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Internal Medicine > Symptom To Diagnosis - Syncope > Flashcards

Symptom To Diagnosis - Syncope Flashcards

1
Q

Consciousness requires the following:

A
  1. Organized cortical electrical activity.
  2. Glucose.
  3. Oxygen.
  4. A functional delivery system to deliver oxygen and glucose.
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2
Q

The evaluation of ALL syncopal patients must include?

A
  1. Thorough history.
  2. Physical exam.
  3. ECG.
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3
Q

Neurocardiogenic (vasovagal) syncope - Textbook presentation:

A

Typically develops in young patients during prolonged standing at times precipitated by pain or anxiety (ie, phlebotomy).
–> Lightheadedness, nausea, and diaphoresis may precede syncope, which is BRIEF.

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4
Q

MCC of syncope:

A

Neurocardiogenic (vasovagal) –> 20-33%.

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5
Q

Pathophysiology of neurocardiogenic syncope:

A
  1. Low preload state due to venous pooling (from prolonged standing) or dehydration.
  2. Superimposed anxiety, pain or fears triggers a sympathetic surge.
  3. Sympathetic surge augments ventricular contraction.
  4. Vigorous contraction coupled with low preload results in LOW ESV, which triggers intracardiac mechanoreceptors.
  5. Mechanoreceptors trigger the vagal reflex.
  6. Vagal reflex triggers bradycardia, vasodilatation, or both, resulting in hypotension and syncope.
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6
Q

EBD of neurocardiogenic syncope - Provocative circumstances:

A 
37% --> Prolonged standing.
42% --> Hot weather.
23% --> Lack of food.
21% --> Fear.
14% --> Acute pain.
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7
Q

EBD of neurocardiogenic syncope - Sensitive finding?

A

NO SINGLE FINDING is very sensitive (14-40%).

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8
Q

EBD of neurocardiogenic syncope - Certain findings are fairly specific and increase the likelihood of neurocardiogenic syncope when present:

A

LR+ 12 –> Feeling warm.
LR+ 9 –> Prolonged standing.
LR+ 8 –> Abdominal discomfort prior to syncope.
LR+ 7 –> Occurring during injection/cannulation.

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9
Q

EBD of neurocardiogenic syncope - Syncope DURING exercise should raise the suspicion of?

A

CARDIOGENIC SYNCOPE.

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10
Q

EBD of neurocardiogenic syncope - Lab and radiologic tests:

A
  1. Typical history, normal physical exam, ECG, + no evidence of heart disease or red flags –> NO FURTHER TESTING.
  2. Atypical history (without a clear precipitant) –> Echocardiogram + occasionally tilt-table testing.
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11
Q

HCM - Textbook presentation:

A

May be asymptomatic and discovered due to a family history of sudden cardiac death, during the evaluation of an asymptomatic systolic murmur, during pre-participation athlete screening, or when symptoms occur (syncope, HF, A-fib, cardiac arrest).

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12
Q

MCC of cardiovascular death among young athletes:

A

HCM.

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13
Q

HCM - Complications:

A
  1. HF.
  2. Angina.
  3. MR.
  4. A-fib.
  5. Stroke.
  6. Syncope.
  7. Sudden cardiac death.
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14
Q

Angina develops in …-…% of patients with HCM.

A

25-30%.

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15
Q

Syncope develops in …-…% of patients with HCM.

A

15-25%.

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16
Q

ANNUAL risk of sudden cardiac death among all patients with HCM:

A

0.6-1%.

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17
Q

Major risk factors for sudden cardiac death in HCM:

A
  1. Prior events –> Prior cardiac arrest + spontaneous sustained VT.
  2. High risk clinical factors:
    a. Family history in 1st degree relative.
    b. Unexplained syncope.
    c. Massive LVH (>3cm).
    d. Abnormal BP response to exercise.
    e. Nonsustained VT on Holter monitoring.
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18
Q

Annual evaluation of patients with HCM:

A
  1. History and physical exam.
  2. Family history.
  3. Echocardiography.
  4. 48h-Holter.
  5. Exercise stress testing –> To assess BP response to exercise and evaluate ischemia.
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19
Q

EBD of HCM - Classic murmur of HCM - Increased and decreased when?

