LOYOLACARDIOLOGY

Henri Matisse: © 2015 Succession H. Matisse / Artists Rights Society (ARS), New York

INTRODUCTIONHenri 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, �ew 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.

Mike Hushion, MD (PGY 6)Chief Cardiology Fellow

Andrew Chen, MD (PGY 3)Internal Medicine Resident

Shermeen Memon, MD (PGY 6)Chief Cardiology Fellow

Ambrose Panico, DO (PGY 5)General Cardiology Fellow

Contributors

Produced and Edited ByChris Latanich, MD (PGY 5)

General Cardiology Fellow

ADMISSIONSAdmissions 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 ACS3) Severe Valvular Disease4) Pericardial Disease5) Post ACS Complications (chest pain, access problems etc...)6) Non-Sustained Ventricular Tachycardia OR <1 ICD shocks7) Cardiac Syncope8) Hypertensive Urgency9) Adult Congenital Heart Disease10) Clinically Signi�cant 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.

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.

Name and contact number of the patient’s primary cardiologist

Angiogram (cath report)

Transthoracic echocardiogram

Stress test

Baseline EKGs (or if a patient is admitted / transferred for VT / AT the arrhythmia in question)

Lipid panel and A1c

Open heart operative reports (bare minimum is the graft anatomy)

Device interrogation report with indication for device implantation

HYPERTENSIONHypertensive 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.

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 �rst 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 di�erence in hypertensive urgency and emergency is the rapidity of rise. Hypertensive emergency is accordingly associated with di�use necortizing vasculitis, arteriolar thrombi and �brin deposition in arteriolar walls whereas urgency is not.

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 �xed dose combinations as there is some data to suggest that compli-ance improves with these formulations. Otherwise the non-compliance rate is generally >30%.

End Organ Damage

Flash pulmonary edemaAcute left ventricular failureMyocardial ischemia / infarctionStrokeSubarachnoid hemorrhageIntracerebral hemorrhageRetinal hemorrhageRetinopathyEclampsiaHypertensive encephalopathyMicroangiopathic hemolytic anemiaAcute kidney injuryAortic dissection / aneurysm rupture

Walmart / Target $4 FormularyBeta Blockers Atenolol (25, 50, 100) Carvedilol (3.125, 6.25, 12.5, 25) Metoprolol Tartrate (25, 50, 100) Nadolol (20, 40) Pindolol (5, 10)Ace Inhbitors Benazepril† (5, 10, 20, 40) Enalapril* (2.5, 5, 10, 20) Lisinopril* (2.5, 5, 10, 20)Thiazide Diuretics Chlorthalidone (25, 50) HCTZ* (12.5, 25, 50)Loop Diuretics Bumetaide (0.5, 1) Furosemide (20, 40, 80)Vasodilators Diltiazem (30, 60, 90, 120) Hydralazine (10, 25) Verapamil (80, 120)*Widely available �xed dose combinations with HCTZ†Widely available �xed dose combinations with amlodipine

Reading an EKG may seem overwhelming at �rst but the following instructions are to help guide your evalua-tion. 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.

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.

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).

No P-wave with a narrow regular QRS complex suggests a junctional rhythm (40 - 60 bpm vs accelerated 60-100 bpm).

No P-wave with a wide QRS complex suggests a ventricular escape rhythm (20-40 bpm).

EKG INTERPRETATION

300 150 100 75 60 50

1 small box = 0.04 s

1 large box = 0.20 s

SA Node

VentricularEscape

AV Node

300 150 100 75 60 50

300 150 100 75 60 50 43

300 150 100 75 60 50 43

EKG INTERPRETATION3. 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 �nd which lead is most isoelectric).

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 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°): - RVH, PE, COPD, lateral MI, WPW, ostium primum ASD- 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.

Step 1: Quadrant

I Normal

Left Axis

Extre

me Right

Right Ax

is

aVF

aVF

I

aVF

I

aVF

I

I isolectric / -90°

-30° II isolectric

I aVF

aVF I isolectric180°

I isolectric / 90°

aVFI

Normal

Left Axis

Extre

me Right

Right Ax

is

I / 90°

I / -90°

aVF / 180°

II / 150°

III / -150°

aVR / 120°

aVL / -120°

0° / aVF

30° / III

-30° / II

60° / aVL

-60° / aVR

Step 2: Find lead whereQRS is most isoeletric.

RR Interval

ST Interval

QT Interval

PR

EKG INTERPRETATION4. Intervals.PR Interval (normal 120 - 200 ms):

- Short PR (<120 ms): Wol�-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 / nonspeci�c 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 INTERPRETATION5. Hypertrophy and Voltage.Atrial Enlargement.

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 e�usions ; obesity ; cardiomyopathies ; CAD with extensive LV infarction ; myxedema

Left Ventricular HypertrophyCornell: R in aVL + S in V3 greater than 28 mm in men / 20 mm in womenAlternate 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 HypertrophyRight 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 identi�cation, 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 signi�cance.

Terminal portion in V1 >1 deep & 1 wide Notched P > 120 ms in II, III or aVF

LA EnlargementNormal

II

>2.5 mm in II, III & aVF>1.5 mm in V1 or V2

RA Enlargement

II V1 II

EKG INTERPRETATION8. Bundle Branch Blocks.

9. ST Segment Changes.ST Segment Identi�cation: Starting 0.06 s after J point and measure in mm relative to TP segment.

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 precor-dial leads in early repolarization.

Diagnosing MI with LBBB (Sgarbossa’s Criteria): Scores ≥ 3 are 80% sensitive and 90% speci�c for AMI

10. Infarct Localization.

ST elevation ≥ 1 mm concordant with QRS in any lead.

