LOYOLA CARDIOLOGY

Housestaff Handbook 2018-2019

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.

ADMISSIONS

Walmart / Target $4 Formulary

Beta 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 fixed dose combinations with HCTZ †Widely available fixed dose combinations with amlodipine

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.

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 compli- ance improves with these formulations. Otherwise the non-compliance rate is generally >30%.

HYPERTENSION

Reading an EKG may seem overwhelming at first 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.

1 small box = 0.04 s

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).

SA Node

Inverted or abnormal P-waves suggest an ectopic atrial rhythm (P:QRS is1:1).

300 150 100 75 60 50

AV Node

Ventricular Escape

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

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

I I

aVF

I

aVF aVF

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).

Step 1: Quadrant Step 2: Find lead where QRS is most isoeletric.

I / -90°

aVF aVL / -120°

III / -150°

-60° / aVR

-30° / II

I aVF / 180° 0° / aVF

II / 150°

aVR / 120°

I / 90°

30° / III

60° / aVL

I isolectric / -90°

I aVF

-30° II isolectric

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.

aVF I isolectric

180°

I

I isolectric / 90°

aVF

RR I nte rva l

ST In ter val PR

QT Int erv al

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.

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

Normal 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.

II V1 II II

EKG INTERPRETATION

I

V, I

V

J poi nt

S T S egmen t

1 2

≥ 5 mm

3 ≥ 1 mm

Septal (LAD)

8. Bundle Branch Blocks.

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

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

V, V

Lead 1: Monophasic R & no Q waves. Lead V,: QS or rS pattern Lead V : Late intrinsicoid deflection, Monophasic R & no Q waves.

Lead 1: Wide S wave. Lead V,: Late intrinsicoid deflection. M-shaped QRS (RSR’). Sometimes wide R or qR Lead V : Early intrinsicoid deflection with a wide S wave.

9. ST Segment Changes.

Normal Variation

ST Segment Identification: 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% specific for AMI

≥ 1 mm

5 Points

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

2 Points ST elevation ≥ 5 mm disconcordant with QRS in any lead.

3 Points ST depression ≥ 1 mm in V1, V2 or V3.

10. Infarct Localization.

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

EKG INTERPRETATION Q

RS

Axi

s

QR

S A

xis

QR

S A

xis

Inferior (PDA)

Anterior (LAD)

Lateral (Circ)

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 finds fast pathway reset, travels retrograde up fast pathway and finds 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.

SA Node

Slow Fast

Adenosine

Block

PAC

PAC

Retrograde P

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).

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.

SA Node

Slow Fast

Accessory Pathway

PAC PAC

Adenosine

Block

Adenosine

Block

Orthodromic Antidromic Orthodromic Antidromic

Retrograde P

PAC

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).

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.

AVNRT vs AVRT A

nti

dro

mic

O

rth

od

rom

ic

a

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.

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.

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 CHA2DS2-VASc Annual Stroke Risk

Heart Failure / L V dysfunction 1 0 Hypertension 1

1 1.3% Age

2 2.2%

65-74 75+ 1

2 3 4 3.2%

Diabetes Mellitus Stroke / TIA PAD / Old MI / Aortic Plaque Female

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

Sinus Beat Multifocal A Tach

P

P1 P P1 P P P P1 P P P1

Sinus Beat 2:1 A Tach

Sinus Beat Focal A Tach

ATRIAL TACHYCARDIAS

4.0% 1

5

6.7% 2

6

9.8%

1

7

9.6% 1

8 9

6.7%

15.2%

1

2

3

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.

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).

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.

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.

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.

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.

Atropine or Isoproterenol

3

Infranodal and Intra-His Mediated Bradycardias

3

2

2

2

1

1

SA and AV Nodally Mediated 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.

BRADYCARDIAS

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.

