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LOYOLA
CARDIOLOGY
Henri Matisse: © 2015 Succession H. Matisse / Artists Rights Society (ARS), New York
INTRODUCTION
Henri Matisse (1869-1954)
The artwork featured on the front of this
reference book was a work created by
Henri Matisse titled “Icarus.” The myth
arises from the story that Daedalus and his
son Icarus, after revealing the secret of the
Labarynth to the people of Greece were
condemned to die in the Labarynth. They
then devised a way to escape the maze by
building wings of feathers and wax, but in
his hubris and excitement, Icarus, failing to
heed the warnings of his father, flew too
close to the sun and the wings melted and
fell to his death. Daedalus, having escaped
to Siciliy, and his son’s body was found by
Heracles who in turn burried him near a
small rock promontory in the Aegean Sea.
Matisse’s work is complex, showing Icarus
in free fall, his death inevitable, but set against the bursts of sunlight and the
surreal calm and peace depicted by the spot of red in place of his heart.
Produced and Edited By
Chris Latanich, MD (PGY 5)
General Cardiology Fellow
Contributors
Shermeen Memon, MD (PGY 6)
Mike Hushion, MD (PGY 6)
Ambrose Panico, DO (PGY 5)
Andrew Chen, MD (PGY 3)
Chief Cardiology Fellow
General Cardiology Fellow
Chief Cardiology Fellow
Internal Medicine Resident
ADMISSIONS
Admissions to the Cardiology Service: The following are guidelines regarding who is
generally appropriate for admission to the cardiology inpatient service (as opposed to a general
medicine service or ICU service), each patient must be evaluated respectively and if there is any
question about the propriety of an admission, it should be discussed with the fellow on service or on
call.
1) Complicated Heart Failure (e.g., severe edema, recurrent admissions or 30 day readmission,
inotropic or LVAD support)
2) Intermediate Risk ACS
3) Severe Valvular Disease
4) Pericardial Disease
5) Post ACS Complications (chest pain, access problems etc...)
6) Non-Sustained Ventricular Tachycardia OR <1 ICD shocks
7) Cardiac Syncope
8) Hypertensive Urgency
9) Adult Congenital Heart Disease
10) Clinically Significant Arrhythmias
Required Information For All Consults and Admissions: For any patient seen by the
cardiology consult service and or admitted to the CCU / HTU / inpatient cardiology service, it is
expected that the following records to have been obtained and in hand within 24 hours of the
consultation / patient admission.
Name and contact number of the patient’s primary cardiologist
Angiogram (cath report)
Transthoracic echocardiogram
Stress test
Lipid panel and A1c
Baseline EKGs (or if a patient is admitted / transferred for VT / AT the arrhythmia in question)
Open heart operative reports (bare minimum is the graft anatomy)
Device interrogation report with indication for device implantation
Ordering of Echocardiograms / Stress Tests: Before ordering a stress test it is
imperative that you can provide some explanation of how the test will change your
management of a given patient (don’t order a stress test on a patient who is 95 years old
and on hospice for example).
For echocardiograms, if one was done within the last six months, there needs to have
been a clear change in clinical status to justify ordering it otherwise the study will not be
reimbursed and the hospital or patient will be stuck with the cost.
HYPERTENSION
Hypertensive Urgency: Systolic BP > 180 mmHg or
diastolic BP >110 mmHg without associated evidence of end
organ damage.
Treatment Goals: Avoid IV agents and high loading doses. Aim
for a reduction in SBP to a target of 160/100 over a period of
6-12 hours then return to normal blood pressure in 24-48 hours
time.
Important to recognize that most of the patients live with very
high blood pressures and so the risk is much higher if you drop
their pressures too rapidly as they will likely have altered cerebral
autoregulation.
End Organ Damage
Flash pulmonary edema
Acute left ventricular failure
Myocardial ischemia / infarction
Stroke
Subarachnoid hemorrhage
Intracerebral hemorrhage
Retinal hemorrhage
Retinopathy
Eclampsia
Hypertensive encephalopathy
Microangiopathic hemolytic anemia
Acute kidney injury
Aortic dissection / aneurysm rupture
Hypertensive Emergency: Systolic BP > 180 mmHg or diastolic BP >110 mmHg with evidence of
end organ damage.
Treatment Goals: Initial reduction of 20-25% in SBP within the first 1-2 hours ; once achieved, further
reduction to a target of 160/100 in 6-12 hours then a return to a normal blood pressure in 24-48
hours.
The primary difference in hypertensive urgency and emergency is the rapidity of rise. Hypertensive
emergency is accordingly associated with diffuse necortizing vasculitis, arteriolar thrombi and fibrin
deposition in arteriolar walls whereas urgency is not.
Walmart / Target $4 Formulary
Beta Blockers
Atenolol
Carvedilol
Metoprolol Tartrate
Nadolol
Pindolol
Ace Inhbitors
Benazepril†
Enalapril*
Lisinopril*
Thiazide Diuretics
Chlorthalidone
HCTZ*
Loop Diuretics
Bumetaide
Furosemide
Vasodilators
Diltiazem
Hydralazine
Verapamil
(25, 50, 100)
(3.125, 6.25, 12.5, 25)
(25, 50, 100)
(20, 40)
(5, 10)
(5, 10, 20, 40)
(2.5, 5, 10, 20)
(2.5, 5, 10, 20)
(25, 50)
(12.5, 25, 50)
(0.5, 1)
(20, 40, 80)
(30, 60, 90, 120)
(10, 25)
(80, 120)
*Widely available fixed dose combinations with HCTZ
†Widely available fixed dose combinations with amlodipine
Antihypertensive Regimen Choice:
When starting patients on an antihypertensive
regimen (including diabetic patients), begin with
either a thiazide diuretic or calcium channel
blocker (Amlodipine or Nifedipine).
As a general principle, try to stick to HCTZ or
Amlodipine (amlodipine is also an anti-anginal)
as both are widely available and come in a wide
range of two drug combinations.
If a second agent is needed, start an ACE or ARB.
Always remain coginizant of how many times a
day the regimen you prescribe needs to be
taken (e.g., Hydralazine TID). When possible,
look into switching to fixed dose combinations
as there is some data to suggest that compliance improves with these formulations.
Otherwise the non-compliance rate is generally
>30%.
EKG INTERPRETATION
Reading an EKG may seem overwhelming at first but the following instructions are to help guide your evaluation. You should approach an EKG systemically every time, making the potential abundance of information
more manageable. Approach them in the following order, even if it appears to be straightforward.
1. Rate.
For a regular rhythm, count the large boxes between two QRS complexes.
1 small box = 0.04 s
For an irregular or severely bradycardic rhythm, count the number of QRS complexes
on the full 12 lead EKG strip and multiplying by 10 yielding the average beats per
minute.
300
150
100
75
60
50
1 large box = 0.20 s
2. Origin of Rhythm.
Assess for the presence of a P-wave before every QRS, and upright P-waves in leads I and II – if present,
the rhythm is likely normal sinus (60 - 100 bpm).
Inverted or abnormal P-waves suggest an ectopic atrial rhythm
(P:QRS is1:1).
SA Node
300
150
100
75
60
50
AV Node
No P-wave with a narrow regular QRS complex suggests a
junctional rhythm (40 - 60 bpm vs accelerated 60-100 bpm).
Ventricular
Escape
300
150
100
75
60
50
43
No P-wave with a wide QRS complex suggests a ventricular escape rhythm (20-40 bpm).
300
150
100
75
60
50
43
EKG INTERPRETATION
3. Axis.
A normal axis is positive in leads I, II and aVF. Determine the quadrant based upon the orientation of
leads I and aVF (to be more precise, then find which lead is most isoelectric).
Rig
h
aVR / 120°
I
aVF
-30° / II
0° / aVF
I / 90°
I isolectric / -90°
-60° / aVR
Left
Ax
Nor
ma
II / 150°
aVF
Extr
em
xis
tA
aVF / 180°
I
e
ht
Rig
is
aVF
I / -90°
aVL / -120°
aVF
III / -150°
No
r
I
Left
Ax
xis
tA
ht
Rig
l
ma
Extr
em
e
is
aVF
Step 2: Find lead where
QRS is most isoeletric.
I
Rig
h
I
l
Step 1: Quadrant
30° / III
60° / aVL
Left Axis Deviation (-30° to -90°):
- LVH, inferior MI, WPW, ostium secundum ASD
- Left anterior fascicular block (-45° to -90°): qR in aVL, no other cause
-30°
II isolectric of left axis deviation. QRS <100 ms unless aberrant conduction
present. You cannot code a LAFB if you have an inferior MI.