≥ 1 mm

QRS

Axi

s

1

5 PointsST elevation ≥ 5 mm disconcordant with QRS in any lead.

≥ 5 mm

QRS

Axi

s

2

2 PointsST depression ≥ 1 mm in V1, V2 or V3.

≥ 1 mm

QRS

Axi

s

3

3 Points

NormalVariation

J point

ST Segment

Septal (LAD)

Lateral (Circ)

Inferior (PDA)

Anterior (LAD)

aVR V1 V4

aVL V2 V5

I

II

III aVF V3 V6

Left Bundle Branch BlockQRS Duration must be > 120 ms (incomplete if QRS is >100 ms but otherwise appears like a LBBB)

Lead 1: Monophasic R & no Q waves.Lead V1: QS or rS patternLead V6: Late intrinsicoid de�ection, Monophasic R & no Q waves.

I V1 V6I V1 V6

Right Bundle Branch BlockQRS Duration must be > 120 ms (incomplete if QRS is >90 ms but otherwise appears like a RBBB)

Lead 1: Wide S wave.Lead V1: Late intrinsicoid de�ection. M-shaped QRS (RSR’). Sometimes wide R or qRLead V6: Early intrinsicoid de�ection with a wide S wave.

AVNRT vs AVRTAV 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).

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

Refractory

SA Node

Slow Fast

Sinus impulse conducted down fast pathway (long

refractory period).

PAC occuring while fast path still refractory and

conducts down slow path.

Impulse from PAC enters ventricles and �nds fast pathway reset, travels retrograde up fast pathway and �nds slow pathway reset and creates a loop.

Termination of AVNRT via Adenosine blockade of AV node (or vagal maneuvers or DCCV). May

terminate in either a ventricular or atrial complex.

PAC

Retrograde P

AdenosineBlock

PAC travels down AV node, through ventricles and retrograde up accessory pathway

establishing loop (orthodromic / typical AVRT).

PAC

Retrograde P

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.

Slow Fast

SA Node

AccessoryPathway

PAC

Orthodromic Antidromic

PAC

Ort

hodr

omic

Ant

idro

mic

Orthodromic

AdenosineBlock

Antidromic

AdenosineBlock

ATRIAL TACHYCARDIAS

Sinus Beat 2:1 A Tach

Sinus Beat Focal A Tach

Sinus Beat Multifocal A Tach

P

P1 P1 P1 P1P2 P2 P2 P2P3 P3

Atrial Tachycardia: Broad term used to describe a complex of atrial tachyarrhythmias including atrial �utter. It encopmasses a discrete atrial ectopic focus driving a tachyarrhythmia and re-entrant tachycardias like atrial �utter.

Multifocal Atrial Tachycardia: Rare arrhythmia. Halmark is the identi�cation of 3+ ectoptic atrial foci driving the tachyarrhtyhmia. Treated in a similar fashion as typical focal atrial tachycardia.

Atrial Flutter: Atrial �utter 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 �utter has sawtooth pattern with negative �utter waves in the inferior leads and positive �utter 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 signi�cant conduction system disease. Do not expect to alway see a �brillating baseline.

CHA2DS2-VASc Scoring SystemHeart Failure / L V dysfunction 1Hypertension 1Age 65-74 1 75+ 2Diabetes Mellitus 1Stroke / TIA 2PAD / Old MI / Aortic Plaque 1Female 1

Lip et. al. Chest. 2010;137(2):263-272

CHA2DS2-VASc Annual Stroke Risk0123456789 15.2%

6.7%9.6%9.8%

6.7%4.0%

3.2%2.2%

1.3%

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.

1

23

SA and AV Nodally Mediated Bradycardias

1

1

Pure sinus bradycardia driven by poor intrinsic SA nodal activity or by excess vagal tone (or drug e�ect). Stimulation with Isoroterenol or Epinepherine or disinhibition with Atropine will raise SA nodal rate.

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 �x 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

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 signi�cant e�ect or may worsen the ventricular response, especially if there is concurrent bundle branch blocks.

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

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.

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.

Atropine orIsoproterenol

WIDE COMPLEX TACHYCARDIA

Regular R-R

1:1 AV Ratio or Unknown

Wide QRS Complex TachycardiaQRS > 120 ms

Irregular R-R

Atrial �brillation / �utter / tachycardia with abberent conduction (BBB, IVCD

or accessory pathway)

Vagal Maneuvers Adenosine IVP

SVT, RBBB / LBBB and antidromic AVRT

QRS identical to resting EKG

Likely VT

QRS di�ers from resting EKG and prior MI or structural disease

< 1:1 AV Ratio

Likely VT Atrial tachycardia / �utter

> 1:1 AV Ratio

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°

Left Ventricular Tachycardia

LBBB Patern R in V1 > 30 ms R to nadir of S in V1 > 60 ms qR or qS in V6

Right Ventricular Tachycardia

V6

V5V4V3V2V1

R to S > 100 ms

I II

aVF V1 V6

I II aVF V1

V6

AmericanHeartAssociation Blomström-Lundqvist et al. JACC. 2003;42:1493–531

CHEST PAIN EVALUATIONDe�nitions of angina:

Typical Angina (De�nite): 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 de�nite or typical angina.

Nonanginal Chest Pain: Chest pain or discomfort that meets one or none of the typical angina characteristics.

ELECTROCARDIOGRAPHY - LEAD PLACEMENT

4th right intercostal space V1

V2 4th left intercostal space Directly between V2 and V4V3

5th left ICS at the MCLV4

V5 5th left ICS at ant ax line5th left ICS at mid ax lineV6

5th right ICS at the MCLV4r

V5r 5th right ICS at ant ax line5th right ICS at mid ax lineV6r Right ArmRA

LA Left ArmLeft LegLL

Right LegRL

Diamond and Forrester Pre-Test Probability of Coronary Artery Disease

<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%

>60 Man >90% 10-90% 10-90%

Woman >90% 10-90% 10-90%

Age (Years) Sex Typical Angina Atypical Angina Nonanginal Chest Pain

ACUTE CORONARY SYNDROMEAlgorithm for the evaluation and management of patients suspected of having ACS