RBBB Patern qR, Rs or Rr’ in V1 Frontal axis +90° to -90°

Left Ventricular Tachycardia

I II

V1

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

Right Ventricular Tachycardia

V1

V6

Vagal Maneuvers Adenosine IVP

aVF V6

I II aVF

American

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

R to S > 100 ms

Concordant precordial leads No RS pattern Onset of R to nadir > 100 ms

Ventricular Tachycardia V1 V2 V3 V4 V

V6

> 1:1 AV Ratio

Atrial tachycardia / flutter

< 1:1 AV Ratio

Likely VT

1:1 AV Ratio or Unknown

QRS differs from resting EKG and prior MI or structural disease

Likely VT

Irregular R-R

Atrial fibrillation / flutter / tachycardia with abberent conduction (BBB, IVCD

or accessory pathway)

Wide QRS Complex Tachycardia QRS > 120 ms

WIDE COMPLEX TACHYCARDIA

Regular R-R

QRS identical to resting EKG

SVT, RBBB / LBBB and antidromic AVRT

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%

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

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

ELECTROCARDIOGRAPHY - LEAD PLACEMENT

V, 4th right intercostal space

V2 4th left intercostal space

V3 Directly between V2 and V4

V4 5th left ICS at the MCL

V5 5th left ICS at ant ax line

V 5th left ICS at mid ax line

V4r 5th right ICS at the MCL

V5r 5th right ICS at ant ax line

V r 5th right ICS at mid ax line RA Right Arm

LA Left Arm

LL Left Leg

RL Right Leg

CHEST PAIN EVALUATION

Possible ACS

Nondiagnostic ECG Normal initial troponin

No recurrent pain; Negative follow-up studies

No ST elevation ST elevation

ST and/or T wave changes

Ongoing pain Positive troponin

Hemodynamic abnormalities

Recurrent ischemic pain or Positive followup studies

Diagnosis of ACS confirmed

American

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

Arrangements for outpatient follow-up Negative Potential diagnoses: nonischemic

discomfort; low-risk ACS

Admit to hospital Manage via acute ischemia pathway

Positive Diagnosis of ACS confirmed

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)

Observe Follow-up at 4-8 hours: ECG , troponin

Activate STEMI Pager

Definite ACS

SYMPTOMS SUGGETIVE OF ACS

Algorithm for the evaluation and management of patients suspected of having ACS

ACUTE CORONARY SYNDROME

Low risk

Immediate angiography 12-24 hour angiography Recurrent

symptoms/ischemia Heart failure

Serious arrhythmia

Patient stabilizes

LVEF <40% LVEF >40%

Not low risk

American

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

Follow on

medical Rx

Stress Test

Evaluate LV Function

Early conservative strategy Early invasive strategy

Aspirin Beta blockers

Nitrates Antithrombin Regimen

GP IIb/IIIa inhibitor Monitoring (rhythm and ischemia)

Recurrent ischemia and / or ST segment shift, or

Deep T-wave inversion, or Positive troponin

ACUTE ISCHEMIA PATHWAY

Supply demand imbalance alone

Vasospasm or endothelial dysfunction

Fixed atherosclerosis and supply demand imbalance

Plaque rupture with thrombus

Troponin without reperfusion

Troponin with reperfusion

CKMB without reperfusion

CKMB with reperfusion

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.

Type 2 Myocardial Infarction (Demand Ischemia)

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.

100

20

10

5

2

1

0

0 1 2 3 4 5 6 7 8

Days from Onset of Infarction

ACUTE CORONARY SYNDROME x

Up

pe

r Li

mit

of

No

rmal

TIMI Risk Score (NSTEMI)

50

40

30

20

10

0

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 years 2) 3+ cardiac risk factors 3) Prior coronary stenosis >50% 4) ST segment deviation on admission ECG 5) >2 anginal events in the last 24 hours 6) Aspirin treatment in the prior 7 days 7) 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 / Enent / Brilinta (P2Y12 inhibi- tors) should not be started unless told to do

0-1 2 3 4 5 6-7 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 forma- tion.

