Grand Rounds Recap 9.7.22
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LVADs WITH DR. VIERECKE
Heartmate II and HeartMate 3
Components:
Pump = provides up to 5 LPM flow, connects LV to aorta
Drive line connects pump to outside world
System controller - user interface with pump
External power source
In the HeartMate 3, cannot see pump connection to the aorta on X-ray
In the HeartMate 2, this connection is visible on X-ray
Indications
Short term mechanical circulatory support for cardiac transplantation candidates with risk of imminent death from nonreversible LV failure
Destination therapy for those with end stage heart failure who are not transplant candidates
Failed optimum medical therapy
Post LVAD Implant Survival
12 mo survival ~90%, 24 mo survival 80%
Driveline
Usually left or right side of the abdomen, should be covered by an aseptic dressing, changed at home
Driveline should always be anchored. Breaking the seal increases the chance of infection
Redness or concern for infection needs to be reported to the LVAD team, will often be treated with antibiotics
LVAD Controller Interface
Look for the green arrows = LVAD is running
Red items indicate emergent alarms (flow alarm, low battery)
Yellow items indicate problems that need to be addressed on a less emergent basis
LVAD Battery
Two batteries carried by the patient
Each lasts 17 hours in HM 3, 12 hours in HM 2
Patients should have 2 extra batteries and an extra controller
LVAD Power Module is used in hospitals or clinic settings to evaluate and monitor LVAD patients
Pump Parameters
Flow rate (LPM)
Must be at least 2.5 LPM, or will produce a low-flow alarm
Pump Speed
This is set by cardiology and can only be changed using the System Monitor
Increased speed = increased flow
Pulsatility Index
Flow pulses measured and averaged over 15 second intervals
Evaluates native LV function
Absolute values are less important, but useful to monitor changes
Useful to assess volume status
Power
Measure of the current and voltage supplied
System Controller Functions
To find LVAD Pump Parameters = Click the square button on the system controller
To evaluate the last 6 LVAD alarms = Click the square button and the bell at the same time
Physiologic States
Hypovolemia
Low power/flow, low PI, no change in speed
Hypertension
Low power/flow, high PI, no change in speed
Sepsis
High power/flow, low PI, no change in speed
VT/VF
Low power/flow, low PI, speed could drop to LL
RV Failure
Low power/flow, low PI, speed could drop to LL
Aortic Insufficiency
May have falsely high power/flow, variable PI, no change in speed
Pump Thrombosis
Falsely high power/flow, high PI, no change in speed
HeartMate Device Assessment
Evaluate pump parameters and alarms
Auscultate pump
Evaluate driveline connection
Ensure two batteries are connected
Assess driveline exit site
Blood Pressure Monitoring
Given continuous flow, difficult to measure BP via traditional korotkoff sounds
Use arterial line or doppler
Goal MAP 65-85 mmHg
MAP > 90 mmHg may lead to decreased forward flow, decrease in pump flow and power, increase in PI
Aortic Insufficiency can lead to decrease in forward flow even after LVAD placement. This can be treated with valve replacement. About 10% of our patients here have their aortic valve oversewn in an attempt to improve AI. Chest compressions are not effective in patients with an oversewn aortic valve.
EKG
Artifacts are common. May see native QRS underneath, but difficult to discern P waves.
For VT/VF, evaluate the patient first, depending on their RV function they may have decent perfusion to maintain mental status despite these rhythms.
Arrhythmias
External defib = does not interrupt pump support
Internal defib = disconnect pump from controller, keep ICD turned on
Prehospital LVAD Guide
LVAD Problems:
Incidence of stroke 12-28%
Incidence of thrombosis 2-13%
Incidence of ICH 10-50%
Incidence of GIB 15-61%; pooled prevalence of 23%
vWF
Heyde syndrome, angiodysplasia
Anticoagulation
Resources:
QI/KT Blunt Cardiac Injury WITH Drs. Haffner and Sobocinski
Definition = cardiac injury sustained from blunt trauma to the thorax
Variable definitions in the literature
Epidemiology
0.3-2.3% of all trauma
Most common in 20-40 year olds
Severe BCI more common in people older than 60
Mechanism
Direct Trauma
Most common injury occurs when ventricles are most distended during end-diastole and therefore most vulnerable to injury
Thought to be most common cause of cardiac contusion
Timing of the force to occur at the precise moment in the cardiac cycle may lead to R on T phenomenon, commotio cordis
Bidirectional Compression
Likely to cause contusion, increased intracardiac pressure against a closed valve may lead to valvular injury
May lead to compression of the LAD and RCA
Acceleration/Deceleration
Ligamentum arteriosum connecting pulmonary trunk and aortic arch. Remnant of ductus arteriosus.