AmericanHeartAssociation Eugene Braunwald et al. Circulation. 2000;102:1193-1209

SYMPTOMS SUGGETIVE OF ACS

Possible ACS De�nite ACS

No ST elevation ST elevation

Activate STEMI Pager

Nondiagnostic ECGNormal initial troponin

ST and/or T wave changesOngoing pain

Positive troponinHemodynamic abnormalities

Recurrent ischemic pain orPositive followup studies

Diagnosis of ACS con�rmed

ObserveFollow-up at 4-8 hours: ECG , troponin

Admit to hospitalManage via acute ischemia pathway

No recurrent pain; Negative follow-up studies

PositiveDiagnosis of ACS con�rmed

NegativePotential diagnoses: nonischemic

discomfort; low-risk ACSArrangements for outpatient follow-up

Stress study to provoke ischemiaConsider evaluation of LV function if

ischemia is present(Tests may be performed either prior to

discharge or as outpatient)

ACUTE ISCHEMIA PATHWAY

Immediate angiography 12-24 hour angiography Recurrent symptoms/ischemia

Heart failureSerious arrhythmia

Not low risk Low risk

Follow on medical Rx

Recurrent ischemia and / or ST segment shift, or

Deep T-wave inversion, or Positive troponin

AspirinBeta blockers

NitratesAntithrombin Regimen

GP IIb/IIIa inhibitorMonitoring (rhythm and ischemia)

Early invasive strategy Early conservative strategy

Patient stabilizes

Evaluate LV Function

LVEF >40%LVEF <40%

Stress Test

AmericanHeartAssociation Eugene Braunwald et al. Circulation. 2000;102:1193-1209

ACUTE CORONARY SYNDROMENot all troponin leaks are secondary to acute myocardial infarction. THINK is the TROPONIN ELEVATION due to PLAQUE RUPTURE or secondary to another underlying cause.

STEMI: Clinical syndrome de�ned 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 LBBB3) ST depression in 2 precordial leads (V1–V4) may indicate transmural posterior injury4) 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 de�ned 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 de�ned by 1) symptoms, 2) absence of persistent ST elevation but can have other ST-T wave changes, and 3) release of cardiac biomarkers.

Type 1 Myocardial Infarction

Type 2 Myocardial Infarction(Demand Ischemia)

Vasospasm or endothelial dysfunction

Fixed atherosclerosis andsupply demand imbalance

Supply demand imbalance alone

Plaque rupture with thrombus

Troponin without reperfusionTroponin with reperfusionCKMB without reperfusionCKMB with reperfusion

x U

pper

Lim

it of

Nor

mal

1

2

5

10

20

100

1 2 3 4 5 6 7 80

Days from Onset of Infarction

0

ACUTE CORONARY SYNDROME

Indicator of 35 day composite events risk (mortality, new or repeat MI, severe recurrent ischemia requiring urgent revascularization through 14 days after admission).

1) Age >65 years2) 3+ cardiac risk factors3) Prior coronary stenosis >50%4) ST segment deviation on admission ECG5) >2 anginal events in the last 24 hours6) Aspirin treatment in the prior 7 days7) Prior congestive heart failure, MI, CABG or PCI

TIMI Risk Score (NSTEMI)

0

10

20

30

40

50

0-1 2 3 4 5 6-7

Com

posi

te R

isk

(%)

Medications to be started immediately (these have survival bene�ts) to be administered to all patients (unless clear contraindication).1. Aspirin 325 mg PO once followed by Aspirin 81 mg PO daily2. Heparin drip (intermediate algorithm with bolus)3. Lipitor 40-80 mg PO QHS4. Plavix / E�ent / Brilinta (P2Y12 inhibi-tors) 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 bene�t 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 bene�t.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 panel2) Hemoglobin A1c3) Transthoracic echocardiogram (with de�nity if a large anterior wall MI or concern for aneurysm formation which could predispose to LV thrombus forma-tion.

CARDIAC CATHETERIZATION

Common Angiographic Views

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 bene�t assessment and the expectation that the information or therapeutics gleaned from the study will o�set the risks of the procedure.

Pericardiocentesis (30 min): E�usion 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.

Left Main

LAD

Circum�ex

RCA

PDA

Left Main

LAD

Circum�ex

RCA

PDAPDA

Left Main

LAD

Circum�ex

RCA

Contraindications

INR > 2

Platelets < 50

AKI (Angiogram)

Hemodynamically Unstable

Active Hemorrhage

Stroke / CNS Bleed

Preprocedure Checklist

BMP

CBCEKG

INR NPO

Consent

Images courtesy of Patrick J. Lynch

VALVULAR HEART DISEASE

Image courtesy of Patrick J. Lynch

AmericanHeartAssociationNishimura et. al. J Am Coll Cardiol. 2014;63(22):e57-e185

Normal Mild Moderate Severe

Aortic Stenosis Velocity (m/s) <2 2.0 - 2.9 3.0 - 3.9 >4.0 Mean Pressure Gradient (mmHg) <10 <20 20 - 39 >40 Valve Area >2 >1.5 1.0 - 1.5 <1.0 Aortic Regurgitation Vena Contracta (cm) <0.3 0.3 - 0.6 >0.6Mitral Stenosis Planimetry MV Area (cm2) >1.5 1.0 - 1.5 <1.0 DIastolic Pressure Half Time (ms) <150 >150 >220 Mean Pressure Gradient (mmHg) <5 5 - 10 >10Mitral Regurgitation Vena Contracta (cm) <0.3 <0.7 >0.7 ERO (cm2) <0.4 >0.4

American Society for Echocardiography Reference Ranges

Medtronic CoreValve Evolut

Medtronic Mosaic Bovine Pericardial

St. Jude Mechanical

CARDIAC DEVICES

Device Program Coding

Dual Chamber Pacemaker RV & RARV & RA

ShockATPPacing

TherapiesSensing

CSRVRA

Device Type Leads

Single Chamber Pacemaker RVRV

Biventricular Pacemaker (CRT-P) RA / BiVRA / RV / CS

Subcutaneous ICD (SC-ICD) SC Coil

Biventricular De�brillator (CRT-D) RA / BiVRA / RV / CS

Dual Chamber De�brillator (ICD) RV & RARV & RA

Single Chamber De�brillator (ICD) RVRV

Designed to treat tachyarrhythmias (primarily VT / VF) most de�brillators also have the ability to treat bradyarrhythmias via a pacing function (with the exception of subcutaneous ICDs which only de�bril-late).