ACUTE CORONARY SYNDROME C

om

po

site

Ris

k (%

)

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.

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

Circumflex

RCA

Left Main

Circumflex

Left Main

RCA

LAD

RCA LAD

LAD

Circumflex

PDA

PDA

PDA

Images courtesy of Patrick J. Lynch

INR > 2 Hemodynamically Unstable

Platelets < 50 Active Hemorrhage

AKI (Angiogram) Stroke / CNS Bleed

Contraindications Preprocedure Checklist

EKG CBC

INR NPO

BMP Consent

CARDIAC CATHETERIZATION

Medtronic Mosaic Bovine Pericardial

Image courtesy of Patrick J. Lynch Medtronic CoreValve Evolut

American Society for Echocardiography Reference Ranges

Normal Mild Moderate Severe Aortic Stenosis

<2

2.0 - 2.9

3.0 - 3.9

>4.0 Velocity (m/s) 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 >0.6

Mitral Stenosis Planimetry MV Area (cm ) >1.5 1.0 - 1.5 <1.0 DIastolic Pressure Half Time (ms) <150 >150 >220 Mean Pressure Gradient (mmHg) <5 5 - 10 >10

Mitral Regurgitation Vena Contracta (cm) <0.3 <0.7 >0.7 ERO (cm ) <0.4 >0.4

American

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

St. Jude Mechanical

VALVULAR HEART DISEASE

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

Coronary Sinus Lead (CS)

(Pace / Sense)

Right Atrial Lead (RA) (Pace / Sense)

Right Ventricular Lead (RV) (Pace / Sense / Defibrillate)

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.

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 tachyar- rhythmias.

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 defibril- late).

Device Type Leads Sensing Therapies

RA RV CS Pacing ATP Shock

Single Chamber Pacemaker RV RV

Dual Chamber Pacemaker RV & RA RV & RA

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

Single Chamber Defibrillator (ICD) RV RV

Dual Chamber Defibrillator (ICD) RV & RA RV & RA

Biventricular Defibrillator (CRT-D) RA / RV / CS RA / BiV

Subcutaneous ICD (SC-ICD) SC Coil

DEFIBRILLATORS PACEMAKERS

Device Program Coding

CARDIAC DEVICES

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. 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 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.

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).

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

Post Device Implantation Checklist

Preprocedure Checklist

Type and Screen CBC NOACs held as directed

INR NPO Coumadin OK to continue

BMP Heparins stopped at least 12 hours earlier

EP PROCEDURES

Diuretic Equivalence

Agent Onset Duration Bioavailability Lasix (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

45 Degrees

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

Volume Status vs Perfusion: Volume status: Jugular vein distention (JVD), hepato- jugular reflux, 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 NYHA Stage 1 Year

Mortality

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

Based on comorbidities

B Structural heart disease without heart failure. I

Asymptomatic 5-10%

C Structural heart disease with prior or active heart failure.

II Symptoms with moderate exertion 15-30%

III Symptoms with minimal exertion

D Refractory heart failure requring specialized interventions. IV

Symptoms at rest 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 volume status. There is currently no well agreed indication for pulmonary artery catheter placement to guide therapy outside of document- ing inotrope dependence.

HEART FAILURE

Reference 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/m

Swan Daily Rounds

Chest XR for catheter position

Assessment of insertion site

a c v y

x

Tricuspid Valve

ECG

RA 25

0 mmHg

RV 25

Closes Tricuspid Valve Opens

0 mmHg

Pulmonic Valve Opens

PA 25

Pulmonic Valve Closes

0 mmHg

a c v

x y

PCWP 25

0 mmHg

Aortic Valve Opens

Ao

Aortic Valve

125

100

Mitral Valve Closes

edp

Closes 75

50

Mitral Valve

Opens LV 25

0 mmHg

C

Aortic Valve B Opens

IABP

125

A E

Systole

Diastole D

Systole

Ao 100

Aortic Valve

Closes 75

50

mmHg

HEMODYNAMICS

Diastole

Systole

Coronary Perfusion Augmentation

Systole Diastole

125

100

75

50 mmHg

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

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

50

40

30

20

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

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

Days after randomisation

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.