Right Axis Deviation (90° to 180°):
aVF I isolectric
- RVH, PE, COPD, lateral MI, WPW, ostium primum ASD
180°
- Left posterior fascicular block: rS in I and aVL and qR in III and
aVF, no other causes of R axis deviation - QRS narrow unless
aberrant conduction present.
4. Intervals.
RR Interval
ST Interval
QT Interval
PR
I
I isolectric / 90°
aVF
EKG INTERPRETATION
4. Intervals.
PR Interval (normal 120 - 200 ms):
- Short PR (<120 ms): Wolff-Parkinson-White, AV nodal rhythm, low atrial ectopic rhythms.
- Long PR (>200 ms): 1° aV block, higher degree heart block, hypokalemia, rheumatic fever, Lyme
disease.
QRS Interval [duration] (normal 60 - 100 ms):
- Narrow QRS (<60 ms): Rarely seen. Hypocalcemia.
- Wide QRS (>120 ms): Bundle branch blocks / nonspecific conduction delays, VT / VF, hyperkalemia,
accessory pathways with preexcitation, ventricular escape rhythms.
QT Interval (normal <450 ms): Varies with heart rate (QTc ). More concerning when QTc >500 ms.
- Prolonged QTc (> 450 ms): Medications (see www.qtdrugs.org), hypocalcemia, hypokalemia,
hypomagnesaemia, ICH, stroke, carotid endarterectomy, neck dissection, congenital long QT (may
not be present on resting EKG), K/Na/Ca channelopathies, CAD, cardiomyopathy, hypothyroidism,
hypothermia.
5. Atrioventricular Blocks.
1° AV Block (Physiologic): PR > 200 ms and P to QRS is 1:1.
- No treatment necessary if seen in isolation
2° AV Block Type I (Wenckebach) (Physiologic): Progressive lengthening of PR interval until impulse
not conducted, exhibits “grouped beating.”
- No treatment necessary unless severely bradycardic or symptomatic
2° AV Block Type II (Mobitz) (Pathologic): Ocasional or repeatedly non-conducted impulses with
consistent PR interval. Level of the block is typically infrahisian.
- Requires pacemaker, often worsens to third degree
3° AV Block (Pathologic): Complete AV dissociation, irregular PR intervals, P waves and QRS
complexes are both regular but indepentent of one another.
- Morphology of QRS complex dependent on origin of escape rhythm
- Requires pacemaker
EKG INTERPRETATION
5. Hypertrophy and Voltage.
Atrial Enlargement.
II
RA Enlargement
>2.5 mm in II, III & aVF
>1.5 mm in V1 or V2
II
V1
Normal
II
LA Enlargement
Terminal portion in V1 >1 deep & 1 wide
Notched P > 120 ms in II, III or aVF
Ventricular Hypertrophy and Low Voltage.
Low Voltage: Requires < 10 mm in all precordial leads and < 5 mm in all limbs.
Seen with chronic lung disease ; pericardial / pleural effusions ; obesity ; cardiomyopathies ; CAD
with extensive LV infarction ; myxedema
Left Ventricular Hypertrophy
Cornell: R in aVL + S in V3 greater than 28 mm in men / 20 mm in women
Alternate criteria for precordial and limb leads (one or more):
1) R in V5 or V6 + S in V1 > 35 mm (40 yrs) ; > 40 mm (30-40 yrs)
2) Maximum R wave + S wave in precordial leads > 45 mm
3) R wave in V5 > 26 mm ; in V6 > 20 mm
4) R wave in I + S in II > 25 mm ; R in I > 14 mm ; aVL > 12 mm ; aVF > 21 mm
Right Ventricular Hypertrophy
Right axis deviation with axis > 100°, downsloping ST depression and T inversions in right
precordial leads and one of the following
1) R / S ratio in V1 >1 or R / S ratio in V5 or V6 < 1
2) R in V1 > 7 mm
3) rSR’ in V1 with R’ > 10 mm
6. R Wave Progression.
R wave amplitude should increase with the progression of the precordial leads assuming appropriate
placement and should be > 3 mm by V3. Poor progression may be caused by anteroseptal MI, LVH,
dilated cardiomyopathy.
7. Q Waves.
Q Waves: <30 ms common but all Q waves in V1-3 and any in I, II, aVL, aVF and V4-6 lasting over 30 ms are
abnormal. For infarct identification, Q waves must be seen in 2 or more contiguous leads.
Isolated Q waves in lead III are not uncommon and do not carry any known prognostic significance.
EKG INTERPRETATION
8. Bundle Branch Blocks.
Left Bundle Branch Block
Right Bundle Branch Block
QRS Duration must be > 120 ms
(incomplete if QRS is >100 ms but
otherwise appears like a LBBB)
I
QRS Duration must be > 120 ms (incomplete if QRS
is >90 ms but otherwise appears like a RBBB)
V6
V1
I
Lead 1: Monophasic R & no Q waves.
Lead V1: QS or rS pattern
Lead V6: Late intrinsicoid deflection,
Monophasic R & no Q waves.
V1
V6
Lead 1: Wide S wave.
Lead V1: Late intrinsicoid deflection. M-shaped
QRS (RSR’). Sometimes wide R or qR
Lead V6: Early intrinsicoid deflection with a wide
S wave.
9. ST Segment Changes.
ST Segment Identification: Starting 0.06 s after J point
and measure in mm relative to TP segment.
J point
Normal
Variation
Normal ST Segments: Usually isoelectric but may vary
from 0.5 mm depression to 1mm elevation in limb leads
and up to 3 mm concave upward elevation in the precordial leads in early repolarization.
ST Segment
Diagnosing MI with LBBB (Sgarbossa’s Criteria):
Scores ≥ 3 are 80% sensitive and 90% specific for AMI
3
QRS Axis
≥ 1 mm
≥ 5 mm
≥ 1 mm
QRS Axis
2
QRS Axis
1
5 Points
2 Points
3 Points
ST elevation ≥ 1 mm
concordant with QRS in
any lead.
ST elevation ≥ 5 mm
disconcordant with QRS
in any lead.
ST depression ≥ 1 mm in
V1, V2 or V3.
10. Infarct Localization.
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Inferior (PDA)
Anterior (LAD)
Lateral (Circ)
Septal (LAD)
AVNRT vs AVRT
AV Nodal Reentrant Tachycardia (AVNRT):
Initiated with a premature complex (PAC / PVC) and can be divided into one of two varieties: 1) typical
AVNRT (antegrade conduction down slow pathand retrograde up fast path): 80-90% of cases and 2)
atypical AVNRT (antegrade down fast path and retrograde up slow path): 10-20% of cases.
Rhythm is rapid and regular with normal QRS duration unless there is co-existing conduction system
disease (RBBB / LBBB or a rate dependent bundle branch block).
Sinus impulse conducted
down fast pathway (long
refractory period).
PAC occuring while fast
path still refractory and
conducts down slow path.
SA Node
Impulse from PAC enters ventricles and finds fast
pathway reset, travels retrograde up fast pathway
and finds slow pathway reset and creates a loop.
PAC
Refractory
Slow
Termination of AVNRT via Adenosine blockade of
AV node (or vagal maneuvers or DCCV). May
terminate in either a ventricular or atrial complex.
Adenosine
Block
Fast
PAC
Retrograde P
AV Reentrant Tachycardia (AVRT):
Initiated with a premature atrial complex (PAC) and can be devided into one of two varieties: 1) typical
/ orthodromic AVRT (antegrade conduction down fast path and retrograde up accessory path (narrow
QRS) 95% of cases and 2) atypical (antidromic) AVRT antegrade down accessory path and retrograde up
AV node (wide QRS) 5% of cases.
Sinus impulse conducted
down fast path and
accessory path.
PAC travels down AV node, through ventricles
and retrograde up accessory pathway
establishing loop (orthodromic / typical AVRT).
PAC
SA Node
Slow
PAC
Fast
Accessory
Pathway
Adenosine
Block
Orthodromic
Orthodromic
Antidromic
Termination of Orthodromic AVRT via Adenosine blockade of AV node (or
vagal maneuvers or DCCV) terminates in an atrial complex. Antidromic AVRT
terminates in a ventricular complex.
Antidromic
PAC
Retrograde P
Orthodromic
Adenosine
Block
Antidromic
ATRIAL TACHYCARDIAS
Atrial Tachycardia: Broad term used to describe a complex of atrial tachyarrhythmias including
atrial flutter. It encopmasses a discrete atrial ectopic focus driving a tachyarrhythmia and re-entrant
tachycardias like atrial flutter.