DEFIBRILLATORSDesigned 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 tachyar-rhythmias.

PACEMAKERS

Right Atrial Lead (RA) (Pace / Sense)

Right Ventricular Lead (RV) (Pace / Sense / De�brillate)

Coronary Sinus Lead (CS) (Pace / Sense)

Pulse Generator

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.

Most common modes:DDD - Paces both RA and RV (sometimes BiV). Monitors RA and RV. Detections may trigger a pacing impulse or inhibit depend-ing upon their timing. VVI - Paces RV. Monitors RV. Detections inhibit pacing.

AAI - Paces RA. Monitors RA. Detections inhibit pacing.

AAI <-> DDD - Converts between modes when in AFib or Flutter.

EP PROCEDURESRoutine 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. Pacemak-ers 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 bene�t 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.

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 �brillation 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.

De�brillator 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 �utter. If onset of atrial �utter is > 48 hours before the procedure or the patient has not been on anticoagulation, they will usually require a TEE �rst.

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 �ushing).

Preprocedure Checklist

BMP

Type and Screen

INR

CBC

NPO

Heparins stopped at least 12 hours earlier

NOACs held as directed

Coumadin OK to continue

Post Device Implantation Checklist

Site dressings managed by EP Service

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

Device interrogation in AM

HEART FAILUREVolume Status vs Perfusion: Volume status: Jugular vein distention (JVD), hepato-jugular re�ux, peripheral edema, orthopnea, PND, rales.

Perfusion: Look for evidence of end organ hypoperfu-sion (cool extremities, renal failure, acidosis, altered mental status etc...).

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

High risk for heart failure but without structural heart disease or symptoms. A

Structural heart disease without heart failure.B

Structural heart disease with prior or active heart failure.C

Refractory heart failure requring specialized interventions.D

I Asymptomatic

II Symptoms with moderate exertion

III Symptoms with minimal exertion

IV Symptoms at rest

NYHA Stage1 Year

Mortality

5-10%

15-30%

50-60%

Based on comorbidities

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 bene�t to the use of pulmonary artery catheters to guide therapy over just clinical assessment of volume status. There is currently no well agreed indication for pulmonary artery catheter placement to guide therapy outside of document-ing inotrope dependence.

Measure JVD in CM above sternal notch (measured + 5).Normal is 7-9

45 Degrees

Agent Onset Duration BioavailabilityLasix (40 mg PO) 30-60 min 6-8 hrs 50%Lasix (20 mg IV) 5 min 2 hrs 100%Bumex (1 mg PO) 10 min 4-6 hrs 80%Demedex (10 mg PO) 1 hr 4-6 hrs 90%Metolazone (PO) 60 min >24 hrs

Diuretic Equivalence

HEMODYNAMICS

ECG25

0mmHg

25

0mmHg

25

0mmHg

av

y

c25

0mmHg

x

Aortic ValveOpens

Mitral ValveCloses

Aortic ValveCloses

Mitral ValveOpens

edp

125

100

75

50

25

0mmHg

125

100

75

50mmHgSystole

DDiastole Systole

E

Aortic ValveOpens

Aortic ValveCloses

A

B

C

Native Pressures

With IABP On

RA

RV

PCWP

Ao

LV

IABP

Ao

PAReference Ranges

Right Atrium a wave 2 - 7 mmHg v wave 2 - 7 mmHg Mean 1 - 5 mmHg

Right Ventricle Systolic 15 - 30 mmHg EDP 1 - 7 mmHg

Pulmonary Artery Systolic 15 - 30 mmHg Diastolic 4 - 12 mmHg Mean 9 - 19 mmHg

Pulmonary Capillary Wedge Mean 4 - 12 mmHg

Left Ventricle Systolic 90 - 140 mmHg EDP 5 - 12 mmHg

Aortic Systolic 90 - 140 mmHg Diastolic 60 - 90 mmHg Mean 70 - 105 mmHg

Cardiac Index > 2.5 L/min/m2

Swan Daily Rounds

Chest XR for catheter position

Assessment of insertion site

Pulmonic ValveOpens

Pulmonic ValveCloses

Tricuspid ValveCloses Tricuspid Valve

Opens

a cx

v y

BALLOON PUMPS

Diastole Systole

0 30 60 90 120 150 180 210 240 270 300 330 360 390 420Days after randomisation

p=0·94; log-rank testRelative risk 1·02, 95% CI 0·88–1·19

0

10

20

30

40

50

60

Mor

talit

y (%

)

IABPControl

All Cause Mortality from SHOCK II Trial (IABP Support in ACS with Cardiogenic Shock)

Systole Diastole

125

100

75

50mmHg

Native Pressures

IABP Augm

entation

Coronary PerfusionAugmentation

Bene�t is garnered by a reduction in the work required by the LV during systole (balloon de�ates providing a partial vacuum into the aorta) and an increase in the diastolic pressure (during coronary perfusion).

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 bene�t as shown above. In the other situations, there is little if any data to assess their value.

Proper placement of IABP with radio-opaque marker just below aortic arch and about the level of the carina.

Balloon Pump (IABP) Daily Rounds

Chest XR to con�rm IABP position

Most recent aPTT and trend

Assessment of IABP insertion site

Assessment of pedal pulses and perfusion

Heparin drip (low dose nomogram)

Balloon Pump (IABP) Anticoagulation

Image redrawn from Jones et. al. J Invasive Cardiol 2012; 24:544-550

LEFT VENTRICULAR ASSIST DEVICES

Inlet (LV) Pressure Outlet (Aortic) Pressure

Pres

sure

(mm

Hg)120

90

60

30

0

Flow

(L/m

in)

8

6

4

2

0

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 cu� and a doppler probe, record the �rst audible sound during de�ation as the MAP (goal is 70-80 mmHg).