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 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)

BALLOON PUMPS M

ort

alit

y (%

)

LVAD Flow and Pressure

Inlet (LV) Pressure Outlet (Aortic) Pressure

8

6

4

2

0

Pump Flow

120

90

60

30

0

Characteristic Electrical Baseline EKG Intereference

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)

Flo

w (

L/m

in)

Pre

ssu

re (

mm

Hg)

PUMP PARAMETER OVERVIEW There are four parameters monitored on the HeartMate II: Speed, Flow, Power, and Pulsatility Index. No single parameter is a surrogate for monitoring a patient’s clinical status. It is important to consider trends. Each patient’s values are specific to their pump. SPEED

• Speed can only be changed using the system monitor o If speed is turned up, more blood is pulled from the LV = ↓LV

chamber size o If speed is turned down, less blood is pulled from the LV = ↑LV

chamber size

• The system monitor displays the pump speed in revolutions per minute (rpm). This value matches the actual speed within ±100 rpm under normal conditions

POWER

• Device power is a direct measurement of pump motor voltage and current. Changes in pump speed, flow, or physiological demand can affect pump power

FLOW

• Flow is an estimate that is derived from a calculation of fixed speed and power

• Flow and power have a linear relationship: ↑Power = ↑Flow estimate ↓Power = ↓Flow estimate

o If the flow estimate falls outside the expected operational range or acceptable linear region, “+++” or “- - -“ is displayed. This prevents the display of inaccurate flow information.

o If flow falls below 2.5 L/min, the device will alarm “low flow”

• Afterload Sensitive: If afterload (blood pressure) is high, the pump will not increase speed to overcome the high outflow pressure. Because power demand is not increased, the displayed flow read out may not change or, potentially, decrease, even though the true flow out of the pump is hindered by the high aortic pressure

• At any given speed, increased blood pressure will decrease flow! PULSATILITY INDEX

• Pulsatility Index (PI) is the left ventricle’s (LV) pulsatile contribution to the pump:

LVAD

HEARTWARE LVAD (HVAD)

LV full → greater stretch → greater contractility = ↑Pulsatility Index LV empty → less stretch → little contractility = ↓Pulsatility Index

• PI as it relates to changes in patient’s status: o Indicative of changes in volume status due to altered preload o Indicative of changes to the natural heart’s contraction

• PI as it relates to changes in pump speed: o As pump speed is increased, the PI goes down o As pump speed is decreased the PI goes up

PI EVENT

• A PI event occurs when there is a 45% + or – change from the previous 15 second running average. Possible causes of events:

Suction Event: the inflow cannula is obstructed

Dehydration Bleeding increased diuresis

Arrhythmia Vasovagal response Right heart failure Increased PA pressure

• If a PI event is detected, the pump speed will automatically reduce to the low speed limit and then gradually ramps back up at 100rpm/sec to the fixed speed.

LOW “FLOW” ALARMS 1. Assess patient – EMERGENTLY (think STEMI page)

a. Are they bleeding? b. What is their blood pressure (mean arterial pressure if no pulse)? c. How do they clinically look like? d. What are the patient’s last lab results?

2. Page the Heart Failure (HF) attending physician a. If no response after 10 minutes, page again b. If STILL no response, page another HF attending OR the CV surgery

fellow on-call c. You may also page the VAD coordinator (all numbers listed in Web

On-Call) 3. Report the following information to attending, fellow, VAD coordinator (get

them ready beforehand) a. Your assessment of patient (see above) b. The latest LVAD parameters (Flow, Speed, Power, PI or PI

amplitudes if HVAD) c. Trends of the MAPs and Flows

d. Urine output e. Most recent last lab results

4. You will likely have to Order the following, plus any other orders rec’d by the attending…

a. New set of labs including PT/INR b. ECHO to assess RV, LV fxn, inlet cannula obstruction

CARDIAC ARREST IN LVAD PATIENT

Garg S, Ayers CR, Fitzsimmons C, et al. In-Hospital Cardiopulmonary Arrests in Patients With Left Ventricular Assist Devices. J Card Fail 2014;20:899-904.