A

Increased –> By maneuvers that DECREASE chamber size (incr. obstruction) - Increases as the patient goes from a squatting to a standing position (sens 95%, spec 84%, LR+ 5.9, LR- 0.06).
Decreased –> Passive leg elevation –> Sens 85%, spec 91%, LR+ 9.4, LR-0.16.

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20
Q

EBD of HCM - ECG findings - Abnormal in?

A

92% (73% in asymptomatic patients without obstruction).

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21
Q

EBD of HCM - ECG abnormalities:

A

Repolarization abnormalities –> ST segment elevation, depression or T wave inversions) are found in 86% of patients although less common in asymptomatic, non obstructed patients (58%).

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22
Q

EBD of HCM - LVH present in …% of obstructed patients and …% of non obstructed.

A

81%.

48%.

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23
Q

EBD of HCM - ECG abnormalities may ?

A

Precede ECHOcardiographic abnormalities and may increase in frequency with age.

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24
Q

Cardiac syncope - Textbook presentation:

A

Elderly patients with known heart disease (ie HF, CAD) who experience sudden syncope, which may occur without warning.
Patients may have palpitations.

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25
Q

What is cardiac syncope?

A

Syncope 2o to a disorder arising within the heart.

  1. Arrhythmias (either tachyarrhythmias or bradyarrhythmias) –> MC.
  2. Occasionally –> Severe valvular heart disease (AS).
  3. Rare causes –> Aortic dissection, cardiac tamponade, atrial myxoma.
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26
Q

Cardiac syncope is associated with increased mortality. 1-yr?

A

1y mortality rate in patients with cardiac syncope is 18-33%, compared with 6% in patients with syncope of unknown cause.

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27
Q

Cardiac syncope - Among patients with DCM, sudden cardiac death (presumably arrhythmogenic) accounts for …% of mortality.

A

30%.

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28
Q

Why most SVTs do not produce syncope?

A

Because the AV node limits the ventricular response rate.

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29
Q

MC tachycardias associated with syncope:

A
  1. VT.

2. SVTs associated with an accessory pathway (ie WPW syndrome).

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30
Q

MC bradycardias associated with syncope:

A

34% of patients with heart disease have significant bradycardias.

  1. Sinus node dysfunction (sinus bradycardia, sinus pauses defined as >3 sec.
  2. AV heart block (2nd or 3rd degree).
  3. A-fib with slow ventricular response.
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31
Q

EBD of cardiac syncope - History - Specific, but not sensitive findings:

A

Syncope while supine –> LR+ 6.
Syncope during exertion –> LR+ 3.5.
Palpitations –> LR+ 5.8.

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32
Q

EBD of cardiac syncope - Certain ECG findings may suggest particular cardiac etiologies:

A
  1. ECG evidence of prior MI or a long QT interval increases the likelihood of VT.
  2. ECG findings of significant bradycardia, 2nd/3rd degree AV block –> Bradycardia.
  3. BBB suggests intermittent AV block.
  4. RV strain (S1Q3T3) or RBBB suggests PE.
  5. Ischemic changes suggest MI.
  6. Delta wave or short PR interval suggest an accessory pathway (WPW syndrome).
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33
Q

VT - Textbook presentation:

A

Patients with VT may be asymptomatic or have symptoms that range from palpitations to lightheadedness, near syncope, syncope, or sudden cardiac death.

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34
Q

VT is associated with CAD in …% of cases.

A

80%.

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35
Q

Other etiologies of VT:

A
  1. HF.
  2. HCM.
  3. Valvular heart disease.
  4. Drugs (antiarrhythmics, antipsychotic, TCA –> Prolong QT interval).
  5. Electrolyte disorder –> HYPOkalemia, HYPOcalcemia, HYPOmagnesemia.
  6. Congenital disorders.
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36
Q

Brugada syndrome as a cause of VT:

A
  1. UNUSUAL disorder 2o to mutation in the Na channel gene, which predisposes patients to polymorphic VT and sudden death.
  2. Suggestive baseline ECG abnormalities include a RBBB pattern with ST elevation in the right precordial leads.
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37
Q

ECG criteria for VT:

A
  1. > 3 CONSECUTIVE wide complex (QRS>0.12 sec) beats.

2. SVTs can also occasionally manifest wide QRS complexes.

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38
Q

ECG criteria that increase the likelihood that the wide complex tachycardia is VT include?

A
  1. Fusion beats.
  2. Capture beats.
  3. AV dissociation.
  4. QRS width >0.14sec.
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39
Q

Sustained VT is defined as VT lasting longer than …sec?