Reported Pump Parameters:

Pump Speed (Set)

Power (Measured)

Flow (Estimated)

Pulse Index (Estimated)

Characteristic Electrical Baseline EKG Intereference

Pump Flow

LVAD Flow and Pressure

HEARTWARE LVAD (HVAD)

4.3L/min

2920RPM

4.2Watts

Fixed

Sx O�

1 2 HeartWareHW123456722:43:56

POD: 8

TimeScale

9 8 7 6 5 4 3 2 1Time (s)

12

8

4Pow

er (W

atts

)

9 8 7 6 5 4 3 2 1Time (s)

12

8

4Flow

(L/m

in)

Critical Alarms

Steady Tone

NO MESSAGE - No power to pump / Pump has stopped

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 sta� has been trained to care for most of these scenarios. In the event of repeated alarms, notify the on call fellow immediately.

Patient System Controller Display(Attached via Driveline)

HeartWare

3000 RPM 5.0 L/min4.8 Watts

Alarm Mute Battery Indicator 2Alarm IndicatorScroll

Battery Indicator 1

Two Tone

Flashing Red

1800 2400 3200 4000

2.5 8.5

103 81.8

Power (Watts)

Set Speed (RPM)

Flow (L/min)

INR 1 2 3 4

HeartWare HVAD Function Reference Ranges

Con�rmation of pump speed

Pump �ow and power trends

Hgb, PLT and LDH trends

Arrhythmia review

Suction event review

INR

HeartWare HVAD Daily Rounds

Aspirin 325 mg PO QD

Coumadin (INR 2-3)

HeartWare HVAD Anticoagulation

Reprinted with the permission of HeartWare ©

HEARTMATE LVAD (LVAD)Clinical Settings Alarms Save Data History Admin

Pump Flow Pump Speed Pulse Index

Display ON/OFF

9500rpm3.6

Pump Power

5.7w

4.5 lpm

Fixed Mode - Speed Setpoint: 9600 rpm

Test SelectButton

Power Symbol Controller CellSymbol

Red HeartSymbol

Silence AlarmButton

Battery Symbol(yellow & red)

Battery Fuel Gauge

Critical AlarmsRed Heart

Steady Tone

Pump �ow < 2.5 Lpm, pump has stopped, perc lead is disconnected, or pump is not working properly.

Red Battery

Steady Tone

< 5 min battery power remains, voltage too low, or the System Controller is not getting enough power.

Yellow Battery

1 Beep Q4 seconds

< 15 min battery power remains, voltage too low, or the System Controller is not getting enough power.

The nursing sta� has been trained to care for most of these scenarios. In the event of repeated alarms, notify the on call fellow immediately.

Patient System Controller Display(Attached via Driveline)

6K 8K 10K 15K

2.5 10

3 102.5

Power (Watts)

Set Speed (RPM)

Flow (L/min)

INR 1 2 3 4

LVAD Functional Reference Ranges

Con�rmation of pump speed

Pump �ow, PI and power trends

Hgb, PLT and LDH trends

Arrhythmia review

PI / Suction event review

INR

HeartMate II LVAD Daily Rounds

Aspirin 325 mg PO QD

Coumadin (INR 2-3)

HeartMate II LVAD Anticoagulation

Reprinted with the permission of Thoratec Corporation ©

PREOPERATIVE EVALUATION

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 strati�cation 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).

JUMPING ROPE

7 MET

8-10 MET

RUNNING

6 MET

CLIMBING STAIRS

EQUIVALENT

1-10 MET

METABOLIC

4 MET

GARDENING

1 MET

READING

UrgencyEmergent Serious threat to life or limb if not in the operating room within <6 hours.

*Provide risk strati�cation but the patient should proceed directly to surgery without delay.

De�nition

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 e�ect outcome.

Elective Any procedure that which can safely be delayed for up to or over 1 year.

Procedural Risk Class

High Risk Emergent surgery Vascular surgery Surgery with large EBL / �uid shift

Intermediate Risk Carotid endarterectomy Head and neck surgery Intraperitoneal surgery Intrathoracic surgery Orthopedic surgery Prostate surgery

Low Risk Endoscopic procedures Super�cial procedure Cataract surgery Breast surgery

Indicator of risk of su�ering perioperative myocardial infarction, pulmonary embolism, VF or other cardiac arrest or complete heart block.

1) Coronary artery disease2) Cardiomyopathy3) History of TIA or stroke4) Insulin dependent diabetes 5) Creatinine > 2.0 mg/dL6) Planned high risk surgical procedure

Revised Cardiac Risk Index

0 1 2 3+0

5

10

15

Com

posi

te R

isk

(%)

AmericanHeartAssociation Lee et al. Circulation. 1999; 100(10): 1043-1049

PREOPERATIVE EVALUATIONAlgorithm for the risk evaluation of patients prior to surgery

AmericanHeartAssociation

Patient scheduled for surgery with known or risk factors for CAD

Estimated perioperative risk of MACE based on combined clinical / surgical

risk (RCRI etc...)

Functional capacity <4 METs or unknown

Will further testing impact decision making or perioperative care?

Pharmacologic stress testing with angiography and

revascularization as indicated

Proceed to surgery or alternate management

as appropriate

Nonemergent surgical case Emergent surgical case

Clinical risk strati�cation and proceed directly to

surgeryClinically stable Acute coronary syndrome

Evaluate and treat accordingly

Low risk (<1%) Elevated risk (>1%)

Functional capacity >4 METs

No further testing

Proceed to surgeryYesNo

PREOPERATIVE CHECKLISTEKG Should be obtained in patients with known CAD/PAD, arrhythmia, cerebro-

vascular disease, or other signi�cant 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 �rst 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 reason-able to continue aspirin if patient at high risk of cardiac events and bene�ts outweighs risk of bleeding.