May lead to aortic dissection/transection which some people would include as a component of BCI
May lead to shearing type injury of the myocardium or coronary vessels
Blast Injury
Septal or ventricular rupture
Hydraulic Pressure
Extreme increase in preload which distends the myocardium and may lead to cardiac wall or septum rupture. If it occurs during diastole may lead to aortic/pulmonary valve injury; during systolic may cause tricuspid or mitral injury
Arrhythmia
BCI can predispose to arrhythmias that can develop hours to days after direct insult
Conduction delays, heart block, VF can be seen
Commotio Cordis
Occurs when non-penetrating blows to the mid-chest trigger ventricular tachycardia/VF in the absence of other thoracic injury
Injury must occur during the 15-30ms window on the upstroke of the T-wave (1% of the cardiac cycle)
Exact mechanism is unknown, but it is thought to increase K+ current leading to arrhythmia
Mostly occurs in healthy young people (mean age 13) due to a thin chest wall and under-developed intercostal musculature
Classically baseball/softball, hockey, lacrosse, football, light boxing, or even being hit in the head by a dog
Treatment is rapid identification followed by CPR and defibrillation
Primarily pre-hospital problem, not included in protocol
Injuries and Factors associated with BCI
Consider in those with:
Chest pain, unexplained tachycardia, heart murmur, sternal fracture, pulmonary injury, dangerous mechanism, depressed GCS
Schultz et al. (2004) meta analysis of patients presenting with BCI
The most common finding associated with BCI was "chest pain"
Other common presenting complaints were dyspnea, chest wall ecchymosis, flail chest, and sternal fractures
Ernet et al (2010) prospective observational trial observing incidence of BCI
Pulmonary contusion OR 7.2 (1.9-27.9)
GCS < 13 OR 7.1 (1.2-42)
Palpitations OR 4.9 (1.7-13.8)
Abnormal ECG OR 3.5 (1.3-9.4)
Sternal Fracture
Ishida et al (2022) retrospective review evaluating association of sternal fracture with BCI
N = 228,51
Incidence of BCI 0.4%
Johnson et al (1993) retrospective review of patients w/ sternal fractures
N = 103
50% of patients were discharged in less than 24 hours, and 80% were discharged in less than 48 hours
No long term sequelae identified in early discharge patients
5 patients had ECG abnormalities, but no patients had any clinical evidence of myocardial dysfunction
Fokin et al (2022) retrospective review of blunt trauma patients admitted to two level 1 Trauma centers over a 5-year period with radiographically confirmed sternal fracture
N = 380
BCI was identified in 19 (5%) patients
Isolated sternal fracture (including displacement or retrosternal hematoma) was not associated with BCI
Sternal fracture with pulmonary co-injury was associated with BCI
Audette et al (2014) Retrospective review of patients evaluated in the ED of 2 academic trauma centers found to have sternal fractures over a 3-year period
N = 54
Only 39 (72%) of patients received an initial ECG
Only 16 (30%) of patients had a Troponin I sent
Two "complex" cases were identified
Abnormal EKG
Concerning findings = unexplained sinus tachycardia, new BBB, new AVB, new arrhythmia, new ST segment or TW changes
Foil et al (1990) Retrospective review of admitted patients with BCI
N= 524
27/28 (96%) patients with cardiac complications had initial abnormal ECGs