A

30seconds.

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40
Q

Evaluation of VT:

A
  1. Obtain a baseline ECG to look for evidence of ischemia, long QT syndrome.
  2. Stress testing (and coronary angiography in selected patients) is recommended for patients with exercise-induced syncope or chest pain or an intermediate or greater probability of CAD.
  3. Obtain an ECHO –> Evaluate LV function + rule out valvular heart disease.
  4. Electrophysiologic testing is recommended for selected patients.
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41
Q

Prognosis of VT:

A
  1. Potentially life-threatening arrhythmia.
  2. Predictors of mortality include:
    a. Prior cardiac arrest.
    b. LV dysfunction.
    c. Post MI.
    d. Inducible VT on EP studies.
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42
Q

Textbook presentation of bradycardia from SSS:

A
  1. Depends on duration and severity of the bradyarrhythmia.
  2. Sudden syncope when bradyarrhythmia severe + prolonged.
  3. Weakness, dyspnea on exertion, angina, TIAs, near syncope when bradycardia is less severe.
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43
Q

What is the MC indication for pacemaker placement?

A

Bradycardia from SSS.

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44
Q

What is the target group of bradycardia from SSS?

A
  1. Often seen in the elderly (mean age 68) due to fibrosis and degeneration of sinus node.
  2. Underlying CAD is common –> Contributes to the pathogenesis of SSS in some patients.
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45
Q

Medications that can depress sinus node function and aggravate SSS:

A
  1. Beta-blockers.
  2. Verapamil.
  3. Diltiazem.
  4. Digoxin.
  5. Clonidine.
  6. Methyldopa.
    + Other antiarrhythmics.
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46
Q

Bradycardia from SSS - Electrical manifestations include:

A
  1. Sinus bradycardia 2sec.
  2. Sinus arrest (with an escape junctional rhythm).
  3. Sinoatrial exit block (inability of the sinus impulse to exit the sinus node).
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47
Q

Concomitant AV conduction disturbances are present in over …% of patients with SSS.

A

50%.

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48
Q

Bradycardia from SSS is associated with supraventricular TACHYarrhythmias in …-…% of patients, particularly A-fib (tachy-brady syndrome).

A

40-60%.

Such patients may complain of palpitations.

49
Q

Is tachy-brady syndrome dangerous?

A

Markedly increases the risk of death or non fatal stroke (2- to 3-fold) compared with SSS alone.

50
Q

EBD of bradycardia from SSS - Simultaneous symptoms and ECG findings (sinus bradycardia, significant pauses or sinus exit block) …?

A

Establish the diagnosis.

51
Q

EBD of bradycardia from SSS - Holter monitoring?

A

May be used but is often non diagnostic due to intermittent nature of the arrhythmia.

52
Q

EBD of bradycardia from SSS - Carotid sinus massage:

A

May cause prolonged pauses in patients with SSS –> >3sec.

53
Q

EBD of bradycardia from SSS - Pharmacologic studies:

A
  1. Adenosine slows sinus node activity.
  2. Small studies suggest patients with SSS have delayed sinus node recovery following adenosine administration.
  3. Diagnostic accuracy is similar to EP studies.
54
Q

EBD of bradycardia from SSS - EP studies:

A

Sinus node recovery time (SNRT) and sinoatrial conduction time (SACT) can be measured.
–> Abnormal responses are 70% sens, 90% specific.
Normal results do NOT rule out SSS.

55
Q

Bradycardia due to AV block - Textbook presentation:

A

Depending on the duration and the severity of the block, patients with AV block may be asymptomatic or complain of syncope, near syncope, palpitations, angina or TIAs.

56
Q

Bradycardia due to AV block is 2o to?

A

Conduction abnormalities in the:

  1. AV node.
  2. Bundle of His.
  3. Bundle branches.
57
Q

Classification of AV block:

A

1st degree –> 1:1 conduction.
2nd degree –> Some P waves are conducted.
3rd degree –> None of the P waves are conducted.

58
Q

1st degree AV block - ECG findings:

A
  1. PR interval >0.2sec.

2. QRS width usually within normal limits.

59
Q

2nd degree (Mobitz I) AV block - ECG findings:

A
  1. Progressive lengthening of PR interval until P wave is not conducted and QRS is absent.
  2. Next PR interval is shorter than PR prior to dropped beat.
  3. QRS width usually within normal limits.
60
Q

2nd degree (Mobitz II) - ECG findings:

A
  1. Intermittent non-conduction of P waves.