4.3 L/min

2920 RPM

4.2 Watts

12

8

4

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

12

8

4

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

Fixed

Sx Off

HeartWare HW1234567 POD: 8

22:43:56 1 2

Reprinted with the permission of HeartWare ©

Patient System Controller Display (Attached via Driveline)

Alarm Mute Battery Indicator 1 Alarm Indicator Battery Indicator 2

Scroll

3000 RPM 5.0 L/min 4.8 Watts

HeartWare

Critical Alarms

NO MESSAGE - No power to pump / Pump has stopped

Steady Tone

Flashing Red VAD STOPPED - Driveline disconnected, fracture or connector malfunction. VAD electrical failure,

Two Tone 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.

HEARTWARE LVAD (HVAD)

HEARTWARE LVAD (HVAD)

Po

wer

(W

att

s)

HeartWare HVAD Daily Rounds

Confirmation of pump speed

INR

Pump flow and power trends

Hgb, PLT and LDH trends

Arrhythmia review

Suction event review

HeartWare HVAD Anticoagulation

Aspirin 325 mg PO QD

Coumadin (INR 2-3)

Flo

w (

L/m

in)

HeartWare HVAD Function Reference Ranges Set Speed (RPM) 1800 2400 3200 4000 Power (Watts) 2.5 8.5 Flow (L/min) 1.8 3 8 10 INR 1 2 3 4

Patient System Controller Display (Attached via Driveline)

Test Select Battery Fuel Gauge Battery Symbol

Button (yellow & red)

Power Symbol Controller Cell Red Heart Silence Alarm

Symbol Symbol Button

Critical Alarms

Red Heart Pump flow < 2.5 Lpm, pump has stopped, perc lead is disconnected, or pump is not working properly.

Steady Tone

Red Battery

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

Steady Tone power.

Yellow Battery

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

1 Beep Q4 seconds 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.

Clinical Settings Alarms Save Data History Admin Pump Flow Pump Speed Pulse Index

4.5 lpm

Display ON/OFF 9500rpm

3.6 Pump Power

Fixed Mode - Speed Setpoint: 9600 rpm 5.7w

Reprinted with the permission of Thoratec Corporation ©

HEARTMATE LVAD (LVAD)

LVAD Functional Reference Ranges Set Speed (RPM) 6K 8K 10K 15K Power (Watts) 2.5 10 Flow (L/min) 2.5 3 10 INR 1 2 3 4

HeartMate II LVAD Daily Rounds

Confirmation of pump speed

INR

Pump flow, PI and power trends

Hgb, PLT and LDH trends

Arrhythmia review

PI / Suction event review

HeartMate II LVAD Anticoagulation

Aspirin 325 mg PO QD

Coumadin (INR 2-3)

METABOLIC

EQUIVALENT

1-10 MET

1 MET

READING

4 MET

GARDENING

6 MET

CLIMBING STAIRS 7 MET

JUMPING ROPE 8-10 MET

RUNNING

Revised Cardiac Risk Index

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.

1) Coronary artery disease 2) Cardiomyopathy 3) History of TIA or stroke 4) Insulin dependent diabetes 5) Creatinine > 2.0 mg/dL 6) Planned high risk surgical procedure

Urgency Definition Emergent 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 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).

Procedural Risk Class

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

Low Risk Endoscopic procedures Superficial procedure Cataract surgery Breast surgery

American

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

PREOPERATIVE EVALUATION

Co

mp

osi

te R

isk

(%)

Clinically stable

Nonemergent surgical case

Acute coronary syndrome

Proceed to surgery or alternate management

as appropriate

Will further testing impact decision making or perioperative care?