Sinus Beat
Focal A Tach
Sinus Beat
2:1 A Tach
Multifocal Atrial Tachycardia: Rare arrhythmia. Halmark is the identification of 3+ ectoptic
atrial foci driving the tachyarrhtyhmia. Treated in a similar fashion as typical focal atrial tachycardia.
Sinus Beat
Multifocal A Tach
P
P1
P2
P1
P2
P3
P3
P1
P2
P2
P1
Atrial Flutter: Atrial flutter rate 240 - 350 with the ventricular rate dependent upon AV conduction
(may be conducting in a set ratio such as 1:4 or have variable AV conduction). Typical atrial flutter has
sawtooth pattern with negative flutter waves in the inferior leads and positive flutter waves in V1.
Atrial Fibrillation: Seemingly chaotic atrial activity (mechanism is a matter of debate). Ventricular
repsonse typically very irregular but may seem regular if very slow (<70 bpm) which is also indicative
of significant conduction system disease. Do not expect to alway see a fibrillating baseline.
CHA2DS2-VASc Scoring System
Heart Failure / L V dysfunction
Hypertension
Age
65-74
75+
Diabetes Mellitus
Stroke / TIA
PAD / Old MI / Aortic Plaque
Female
CHA2DS2-VASc Annual Stroke Risk
1
1
1
2
1
2
1
1
Lip et. al. Chest. 2010;137(2):263-272
0
1
2
3
4
5
6
7
8
9
1.3%
2.2%
3.2%
4.0%
6.7%
9.8%
9.6%
6.7%
15.2%
BRADYCARDIAS
Before attempting to treat a patient for symptomatic bradycardia it is imperative that you
understand the pathology driving their bradycardia as medications such as Isoproterenol, Atropine
and Epinepherine can paradoxically worsen high grade heart block.
SA and AV Nodally Mediated Bradycardias
1
2
3
1
Pure sinus bradycardia driven by poor intrinsic SA nodal activity or by
excess vagal tone (or drug effect). Stimulation with Isoroterenol or
Epinepherine or disinhibition with Atropine will raise SA nodal rate.
1
Sinus bradycardia driven by excess vagal tone (e.g. untreated OSA).
Progressive RR prolongation before potentially very long sinus pauses
(sometimes 6+ seconds) while sleeping. Stimulation with Isoroterenol or
Epinepherine or disinhibition with Atropine will raise SA nodal rate and
improve AV nodal conduction, but typically the goal is to fix the
underlying problem (e.g. CPAP).
2
Second Degree AV Block type I (Wenckebach) driven by intrinsic AV nodal delays, typically physiologic but may also
be a manifestation of nodal ischemia or valvular disease. Stimulation with Isproterenol or Epinepherine or
disinhibition with Atropine will typically improve AV nodal conduction but this is rarely needed.
2
Atrial Fibrillation with Slow Ventricular Response. Slow ventricular rates a manifestation of either high frequency
stimulation of the AV node with and longer refractory periods and or of infranodal disease. Stimulation with
Isproterenol or Epinepherine or disinhibition with Atropine will probably not have any significant effect or may
worsen the ventricular response, especially if there is concurrent bundle branch blocks.
2
Complete Heart Block. Slow ventricular rate a manifestation of the secondary pacemaker site (narrow QRS
junctional, wide QRS may be fascicular or ventricular). Stimulation with Isproterenol or Epinepherine or disinhibition
with Atropine may accelerate the secondary pacemaker but if the patient is in any way unstable should have
transcutaneous pacing preferentially.
Infranodal and Intra-His Mediated Bradycardias
3
Atrial Fibrillation with Slow Ventricular Response and RBBB. Slow ventricular rates likely a manifestation of high
frequency stimulation of the AV node compounded by concurrent infranodal disease with hyperpolarization of the
his bundles causing longer refractory periods. Stimulation with Isproterenol or Epinepherine or disinhibition with
Atropine may worsen the bradycardic response by augmenting the his bundle hyperpolarization and refractoriness.
3
Atropine or
Isoproterenol
Second Degree AV Block type II (Mobitz) driven by infrahisian conductoin system disese. Stimulation with
Isproterenol or Epinepherine or disinhibition with Atropine may worsen the bradycardic response by augmenting
the his bundle hyperpolarization and refractoriness.
WIDE COMPLEX TACHYCARDIA
Wide QRS Complex Tachycardia
QRS > 120 ms
Regular R-R
Irregular R-R
Atrial fibrillation / flutter / tachycardia
with abberent conduction (BBB, IVCD
or accessory pathway)
QRS identical to resting EKG
SVT, RBBB / LBBB and
antidromic AVRT
Vagal Maneuvers
Adenosine IVP
QRS differs from resting EKG and
prior MI or structural disease
Likely VT
1:1 AV Ratio or
Unknown
Concordant precordial leads
No RS pattern
Onset of R to nadir > 100 ms
Ventricular Tachycardia
RBBB Patern
qR, Rs or Rr’ in V1
Frontal axis +90° to -90°
< 1:1 AV Ratio
> 1:1 AV Ratio
Likely VT
Atrial tachycardia / flutter
R to S > 100 ms
V1
V2
V3
V6
I
II
Left Ventricular Tachycardia
LBBB Patern
R in V1 > 30 ms
R to nadir of S in V1 > 60 ms
qR or qS in V6
aVF
I
II
Right Ventricular Tachycardia
American
Heart
V5
V4
Association Blomström-Lundqvist et al. JACC. 2003;42:1493–531
aVF
V1
V6
V1
V6
CHEST PAIN EVALUATION
Definitions of angina:
Typical Angina (Definite):
Substernal chest pain or discomfort that is 1) provoked by
exertion or emotional stress and 2) relieved by rest and/or
nitroglycerin.
Atypical Angina (Probable): Chest pain or discomfort that lacks one of the
characteristics of definite or typical angina.
Nonanginal Chest Pain:
Chest pain or discomfort that meets one or none of
the typical angina characteristics.
Diamond and Forrester Pre-Test Probability of Coronary Artery Disease
Age (Years)
Sex
Typical Angina
Atypical Angina Nonanginal Chest Pain
<40
Man
10-90%
10-90%
<10%
Woman
10-90%
<5%
<5%
40-49
Man
>90%
10-90%
10-90%
Woman
10-90%
<10%
<5%
50-59
Man
>90%
10-90%
10-90%
Woman
10-90%
10-90%
<10%
Man
>90%
10-90%
10-90%
Woman
>90%
10-90%
10-90%
>60
ELECTROCARDIOGRAPHY - LEAD PLACEMENT
V1
V2
V3
V4
V5
V6
V4r
V5r
V6r
4th right intercostal space
4th left intercostal space
Directly between V2 and V4
5th left ICS at the MCL
5th left ICS at ant ax line
5th left ICS at mid ax line
5th right ICS at the MCL
5th right ICS at ant ax line
5th right ICS at mid ax line
RA
LA
LL
RL
Right Arm
Left Arm
Left Leg
Right Leg
ACUTE CORONARY SYNDROME
Algorithm for the evaluation and management of patients suspected of having ACS
SYMPTOMS SUGGETIVE OF ACS
Possible ACS
Definite ACS
ST elevation
No ST elevation
Activate STEMI
Pager
Nondiagnostic ECG
Normal initial troponin
ST and/or T wave changes
Ongoing pain
Positive troponin
Hemodynamic abnormalities
Observe
Follow-up at 4-8 hours: ECG , troponin
No recurrent pain;
Negative follow-up studies
Stress study to provoke ischemia
Consider evaluation of LV function if
ischemia is present
(Tests may be performed either prior to
discharge or as outpatient)
Negative
Potential diagnoses: nonischemic
discomfort; low-risk ACS
Recurrent ischemic pain or
Positive followup studies
Diagnosis of ACS
confirmed
Positive
Diagnosis of ACS confirmed
Arrangements for outpatient follow-up
American
Heart
Association Eugene Braunwald et al. Circulation. 2000;102:1193-1209
Admit to hospital
Manage via acute
ischemia pathway
ACUTE ISCHEMIA PATHWAY
Recurrent ischemia and /
or ST segment shift, or
Deep T-wave inversion, or
Positive troponin
Aspirin
Beta blockers
Nitrates
Antithrombin Regimen
GP IIb/IIIa inhibitor
Monitoring (rhythm and ischemia)
Early invasive strategy
Immediate angiography
12-24 hour angiography
Early conservative strategy
Recurrent
symptoms/ischemia
Heart failure
Serious arrhythmia
Patient stabilizes
Evaluate LV Function
LVEF <40%
LVEF >40%
Stress Test
Not low risk
Low risk
Follow on
medical Rx
American
Heart
Association Eugene Braunwald et al. Circulation. 2000;102:1193-1209
ACUTE CORONARY SYNDROME
Not all troponin leaks are secondary to acute myocardial infarction. THINK is the
TROPONIN ELEVATION due to PLAQUE RUPTURE or secondary to another underlying
cause.
