Endocrinology: Physiological Basis of Collapse Flashcards
What is syncope?
sudden and temporary loss of consciousness
commonly includes cerebral hypoperfusion
What groups are syncope more common in?
More common in folks ~20 and ~80 years (bimodal distribution) and accounts for ~6% of hospital admissions in developed countries (common)
When does syncope often occur?
- When syncope occurs, it is most common for the head and heart to be at the same level, this typically permits adequate perfusion to the brain and consciousness
- Exceptions: syncope while sitting
Requirements for consciousness
- Adequate perfusion of brain with oxygenated blood
- Adequate delivery of glucose for cellular metabolism
- Adequate neural activity and connection of sensors and effectors
- Changes in pH, electrolytes, temperature, pressure, and metabolism can have a negative impact on consciousness
Basic reflex mechanisms that help maintain consciousness
The cortex of the brain is important for all forms of perception and control of voluntary movements so when there is inadequate perfusion, many things become dysregulated.
Basic reflex mechanisms that help maintain consciousness
- Cerebrovascular autoregulation: aims to maintain BP within a narrow range, when cerebrovascular blood pressure drops below 70mmHg cerebral ischemia typically occurs
- Unhealthy ageing and some medical disorders can decrease the sensitivity of the cardiovagal baroreflex predisposing onto syncope of presyncope (dizziness)
- The baroreceptor reflex is a neurocardiovascular reflex that aims to maintain arterial BP/ cerebral perfusion
- Physical activity, digestion, mental state and changes in posture can alter cardiovascular homeostasis
E.g., on standing the distensible veins the dependent limbs can hold an additional 500-800mLs of blood
- Pressure sensors (baroreceptors) in the aortic arch and carotid sinus detect the decrease in BP and relay to the CNS to decrease parasympathetic tone and increase sympathetic tone
- Withdrawal of PNS (vagal tone) increases HR and rise in SNS increases noradrenaline secretion increasing peripheral vasoconstriction
- Together this increases BP and cerebral perfusion
- When these responses are slow and sluggish this can lead to syncope
Some causes of syncopal collapse
- Situational: pain, stress or emotion, dehydration, blood loss, postprandial state, cough or sneeze, hair brushing/ shaving, cold liquids, stretching
- Reflex (neurally mediated syncope): vasovagal syncope (most common), postural orthostatic tachycardia (POTS), orthostatic hypotension
- Cardiac: arrhythmia, bradycardia or tachycardia, structural cardiac disorders, myocardial infraction (as a group second most common)
- Psychogenic: anxiety disorder, depressive disorder, conversion disorder, attention seeking behaviour, Munchausen syndrome
- Metabolic/ other: hypoglycaemia, anorexia, pregnancy, hyperventilation/ holding breath, anaemia, alcohol/ drugs, failure of venous return, blood loss hypovolaemia, autonomic dysfunction
- Neurologic: seizures, migraines, brain tumour, cerebrovascular occlusive disease, arteriovenous malformation
Example mechanism for reflex or neurally-mediated syncope
- Anxiety, emotion, stress can trigger cortical sites to generate exaggerated sympathetic nervous activity followed by an increase in parasympathetic tone, and SNS withdrawal effectively generating a rapid up down response; this is the cause of the prodromal (preceding) signs and symptoms of reflex syncope: diaphoresis (sweating), dizziness, nausea, epigastric pain
- Syncope can be avoided by moving the individual to a supine position with the heart and head at an equal level
- Cause: the transient shift in autonomic response leads to trigger vasodilation and reduced CO
- These responses are more common in young adults and over 70
- Situational syncope is typically associated with events that increase parasympathetic (vagal) output
- Increases in intrathoracic pressure, e.g., Valsalva manoeuvre, holding ones breath, coughing, sneezing, heaving lifting, results in compression of the vena cava, reduced venous returned, reduced cardiac filling, reduced CO and decrease in BP – this triggers a reflex increase in SNS output
- Resumption of breathing generates increased negative pressure, and along with vis a tergo in the venous system improves cardiac filling, transiently, above normal resulting in a transient increase in BP – this triggers an increase in parasympathetic drive – bradycardia – and a reduction in BP And hence decreased cerebral perfusion/ syncope