CARDIAC IMAGINGModality Advantages Limitations / Contraindication

Ideal in low to intermediate risk patients who can exercise enough to get to target heart rate and have an interpretable ECG.

Provides functional capacity.

Cannot use if patient has baseline LBBB or paced rhythm.

Cannot perform in a patient having ACS or recent MI, severe symptomatic AS, aortic dissections, or acute PE.

Exercise ECGExercise should be attempted in any stress modality which its felt the patient can reasonably achieve target heart rate.

Appropriate in wide range of pre-test probability patients.

Can assess viability

Balanced ischemia in triple vessel disease may lead to false negatives.

Cannot use in pregnant patients, with hypotension (SBP<90), high degree AV block, active wheezing.

Myocardial Perfusion ImagingRegadenoson or Adenosine

No radiation exposure

Appropriate in a wide range of pre-test probability patients.

Can assess viability

Can obtain additional hemody-namic data during stress.

Can be limited by poor patient echo windows – obese patients, etc.

Cannot use in symptomatic severe AS, aortic dissection, ACS.

Stress EchoDobutamine

Contraindicated in patients with recent ACS, tachyarrhythmias, uncontrolled hypertension (SBP>200/110), aortic dissections and large aneurysms.

No radiation exposure

Can assess for viability/scar

Excellent structure/anatomy imaging

Appropriate in intermediate and high pretest risk patents.

Requires high technical skill

Needs optimal heart rate and should be able to participate in breath holds.

No functional capacity is obtained.

Stress MRIGFR must be >30

ICD/Pacemakers limit study quality.

Option for low to intermediate risk patients with normal ECG and normal cardiac biomarkers.

Excellent tool for assessing anatomy of coronary arteries.

High negative predictive value

Contrast dye exposure

Limited to larger caliber more proximal vessels.Patient will need to perform breath holds and have a controlled heart rate.

Cannot use in pregnancy

Coronary CTACan potentially end up with double contrast dye exposure if positive.

Functional assessment with CT-FFR.

NOT a stress test

Optimal test for high pretest probability, positive stress tests, and those with acute coronary syndromes.

Invasive with risks of complications such as bleeding

Contrast dye exposure

Cardiac CathGold standard study for CAD.

SYNCOPE

<40 40-60 >60Age (Years)

100%

0%

20%

40%

60%

80%

Etio

logy

of S

ynco

pe (%

)

Structural Disease

Arrhythmia

Orthostatic

Neurally Mediated

Inappropriate Re�ex

CerebralHypoperfusion

Low Vasc

ular

Res

istan

ce Low Cardiac O

utput

Cardiac (Pulmonary)

Poor Venous Return

Autonomic Failure

Norm

al A

uton

oics

Arrhythmia

StructuralO

ther

Secondary ANF

Primary ANF

MixedCard Inhib

Vaso

depressor

Drug

Indu

ced

Dys

auto

nom

ia

Volume LowVenous P

ool

Orthostatic Hypotens

ion

Cardiac Syncope

Re�ex Syncope

Physiologic Basis of Syncope: Any mechanism which causes a transient drop in cerebral blood �ow below 50-60 mL/min for at least 6-8 seconds can result in syncope.

*Syncopized is not a word. Syncopated refers to accentuating the o� 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 o�ending drugs like alpha blockers etc...)

Re�ex Syncope: Drop in CBF via sudden changes in e�erent autonomic activity, especially parasympa-thetic, 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

TelemetryEchocardiogram with dopplerOrthostatic Vital Signs EKG

Initial Diagnostic Evaluation

Clearly documented that patient is restricted from driving if no immediately reversible cause is identi�ed

Driving Restrictions

INO

TRO

PIC

AG

ENTS

Age

nt (M

OA

)D

ose

Rang

e

Milr

inon

e (c

GM

P / P

DE3

)0.

20 -

0.50

mcg

/ kg

/ m

in

Clea

ranc

e (t

½)

Rena

l ~80

% (2

.3 h

rs)

PDE3

- cG

MP

med

iate

d in

crea

se in

in

trac

ellu

lar i

ntra

cellu

lar C

a++

conc

entr

atio

n an

d co

nseq

uent

rise

in

con

trac

tility

and

CI.

Dec

reas

es

SVR

/ PVR

.

Prim

ary

Act

ivit

y

Dob

utam

ine

(β1 +

+ / β

2 +)

2.5

- 10

mcg

/ kg

/ m

inRe

nal (

2 m

inut

es)

Beta

1 re

cept

or m

edia

ted

incr

ease

in

car

diac

con

trac

tility

and

HR.

D

ecre

ase

in S

VR v

ia B

eta

2 m

edi-

ated

vas

odila

tion.

Epin

ephe

rine

(β1

/ β2 /

α1)

1 - 2

0 m

cg /

min

Rena

l 100

% (1

min

)Be

ta 1

rece

ptor

med

iate

d in

crea

se

in c

ardi

ac c

ontr

actil

ity a

nd H

R.

Incr

ease

s SV

R vi

a po

tent

Alp

ha

activ

ity.

Nor

epin

ephe

rine

(β1

/ α1)

0.02

- 1.

0 m

cg /

kg /

min

Rena

l 100

% (1

min

)Be

ta 1

rece

ptor

med

iate

d in

crea

se

in c

ardi

ac c

ontr

actil

ity a

nd H

R.

Incr

ease

s SV

R vi

a po

tent

Alp

ha

activ

ity.

VASO

PRES

SOR

AG

ENTS

Age

nt (M

OA

)D

ose

Rang

e

Nor

epin

ephr

ine

(β1

/ α1)

0.02

- 1.

0 m

cg /

kg /

min

Clea

ranc

e (t

½)

Rena

l 100

% (1

min

)Be

ta 1

rece

ptor

med

iate

d in

crea

se

in c

ardi

ac c

ontr

actil

ity a

nd H

R.

Incr

ease

s SV

R vi

a po

tent

Alp

ha

activ

ity.