Supply demand imbalance alone
Vasospasm or endothelial dysfunction
Type 2 Myocardial Infarction
(Demand Ischemia)
Fixed atherosclerosis and
supply demand imbalance
Plaque rupture with thrombus
Type 1 Myocardial Infarction
STEMI: Clinical syndrome defined by 1) symptoms of myocardial ischemia in association with 2)
persistent ECG ST elevation and 3) subsequent release of biomarkers of myocardial necrosis.
1) New ST elevation at the J point in at least 2 contiguous leads of 2+ mm in men or 1.5+ mm in
women in leads V2–V3 and or of 1 mm in other contiguous chest leads or the limb leads.
2) New or presumably new LBBB
3) ST depression in 2 precordial leads (V1–V4) may indicate transmural posterior injury
4) Multilead ST depression with coexistent ST elevation in lead aVR has been described in
patients with left main or proximal left anterior descending artery occlusion.
5) Hyperacute T-wave changes may be observed in the very early phase of STEMI, before the
development of ST elevation
NSTEMI: Clinical syndrome defined by 1) symptoms, 2) absence of persistent ST elevation but can
have other ST-T wave changes, and 3) release of cardiac biomarkers (2 of 3 criteria must be met).
Unstable Angina: Clinical syndrome defined by 1) symptoms, 2) absence of persistent ST elevation
but can have other ST-T wave changes, and 3) release of cardiac biomarkers.
x Upper Limit of Normal
100
Troponin without reperfusion
Troponin with reperfusion
CKMB without reperfusion
CKMB with reperfusion
20
10
5
2
1
0
0
1
2
3
4
5
Days from Onset of Infarction
6
7
8
ACUTE CORONARY SYNDROME
TIMI Risk Score (NSTEMI)
Composite Risk (%)
50
40
30
20
10
0
0-1
2
3
4
5
6-7
Indicator of 35 day composite events risk (mortality, new or
repeat MI, severe recurrent ischemia requiring urgent
revascularization through 14 days after admission).
1)
2)
3)
4)
5)
6)
7)
Age >65 years
3+ cardiac risk factors
Prior coronary stenosis >50%
ST segment deviation on admission ECG
>2 anginal events in the last 24 hours
Aspirin treatment in the prior 7 days
Prior congestive heart failure, MI, CABG or PCI
Medications to be started immediately
(these have survival benefits) to be
administered to all patients (unless clear
contraindication).
1. Aspirin 325 mg PO once followed by
Aspirin 81 mg PO daily
2. Heparin drip (intermediate algorithm
with bolus)
3. Lipitor 40-80 mg PO QHS
4. Plavix / Effient / Brilinta (P2Y12 inhibitors) should not be started unless told to do
so explicitly by the cardiology fellow or
attending. If started before you know if the
patient will need CABG it may delay surgery
for a week. If they are already taking one of
these agents however`, they should be
continued.
Medications to be started before discharge (these have survival benefit but do
not need to be started immediately).
5. Beta blocker (typically Metoprolol or Carvedilol)
6. Ace inhibitor / ARB if LVEF <40%, comorbid hypertension, diabetes or CKD
Medications for symptomatic relief or minimal if any survival benefit.
7. Nitroglycerin 0.3 - 0.4 mg SL Q5min x 3 PRN for continuing angina and
consider starting IV nitroglycerin.
8. Supplemental oxygen only if SaO2 <90% or respiratory distress
Ancillary testing to be obtained on all patients admitted with an acute
coronary syndrome:
1) Lipid panel
2) Hemoglobin A1c
3) Transthoracic echocardiogram (with definity if a large anterior wall MI or
concern for aneurysm formation which could predispose to LV thrombus formation.
CARDIAC CATHETERIZATION
Routine cardiac catheterizations are performed Monday through Friday (7:00 am to 5:00 pm) urgent
and emergent cases are performed after hours. Cases typically performed with local anaesthesia and
light conscious sedation (Versed and Fentanyl).
Before requesting a procedure be done for a patient, there must be a reasonable risk benefit assessment
and the expectation that the information or therapeutics gleaned from the study will offset the risks of the
procedure.
Preprocedure Checklist
Contraindications
EKG
CBC
INR > 2
Hemodynamically Unstable
INR
NPO
Platelets < 50
Active Hemorrhage
BMP
Consent
AKI (Angiogram)
Stroke / CNS Bleed
Pericardiocentesis (30 min): Effusion must be accessible by a subcostal or apical approach.
Right heart catheterization (10-15 min): With shunt run this becomes much longer, usually
around 45 minutes to 1 hour.
Left heart catheterization (30 - 60 min): If done as part of an aortic valve study (with or without
dobutamine) it will add roughtly another 30 min. Stenting can usually be done at the same time as the
angiogram but the time it takes to complete varies greatly with complexity of the intervention.
Balloon Pump Placement (15 - 45 min): If removing a prior balloon pump, add another 30
minutes to the procedure to achieve hemostasis.
Common Angiographic Views
Left Main
RCA
Left Main
Left Main
Circumflex
Circumflex
RCA
LAD
LAD
RCA
Circumflex
LAD
PDA
PDA
Images courtesy of Patrick J. Lynch
PDA
VALVULAR HEART DISEASE
St. Jude Mechanical
Medtronic Mosaic Bovine Pericardial
Medtronic CoreValve Evolut
Image courtesy of Patrick J. Lynch
American Society for Echocardiography Reference Ranges
Aortic Stenosis
Velocity (m/s)
Mean Pressure Gradient (mmHg)
Valve Area
Aortic Regurgitation
Vena Contracta (cm)
Mitral Stenosis
Planimetry MV Area (cm2)
DIastolic Pressure Half Time (ms)
Mean Pressure Gradient (mmHg)
Mitral Regurgitation
Vena Contracta (cm)
ERO (cm2)
Normal
Mild
Moderate
Severe
<2
<10
>2
2.0 - 2.9
<20
>1.5
3.0 - 3.9
20 - 39
1.0 - 1.5
>4.0
>40
<1.0
<0.3
0.3 - 0.6
>0.6
>1.5
<150
<5
1.0 - 1.5
>150
5 - 10
<1.0
>220
>10
<0.3
American
Heart
AssociationNishimura et. al. J Am Coll Cardiol. 2014;63(22):e57-e185
<0.7
<0.4
>0.7
>0.4
CARDIAC DEVICES
Device Program Coding
Standard coding involves three
letters. 1st denotes which
chambers are paced. 2nd denotes
which chambers are monitored
for intrinsic activation. 3rd
denotes the response to a native
activation.
Pulse Generator
Most common modes:
DDD - Paces both RA and RV
(sometimes BiV). Monitors RA and
RV. Detections may trigger a
pacing impulse or inhibit depending upon their timing.
Coronary Sinus Lead (CS)
(Pace / Sense)
Right Atrial Lead (RA)
VVI - Paces RV. Monitors RV.
Detections inhibit pacing.
(Pace / Sense)
Right Ventricular Lead (RV)
(Pace / Sense / Defibrillate)
AAI - Paces RA. Monitors RA.
Detections inhibit pacing.
AAI <-> DDD - Converts between
modes when in AFib or Flutter.
PACEMAKERS
DEFIBRILLATORS
Designed to treat bradyarrhythmias. They
only pace when the patient’s intrinsic
heart rate is less than the programmed
lower rate limit. They do not treat tachyarrhythmias.
Designed to treat tachyarrhythmias
(primarily VT / VF) most defibrillators also
have the ability to treat bradyarrhythmias
via a pacing function (with the exception
of subcutaneous ICDs which only defibrillate).
Device Type
Leads
Sensing
RA RV CS
Single Chamber Pacemaker
Dual Chamber Pacemaker
Biventricular Pacemaker (CRT-P)
Single Chamber Defibrillator (ICD)
Dual Chamber Defibrillator (ICD)
Biventricular Defibrillator (CRT-D)
Subcutaneous ICD (SC-ICD)
Therapies
Pacing ATP
RV
RV
RV & RA
RV & RA
RA / RV / CS RA / BiV
RV
RV
RV & RA
RV & RA
RA / RV / CS RA / BiV
SC Coil
Shock
EP PROCEDURES
Routine electrophysiology procedures (device implantations and ablations) are performed Monday
through Friday (7:00 am to 5:00 pm) urgent and emergent cases are performed after hours. Pacemakers are often performed with local anaesthesia and conscious sedation (Versed and Fentanyl) but
more complex procedures will typically be performed with anaesthesia.
