Cardiology Review
6/3/2009
A 28 yom is evaluated for palpitations. He reports a 5 year history of
palpitations. These episodes used to occur once or twice a year, but over the
past 6 months, he has been experiencing them on a monthly basis. He reports
that his heart starts racing suddenly for no reason, and the episode usually
terminates abruptly after he takes a few deep breaths. Episodes typically last 10
to 15 minutes, although one episode last month lasted 30 minutes. He is
otherwise healthy, denies other symptoms, and takes no medications. Results of
his physical examination are within normal limits. A baseline EKG is obtained
and shown. The ECHO demonstrated a subtle anterior wall motion abnormality
but is otherwise WNL. A 24 hr holter demonstrates a narrow complex regular
tachycardia with rate of 205 during an episode of palpitations.
What is the next step?
RF ablation
metoprolol
stress test
verapamil
WPW
A 28 yom is evaluated for palpitations. He reports a 5 year history of
palpitations. These episodes used to occur once or twice a year, but over the
past 6 months, he has been experiencing them on a monthly basis. He reports
that his heart starts racing suddenly for no reason, and the episode usually
terminates abruptly after he takes a few deep breaths. Episodes typically last 10
to 15 minutes, although one episode last month lasted 30 minnutes. He is
otherwise healthy, denies other symptoms, and takes no medications. Tesults of
his physical examination are within normal limits. A baseline EKG is obtained
and shown. The EKG demonstrated a subtle anterior wall motion abnormality
but is otherwise WNL. A 24 hr holter demonstrates a narrow complex regular
tachycardia with rate of 205 during an episode of palpitations.
What is the next step?
RF ablation
metoprolol
stress test
verapamil
WPW

Short PR interval +delta wave +h/o tachycardia = WPW

Two circuits:
1.
2.
AV node
retrograde accessory pathway

QRS in narrow since there is conduction via AV node

The WMA is a result of abnormal depolarization via the accessory pathway.

RF ablation is first line

Avoid metoprolol, CCB, and adenosine; they blocks the AV node but not
the accessory.

Use Procainamide
A 45 yof is evaluated in the emergency department for
palpitations. She has no history of CV disease but does have a h/o
intermittent palpitations. This is her first prolonged episode, and
cough and strain maneuvers that she has used in the past to terminate
the episodes have been ineffective this time. PE is unremarkable
with the exception of tachycardia. The BP is 110/70. EKG shown.
What is the diagnosis:
AV nodal reentrant tachycardia
AV reentrant tachycardia
ectopic atrial tachycardia
multifocal atrial tachycardia
a flutter
A 45 yof is evaluated in the emergency department for palpitations. She has
no history of CV disease but does have a h/o intermittent palpitations. This is
her first prolonged episdoe, and the cough and strain maneuvers that she has
used in the past to terminate the episodes have been ineffective this time. PE
is unremarkable with the exception of tachycardia. The BP is 110/70. EKG
shown.
What is the diagnosis:
AV nodal reentrant tachycardia
AV reentrant tachycardia
ectopic atrial tachycardia
multifocal atrial tachycardia
a flutter
AVNRT
Narrow
No
P waves; buried in the QRS complex
Usual
Tx
complex tachycardia
rate 160-180
with IV adenosine
Compare


to:
AVRT- P waves are visible
MAT- irregular with 3 P wave morphologies.
AV Nodal Block

1st degree:



2nd degree:




prolonged PR
Look for drug effect (dig, beta blocker, CCB)
Mobitz I: PR progressively lengthens, then a dropped beat
Mobitz II: Intermittent non-conducted beats
3rd degree: complete dissociation
PM: asymptomatic Mobitz II and complete block.
Torsades




Atypical Vtach
Look for hypoK or hypoMg
Worse prognosis than V tach
Management is different from other VTs