Prim

ary

Act

ivit

y

Epin

ephr

ine

(β1

/ β2 /

α1)

1 - 2

0 m

cg /

min

Rena

l 100

% (1

min

)Be

ta 1

rece

ptor

med

iate

d in

crea

se

in c

ardi

ac c

ontr

actil

ity a

nd H

R.

Incr

ease

s SV

R vi

a po

tent

Alp

ha

activ

ity.

Vaso

pres

sin

(V1)

0.03

uni

ts /

min

Rena

l 10-

15%

(10-

20

min

)Va

sopr

essi

n 1

rece

ptor

med

iate

d va

soco

nstr

ictio

n.

Dop

amin

e (β

1 / α

1) 0.

5 - 2

0 m

cg /

kg /

min

Rena

l 80%

(2 m

in)

Dos

e de

pend

ent e

�ect

. Alp

ha 1

an

d Be

ta 1

dom

inan

t act

ivity

at

dose

s ab

ove

10 m

cg /

kg /

min

.

Phen

ylep

hrin

e (α

1)1

- 10

mcg

/ kg

/ hr

Hep

atic

(2-3

hrs

)Pu

re A

lpha

1 m

edia

ted

vaso

con-

stric

tion

Age

ntD

ose

Rang

e

Hyd

rala

zine

O

nset

: 10

- 20

min

D

urat

ion:

1

- 4 h

ours

10 -

20 m

g IV

P

Adv

erse

e�e

cts

Tach

ycar

dia,

hea

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e, �

ushi

ng,

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acra

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pre

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e or

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a

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rain

dica

tions

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l

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et:

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in

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n:

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hou

rs

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80 m

g IV

P Q

10 m

in (

max

300

mg)

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chos

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rt b

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dec

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h gr

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gni�

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br

adyc

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a

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opru

ssid

e

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et:

1 m

in

Dur

atio

n:

1 - 1

0 m

in

0.1

- 10

mcg

/ kg

/ m

inCy

anid

e an

d th

yocy

anat

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xici

ty,

naus

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omiti

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uscl

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ogly

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et:

2 - 5

min

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urat

ion:

5

- 10

min

5 - 2

00 m

cg /

min

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ardi

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ethe

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ia

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se o

f PD

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a�l).

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r mon

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nset

: 5

-15

min

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urat

ion:

1.

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r +Δ

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min

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april

at

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30 m

in

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atio

n:

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2 ho

urs

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mg

– 5

mg

Q6H

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t dos

e hy

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and

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nal f

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A)

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e Ra

nge

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ogly

cerin

e5

- 200

mcg

/ m

in

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ranc

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½)

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atic

/ RB

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- 3

min

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nver

ted

to N

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rom

otin

g ve

nous

(pre

load

) rel

axat

ion.

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all a

fter

load

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cing

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ct.

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ary

Act

ivit

yCo

ntra

indi

catio

ns

Acut

e in

ferio

r MI

HO

CM

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opru

ssid

e0.

1 - 1

0 m

cg /

kg /

min

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atic

/ RB

Cs (1

- 3

min

)Sm

all v

esse

l vas

odila

tion

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ar-

ily a

fter

load

redu

ctio

n.St

roke

/ TI

ACo

arct

atio

nVS

D

HEA

RT F

AIL

URE

AG

ENTS

Age

nt (M

OA

)

ACE

Inhi

bito

rs

Capt

opril

En

alap

ril

Lisi

nopr

il

50 m

g PO

TID

10 m

g PO

BID

40 m

g PO

QD

Vaso

dila

tors

H

ydra

lazi

ne

Isor

dil

Im

dur

50-7

5 m

g PO

TID

20-8

0 m

g PO

TID

60-1

20 m

g PO

QD

Targ

et D

ose

Age

nt (M

OA

)Ta

rget

Dos

e

Beta

Blo

cker

s

Carv

edilo

l

Met

opro

lol X

L (n

ot L

opre

ssor

)25

mg

PO B

ID20

0 m

g PO

QD

Ald

oste

rone

Ant

agon

ist

Sp

irono

lact

one

25 m

g PO

QD

Ang

iote

nsin

Rec

epto

r Blo

cker

s V

alsa

rtan

80-1

60 m

g Q

D -

BID

NO

VEL

ORA

L A

NTI

COA

GU

LAN

TS

Dab

igat

ran

(Pra

daxa

)

Dire

ct T

hrom

bin

Inhi

bito

r

Ons

et:

90 m

in

Clea

ranc

e: R

enal

(12-

27 h

rs)

Re

vers

al:

Prax

bind

Non

-Val

vula

r AF

G

FR >

30:

150

mg

PO B

ID

GFR

15-

30:

75 m

g PO

BID

DVT

/ PE

Tre

atm

ent

G

FR >

30:

150

mg

PO B

ID

Mus

t not

ope

n ca

psul

es.

Avoi

d us

ing

with

am

ioda

rone

, dro

nade

rone

, ve

rapa

mil,

ket

ocon

azle

, cla

rithr

omyc

in, q

uini

dine

.

Cons

ider

atio

ns

Ok

to c

rush

tabl

ets

and

mix

with

app

le s

auce

.

Avoi

d us

ing

in p

atie

nts

with

mod

erat

e to

sev

ere

liver

dy

sfun

ctio

n.

Api

xaba

n (E

liqui

s)

Fact

or X

a In

hibi

tor

O

nset

: 3-

4 ho

urs

Cl

eara

nce:

Hep

atic

(12

hrs)

Re

vers

al:

KCen

tra

Non

-Val

vula

r AF:

5 m

g PO

BID

but

if tw

o or

mor

e co

nditi

ons

appl

y

(C

r >1.

5, A

ge >

80, w

t< 6

0 kg

) the

n 2.

5 m

g PO

BID

DVT

/ PE

Tre

atm

ent

10

mg

PO B

ID x

7 d

ays

then

5 m

g PO

BID

Ok

to c

rush

and

sus

pend

in D

5W 6

0 m

L if

give

n im

med

iate

ly.

Avoi

d in

sev

ere

hepa

tic im

pairm

ent.