Before consulting the electrophysiology service there must be a risk benefit assessment and a reasonable
expectation of quality and life and expected survival of at least one year from any device implantation or
upgrade. Similarly if the patient has bradycardia or other arrhythmias due to reversible causes or
remediable problems such as electrolye derrangements, sleep apnea or digoxin toxicity, they are generally
not appropriate candiates for device implantation.
Preprocedure Checklist
Type and Screen
CBC
NOACs held as directed
INR
NPO
Coumadin OK to continue
BMP
Heparins stopped at least 12 hours earlier
Single or Dual Chamber Pacemaker Implantation (60 min): Indicated for 1) symptomatic
bradycardia or chronotropic incompetence, 2) high grade heart block, 3) alternating bundle branch
blocks, 4) sinus pauses while awake of >3 seconds and 5) atrial fibrillation conversion pauses while
awake of >5 seconds.
Cardiac Resynchronization Therapy (CRT-P / CRT-D) (1 - 3 hours): Indicated for patients with
an LVEF <35% and a QRS duration >120 ms in sinus rhythm with class III or ambulatory class IV heart
failure despite optimal medical therapy.
Defibrillator Implantation (60 min): Indicated for 1) patients who survived a cardiac arrest from
VF / VT or sustained VT after exclusion of reversible causes and 2) patients with an LVEF <35% (and at
least 40 days post MI if their heart failure is ischemic in nature) and are in NYHA class I-III heart failure.
Atrial Flutter Ablation (1 - 2 hours): Indicated as front line therapy for treatment of typical atrial
flutter. If onset of atrial flutter is > 48 hours before the procedure or the patient has not been on
anticoagulation, they will usually require a TEE first.
Atrial Fibrillation Ablation (4 - 6 hours): Typically this is a very complicated procedure and
generally only done as an outpatient.
Ventricular Tachycardia Ablation (4 - 8 hours): Potentially a very complicated procedure and
given the length of the procedure usually requires 2-3+ L of IVF being given to prevent thermal burns
from the ablation catheters (require continuous flushing).
Post Device Implantation Checklist
Do NOT restart any heparins or NOACs (this includes DVT prophylaxis) for 1-2 weeks
Coumadin OK to continue
Chest XR ( PA / Lateral) in AM
Site dressings managed by EP Service
Device interrogation in AM
HEART FAILURE
Volume Status vs Perfusion:
Measure JVD in CM above
sternal notch (measured + 5).
Normal is 7-9
Volume status: Jugular vein distention (JVD), hepatojugular reflux, peripheral edema, orthopnea, PND, rales.
Perfusion: Look for evidence of end organ hypoperfusion (cool extremities, renal failure, acidosis, altered
mental status etc...).
45 Degrees
It is extremely important to remember that these are not problems
occuring in isolation and in most patients, there is a mix of both
problems at any one given time.
ACC / AHA Stage
NYHA Stage
A
High risk for heart failure but without
structural heart disease or symptoms.
B
Structural heart disease without
heart failure.
I
C
Structural heart disease with prior or
active heart failure.
II
III
Symptoms with moderate exertion
D
Refractory heart failure requring
specialized interventions.
IV
Symptoms at rest
1 Year
Mortality
Based on
comorbidities
Asymptomatic
Symptoms with minimal exertion
5-10%
15-30%
50-60%
Documentation:
Your note must stipulate acute, chronic or acute on chronic systolic or diastolic heart failure. Terms such
as HFpEF and HFrEF are not acceptable. After establishing the etiology (if known), you need to note the
ACC and NYHA stage as detailed above.
Initial Management:
Once you identify the major problem (volume overload and or poor stroke volume) tailor treatment
accordingly (diuretics or dialysis for volume overload and inotropes, balloon pumps and LVADs for
poor LV function).
Right Heart Catheterization:
The use of pulmonary artery catheters to guide heart failure managment was formally evaluated in the
ESCAPE trial (PMID 16204662). This study failed to show any benefit to the use of pulmonary artery
catheters to guide therapy over
just clinical assessment of
Diuretic Equivalence
volume
status. There
is
Agent
Onset
Duration Bioavailability
currently no well agreed
Lasix (40 mg PO)
30-60 min 6-8 hrs
50%
indication for pulmonary artery
Lasix (20 mg IV)
5 min
2 hrs
100%
catheter placement to guide
Bumex (1 mg PO)
10 min
4-6 hrs
80%
therapy outside of documentDemedex (10 mg PO) 1 hr
4-6 hrs
90%
ing inotrope dependence.
Metolazone (PO)
60 min
>24 hrs
HEMODYNAMICS
ECG
RA
a c
v
x
25
y
0
mmHg
RV
Tricuspid Valve
Closes
25
Tricuspid Valve
Opens
0
mmHg
Reference Ranges
Right Atrium
a wave
v wave
Mean
2 - 7 mmHg
2 - 7 mmHg
1 - 5 mmHg
Right Ventricle
Systolic
EDP
15 - 30 mmHg
1 - 7 mmHg
Pulmonary Artery
Systolic
Diastolic
Mean
15 - 30 mmHg
4 - 12 mmHg
9 - 19 mmHg
25
Pulmonic Valve 0
mmHg
Closes
a
c
PCWP
v
x
0
mmHg
125
Aortic Valve
Opens
Aortic Valve
Closes
Ao
90 - 140 mmHg
60 - 90 mmHg
70 - 105 mmHg
Cardiac Index
> 2.5 L/min/m2
100
75
90 - 140 mmHg
5 - 12 mmHg
Aortic
Systolic
Diastolic
Mean
25
y
Pulmonary Capillary Wedge
Mean
4 - 12 mmHg
Left Ventricle
Systolic
EDP
PA
Pulmonic Valve
Opens
50
Mitral Valve
Closes
Mitral Valve
Opens
LV
edp
25
0
mmHg
IABP
B
A
E
125
Aortic Valve
Opens
Pres
s
Ao
On
Swan Daily Rounds
Nativ
e
P
IAB
ith
W
C
ures
Aortic Valve
Closes
Chest XR for catheter position
Assessment of insertion site
Systole
Diastole
D
Systole
100
75
50
mmHg
BALLOON PUMPS
PA
IAB
Coronary Perfusion
Augmentation
Systole
Diastole
Systole
Image redrawn from Jones et. al. J Invasive Cardiol 2012; 24:544-550
ti
ta
en
m
ug
Nativ
e
125
Pres
sures
100
on
75
50
mmHg
Diastole
Benefit is garnered by a reduction in the work
required by the LV during systole (balloon deflates
providing a partial vacuum into the aorta) and an
increase in the diastolic pressure (during coronary
perfusion).
All Cause Mortality from SHOCK II Trial (IABP Support in ACS with Cardiogenic Shock)
60
IABP
Control
Mortality (%)
50
40
30
20
10
0
p=0·94; log-rank test
Relative risk 1·02, 95% CI 0·88–1·19
0
30
60
90
120
150
180
210
240
270
Days after randomisation
300
330
360
390
420
The use of intraaortic balloon pumps for the treatment of acute cardiogenic shock has mostly been studied in cases of an
acute coronary syndrome (such was the subject of the SHOCK II trial). They are also commonly used in cases of cardiogenic
shock from other etiologies such as fulminant myocarditis or acute on chronic systolic heart failure. In ACS patients their
use has failed to show benefit as shown above. In the other situations, there is little if any data to assess their value.
Balloon Pump (IABP) Daily Rounds
Chest XR to confirm IABP position
Most recent aPTT and trend
Assessment of IABP insertion site
Assessment of pedal pulses and perfusion
Balloon Pump (IABP) Anticoagulation
Heparin drip (low dose nomogram)
Proper placement of
IABP with radio-opaque
marker just below aortic
arch and about the level
of the carina.
LEFT VENTRICULAR ASSIST DEVICES
Two models in use are the
Heartmate II and HeartWare.
Both have a mechanical
pump which draws blood
from the LV cavity at the apex
and shunts it to the aortic
root.
This augments the
native LV function and there is
usually a pulse during systole.
Occasionally, the residual LV
function is so poor that there
is no palpable pulse and the
aortic valve does not open.
To measure blood pressure in
these patients use a manual
cuff and a doppler probe,
record the first audible sound
during deflation as the MAP
(goal is 70-80 mmHg).