Avoid Class I, Ic or III antiarrhythmics (prolong QT)
Give Magnesium acutely
Things that cause torsades: arsenic, ciapride,
droperidol, Li, methadone, fluoroquinolones
A 79 yof is seen for an annual examination. She is in good health except for osteopenia, for
which she takes Ca and VitD supplements. She walks regularly to and from the bus stop
several times per week. It now takes her 25 min to get to the bus stop; whereas it only took her
10 min a year ago. She describes dyspnea midway in her walk, causing her to stop and catch
her breath. She denies angina, presyncope, syncope or pedal edema. PE: HR 80, BP 165/86.
Lungs CTAB, carotid upstrokes delayed. S1 nl, single S2, and S4. Grade 3/6 late peaking
systolic murmur at R 2nd intercostal, radiates to R carotid. TTE with concentric LVH. EF
69%, no WMA. Trileaflet AV with heavy calcification, aortic jet 4.8/ m/sec, peak transaortic
gradient of 92, valve area of 0.7 cm2.
What will improve her quality of life?
Begin ACEI
Percutaneous aortic balloon valvuloplasty
AVR
Cardiac rehab
Stop Calcium supplement
AS
A 79 yof is seen for an annual examination. She is in good health except for osteopenia, for
which she takes Ca and VitD supplements. She walks regularly to and from the bus stop
several times per week. It takes her 25 mimn to get to the bus stop whereas it only took her 10
min a year ago. She describes dyspnea midway in her walk, causing her to stop and catch her
breath. She denies angina, presyncope, syncope or pedal edema. PE: HR 80, BP 165/86. Lungs
CTAB, carotid upstrokes delayed. S1 nl, single S2, and S4. Grade 3/6 late peaking systolic
murmur at R 2nd intercostal, radiates to R carotid. TTE with concentric LVH. EF 69%, no
WMA. Trileaflet AV with heavy calcification, aortic jet 4.8/ m/sec, peak transaortic gradient
of 92, valve area of 0.7 cm2.
What will improve quality of life?
Begin ACEI
Percutaneous aortic balloon valvuloplasty
AVR
Cardiac rehab
Stop Calcium supplement
Aortic Stenosis
Severe
AS: valve area below 0.8
Most common cause: progressive valvular Ca
Initial compensatory mechanism is myocardial hypertrophy
Indication


onset of cardiac symptoms
NOT prophylactically
Triad



for AVR:
of symptoms:
Angina
CHF
Syncope
ACEIs
contraindicated: afterload reduction may increase effective pressure
gradient across stenotic valve.
Murmurs
Sounds
Maneuvers
Other
Mitral
Stenosis
Mitral Regurg
Opening snap following
S2 on LSB or apex.
Middiastolic rumble.
Loudest after exercise.
RAD, negative biphasic
P in V1
Aortic
stenosis
Harsh,
crescendo/decrescendo,
at R 2nd intercostal
Paradoxical splitting of
S2, radiates to carotids
with slow upstoke,
louder with squatting or
expiration.
LVH
Aortic regurg
Faint, blowing between
S2 and S1, diastolic, at
LSB 3/4th intercostal
Wide pulse pressure,
prominent carotid
pulses.
LVH
VSD
Holosystolic at LLSB
Louder with handgrip
ASD
Fixed split S2
Primum: LAD, RBBB
Secundum: RAD, RBBB
Holosystolic, blowing,
over PMI, radiates to L
axilla
LAD, LVH,
Primum needs Abx
prophy
Primum may have AV
block
42 yof with recent onset of exertional dyspnea and occasional
palpitations. She has been told for many years that she has a heart
murmur. PE: BP 129/78 in both upper extremities, JVP elevated with both a
and v waves. Apical pulse unremarkable. Parasternal impulse present. 2/6
midsystolic murmur noted at 2nd L intercostal and 2/6 holosystolic murmur at
the apex and L sternal border. Fixes splitting of S2.
Which is the most likely cause of the symptoms?
secundum atrial septal defect
primum atrial septal defect
PFO
sinus venosus atrial septal defect
ASD
42 yof with recent onset of exertional dyspnea and occasional
palpitations. She has been told for many years that she has a heart
murmur. PE: BP 1269/78 in both upper extremities, JVP elevated with both a
and v waves. Apical pulse unremarkable. Parasternal impulse present. 2/6
midsystilic murmur noted at 2nd L intercostal and 2/6 holosystolic murmur at
the apex and L sternal border. Fixes splitting of S2.
Which is the most likely cause of the symptoms?
secundum atrial septal defect
primum atrial septal defect
PFO
sinus venosus atrial septal defect
ASD
Fixed
splitting of S2: hallmark of ASD
Exam:




Parasternal impulse: R sided cardiac enlargement (also seen on CXR)
Systolic murmur at the apex: mitral regurg
L sternal border: TVR
midsystolic murmur: flow across the pulmonary valve.
EKG
PE
shows first degree AV vlock and LAD= primum
for PFO is normal
Why
does this matter: Secundum and PFO can be treated with percutaneous
devices.
69 yom is evaluated in the ED for acute onset of substernal CP radiating to the
L arm. Former smoker and PMH of HTN. PE 210/95 R arm, 164/56 L arm,
HR 90, RR 20, dullness half way up the R posterior thorax, 2/6 diastolic
murmur at RUSB, EKG with NSR, 2-3 mm inferior ST segment elevation.
What is the most appropriate med to administer?
ASA
IV heparin
Thrombolytic
Beta blocker
ACEI
Dissection
69 yom is evaluated in the ED for acute onset of substernal CP radiating to the
L arm. Former smoker and PMH of HTN. PE 210/95 R arm, 164/56 L arm,
HR 90, RR 20, dullness half way up the R posterior thorax, 2/6 diastolic
murmur at RUSB, EKG with NSR, 2-3 mm inferior ST segment elevation.
What is the most appropriate med to administer?
ASA
IV heparin
Thrombolytic
Beta Blocker
ACEI
Aortic Dissection
Disparate
blood pressures + diastolic murmur of AR
= acute ascending aortic dissection (involves the AV)
Dullness
RCA
in R lung = hemothorax (complication of dissection)
is the most common involved coronary with dissection,
ischemia (STEMI).
Initial


Treatment
beta blockade (decrease shear stress)
Start BB before afterload reduction.
Avoid:

ASA, heparin, thrombolytics
Increased risk of: periaortic hemorrhage, aortic rupture, and cardiac tamponade
Studies:
TEE, chest CT with contrast, contrasted MR.
A 68 yom is evaluated in the ED for chest pain that has lasted 90 min. He was
eating when he developed sudden onset of sharp precordial pain radiating
toward both shoulders and back. The pain is 9/10. PMH for HTN and
dyslipidemia. PE: HR 90, RR 19 BP 110/60, O2 sat 94% on RA. Lungs:
bibasilar crackles. Heart sounds distant, nl S1, S2, no S4 or S3. 3/6 diastolic
murmur at the RUSB, radiates across L precordium. No abdominal
bruits. Trace pedal edema. P CXR with prominent thoracic aorta and
widening of the mediastinum.
Next step?
cath
fibrinolytic therapy
VQ scan
CT chest
balloon pump
Aortic dissection with AR
A 68 yom is evaluated in the ED for chest pain that has lasted 90 min. He was
eating when he developed sudden onset of sharp precordial pain radiating
toward both shoulders and back. The pain is 9/10. PMH for HTN and
dyslipidemia. PE: HR 90, RR 19 BP 110/60, O2 sat 94% on RA. Lungs:
bibasilar crackles. Heart sounds distant, nl S1, S2, no S4 or S3. 3/6 diastolic
murmur at the RUSB, radiates across L precordium. No abdominal
bruits. Trace pedal edema. P CXR with prominent thoracic aorta and
widening of the mediastinum.
Next step?
cath
fibrinolytic therapy
VQ scan
CT chest
balloon pump – This would exacerbate the acute AR
Ascending Dissection with Acute AR
Aortic
Risk





Regurg: Diastolic murmur
Factors:
age
HTN
bicuspid aortic valve
Coarctations
3rd trimester pregnancy and Marfans)
Possible



imaging include:
CT chest with contrast
MRI with contrast
TEE
Complications:




MI from anterograde propogation,
Tamponade
limb ischemia (if great vessels involved)
aortic rupture
Ascending vs Descending
Ascending dissections are high risk for complications.
Do not pass go, instead… go directly to surgery.
Descending dissections treat medically (Beta Blockers
and nitroprusside-if needed), and if pain persists, it is
due to extension of dissection, then go to surgery.
Even with repair mortality is 26%, without 55%
AAA



Screen all men with smoking hx after age
65 (medicare pays for this)
AAA, DM are both CAD equivalents
Surgery




Men >5 cm
Women >4.5
Marfans >4.5
expands more than 0.5/year
64 yof presents 6 hrs after onset of severe crushing chest pain associated with
diaphoresis, n/v. She has a h/o mild hyperlipidemia, meds include atorvastatin
and ASA. BP 140/88, HR 88, lungs clear, no murmurs, abd and extremities
normal. EKG 3 mm ST elevation in leads II, III, and aVF, occasional
PVCs. No cath lab facilities are present, fibrinolytics are given and transferred
to ICU. CP resolves. 2 episodes of 6-10 beats of Vtach noted with stable
hemodynamics. EKG now shows <0.5 mV ST segment elevation.
In addition to heparin ans ASA, which is the next appropriate step?
Cath
Plavix
Beta blocker
amiodarone
DSE
64 yow presents 6 hrs after onset of severe crushing chest pain associated with
diaphoresis, n/v. She has a h/o mild hyperlipidemia, meds in clude atorvastatin
and ASA. BP 140/88, HR 88, lungs clear, no murmurs, abd and extremities
normal. EKG 3 mm ST elevation in leads II, III, and aVF, occasional
PVCs. No cath lab facilities are present, fibrinolytics are given and transferred
to ICU. CP resolves. 2 episodes of 6-10 beats of Vtaqch noted with stable
hemodynamics. EKG now shows <0.5 mV ST segment elevation.
In addition to heparin ans ASA, which is the next appropriate step?
Cath
Plavix
Beta blocker
amiodarone
DSE
Inferior STEMI
Medical




management After MI:
ASA
beta blockers
ACEI
Statin
Reperfusion
arrhythmias usu do not require additional
antiarrhythmic therapy.
Immediate




cath after STEMI for:
recurrent ischemia
persistent ST elevation
hemodynamic instability
CHF
ACS Treatment for the Boards








ASA
Plavix (with, or prior to, PCI- CURE trial),
Lovenox (more effective than heparin)
beta blocker
ACEI
IIbIIIa for PCI but NOT without PCI
Statin
smoking cessation.
78 yom brought to the ED for malaise, fatigue and mild dyspnea on
exertion. Intermittent CP for 5 days, with the most severe episode 2 days
ago. Pain free since then. PMH: HTN, DM type 2, meds: ACEI and
metformin. BP 112/82, HR 92, JVP is 5 mmHg, no carotid bruits, lungs
clear. CV nl S1/S2, 2/6 holosystoloic murmur at apex to axilla, diminished leg
pulses, no edema. EKG with sinus tach, Q waves in V1-4. Renal fn and Hct
are normal. CK 120, Troponin 6.8. CXR with mild pulmonary edema. Pt is
started on lovenox and ASA.
Next appropriate therapeutic approach is?
plavix
glycoprotein receptor blocker
fibrinolysis
urgent cath
beta blocker
Anterior STEMI
78 yom brought to the ED for malaise, fatigue and mild dyspnea on
exertion. Intermittent Cp for 5 days, most severe episode 2 days ago. Pain
free since then. PMH: HTN, DM type 2, meds: ACEI and metformin. BP
112/82, HR 92, JVP is 5 mmHg, no carotid bruits, lungs clear. CV nl S1/S2,
2/6 holosystoloic murmur at apex to axilla, diminished leg pulses, no
edema. EKG with sinus tach, Q waves in V1-4. Renal fn and Hct are
normal. CK 120, Troponin 6.8. CXR with mild pulmonary edema. Pt is
started on lovenox and ASA.
Next appropriate therapeutic approach is?
plavix
glycoprotein receptor blocker
fibrinolysis
urgent cath
beta blocker
Anterior STEMI
Beta
Blockers are always a good answer.
Unless signs of persistent ischemia, cath is not urgently indicated.
Late fibrinolysis not beneficial, and increases risk of hemorrhage in the
infarcted zone.
No benefit of plavix added to ASA if there are no plans on PCI
IIbIIIa
is indicated for patients who are going to cath/PCI, if there are high
risk factors such as:







TIMI>3
elevated troponin
ongoing ischemia
new ST changes
CHF or DM
hemodynamic instability
PCI within the past 6 months
42 yom evaluated in Halifax Regional for L shoulder chest pain that radiates to
the jaw, associated with diaphoresis and mild dyspnea. No PMH, no meds. FH
of CAD in first degree relatives. ED administered IV heparin, atenolol,
ASA. BP 100/79, HR 61, no JVD, no carotid bruits, lungs clear, nl S1/S2, no
murmurs. Abd and extremities wnl. No cath lab at the OSH, UNC is 62 miles
away, and will take 2 hours.
Before transfer you should give…..
2b3a receptor blocker
plavix
esmolol
fibrinolytic therapy
NTG
STEMI with no Cath Lab
42 yom evaluated in rural ED for L shoulder chest pain that radiates to the jaw,
associated with diaphoresis and mild dyspnea. No PMH, no meds. FH of
CAD in first degree relatives. ED administered IV heparin, atenolol,
ASA. BP 100/79, HR 61, no JVD, no carotid bruits, lungs clear, nl S1/S2, no
murmurs. Abd and extremities wnl. No cath lab at the OSH, UNC is 62 miles
away, and will take 2 hours.
Before transfer you should give…..
2b3a receptor blocker
plavix
esmolol
fibrinolytic therapy
NTG
STEMI and Fibrinolytics
The
best answer is always CATH
Second best is FIBRINOLYSIS
Fibrinolysis


Given within 30 minutes of arrival to ED
DO NOT give if >12 hours after onset of symptoms and
asymptomatic (this pt is less than 12 hours)
Contraindications:






recent surgery
CVA
Bleeding
uncontrolled HTN
PUD
cardiogenic shock
68 yom seen 14 hrs after onset of substernal CP that lasted for 2 hrs. 6 hrs
prior to presentation he experienced 2 additional shorter episodes of CP, each
10 min in duration. CP associated with diaphoresis, no dyspnea, palpitations,
or dizziness. H/o HTN, DM, active smoker 40 pack year hx. Home meds:
ASA, norvasc, metoprolol and glyburide. PE: normotensive, NAD, enlarged
PMI. CK and troponins elevated, EKG with small R waves in V1-3,
unchanged by day 3 of hospitalization. ECHO with severe hypokinetic LV
anterior wall, moderate hypokinesis of the inferior wall and LVEF
38%. Current meds: metoprolol, asa, NTG, plavix, lipitor, lisinopril,
heparin. What is the most appropriate evaluation prior to discharge?
24 hr EKG
low level treadmill stress test
dobutamine viability study
cath
68 yom seen 14 hrs after onset of substernal CP that lasted for 2 hrs. 6 hrs
prior to presentation he experienced 2 additional shorter episodes of CP, each
10 min in duration. CP associated with diaphoresis, no dyspnea, palpitations,
or dizziness. H/o HTN, DM, active smoker 40 pack year hx. Home meds:
ASA, norvasc, metoprolol and glyburide. PE: normotensive, NAD, enlarged
PMI. CK and troponins elevated, EKG with small R waves in V1-3,
unchanged by day 3 of hospitalization. ECHO with severe hypokinetic LV
anterior wall, moderate hypokinesis of the inferior wall and LVEF
38%. Current meds: metoprolol, asa, NTG, plavix, lipitor, lisinopril,
heparin. What is the most appropriate evaluation prior to discharge?
24 hr EKG
low level treadmill stress test
dobutamine viability study
cath
>12 Hours out from an Anterior MI
Patient
did not get revascularization or thrombolytics. By ECHO pt has
decreased EF and 2 areas of WMA with TIMI 5
High





