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Vasovagal Reflex Syndrome Post


Percutaneous Coronary Intervention (PCI)
Supervisor
Prihati Pujowaskito, dr., Sp.JP(K), MMRS
Created By :
Jalalludin I11108074
Chandra I11112028
Samialhuda R Fitria I11110060

CARDIOLOGY DEPARTMENT
Faculty of Medicine, Tanjungpura University
Dustira Hospital, Cimahi
2018
Acute Coronary Syndrome
(ACS)
What is ACS?
Stable Angina Unstable Angina NSTEMI STEMI
Definitions
• Unstable angina:
• An unprovoked or prolonged episode of chest pain raising suspicion of acute
myocardial infarction (AMI)
• Without definite ECG or laboratory evidence
• NSTEMI:
• Chest pain suggestive of AMI
• Non-specific ECG changes (ST depression/T inversion/normal)
• Laboratory tests showing release of troponins
• STEMI:
• Sustained chest pain suggestive of AMI
• Acute ST elevation or new LBBB
Percutaneous Coronary Intervention
(PCI)
Defenition
• Percutaneous coronary intervention (PCI), also known as coronary
angioplasty, is a nonsurgical technique for treating obstructive
coronary artery disease, including unstable angina, acute myocardial
infarction (MI), and multivessel coronary artery disease (CAD).
Indications
• Clinical indications for PCI include the following:
• Acute ST-elevation myocardial infarction (STEMI)
• Non–ST-elevation acute coronary syndrome (NSTE-ACS)
• Unstable angina
• Stable angina
• Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
• High risk stress test findings
Stable angina
• In patients with stable angina, medical therapy is recommended as
first-line therapy unless one or more of the following indications for
cardiac catheterization and PCI or coronary artery bypass grafting
(CABG) are present:
• Severe symptoms
• A change in symptom severity
• Failed medical therapy
• High-risk coronary anatomy
• Worsening left ventricular (LV) dysfunction
NSTE-ACS
For patients with NSTE-ACS, American College of Cardiology Foundation (ACCF)/American
Heart Association (AHA) guidelines on the management of NSTE-ACS (updated in 2014 [1] )
recommend an early invasive strategy in most cases, with timing as follows:
Immediate (within 2 hours) - Patients with refractory angina, recurrent angina after initial
treatment, signs/symptoms of heart failure, new/worsening mitral regurgitation, hemodynamic
instability, sustained ventricular tachycardia, or ventricular fibrillation
Early (within 24 hours) - None of the immediate characteristics but new ST-segment
depression, a GRACE risk score >140, or temporal change in troponin
Delayed invasive (within 25-72 hours) - None of the immediate or early characteristics but
renal insufficiency (glomerular filtration rate [GFR] <60 mL/min/1.73 m 2), left ventricular
ejection fraction (LVEF) <40%, early postinfarct angina, history of PCI within the preceding 6
months, prior CABG, GRACE risk score of 109-140, or TIMI score of 2 or higher
Ischemia-guided approach is recommended for patients with a low-risk score (TIMI 0 or 1,
GRACE <1).
Contraindications
Relative angiographic contraindications include the following:
Arteries <1.5 mm in diameter
Diffusely diseased saphenous vein grafts
Other coronary anatomy not amenable to PCI
Vasovagal Reflex Syndrome
Definition
• A vasovagal reaction is a sudden drop in blood pressure, heart rate and
cardiac output. It is the result of the stimulation of the parasympathetic
nervous systems and its physical responses are manifested by
activation of the vagus nerve.
• Fainting, also known as vasovagal syncope, is the most common out-
of-hospital vagal reaction, often brought on by visual stimuli (e.g.
Blood, injection), emotional stimuli, or positional orthostasis.
Sign and Symptoms
• Prior to significant, vagally-mediated hypotension, patients often
experience a prodrome of lightheadedness, nausea, the feeling of being
extremely hot (accompanied by sweating), ringing in the ears
(tinnitus), chest discomfort, confusion, a slight inability to speak or
form words, weakness, visual disturbances such as lights seeming too
bright, fuzzy or tunnel vision, yawning or anxiety.
• These symptoms last for at least a few seconds before the blood
pressure falls, often (but not always) in conjunction with marked
slowing of the heart rate, which often proceeds the fall in BP.
Mechanisms
• When the vagus nerve is stimulated, outgoing (efferent) impulses
travel from the brain stem via the vagal nerve to the heart.
• The vagal nerve fiber causes slowing of the heart rate via the sinus
node, and vasodilation of the systemic circulation through cardiac
baro-receptor and arterial baro-receptor activation.
• Other organs are also affected, resulting in nausea, pallor, diaphoresis,
yawning, and the like.
• 3 common hemodynamic presentations:
• The cardioinhibitory response, characterized by a drop in heart rate
(negative chronotropic effect) and in contractility (negative inotropic
effect), leading to a decrease in cardiac output and a drop in blood
pressure. This response results primarily from enhancement in
parasympathetic tone.
• The vasodepressor response, a drop in blood pressure without much
change in heart rate. This manifestation is due to vasodilation (loss of
vessel tone) as a result of withdrawal of sympathetic nervous system
tone.
• The mixed vasodepressor and cardioinhibitory response having
characteristics of both reactions 1 and 2 above. The majority of people
with a significant vagal reaction have this response.
Treatment
• Treatment for vasovagal syncope focuses on avoidance of triggers, volume
repletion for relative hypovolemia, and medications that interrupt the
pathophysiologic mechanisms.
• Atropine is used to block vagally-induced slowing of the heart rate and
hypotension. Doses of 0.6 to 1.2 mg IV can be given immediately and
reverse bradycardia and hypotension within 2 minutes.
• This low blood pressure can be alleviated by the administration of
intravenous atropine and normal saline. In the rare patient in whom
intravenous access is not immediately available, intra-aortic atropine can be
administered.
• Vasoconstrictors are reserved for persistent hypotension after recovery of
heart rate.
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