Reported Pump Parameters:
Pump Speed (Set)
Power (Measured)
Flow (Estimated)
Pulse Index (Estimated)
Flow (L/min)
8
Inlet (LV) Pressure
Outlet (Aortic) Pressure
Pump Flow
120
6
90
4
60
2
30
0
0
Characteristic Electrical Baseline EKG Intereference
Pressure (mmHg)
LVAD Flow and Pressure
L/min
2920
RPM
4.2
Watts
Power (Watts)
4.3
12
Flow (L/min)
HEARTWARE LVAD (HVAD)
12
Fixed
4
POD: 8
1
9
8
7
6 5 4
Time (s)
3
2
1
9
8
7
6 5 4
Time (s)
3
2
1
8
4
Time
Scale
Sx Off
HW1234567
22:43:56
8
HeartWare
2
Reprinted with the permission of HeartWare ©
HeartWare HVAD Function Reference Ranges
Set Speed (RPM) 1800 2400
INR
Patient System Controller Display
(Attached via Driveline)
Alarm Mute
2.5
8.5
1.8
3
8
10
1
2
3
4
Power (Watts)
Flow (L/min)
3200 4000
Battery Indicator 1 Alarm Indicator Battery Indicator 2
Scroll
3000 RPM 5.0 L/min
4.8 Watts
HeartWare
Critical Alarms
HeartWare HVAD Daily Rounds
Confirmation of pump speed
INR
Pump flow and power trends
NO MESSAGE - No power to pump /
Pump has stopped
Steady Tone
Flashing Red
Hgb, PLT and LDH trends
Arrhythmia review
Suction event review
HeartWare HVAD Anticoagulation
Aspirin 325 mg PO QD
Coumadin (INR 2-3)
Two Tone
VAD STOPPED - Driveline
disconnected, fracture or connector
malfunction. VAD electrical failure,
Controller / VAD Failure. Thrombus or
other material in device.
CONTROLLER FAILED - Controller
Component Failed
CRITICAL BATTERY - Limited battery
life remaining or malfunction.
The nursing staff has been trained to care for most of these scenarios. In the event of
repeated alarms, notify the on call fellow immediately.
HEARTMATE LVAD (LVAD)
Clinical
Settings
Pump Flow
Alarms
Save Data
History
Pump Speed
4.5 9500
lpm
Admin
Pulse Index
rpm
Display ON/OFF
Fixed Mode - Speed Setpoint: 9600 rpm
3.6
Pump Power
5.7
w
Reprinted with the permission of Thoratec Corporation ©
LVAD Functional Reference Ranges
Set Speed (RPM)
6K
8K
10K 15K
2.5
10
2.5
3
10
1
2
3
Power (Watts)
Flow (L/min)
INR
Patient System Controller Display
(Attached via Driveline)
Test Select
Button
Battery Fuel Gauge
Battery Symbol
(yellow & red)
4
Power Symbol
Controller Cell
Symbol
Red Heart
Symbol
Silence Alarm
Button
Critical Alarms
HeartMate II LVAD Daily Rounds
Red Heart
Confirmation of pump speed
INR
Pump flow, PI and power trends
Steady Tone
Red Battery
Hgb, PLT and LDH trends
Arrhythmia review
PI / Suction event review
Steady Tone
Yellow Battery
HeartMate II LVAD Anticoagulation
Aspirin 325 mg PO QD
Coumadin (INR 2-3)
Pump flow < 2.5 Lpm, pump has
stopped, perc lead is disconnected, or
pump is not working properly.
1 Beep Q4 seconds
< 5 min battery power remains,
voltage too low, or the System
Controller is not getting enough
power.
< 15 min battery power remains,
voltage too low, or the System
Controller is not getting enough
power.
The nursing staff has been trained to care for most of these scenarios. In the event of
repeated alarms, notify the on call fellow immediately.
PREOPERATIVE EVALUATION
Urgency
Emergent
Definition
Serious threat to life or limb if not in the operating room within <6 hours.
*Provide risk stratification but the patient should proceed directly to surgery
without delay.
Urgent
Serious threat to life or limb if not in the operating room within 6-24 hours.
Time Sensitive No immediate threat to life or limb but excess delay for clinical evaluation (>6
weeks) will negatively effect outcome.
Elective
METABOLIC
EQUIVALENT
1-10 MET
1 MET
Any procedure that which can safely be delayed for up to or over 1 year.
Routine Preoperative Evaluation:
There are many conditions which supercede routine perioperative risk
evaluation for non-emergency surgery and require further stabilization prior to
proceeding to the operating room this includes problems such as complete
heart block, symptomatic bradycardia, an acute coronary syndrome etc...
Several risk stratification models are in use but the most dominant is the
revised cardiac risk index (RCRI) but several other models also are in use such
as the ACS NISQP Surgical Risk Calculator (riskcalculator.facs.org) and the ACS
NSQIP MICA Calculator: (surgicalriskcalculator.com/miorcardiacarrest).
READING
Revised Cardiac Risk Index
4 MET
GARDENING
6 MET
Composite Risk (%)
15
10
5
0
0
1
2
3+
Indicator of risk of suffering perioperative myocardial
infarction, pulmonary embolism, VF or other cardiac
arrest or complete heart block.
JUMPING ROPE
8-10 MET
1)
2)
3)
4)
5)
6)
High Risk
Emergent surgery
Vascular surgery
Surgery with large EBL / fluid shift
Intermediate Risk
Carotid endarterectomy
Head and neck surgery
Intraperitoneal surgery
Intrathoracic surgery
Orthopedic surgery
Prostate surgery
CLIMBING STAIRS
7 MET
Procedural Risk Class
Low Risk
Endoscopic procedures
Superficial procedure
Cataract surgery
Breast surgery
Coronary artery disease
Cardiomyopathy
History of TIA or stroke
Insulin dependent diabetes
Creatinine > 2.0 mg/dL
Planned high risk surgical procedure
American
RUNNING
Heart
Association Lee et al. Circulation. 1999; 100(10): 1043-1049
PREOPERATIVE EVALUATION
Algorithm for the risk evaluation of patients prior to surgery
Patient scheduled for surgery with
known or risk factors for CAD
Nonemergent surgical case
Clinically stable
Emergent surgical case
Clinical risk stratification
and proceed directly to
surgery
Acute coronary syndrome
Evaluate and treat
accordingly
Estimated perioperative risk of MACE
based on combined clinical / surgical
risk (RCRI etc...)
Low risk (<1%)
Elevated risk (>1%)
Functional capacity <4
METs or unknown
Functional capacity
>4 METs
Will further testing impact
decision making or
perioperative care?
No further testing
Yes
No
Proceed to surgery
Pharmacologic stress testing
with angiography and
revascularization as indicated
American
Heart
Association
Proceed to surgery or
alternate management
as appropriate
PREOPERATIVE CHECKLIST
EKG
Should be obtained in patients with known CAD/PAD, arrhythmia, cerebrovascular disease, or other significant structural disease except those
undergoing low risk surgery.
It should also be considered in patients without above risks factors except
those undergoing low risk surgery
Echocardiogram Pre-operative echo should be obtained in patients with dyspnea of
unknown origin to assess LV function, known heart failure with change in
clinical status, re-assessment of LV function in clinically stable patients with
previously documented decreased LV function if there has been no
assessment within a year.
Stress Test
Reasonable for patients at elevated risk for noncardiac surgery with poor
functional capacity to undergo either exercise/dobutamine stress echo or
myocardial perfusion scan if it will change management
Please refer to stress testing and ACC pre-operative algorithm.
Angiogram
Routine preoperative coronary angiography is not recommended per ACC
guidelines
Beta Blockers
Continue beta blockers in patients on them chronically. In patients with
intermediate or high preoperative test (RCRI>3), it may be reasonable to
begin beta blockers prior to surgery.
Do not initiate beta blockers in the immediate pre-operative period (at least
2-7 days prior to surgery).
Statins
Continue statins in patients on them chronically. Consider initiating statins
before vascular surgery or those with one clinical risk factor. Can consider
initiating prior to elevated risk surgery in patients who already meet an
indication for statin therapy.
ACE / ARB
Reasonable to continue perioperatively if already on them chronically. If
held, restart as soon as safe following surgery.
Antiplatelets
Continue DAPT in patients undergoing urgent noncardiac surgery in the
first 4 to 6 weeks after BMS or DES implantation, unless risks of bleeding
outweigh risk of stent thrombosis. Patients with stents undergoing surgery
that requires discontinuation of P2Y12 inhibitors, continue aspirin and
restart P2Y12 inhibitor as soon as possible following surgery. In those
undergoing nonurgent surgery and without prior stents, it may be reasonable to continue aspirin if patient at high risk of cardiac events and benefits
outweighs risk of bleeding.