Dysrhythmia, infarction, effusion, hemodynamic instability, CPK elevation, abnormal chest radiography
No complications in patients with normal ECG on admission and at 4 hours
García-Fernández (1998) prospective observational trial evaluating patients with abnormal traumatic findings on TEE
N = 134 with BCI, 66 with abnormal TEE
Abnormal ECG in 59% with BCI found on TTE vs 24% without abnormal ECG
ECG sensitivity 59% specificity 73 % compared to TEE
Given limited sensitivity of EKG, if EKG is normal, we must evaluate hsTnT
If HsTnT is negative (per gender average; male 20, female 14), can exclude BCI
Salim et al (2001) and Velmahos et al (2003)
Prospective observational studies of patients with thoracic trauma (n = 115, n = 333) demonstrating NPV of normal ECG and TnTI of 100% for BCI
Multiple studies have shown that patients may present with elevated HsTrop, and thus may not be specific for BCI
Role of Imaging
Posterior myocardial enhancement on CT can be seen with myocardial contusion
Poorly sensitive for RV and LV contusion, though specificity of 95% (Hammer et al, 2016)
For unstable patients with concern for BCI
Limited data
For patients presenting with heart block, 20% resolved within 72 hours (Ali et al 2017)
50% ultimately required pacemaker placement at discharge
Retrospective observational study of ~100,000 patients in Oklahoma trauma registry over 10 years showed mortality of BCI 26.3% and 51.2% in penetrating cardiac injury (Tran et al 2020)
Summary of BCI
Patients with possible BCI should receive an ECG and troponin assay
Normal ECG and troponin have a NPV of 100% for BCI
Patients with an abnormal finding should be admitted for telemetry monitoring and receive a comprehensive echocardiogram
Unstable blunt trauma patients should receive a bedside E-FAST and possible echocardiogram
Hypotension should be managed with blood products initially
Grand Rounds Rant: Cardiac Arrest WITH Dr. Benoit
V-Fib Arrest is CAD until proven otherwise
PROCAT Study (Dumas et al, 2010)
EKG is specific for significant coronary lesion (95%) but not sensitive (42%)
CARES Study (Vyas et al, 2015)
Among survivors of OHCA, early coronary angiography was associated with higher odds of survival to discharge and favorable neurological outcome
TOMAHAWK Trial
Immediate angiography after OHCA without ST segment elevation did not show benefit over delayed angiography with respect ot 30 day risk of death from any cause
Berlemont et al, 2022
RCT demonstrating patients with OHCA without STE, delayed angiography was not inferior to immediate angiography
Cohort had significant CAD with ~20-30% receiving PCI in both groups
Multiple studies show that shockable rhythms have high incidence of CAD, but jury is still out on whether or not immediate cath is beneficial
Do not allow neuroprognostication in the ED
Pittsburgh Cardiac Arrest Category
Tool to help achieve prognostication following cardiac arrest
However, in PCAC 4 (worst category, coma with absent corneal or pupil reflexes), 10% have survival
AHA recommendations agree that the utility of immediate neurologic prognostication is low
Class 1 Recommendation, Level B evidence
Use of Hypothermia post Cardiac Arrest
TTM-2
Critique: Population has high incidence of bystander CPR, shockable rhythms, with only moderate acidosis (average pH 7.2)
Different cohort relative to post-arrest patients in Cincinnati, Ohio
Adverse event associated with hypothermia is arrhythmia, often bradycardia.