Edox

aban

(Sav

aysa

)

Fact

or X

a In

hibi

tor

O

nset

: 1-

2 ho

urs

Cl

eara

nce:

Ren

al 5

0% (1

2 hr

s)

Reve

rsal

: KC

entr

a

Non

-Val

vula

r AF

G

FR 9

5-50

: 60

mg

PO Q

D

GFR

50-

15:

30 m

g PO

QD

Avoi

d in

pat

ient

s w

ith v

ery

high

func

tioni

ng k

idne

ys

due

to e

xces

sivl

y ra

pid

clea

ranc

e.

Avoi

d us

ing

in p

atie

nts

with

mod

erat

e to

sev

ere

liver

dy

sfun

ctio

n.

Age

nt (M

OA

)D

osin

g

Riva

roxa

ban

(Xar

elto

)

Fact

or X

a In

hibi

tor

O

nset

: 2-

3 ho

urs

Cl

eara

nce:

Ren

al 6

6% (5

-9 h

rs)

Re

vers

al:

KCen

tra

Non

-Val

vula

r AF

G

FR >

15:

20 m

g PO

QD

DVT

/ PE

Tre

atm

ent

G

FR >

15:

15 m

g PO

BID

x 2

1d th

en 2

0 m

g Q

D

LANDMARK CLINICAL TRIALSTopic Trial Name (PMID) Brief FindingsAtrial Fibrillation Anticoalguation Apixiban (Eliquis) ARISTOTLE (21870978) Apixiban superior to coumadin for stroke prevention (NNT 300) Dabigatran (Pradaxa) RE-LY (19717844) Dabigatran non-inferior to coumadin for stroke prevention Rivaroxiban (Xarelto) ROCKET-AF (21830957) Rivaroxiban non-inferior to coumnadin for stroke prevention Rate Control Threshold RACE-II (20231232) Lenient HR control (<110) non-inferior to strict (<80 bpm) for risk of MACE Rate vs Rhythm Control AFFIRM (12466507) Rate control non-inferior to rhythm control for risk of MACE

Ischemic Heart Disease Antiplatelet and Anticoagulant Therapy ASA ISIS-2 (2899772) ASA reduces reinfarct and death [very old study] (NNT 20) Clopidogrel CURE (11519503) Addition of Clopidogrel to ASA reduces MACE (NNT 50) Prasugrel TRITON TIMI 38 (17982182) Prasugrel superior to clopidogrel with PCI (NNT 50) Ticagrelor PLATO (20079528) Ticagrelor superior to clopidogrel with PCI (NNT 60) Revascularization Paclitaxel DES in STEMI HORIZONS AMI (19420364) DES in STEMI reduced TVR but not MACE (NNT 35) Compl. Revasc STEMI PRAMI (23991625) Non-infarct artery PCI reduces death / MI (NNT 7) PCI in UA / NSTEMI RITA-3 (16154018) PCI in high risk pts over OMT alone reduces 5 yr MACE (NNT 30) DES PCI vs CABG SYNTAX (19228612) CABG in LM or 3v CAD superior to PCI (e�ect rises with SYNTAX score) FREEDOM (23121323) CABG superior to PCI in diabetic pts to reduce MACE at 5 years (NNT 12) PCI vs OMT COURAGE (17387127) OMT non-inferior to BMS PCI for stable CAD for 5 year MACE FAME-2 (22924638) FFR guided PCI v OMT in stable CAD reduced urg revasc but not MI or death Access Radial vs Femoral RIVAL (21470671) Radial approach reduced hemorrhagic complications (NNT 500)

Heart failure Enalapril CONSENSUS (2883575) Enalapril in NYHA class IV reduced death(NNT 6) SOLVD (1463530) Enalapril in NYHA class II+ reduced hospitalization, not death (NNT 25) Valsartan ValHeFT (11759645) Valsartan in NYHA class II+ reduced hospitalizatoin (NNT 25) Spironolactone RALES (10471456) Spironolactone in NYHA class III+ reduced death(NNT 9) Carvedilol COMET (12853193) Carvedilol superior to Mortality in NYHA class II+ in reducing death (NNT 18) Digoxin Dig (9036306) Digoxin in Systolic HF reduced hospitalization but not death. Ivabradine BEAUTIFUL (18757088) Ivadribine in stable CAD + HR >70 reduced ACS admits (NNT 50) SHIFT (20801500) Ivadribine in stable CAD + HR >70 reduced ACS and Death (NNT 20 / 50) Dialysis with UF CARRESS-HF (23131078) Ultra�ltration “inferior” really equivalent to diuresis in NYHA class IV

Hypertension Benazepril + Amlodipine ACCOMPLISH (19052124) Benazepril+CCB reduced death / MI v Benazepril+HCTZ (NNT 50) Benazepril + HCTZ ACCOMPLISH (19052124) See above Lisinopril ALLHAT (12479763) Amlodipine v Chlorthalidone v Lisinopril all equal for ACS risk Amlodipine ALLHAT (12479763) See above VALUE (15207952) Amlodipine reduced MI but not mortality compared to Valsartan (NNT 140) Chlorthalidone ALLHAT (12479763) See above Losartan LIFE (11937178) Losartan reduced risk of stroke but not death or MI vs atenolol (NNNT 50) Valsartan VALUE (15207952) 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 JUPITER (18997196) Rosuvastatin in patients with CRP >2 mg/L reduced MACE (NNT 150) Secondary Prevention Rosuvastatin SATURN (22085316) Rosuvastatin 40 and Atorvastatin 80 both promoted atheroma regression Atorvastatin PROVE-IT (15007110) Atorvastatin reduced death / repeat ACS compared to Pravastatin (NNT 25) Ezetimibe IMPROVE-IT (18376000) Ezetimibe +Simvastatin in FHL did not reduce CIMT over Simvastatin alone. Niacin AIM-HIGH (22085343) No bene�t 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.

AmericanHeartAssociation

AM

ERICAN COLLEGE

OF CARDIOLOGY