Pharmacologic stress testing with angiography and

revascularization as indicated

No Yes

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

Functional capacity

>4 METs

Functional capacity <4 METs or unknown

Heart Association

American

Proceed to surgery

No further testing

Estimated perioperative risk of MACE based on combined clinical / surgical

risk (RCRI etc...)

Evaluate and treat accordingly

Emergent surgical case

Clinical risk stratification and proceed directly to

surgery

Patient scheduled for surgery with known or risk factors for CAD

Algorithm for the risk evaluation of patients prior to surgery

PREOPERATIVE EVALUATION

PREOPERATIVE CHECKLIST

EKG Should be obtained in patients with known CAD/PAD, arrhythmia, cerebro- vascular 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 reason- able to continue aspirin if patient at high risk of cardiac events and benefits outweighs risk of bleeding.

Modality Advantages Limitations / Contraindication

Exercise ECG Ideal in low to intermediate risk Cannot use if patient has baseline LBBB or

patients who can exercise enough to paced rhythm.

Exercise should be attempted get to target heart rate and have an its felt the patient can interpretable ECG. recent MI, severe symptomatic AS, aortic

reasonably achieve target Provides functional capacity. dissections, or acute PE. heart rate.

Myocardial Appropriate in wide range of Balanced ischemia in triple vessel disease Perfusion Imaging pre-test probability patients. 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 Can be limited by poor patient echo Dobutamine Appropriate in a wide range of windows – obese patients, etc.

Contraindicated in patients with pre-test probability patients. Cannot use in symptomatic severe AS, recent ACS, tachyarrhythmias, Can assess viability aortic dissection, ACS.

and large aneurysms. Can obtain additional hemody-

namic data during stress.

Stress MRI

GFR must be >30

ICD/Pacemakers limit study quality.

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.

Coronary CTA Option for low to intermediate risk Contrast dye exposure

patients with normal ECG and

Can potentially end up with normal cardiac biomarkers. Limited to larger caliber more proximal if positive.

vessels.

Excellent tool for assessing anatomy Patient will need to perform breath holds

Functional assessment with of coronary arteries. and have a controlled heart rate. CT-FFR.

NOT a stress test High negative predictive value Cannot use in pregnancy

Cardiac Cath Optimal test for high pretest Invasive with risks of complications such as

probability, positive stress tests, and bleeding

Gold standard study for CAD. those with acute coronary

syndromes. Contrast dye exposure

CARDIAC IMAGING

<40 40-60 >60

x

i

Cerebral Hypoperfusion

100%

80%

60%

40%

20%

0%

Age (Years)

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.

Orthostatic

Neurally Mediated

Structural Disease

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 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

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

SYNCOPE

Etio

log

y o

f S

ynco

pe

(%

)

n

ct

ul D

A

INOTROPIC AGENTS

Agent (MOA) Dose Range Clearance (t½) Primary Activity

Milrinone (cGMP / PDE3) 0.20 - 0.50 mcg / kg / min Renal ~80% (2.3 hrs) PDE3 - cGMP mediated increase in intracellular intracellular Ca++ concentration and consequent rise in contractility and CI. Decreases SVR / PVR.

Dobutamine (β1 ++ / β2 +) 2.5 - 10 mcg / kg / min Renal (2 minutes) Beta 1 receptor mediated increase in cardiac contractility and HR. Decrease in SVR via Beta 2 medi- ated vasodilation.

Epinepherine (β1 / β2 / α1) 1 - 20 mcg / min Renal 100% (1 min) Beta 1 receptor mediated increase in cardiac contractility and HR. Increases SVR via potent Alpha activity.

Norepinepherine (β1 / α1) 0.02 - 1.0 mcg / kg / min Renal 100% (1 min) Beta 1 receptor mediated increase in cardiac contractility and HR. Increases SVR via potent Alpha activity.