CARDIAC IMAGING
Modality
Advantages
Limitations / Contraindication
Exercise ECG
Ideal in low to intermediate risk
patients who can exercise enough to
get to target heart rate and have an
interpretable ECG.
Cannot use if patient has baseline LBBB or
paced rhythm.
Exercise should be attempted
in any stress modality which
its felt the patient can
reasonably achieve target
heart rate.
Provides functional capacity.
Cannot perform in a patient having ACS or
recent MI, severe symptomatic AS, aortic
dissections, or acute PE.
Myocardial
Perfusion Imaging
Appropriate in wide range of
pre-test probability patients.
Balanced ischemia in triple vessel disease
may lead to false negatives.
Regadenoson or Adenosine
Can assess viability
Cannot use in pregnant patients, with
hypotension (SBP<90), high degree AV
block, active wheezing.
Stress Echo
No radiation exposure
Dobutamine
Appropriate in a wide range of
pre-test probability patients.
Can be limited by poor patient echo
windows – obese patients, etc.
Contraindicated in patients with
recent ACS, tachyarrhythmias,
uncontrolled hypertension
(SBP>200/110), aortic dissections
and large aneurysms.
Can assess viability
Can obtain additional hemodynamic data during stress.
Stress MRI
No radiation exposure
GFR must be >30
Can assess for viability/scar
ICD/Pacemakers limit study
quality.
Excellent structure/anatomy
imaging
Appropriate in intermediate and
high pretest risk patents.
Coronary CTA
Can potentially end up with
double contrast dye exposure
if positive.
Cannot use in symptomatic severe AS,
aortic dissection, ACS.
Option for low to intermediate risk
patients with normal ECG and
normal cardiac biomarkers.
Requires high technical skill
Needs optimal heart rate and should be
able to participate in breath holds.
No functional capacity is obtained.
Contrast dye exposure
Excellent tool for assessing anatomy
of coronary arteries.
Limited to larger caliber more proximal
vessels.
Patient will need to perform breath holds
and have a controlled heart rate.
NOT a stress test
High negative predictive value
Cannot use in pregnancy
Cardiac Cath
Optimal test for high pretest
probability, positive stress tests, and
those with acute coronary
syndromes.
Invasive with risks of complications such as
bleeding
Functional assessment with
CT-FFR.
Gold standard study for CAD.
Contrast dye exposure
SYNCOPE
Reflex Syncope
w
Cerebral
Hypoperfusion
tu
ic F
a il u re
Sec
onda
ry
ANF
no
Poor Ve
us
Re
Low
Volume
Va
so
d
80%
60%
40%
20%
sP
oo
l
om
rn
Lo
ar
m
Pri
yA
NF
t
t
on
ia
Card c Outp
u
scular Resista
Va
n
ow
mal Autonoics
Nor
L
iac Syncope
Card
ce
nh
ib
ctu
ia Stru ral Othe
thm
r
rhy
Ar
Pulmonar
y)
diac (
Car
priate Refl
ppro
ex
Ina
Au
n
sio
uced Dysautonom
ten
g Ind
o
ia
p
Dru
sor
res
ep
Car
dI
Etiology of Syncope (%)
100%
Mixed
u
no
Ve
Orth
o
s
t
ati
cH
y
Physiologic Basis of Syncope: Any mechanism which causes a
transient drop in cerebral blood flow below 50-60 mL/min for at
least 6-8 seconds can result in syncope.
0%
<40
40-60
>60
Age (Years)
Orthostatic
Structural Disease
Neurally Mediated
Arrhythmia
*Syncopized is not a word. Syncopated refers to accentuating the off beats in music. Neither refers to
syncope. Don’t ever say it again.
Orthostatic Hypotension: Drop in CBF because of either volume depletion, excess venous pooling or a
failure of compensatory vasoconstriction. Further deliniation requires closer assessment of autonomic
function and volume status.
-Compression stockings
-Fludricortisone
-Medication review (may need to stop offending drugs like alpha blockers etc...)
Reflex Syncope: Drop in CBF via sudden changes in efferent autonomic activity, especially parasympathetic, causing bradycardia and a release of sympathetic tone causing a drop in vascular resistance (in
other words vasodilation). Look for common triggers like going to the bathroom or around the time of
procedures (EGD, C-scope, cystoscopy, carotid massage etc...) or psychologic stress like seeing blood or
extreme fear.
-Increased salt and water intake
-Counterpressure maneuvers
-No data to support use of any medications except possibly beta blockers in patients over 40
Cardiac Syncope: Drop in CBF Pretty straight forward subgroup with either structural lesions (HOCM or
severe AS) or arrhythmias as the mechanism.
-Treatment of underlying process
Initial Diagnostic Evaluation
Orthostatic Vital Signs
Echocardiogram with doppler
EKG
Telemetry
Driving Restrictions
Clearly documented that patient is restricted from driving if no immediately reversible cause is identified
Renal 100% (1 min) Beta 1 receptor mediated increase
in cardiac contractility and HR.
Increases SVR via potent Alpha
activity.
Renal 100% (1 min) Beta 1 receptor mediated increase
in cardiac contractility and HR.
Increases SVR via potent Alpha
activity.
Epinepherine (β1 / β2 / α1) 1 - 20 mcg / min
Norepinepherine (β1 / α1) 0.02 - 1.0 mcg / kg / min
Beta 1 receptor mediated increase
in cardiac contractility and HR.
Decrease in SVR via Beta 2 mediated vasodilation.
Renal ~80% (2.3 hrs) PDE3 - cGMP mediated increase in
intracellular intracellular Ca++
concentration and consequent rise
in contractility and CI. Decreases
SVR / PVR.
Primary Activity
Renal (2 minutes)
0.20 - 0.50 mcg / kg / min
Milrinone (cGMP / PDE3)
Clearance (t½)
Dobutamine (β1 ++ / β2 +) 2.5 - 10 mcg / kg / min
Dose Range
Agent (MOA)
INOTROPIC AGENTS
Dose Range
0.02 - 1.0 mcg / kg / min
1 - 20 mcg / min
0.03 units / min
1 - 10 mcg / kg / hr
0.5 - 20 mcg / kg / min
Agent (MOA)
Norepinephrine (β1 / α1)
Epinephrine (β1 / β2 / α1)
Vasopressin (V1)
Phenylephrine (α1)
Dopamine (β1 / α1)
Primary Activity
Renal 80% (2 min)
Hepatic (2-3 hrs)
Dose dependent effect. Alpha 1
and Beta 1 dominant activity at
doses above 10 mcg / kg / min.
Pure Alpha 1 mediated vasoconstriction
Renal 10-15% (10-20 Vasopressin 1 receptor mediated
min)
vasoconstriction.
Renal 100% (1 min) Beta 1 receptor mediated increase
in cardiac contractility and HR.
Increases SVR via potent Alpha
activity.
Renal 100% (1 min) Beta 1 receptor mediated increase
in cardiac contractility and HR.
Increases SVR via potent Alpha
activity.
Clearance (t½)
VASOPRESSOR AGENTS
5 - 200 mcg / min
0.1 - 10 mcg / kg / min
Onset:
15 - 30 min
Duration: 6 - 12 hours
Enalaprilat
1.25 mg – 5 mg Q6H
5 - 15 mg / hr
+Δ 2.5 mg Q15 min
Onset:
5 -15 min
Duration: 1.5 - 4 hours
Nicardipine
Onset:
2 - 5 min
Duration: 5 - 10 min
Nitroglycerine
Onset:
1 min
Duration: 1 - 10 min
Nitroprusside
Onset:
5 -10 min
Duration: 2 - 4 hours
Labetalol
20 - 80 mg IVP Q10 min
(max 300 mg)
10 - 20 mg IVP
Hydralazine
Onset:
10 - 20 min
Duration: 1 - 4 hours
Dose Range
Agent
First dose hypotension in high renin
states, headache, dizziness
Tachycardia, dizziness, flushing,
nausea, headache, phlebitis, edema
Reflex tachycardia, tachyphylaxis,
nausea, headache, vomiting, flushing,
methemoglobinemia
Cyanide and thyocyanate toxicity,
nausea, vomiting, muscle spasm,
sweating, increased intracranial
pressure
Bronchospasm, heart block, nausea,
paresthesias, dizziness
Tachycardia, headache, flushing,
nausea
Adverse effects
Pregnancy and acute renal failure
Need an arterial line for monitoring.
Decompensated heart failure.
Need an arterial line for monitoring.
Recent use of PDE-5 inhibitors (i.e Sildenafil).
Need an arterial line for monitoring.
Acute MI, significant CAD, stroke, increased ICP,
renal or hepatic failure.