TTM for OHCA in Children (Moler et al, 2015)
Supplementary materials contains survival curve showing difference between two groups
HYPERION Trial
TTM demonstrated benefit over targeted normothermia, may be more applicable to our population
ACLS is basic
ACLS algorithms are broad and do not apply specificity to differing etiologies of cardiac arrest
We should not think about ACLS as only “shockable” or “non-shockable”
Cincy BEARCAT trial - collect blood samples during prehospital arrest to help us differentiate cardiac arrest treatment
Orthopedics in the Community WITH Drs. Milligan, Gawron, Betz
Clavicle Fracture
Discharge w/ sling (unless skin tenting, neurovascular compromise)
Sternoclavicular joint evaluation is part of exam; consider CT if medial fracture given difficulty to visualize posterior dislocation
Follow up in 1 week, early passive range of motion in 2 weeks
Radial Head Fracture
Discharge with sling vs posterior splint
Management based on Mason classification
Type 1: sling
Type 2&3: posterior splint
Type 4: reduction and posterior splint
Elbow x-rays → alignment and fat pads
Evaluate alignment with anterior humeral line and radiocapitellar line
Anterior humeral line = Line drawn down the anterior surface of the humerus should pass through the middle to anterior third of the capitellum
Radiocapitellar line = Line drawn through middle of the radius should pass through middle of the capitellum
Fat Pads
Anterior fat pad: small stripe normal, sail sign abnormal
Posterior fat pad: always abnormal
Monteggia/Galleazi
Admit for ORIF or transfer
Obtain dedicated film for secondary injury (elbow for Monteggia, wrist for Galleazi)
Bennett/Rolando Fracture
Intra-articular fractures at base of metacarpal typically require surgical fixation (exception is Bennett <1mm displacement)
Splint in thumb spica
Knee dislocation
50% reduce prior to arrival to ED
40% with popliteal a. injury
Admit or transfer
Need to evaluate for vascular injury
CTA most sensitive
Admit for serial ABI’s if no CTA performed
Differential of negative knee x-ray
Spontaneously reduced dislocation
ACL tear
Meniscus tear
Occult tibial plateau fx
Quad/patella tendon rupture
Compartment syndrome
Referred pain (hip, ankle)
Maisonneuve injury
Discharge in posterior splint
Evaluate common peroneal nerve for injury
Motor: dorsiflexion (deep peroneal) and eversion (superficial peroneal) of ankle
Sensory: skin between 1st/2nd toes (deep peroneal)
Fibular head is part of ankle exam
Limitations of Ottawa Ankle Rules
No palpation of medial ligaments/deltoid complex
No proximal fibular tenderness (ex Maissoneuve fx)
No palpation of anterior tibiotalar joint (ex talar dome fx)
No palpation of 1st/2nd metatarsal base (ex Lisfranc fx)
Ankle Injury Classification
Danis-Weber Classification: based on location of fibula injury compared to the level of the ankle mortise (distal tibiofibular syndesmosis)
Weber A: fibula fracture below the level of the ankle mortise
Follow-up in 1 week, likely will be transitioned to a walking boot as outpatient
Weber B: fibula fracture at the level of the ankle mortise
Will get stress views in orthopedics office, don’t need to in ED
Place in posterior splint and follow-up within 1 week
Weber C: fibula fracture above the level of the ankle mortise
Do not need to wake up orthopedist in the middle of the night
Will require surgery, try to arrange rapid follow up in next few days
Place in posterior splint
5th metatarsal fracture
Discharge with hard sole shoe vs posterior splint
3 zones; jones vs pseudo-jones
Zone 1 (90%): Tuberosity only
Nondisplaced can treat conservatively w/ protected weight-bearing in hard-soled shoe, WBAT as pain subsides, f/u with ortho in 1 week
Displaced >30% articular surface or >2 mm articular step off can be operative,
F/u with ortho to in 1 week
Zone 2: Metaphyseal/diaphyseal junction (Fx: Jones)
Vascular watershed → Nonunion rate of 15-30%
Zone 2&3 fx higher rates of nonunion due to vascular supply
Terminal branches DP/PT arteries supply proximal end/tuberosity, nutrient arteries supply diaphysis → metaphysis (4/5th MT joint area) is a watershed
Nondisplaced: 6-8 weeks NWB in boot or posterior splint, weight-bearing advanced as evidence of bone healing (around 4-6 weeks)
Close ortho f/u within 5-7 days
Surgery can be considered in competitive athletes
Zone 3: Diaphyseal area, fracture distal to 4th/5th MTP joint
Trial of conservative mgmt w/ NWB in short leg splint/cast 6-8 weeks, healing can take several months, still may fail conservative mgmt
Operative may be recommended for all in professional athletes/high-demand pts to hasten return to play
Lisfranc injury
Lisfranc joint = Tarsometatarsal joints and ligaments that stabilize the midfoot
Mechanism of injury: generally a twist or axial load on a plantar-flexed foot or direct blow to foot
Presentation: midfoot pain, swelling, difficulty bearing weight and standing on toes secondary to pain
Treatment: Non-weight bearing in short leg/posterior splint or boot and f/u with ortho in 1 week
Stability of fracture with delayed weight-bearing views generally determines need for operative management
Follow up within one week unless dislocation, splint. No need to transfer.