VASOPRESSOR AGENTS

Agent (MOA) Dose Range Clearance (t½) Primary Activity

Norepinephrine (β1 / α1) 0.02 - 1.0 mcg / kg / min Renal 100% (1 min) Beta 1 receptor mediated increase

in cardiac contractility and HR.

Increases SVR via potent Alpha

activity.

Epinephrine (β1 / β2 / α1) 1 - 20 mcg / min Renal 100% (1 min) Beta 1 receptor mediated increase

in cardiac contractility and HR.

Increases SVR via potent Alpha

activity.

Vasopressin (V1) 0.03 units / min Renal 10-15% (10-20 Vasopressin 1 receptor mediated

min) vasoconstriction.

Phenylephrine (α1) 1 - 10 mcg / kg / hr Hepatic (2-3 hrs) Pure Alpha 1 mediated vasocon-

striction

Dopamine (β1 / α1) 0.5 - 20 mcg / kg / min Renal 80% (2 min) Dose dependent effect. Alpha 1

and Beta 1 dominant activity at

doses above 10 mcg / kg / min.

IV ANTIHYPERTENSIVES

Agent Dose Range Adverse effects Contraindications

Hydralazine 10 - 20 mg IVP Tachycardia, headache, flushing, Increased intracranial pressure or glaucoma Onset: 10 - 20 min nausea Duration: 1 - 4 hours

Labetalol 20 - 80 mg IVP Q10 min Bronchospasm, heart block, nausea, Cocaine intoxication, decompensated heart Onset: 5 -10 min (max 300 mg) paresthesias, dizziness failure, high grade AV blocks, significant Duration: 2 - 4 hours bradycardia

Nitroprusside Onset: 1 min Duration: 1 - 10 min

0.1 - 10 mcg / kg / min Cyanide and thyocyanate toxicity, nausea, vomiting, muscle spasm, sweating, increased intracranial pressure

Acute MI, significant CAD, stroke, increased ICP, renal or hepatic failure.

Need an arterial line for monitoring.

Nitroglycerine 5 - 200 mcg / min Reflex tachycardia, tachyphylaxis, Recent use of PDE-5 inhibitors (i.e Sildenafil). Onset: 2 - 5 min nausea, headache, vomiting, flushing, Duration: 5 - 10 min methemoglobinemia Need an arterial line for monitoring.

Nicardipine 5 - 15 mg / hr Tachycardia, dizziness, flushing, Decompensated heart failure. Onset: 5 -15 min +11 2.5 mg Q15 min nausea, headache, phlebitis, edema Duration: 1.5 - 4 hours

Need an arterial line for monitoring.

Enalaprilat 1.25 mg – 5 mg Q6H First dose hypotension in high renin Pregnancy and acute renal failure Onset: 15 - 30 min states, headache, dizziness Duration: 6 - 12 hours

VASODILATORS AGENTS

Agent (MOA) Dose Range Clearance (t½) Primary Activity Contraindications

Nitroglycerine 5 - 200 mcg / min Hepatic / RBCs (1 - 3 Converted to NO promoting min) venous (preload) relaxation.

Small afterload reducing effect.

Acute inferior MI HOCM

Nitroprusside 0.1 - 10 mcg / kg / min Hepatic / RBCs (1 - 3 Small vessel vasodilation primar- Stroke / TIA min) ily afterload reduction. Coarctation

VSD

HEART FAILURE AGENTS

Agent (MOA) Target Dose Agent (MOA) Target Dose

ACE Inhibitors Captopril 50 mg PO TID Enalapril 10 mg PO BID Lisinopril 40 mg PO QD

Vasodilators

Hydralazine 50-75 mg PO TID Isordil 20-80 mg PO TID Imdur 60-120 mg PO QD

Beta Blockers Carvedilol Metoprolol XL (not Lopressor)