2. More severe INFRANODAL damage, QRS may be widened, BBB may be seen.

61
Q

3rd degree AV block - ECG findings:

A
  1. P waves not conducted.
  2. Complete AV disassociation.
  3. Ventricular rate depends on escape pacemakers.
62
Q

1st degree AV block - Clinical findings:

A

NONE.

63
Q

2nd degree AV block (Mobitz I) - Clinical findings:

A
  1. Associated with inferior MI.

2. RARELY progresses to 3rd degree AV block.

64
Q

2nd degree AV block (Mobitz II) - Clinical findings:

A
  1. Associated with anterior MI.

2. Often progresses to 3rd degree AV block.

65
Q

3rd degree AV block - Clinical findings:

A

Associated with CAD, drugs, degeneration, abnormal electrolytes, bradycardia, hypotension.

66
Q

Which AV blocks do we treat with pacemaker?

A

2nd degree (Mobitz II) + 3rd degree.

67
Q

Etiology of bradycardia due to AV block:

A
  1. Fibrosis of the conduction system.
  2. Ischemic heart disease.
  3. Drugs (beta blockers, verapamil, diltiazem, digoxin, amiodarone).
  4. Hyperkalemia.
  5. Valvular heart disease (due to extension of calcification into the conducting system).
  6. Increased vagal tone.
  7. Miscellaneous other causes (Lyme, sarco).
68
Q

Is PE a usual cause of syncope?

A

NO - 1%.

69
Q

Between …% and …% of patients with PE experience syncope.

A

9% and 14%.

Usually 2o to MASSIVE embolization involving more than 50% of the pulmonary vascular bed.

70
Q

What should be asked in patients with syncope?

A

“What was the next thing you remember?”

Patients who do not remember the ambulance ride or suffer a period of amnesia following the event (>5min) should be evaluated for SEIZURES.

71
Q

Seizures - Textbook presentation:

A

Generalized seizures classically present with tonic-clonic activity, loss of postural tone, incontinence, and a prolonged postictal period of lethargy.

72
Q

…% of US population suffers a seizure in their lifetime.

A

3%.

73
Q

Seizures are the cause of syncope in …-…% of patients.

A

1-7%.

74
Q

Etiology of seizure and prevalence in patients over 60:

A 
35% --> Idiopathic.
49% --> Ischemic.
11% --> Tumors (primary 35%, metastatic 59%).
3% --> Trauma.
2% --> Infection.
\+ Metabolic disturbances
\+Medications
\+Illicit drugs
\+Withdrawal states.
75
Q

Etiology of seizure - Metabolic disturbances:

A
  1. Hypoglycemia + hyperglycemia (marked).
  2. Hypoxia.
  3. Hyponatremia.
  4. Hypocalcemia.
  5. Uremia.
76
Q

Etiology of seizures - Medications:

A 
Numerous have been implicated.
Some common drugs that RARELY cause seizures:
1. Cyclosporine.
2. Fentanyl.
3. Meperidine.
4. Lidocaine.
5. Phenothiazines.
6. Quinolones.
7. Theophylline.
8. TCAs.
9. Bupropion.
77
Q

EBD of seizure - Most SENSITIVE finding:

A

Postictal confusion.

Absence of it makes seizures an unlikely cause of syncope (sens 94%, LR- 0.09).

78
Q

EBD of seizure - Most SPECIFIC findings:

A
  1. Tongue laceration.
  2. Head turning.
  3. Unusual posturing.
    Spec 97%, LR+12-15.
79
Q

EBD of seizures - Certain symptoms are unusual in patients with seizures and reduce the likelihood of seizures:

A
  1. Diaphoresis preceding spell - LR 0.17.
  2. Chest pain preceding spell - LR 0.15.
  3. Palpitations - LR 0.12.
  4. Dyspnea prior to spell - LR 0.08.
  5. CAD - LR 0.08.
  6. Syncope with prolonged standing - LR 0.05.
80
Q

…-…% of patients with syncope NOT related to seizures experience LIMB JERKING, a phenomenon referred to as … .

A

15-90%.

CONVULSIVE syncope.

81
Q

Limb jerking due to syncope is associated with …?

A

Myoclonic jerks, which should be distinguished from tonic-clonic activity.