- Less common forms of reflex syncope include: nasopharyngeal stimulation swallow, glossopharyngeal and trigeminal neuralgia syncope. Stimulation of the urinary tract can stimulate post micturition syncope. Retrograde GI stimulation can also trigger syncope
- Carotid sinus hypersensitivity; in 30% of older folks, pressure against the carotid sinus (above the bifurcation of the common carotid artery) produces a strong cardioinhibitory vasodepressor reflex and syncope
Orthostatic hypotension/ syncope
- Syncope can occur rapidly upon standing due to: actual or relative volume depletion (dehydration, excessive diuresis, GI bleeding, vasodilatory anti-hypertensive drugs)
- Abnormal vasomotor compensatory mechanisms to an orthostatic challenge
- Not associated with vagal hyperactivity – rather an insufficient (baroreceptor-mediated) sympathetic response to standing
- Older pts increased risk of orthostatic hypotension and syncope because of altered baroreceptor responsiveness, polypharmacy, and increased risk of volume depletion
Cardiac syncope
- A consequence of inadequate effective CO and may reflect serious underlying structural heart disease
- Rhythm/ conductivity disorders: arrhythmias, sinus node problems, heart block
- Mechanical obstruction/ failure: aortic stenosis, pulmonary embolism, prosthetic valve dysfunction, severe mitral stenosis, left atrial myxoma (cardiac tumour)
- Congenital heart condition (rare): young people without a prior history of heart disease may experience fainting as the first clinical symptom
Neurological disease and syncope
- Cerebrovascular occlusive disease can cause collapse
- Transient ischaemic attacks caused by vertebrobasilar insufficiency may cause syncope – tend to be elderly men with ischaemic heart disease
- Distinguishing seizures from syncope can be difficult – especially if cerebral hypoxia secondary to cerebral hypoperfusion causes ‘convulsive syncope’ – similar movements to tonic-clonic seizure activity
- Localised seizure activity may also initiate the autonomic reflex arc leading to hypotension and bradycardia
- Neurodegeneration associated with Parkinson’s disease can increase risk of orthostatic hypotension
Psychiatric disease and syncope
- Vasovagal syncope can be caused by acute stress or fear and is therefore implicated in anxiety, panic, and major depressive disorders
- Hyperventilation, particularly in panic disorder, leads to hypocapnia, causing a transient increase in cerebrovascular resistance coupled with simultaneous peripheral vasodilation
- Psychogenic syncope – recurrent unexplained syncope despite thorough investigation. Some may experience syncope during tilt testing, with no measurable change in BP, HR, EEG pattern or transcranial blood flow
- Of patients with syncope of unknown origin, estimated >20% have psychiatric illness
Describe the physiology/ pathophysiology associated with diabetic clients that may contribute to collapse
Hypoglycaemia and CNS dysfunction: hypoglycaemia leads to symptoms of sympathetic nervous system stimulation or of CNS dysfunction, can result in a transient loss of consciousness that mimics syncope; however can occur without acute, transient, and reversible hypotension and cerebral hypoperfusion
This can occur when taking glucose lowering drugs, i.e., in diabetics
Insulin-deficient diabetic can have reduced sympathoadrenal response to hypoglycaemia, with attenuated awareness and defective glucose counterregulatory mechanisms – can lead to recurrent hypoglycaemia
Identify why pregnancy is often associated with presyncope symptoms
Progesterone (higher levels during pregnancy) promotes vasodilation –> systolic BP can decrease by 5-10mmHg, diastolic by ~15mmHg. This increases the likelihood of orthostatic hypotension
Feeling dizzy/ light-headed can also be exacerbated by:
- Dyspnoea (breathlessness) as a common side-effect of pregnancy
- Heat: more blood directed to the skin
- Iron deficiency (or other forms of) anaemia: reduced total RBC compared to metabolic need, can cause a reduction in O2 delivery
- Vomiting and nausea due to morning sickness: not eating due to morning sickness –> hypoglycaemia, vomiting can cause dehydration, sweating, anxiety
- Dehydration
Vary rarely, fainting and dizziness may suggest more serious problems, such as bleeding from the placenta.
Late pregnancy (3rd trimester) – gravid uterus can occlude major vessels in legs, pelvis and trunk (particularly vena cava), particularly in supine position –> supine hypotensive syndrome
- Reduced CO, squeezing aorta
- Vena cava compressed against vertebrae
- Reduced venous return, reduced profusion