Aldosterone Antagonist

Spironolactone

Angiotensin Receptor Blockers

Valsartan

25 mg PO BID 200 mg PO QD

25 mg PO QD

80-160 mg QD - BID

NOVEL ORAL ANTICOAGULANTS

Agent (MOA) Dosing Considerations

Dabigatran (Pradaxa) Non-Valvular AF Must not open capsules. Direct Thrombin Inhibitor GFR >30: 150 mg PO BID Onset: 90 min GFR 15-30: 75 mg PO BID Avoid using with amiodarone, dronaderone, Clearance: Renal (12-27 hrs) DVT / PE Treatment verapamil, ketoconazle, clarithromycin, quinidine. Reversal: Praxbind GFR >30: 150 mg PO BID

Rivaroxaban (Xarelto) Non-Valvular AF Ok to crush tablets and mix with apple sauce. Factor Xa Inhibitor GFR >15: 20 mg PO QD Onset: 2-3 hours DVT / PE Treatment Avoid using in patients with moderate to severe liver Clearance: Renal 66% (5-9 hrs) GFR >15: 15 mg PO BID x 21d then 20 mg QD dysfunction. Reversal: KCentra

Apixaban (Eliquis) Non-Valvular AF: Ok to crush and suspend in D5W 60 mL if given Factor Xa Inhibitor 5 mg PO BID but if two or more conditions apply immediately. Onset: 3-4 hours (Cr >1.5, Age >80, wt< 60 kg) then 2.5 mg PO BID Clearance: Hepatic (12 hrs) DVT / PE Treatment Avoid in severe hepatic impairment. Reversal: KCentra 10 mg PO BID x 7 days then 5 mg PO BID

Edoxaban (Savaysa) Non-Valvular AF Avoid in patients with very high functioning kidneys Factor Xa Inhibitor GFR 95-50: 60 mg PO QD due to excessivly rapid clearance. Onset: 1-2 hours GFR 50-15: 30 mg PO QD

Clearance: Renal 50% (12 hrs) Avoid using in patients with moderate to severe liver Reversal: KCentra dysfunction.

Topic Trial Name (PMID) Brief Findings Atrial 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 (effect 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) Ultrafiltration “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 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.

LANDMARK CLINICAL TRIALS

Mortality

Risk High Intermediate

– High Intermediate

– Low Low

SBP<90 for

>15 min or

Vasopressor/

Inotrope use

(+)

(-)

(-)

(-)

PESI Class

III-V or

sPESI>1

(+)

(+)

(+)

(-)

RV:LV ratio

>0.9 on CT (or

TTE)

(+)

Imaging AND

Lab positive

Imaging OR

Lab positive

(-) Elevated Trop

or BNP (+)

First Line

Therapy

Systemic tPA UFH (Rescue

tPA or CDT) LMWH or

UFH LMWH or UFH

or NOAC PERT Team

Activation

Yes

Yes

Yes

Consider

Preferred Unit

ICU

ICU

Tele Floor,

consider early

discharge

ABSOLUTE CONTRAINDICATIONS TO

THROMBOLYSIS

• Hemorrhagic stroke or stroke of unknown origin at any time

• Ischemic stroke in preceding 6 months

• CNS damage or neoplasms or AVMs

• Recent brain or spinal surgery

• Recent major trauma/surgery/head injury (within preceding 3 weeks)

• Gastrointestinal bleeding within the last month

• Known bleeding

• Suspected aortic dissection

RELATIVE CONTRAINDICATIONS

TO THROMBOLYSIS

• Age >75 years

• TIA in preceding 6 months

• Oral anticoagulant therapy

• Pregnancy or within 1 week post partum

• Non-compressible puncture

• Trauma resuscitation

• Refractory hypertension (systolic blood pressure >180 mmHg)

• Advanced liver disease

• Infective endocarditis

• Active peptic ulcer

QUESTIONS? Please contact:

• Dr. Eugene Brailovsky, Pager 15332, yevgeniy.brailovsky@lumc.edu

• Dr. Amir Darki, Pager 15450, adarki@lumc.edu

Pulmonary Embolism Response Team (PERT)

American

Heart Association