risk factors for complications after MI:
Multivessel CAD
anterior MI
EF <40%
CHF
recurrent ischemia
Never
subject a high risk pt to stress testing even if submaximal stress.
Post-MI complications
1. Recurrent ischemia: 1/3 of patients, and more common in NSTEMI
rather than STEMI.
2. Arrhythmias: bradycardia, SVT/atrial fibrillation, ventricular
arrhythmias (mostly in the first few hours), AV block,
3. CHF
4. Myocardial rupture: rupture of the LV, 1% of pts, 2-7 days
(pseudoaneurysm- rupture sealed by pericardium)
5. LV aneursym: from scar, predisposed to CHF, thrombus, and
arrhythmias
6. Papillary muscle rupture: posteromedial papillary muscle is more
common b/c single blood supply from RCA. Classic case: inferior MI,
later becomes hypotensive, large V waves in PA wedge tracing, new
holosytolic murmur at the apex.
7. Mural thrombi (in anterior and apical STEMI)
8. pericarditis
45 yom brought by EMS for severe CP. Pain similar to prior episode when he
underwent angioplasty 8 m ago. H/O HTN, on beta blocker, also takes ASA
81 mg q day. Nl serum CH and no h/o DM, DOE or claudication. PE: BP
90/60, HR 59, no JVD, no bruits, lungs clear, Nl S1, S2. S4 present with 1/6
SEM at LSB, nonradiating. Abd and extremities nl. EKG with ST depression
in II, III, and aVF. Admitted and placed on plavix, nitrates, and
lovenox. Troponin 0.8 (nl <0.5).
What is the next appropriate step?
Heparin
esmolol
abciximab
NTG
USA
45 yom brought by EMS for severe CP. Pain similar to prior episode when he
underwent angioplasty 8 m ago. H/O HTN, on beta blocker, also takes ASA
81 mg q day. Nl serum CH and no h/o DM, DOE or claudication. PE: BP
90/60, HR 59, no JVD, no bruits, lungs clear, Nl S1, S2. S4 present with 1/6
SEM at LSB, nonradiating. Abd and extremities nl. EKG with ST depression
in II, III, and aVF. Admitted and placed on plavix, nitrates, and
lovenox. Troponin 0.8 (nl <0.5).
What is the next appropriate step?
Heparin
esmolol
abciximab
NTG
USA and NSTEMI
IIbIIIa:


beneficial with pts going to PCI
associated with increased mortality for those not going to PCI
Who








should get it:
TIMI >3
recurrent angina
elevated troponin
new ST depressions
prior CABG
percutaneous intervention within 6 months
VTach
hemodynamic instability
Plavix
is also indicated, but usually held if going to cath in case CABG
needed.
49 yom presents to the ED with mild chest discomfort, with nausea and
dyspnea for 2 hours. No relief with antacids. No PMH, no meds. Older
brother with an MI 9 months earlier, father with CABG 12 years ago. BP
109/78, HR 88, no jvd, no carotid bruits, nl S1/S2, no m/r/g, lungs, abd,
extremities wnl. Troponin of 6. EKG with 1mV ST elevation in II, III and
aVF. Started on lovenox, asa, metoprolol, and IIbIIIa, and sent to cath. DES
placed in subtotally occluded RCA. ECHO on d#2 shows nl LV, no MR, no
effusion. D#4 no complications, and plan on d/c.
In addition to ASA, plavix, and metoprolol what should be given?
Lipitor
lisinopril
warfarin
niacin
49 yom presents to the ED with mild chest discomfort, with nausea and
dyspnea for 2 hours. No relief with antacids. No PMH, no meds. Older
brother with an MI 9 months earlier, father with CABG 12 years ago. BP
109/78, HR 88, no jvd, no carotid bruits, nl S1/S2, no m/r/g, lungs, abd,
extremities wnl. Troponin of 6. EKG with 1mV ST elevation in II, III and
aVF. Started on lovenox, asa, metoprolol, and IIbIIIa, and sent to cath. DES
placed in subtotally occluded RCA. ECHO on d#2 shows nl LV, no MR, no
effusion. D#4 no complications, and plan on d/c.
In addition to ASA, plavix, and metoprolol what should be given?
Lipitor
lisinopril
warfarin
niacin
Statins
are given regardless of cholesterol level after
MI because they reduce late CV events.
PROVE-IT
TIMI 22: showed high dose atorvastatin
80 was superior to pravastatin 40 with a 16%
reduction of a composite endpoint.
Dyslipidemia