82
Q

Difference between myoclonic jerks and tonic-clonic activity:

A
  1. Myoclonic jerks tend to be arrhythmic and asymmetric, whereas the opposite is true of tonic-clonic activity.
  2. Myoclonic jerks tend to be briefer than tonic-clonic activity (average 6.6sec).
  3. Myoclonic jerks never precede collapse, whereas tonic-clonic activity may precede collapse.
83
Q

Postictal period in convulsive syncope?

A

NOT significant (<1min).

84
Q

EBD of seizure - Evaluation includes:

A
  1. EEG.
  2. Neuroimaging.
  3. Na, Ca, glucose, BUN, Cr.
  4. SaO2.
  5. Lumbar puncture.
  6. Toxicology screen.
85
Q

EBD of seizure - EEG:

A
  1. Sens (between episodes) of the spike and wave pattern is …-…% (increased with sleep deprivation).
  2. Spec is 98%.
  3. Indicated in the evaluation of patients with possible seizures.
86
Q

EBD of seizure - Neuroimaging:

A
  1. 37% of adults with new-onset seizures have structural lesions (eg tumors, strokes.
  2. 15% of adults with new-onset seizures and non focal neurologic exams have structural lesions on neuroimaging.
  3. Indicated in ALL adults with new-onset seizures.
  4. In acute cases, a non contrast CT is often performed to rule out an intracranial bleed.
  5. Follow-up MRI is recommended due to its increases sensitivity for both tumor and stroke.
87
Q

EBD of seizure - When to consider LP?

A

If CNS infection is suspected.

  • -> Elevated intracranial pressure should be excluded prior to LP –> Prevent LP-induced herniation.
  • -> Platelet count, PT, PTT should be checked PRIOR to LP –> Hemorrhage may compress spinal cord.
88
Q

Orthostatic hypotension - Textbook presentation:

A

Distinguishing feature of orthostatic hypotension is the occurrence of syncope or symptoms (near syncope, visual blurring) when arising.
–> Patients often have obvious sources of fluid or blood loss.

89
Q

Orthostatic hypotension accounts for …-…% of patients with syncope.

A

20-30%.

90
Q

Orthostatic hypotension - Definition:

A
  1. > 20mmHg decrease in SBP within 3min of standing.
  2. > 10mmHg decrease in DBP within 3min of standing.
  3. > 30bpm increase in pulse within 3min of standing.
91
Q

Orthostatic hypotension - Etiology:

A
  1. Dehydration.
  2. Hemorrhage.
  3. Medications.
  4. Prolonged bed rest.
  5. Autonomic insufficiency.
  6. Elderly (20-30% over 65).
  7. Postprandial hypotension (common in elderly).
  8. Hot environments (hot tubs, baths, saunas).
92
Q

Etiology of orthostatic hypotension (OH) - Dehydration:

A
  1. Decr. oral intake.
  2. GI losses (vomiting, diarrhea).
  3. Urinary losses:
    a. Uncontrolled DM.
    b. Salt-losing nephropathy.
    c. Adrenal insufficiency.
  4. Over-dialysis.
93
Q

Etiology of OH - Hemorrhage:

A
  1. GI.
  2. Ruptured AAA.
  3. Ruptured spleen.
  4. Ruptured ectopic pregnancy.
94
Q

Etiology of OH - Medications:

A
  1. Alpha-blockers.
  2. Diuretics.
  3. Vasodilators (nitrates, CCBs).
  4. TCAs.
  5. Phenothiazines.
  6. Alcohol and opioids.
95
Q

Etiology of OH - Autonomic insufficiency (characterized by a fall in BP upon standing WITHOUT a concomitant increase in pulse):

A
  1. DM.

2. Other neurologic disorders (Parkinson, MS, numerous others).

96
Q

EBD of OH - Accuracy of physical exam for large blood loss (630-1150mL) - Postural increase in pulse >30bpm:

A

Sens 97%.
Spec 98%.
LR+ 48.
LR- 0.03.

97
Q

EBD of OH - Accuracy of physical exam for large blood loss (630-1150mL) - Supine HR >100bpm:

A

Sens 12%.
Spec 96%.
LR+ 3.
LR- 0.9.

98
Q

EBD of OH - Accuracy of physical exam for large blood loss (630-1150mL) - Supine hypotension <95mmHg:

A

Sens - 33%.
Spec - 97%.
LR+ 11.
LR - 0.7.