Cocaine intoxication, decompensated heart
failure, high grade AV blocks, significant
bradycardia
Increased intracranial pressure or glaucoma
Contraindications
IV ANTIHYPERTENSIVES
Target Dose
50 mg PO TID
10 mg PO BID
40 mg PO QD
50-75 mg PO TID
20-80 mg PO TID
60-120 mg PO QD
Agent (MOA)
ACE Inhibitors
Captopril
Enalapril
Lisinopril
Vasodilators
Hydralazine
Isordil
Imdur
Angiotensin Receptor Blockers
Valsartan
Aldosterone Antagonist
Spironolactone
Beta Blockers
Carvedilol
Metoprolol XL (not Lopressor)
Agent (MOA)
HEART FAILURE AGENTS
80-160 mg QD - BID
25 mg PO QD
25 mg PO BID
200 mg PO QD
Target Dose
Nitroprusside 0.1 - 10 mcg / kg / min Hepatic / RBCs (1 - 3 Small vessel vasodilation primar- Stroke / TIA
Coarctation
min)
ily afterload reduction.
VSD
Hepatic / RBCs (1 - 3 Converted to NO promoting
Acute inferior MI
HOCM
min)
venous (preload) relaxation.
Small afterload reducing effect.
Contraindications
Nitroglycerine 5 - 200 mcg / min
Primary Activity
Clearance (t½)
Agent (MOA) Dose Range
VASODILATORS AGENTS
Non-Valvular AF
Non-Valvular AF:
5 mg PO BID but if two or more conditions apply
(Cr >1.5, Age >80, wt< 60 kg) then 2.5 mg PO BID
Apixaban (Eliquis)
Factor Xa Inhibitor
Onset:
1-2 hours
Clearance: Renal 50% (12 hrs)
Reversal: KCentra
Edoxaban (Savaysa)
Factor Xa Inhibitor
Onset:
3-4 hours
Clearance: Hepatic (12 hrs)
Reversal: KCentra
Non-Valvular AF
GFR 95-50: 60 mg PO QD
GFR 50-15: 30 mg PO QD
DVT / PE Treatment
10 mg PO BID x 7 days then 5 mg PO BID
GFR >15: 20 mg PO QD
Factor Xa Inhibitor
Onset:
2-3 hours
DVT / PE Treatment
Clearance: Renal 66% (5-9 hrs) GFR >15: 15 mg PO BID x 21d then 20 mg QD
Reversal: KCentra
Rivaroxaban (Xarelto)
DVT / PE Treatment
GFR >30: 150 mg PO BID
Non-Valvular AF
GFR >30: 150 mg PO BID
GFR 15-30: 75 mg PO BID
Dabigatran (Pradaxa)
Direct Thrombin Inhibitor
Onset:
90 min
Clearance: Renal (12-27 hrs)
Reversal: Praxbind
Dosing
Agent (MOA)
Avoid using in patients with moderate to severe liver
dysfunction.
Avoid in patients with very high functioning kidneys
due to excessivly rapid clearance.
Avoid in severe hepatic impairment.
Ok to crush and suspend in D5W 60 mL if given
immediately.
Avoid using in patients with moderate to severe liver
dysfunction.
Ok to crush tablets and mix with apple sauce.
Avoid using with amiodarone, dronaderone,
verapamil, ketoconazle, clarithromycin, quinidine.
Must not open capsules.
Considerations
NOVEL ORAL ANTICOAGULANTS
LANDMARK CLINICAL TRIALS
Topic
Trial Name (PMID)
Brief Findings
Atrial Fibrillation
Anticoalguation
Apixiban (Eliquis)
Dabigatran (Pradaxa)
Rivaroxiban (Xarelto)
Rate Control Threshold
Rate vs Rhythm Control
ARISTOTLE (21870978)
RE-LY (19717844)
ROCKET-AF (21830957)
RACE-II (20231232)
AFFIRM (12466507)
Apixiban superior to coumadin for stroke prevention (NNT 300)
Dabigatran non-inferior to coumadin for stroke prevention
Rivaroxiban non-inferior to coumnadin for stroke prevention
Lenient HR control (<110) non-inferior to strict (<80 bpm) for risk of MACE
Rate control non-inferior to rhythm control for risk of MACE
Ischemic Heart Disease
Antiplatelet and Anticoagulant Therapy
ASA
ISIS-2 (2899772)
Clopidogrel
CURE (11519503)
Prasugrel
TRITON TIMI 38 (17982182)
Ticagrelor
PLATO (20079528)
Revascularization
Paclitaxel DES in STEMI HORIZONS AMI (19420364)
Compl. Revasc STEMI
PRAMI (23991625)
PCI in UA / NSTEMI
RITA-3 (16154018)
DES PCI vs CABG
SYNTAX (19228612)
FREEDOM (23121323)
PCI vs OMT
COURAGE (17387127)
FAME-2 (22924638)
Access
Radial vs Femoral
RIVAL (21470671)
Heart failure
Enalapril
Valsartan
Spironolactone
Carvedilol
Digoxin
Ivabradine
Dialysis with UF
Hypertension
Benazepril + Amlodipine
Benazepril + HCTZ
Lisinopril
Amlodipine
Chlorthalidone
Losartan
Valsartan
ASA reduces reinfarct and death [very old study] (NNT 20)
Addition of Clopidogrel to ASA reduces MACE (NNT 50)
Prasugrel superior to clopidogrel with PCI (NNT 50)
Ticagrelor superior to clopidogrel with PCI (NNT 60)
DES in STEMI reduced TVR but not MACE (NNT 35)
Non-infarct artery PCI reduces death / MI (NNT 7)
PCI in high risk pts over OMT alone reduces 5 yr MACE (NNT 30)
CABG in LM or 3v CAD superior to PCI (effect rises with SYNTAX score)
CABG superior to PCI in diabetic pts to reduce MACE at 5 years (NNT 12)
OMT non-inferior to BMS PCI for stable CAD for 5 year MACE
FFR guided PCI v OMT in stable CAD reduced urg revasc but not MI or death
Radial approach reduced hemorrhagic complications (NNT 500)
CONSENSUS (2883575)
SOLVD (1463530)
ValHeFT (11759645)
RALES (10471456)
COMET (12853193)
Dig (9036306)
BEAUTIFUL (18757088)
SHIFT (20801500)
CARRESS-HF (23131078)
Enalapril in NYHA class IV reduced death(NNT 6)
Enalapril in NYHA class II+ reduced hospitalization, not death (NNT 25)
Valsartan in NYHA class II+ reduced hospitalizatoin (NNT 25)
Spironolactone in NYHA class III+ reduced death(NNT 9)
Carvedilol superior to Mortality in NYHA class II+ in reducing death (NNT 18)
Digoxin in Systolic HF reduced hospitalization but not death.
Ivadribine in stable CAD + HR >70 reduced ACS admits (NNT 50)
Ivadribine in stable CAD + HR >70 reduced ACS and Death (NNT 20 / 50)
Ultrafiltration “inferior” really equivalent to diuresis in NYHA class IV
ACCOMPLISH (19052124)
ACCOMPLISH (19052124)
ALLHAT (12479763)
ALLHAT (12479763)
VALUE (15207952)
ALLHAT (12479763)
LIFE (11937178)
VALUE (15207952)
Benazepril+CCB reduced death / MI v Benazepril+HCTZ (NNT 50)
See above
Amlodipine v Chlorthalidone v Lisinopril all equal for ACS risk
See above
Amlodipine reduced MI but not mortality compared to Valsartan (NNT 140)
See above
Losartan reduced risk of stroke but not death or MI vs atenolol (NNNT 50)
See above
Trans-Catheter Aortic Valve Implantation (TAVI)
TAVI in Surg High Risk
PARTNER (22443479)
Stroke and MI similar in both arms at 2 years.
Dyslipidemia
Primary prevention
Rosuvastatin
Secondary Prevention
Rosuvastatin
Atorvastatin
Ezetimibe
Niacin
JUPITER (18997196)
Rosuvastatin in patients with CRP >2 mg/L reduced MACE (NNT 150)
SATURN (22085316)
PROVE-IT (15007110)
IMPROVE-IT (18376000)
AIM-HIGH (22085343)
Rosuvastatin 40 and Atorvastatin 80 both promoted atheroma regression
Atorvastatin reduced death / repeat ACS compared to Pravastatin (NNT 25)
Ezetimibe +Simvastatin in FHL did not reduce CIMT over Simvastatin alone.
No benefit to addition of Niacin to Statin, trend toward increase stroke.
*The above information is only an extremely condensed version of the full trial details. Please see the full paper for further details.
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Heart
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Association
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American
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