Develop more side
effects on statins
when you are
concurrently on
fibrates or niacin.
Goals: ATP III-R 2005
RF: tobacco, HTN,
Family history, AGE
(men>45, women
>55)
LDL
goal
NonHDL
goal
CAD or <70
equivele
nt (DM)
<130
2+ RF
<100
<160
0-1 RF
<130
<190
23 yof is brought to the ED after a witnessed syncopal event. The patient
reports having been at church where she DFO, after standing for 45 minutes.
She noted feeling sweaty and lightheaded and seeing spots. She was aware of
the sensation of her heart beating and then developed LOC. After the fall,
witnessed said she had a thready pulse and urinary incontinence. She regained
consciousness within 3 minutes.
Which of the following aspects of the hx is not consistent with
neurocardiogenic syncope?
Urinary incontinence
Prodrome of seeing spots, diaphoresis and lightheadedness
Thready pulse
None of the above
23 yof is brought to the ED after a witnessed syncopal event. The patient
reports having been at church where she DFO, after standing for 45 minutes.
She noted feeling sweaty and lightheaded and seeing spots. She was aware of
the sensation of her heart beating and then developed LOC. After the fall,
witnessed said she had a thready pulse and urinary incontinence. She regained
consciousness within 3 minutes.
Which of the following aspects of the hx is not consistent with
neurocardiogenic syncope?
Urinary incontinence
Prodrome of seeing spots, diaphoresis and lightheadedness
Thready pulse
None of the above
Neurocardiogenic syncope
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vasovagal and vasodepressor:
 Lose of sympathetic tone with vasodilation.
 with vasovagal there is bradycardia (due to increased vagal
tone)
Look for situational stressors: hot, crowded spaces, stressful
environment, long period of standing, hunger, pain.
Prodrome:
 light-headedness
 Diaphoresis
 Nausea
 Weakness
 visual changes
 pallor
Incontinence suggests seizure
Cardiogenic syncope
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Arrhythmia: Bradyarrhythmia, ventricular
arrhythmia or V fib, AV node block
Mechanical: Aortic valve (AS) or HOCM
Absence of premonitory symptoms,
usually exertional
Quick recovery
Orthostatic syncope
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1st- Dehydration
2nd- polypharmacy
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AV nodal blockade (BB, CCB)
Anticholinergics
3rd- autonomic insufficiency- DM
HTN-JNC7
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Treatment of HTN benefits are greater in the older
patients compared to young patients. Reduces CVA,
CHF and CV events, but not overall mortality
Isolated systolic HTN is still high risk, even in the
elderly, and should be treated.
Wide pulse pressure is a risk factor for CHF.
All patients:

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weight loss
stop EtOH,
limit Na,
exercise
HTN-JNC 7
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
1.
2.
3.
4.
5.
6.
Stage 1: 140-159/90-99
Stage II: >160/100
Goal: treat to < 140/90 or <130/80 if DM
Always start with a thiazide unless Post MI or CKD
 The number one reason for failure to control hypertension despite
multiple agents is the failure to use a thiazide diuretic.
CHF: thiazide, BB, ACEI, ARB, spironolactone
POST MI: BB, ACEI, spironolactone
DM: thiazide, BB< ACEI, ARB, CCB
CKD: ACEI, ARB
Recurrent CVA: thiazide, ACEI
High CVD risk: thiazide, BB, ACEI, CCB