99
Q

Aortic stenosis - Textbook presentation:

A

Usually diagnosed incidentally during routine exam rather than due to symptoms.

  • -> When severe –> Patients may have ANY of the 3 cardinal symptoms:
    a. HF (dyspnea).
    b. Syncope.
    c. Angina.
100
Q

Aortic stenosis - Prevalence in patients over 75:

A

3%.

101
Q

Aortic stenosis - Etiology:

A
  1. Degeneration of a previously normal valve.
  2. Congenital bicuspid valve.
  3. Rheumatic heart disease.
102
Q

Severe aortic stenosis is characterized by valve area …mmHg.

A

40mmHg.

103
Q

Aortic stenosis - Prognosis:

A

Aortic stenosis + angina –> 50% 5y mortality.
Aortic stenosis + syncope –> 50% 3y mortality.
Aortic stenosis + dyspnea –> 50% 2y mortality.

104
Q

Other LATE manifestations of aortic stenosis:

A
  1. A-fib (which is poorly tolerated).

2. Increased bleeding tendency 2o to disruption of large vWF multimers by the abnormal aortic valve.

105
Q

EBD of aortic stenosis - Findings that help rule IN aortic stenosis:

A
  1. Effort syncope in patients with a systolic murmur (LR+ 1.3-Infinitum, LR- 0.76).
  2. Slow carotid upstroke (sens 15-42%, spec 95-100%, LR+ 9.2-infinitum).
  3. Murmur radiating to right carotid (sens 71-73%, spec 90%, LR+ 7.5).
106
Q

EBD of aortic stenosis - Findings that help rule OUT aortic stenosis:

A
  1. Absence of any murmur (LR- 0).

2. Absence of murmur below right clavicular head (LR- 0.1).

107
Q

EBD of aortic stenosis - Initial test of choice:

A

Doppler echo.
Mild if –> Valve area is >1.5cm2.
Moderate if –> Valve area is 1-1.5cm2.
Severe if –> Valve area is <1cm2.

108
Q

What is the situational syncope?

A

A variant of neurocardiogenic syncope - Syncope occurs during or immediately after:

a. Micturition.
b. Defecation.
c. Swallowing.
d. Coughing.

109
Q

Carotid sinus syndrome - Textbook presentation:

A

Another variant of neurally mediated syncope.
In affected individuals pressure is applied to the carotid (eg head turning, buttoning collar, shaving or cervical motion) produces bradycardia and/or hypotension with syncope or near-syncope.

110
Q

Carotid sinus syndrome - …% report symptoms precipitated by head movement of looking upward.

A

47%.

111
Q

Carotid sinus syndrome - More common in the elderly in whom it may account for …% of recurrent syncopal events.

A

15%.

112
Q

Carotid sinus syndrome - …-…% of affected individuals experience retrograde amnesia and complain of falls but deny syncope.

A

15-56%.

113
Q

One study demonstrated carotid hypersensitivity in …% of patients presenting with NON accidental falls (compared with …% in patients with accidental falls).

A

46%.

11%.

114
Q

WPW syndrome - Textbook presentation:

A 
May be asymptomatic or present with:
1. Palpitations.
2. Near syncope.
3. Syncope.
4. Sudden death.
In asymptomatic cases, the diagnosis may only be made after typical findings are discovered on an ECG performed for some other reason.
115
Q

WPW syndrome - What happens?

A

A congenital disorder in which an accessory bundle directly connects the atria and ventricular muscle bypassing the AV node.

116
Q

WPW syndrome - A variety of life-threatening arrhythmias may develop that cause syncope or sudden cardiac death:

A
  1. Antidromic tachycardia.
  2. Reentrant loop may run in the opposite direction –> Orthodromic tachycardia.
  3. A-fib or flutter can develop.
117
Q

EBD of WPW syndrome - Baseline ECG abnormalities:

A

Baseline ECG abnormalities during normal sinus rhythm may reveal a combination of a short PR interval + a delta wave.

118
Q

Obstruction of the anterior or the posterior circulation of the brain is more important in syncope?

A

The posterior –> Reticular activating system.

119
Q

What is syncope?

A

Abrupt, transient complete loss of consciousness and postural tone.
–> May be a warning sign that the patient is at risk for sudden cardiac death –> Needs careful evaluation.

Internal Medicine (106 decks)

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