerful
vasodilatator is released.
Two forms (phases) of septic shock
• Early, hyperdynamic phase of septic shock
– Tachycardia, normal or elevated cardiac output, reduced
systemic vascular resistance
– Extremities are warm, however the visceral flow is decreased
– Increased capillary permeability and continued loss of
intravascular volume
– The venous oxygen saturation may be normal while oxygen
extraction is reduced because of impaired microcirculation and
impaired mitochondrial utilization.
• Late, hypodynamic phase of septic shock
– Vasoconstriction occurs and the cardiac output declines.
Oliguria, renal failure and hypothermia.
– There may be striking increase in serum lactate
Treatment: Aggressive volume expansion with crystalloid solution.
Inotropic support, High-dose of activated protein C, Antibiotics
Specific forms of shock
• Hypoadrenal shock
– Occurs in settings in which unrecognized
adrenal insufficiency complicates the host
response to stress induced by acute illnes or
major surgery.
• Charachterized by reductions in systemic vascular
resistance, hypovolemia, and reduced cardiac
output
Treatment: 100 mg hydrocortisone every 6 to 8 h,
volume repletion, pressor support, antibiotics.
Aproach to the patient with shock
• Patients in shock require care in an
intensive care unit
– Continuous assessment of the physiologic
status is necessery:
• Central venous pressure, Cardiac output, Systemic
vascular reistance, Venous O2 saturation, and
Stroke volume,, Pulmonary vascular resistance,
Pulmonary capillary wedge pressure, oxygen
uptake, arterial oxygen concentration etc.
Approach to the patient with shock
Shock
Warm extremities
Cold extremities
Low cardiac output
Jugular vein distension,
rales,crepitation
Congestion
High cardiac output
Decreased CVP,
orthostasis
Septic shock,
Liver disease
„Empty heart”
Cardiogenic shock Hypovolemic shock
Evaluation of myocardial
ischemia
Volume
supplemetation
No improvement
Harrison (2007) Int Med, modified
Hypadrenic crisis?
Pericardial fluid?