Tag Archives: Cardiology

RCA infarct, bradycardia, & hyperkalemia!

Today, we discussed the case of an elderly woman with significant history of vasculopathy and ESRD who presented with weakness, found to be bradycardic to 30s, hypotensive, and hyperkalemic to 7.2.  Her hyperkalemia was treated with dialysis but she underwent cardiac cath due to up trending troponins, found to have a 100% occlusion of the RCA!


Clinical Pearls

  • First step in managing a patient with bradycardia is ABCs!
  • First medication for symptomatic bradycardia is atropine.  Remember that atropine works at the level of the AV node and higher so if the block is occurring somewhere below the AV node, then atropine will not be effective.
  • Other pharmaceutical agents are dopamine, epi, or isoproterenol
  • Anyone with bradycardia and unstable hemodynamics in spite of above treatments should receive transcutaneous pacing.  This buys you time until you can place a transvenous pacemaker (less painful, more effective)
  • ECG has a low sensitivity but high specificity for hyperkalemia-induced cardiomyocyte instability.
  • ECG changes associated with hyperkalemia in progressive severity:
    • Peaked T waves
    • P wave widening, PR prolongation, P wave disappearance
    • QRS widening, AV block, bradycardia
    • Sine wave
    • VF/asystole/PEA

Bradycardia approach

1. ABCs!

  • Pharmaceutical agents
  • Atropine (0.5 mg – 1 mg q3-5 mins for a total of 0.03 mg/kg)
  • If no improvement, consider dopamine or epi
  • If still symptomatic, then start transcutaneous pacing

2. Find underlying cause and treat it 

  • Meds: BB, CCB, amio, digoxin, clonidine, lithium, acetylcholinesterase inhibitors
  • Ischemia (up to 25% of patient with acute MI present with bradycardia)
  • ↑ vagal tone: if young, athlete
  • Metabolic: hypoxia, sepsis, ↓T4, hypothermia, hypoglycemia, hyperkalemia
  • OSA
  • Elevated ICP
  • Infections: legionella, lyme, Q fever, typhoid, malaria, RMSF, yellow fever, leptospirosis, dengue, Chagas disease
  • Infiltrative processes: sarcoid, amyloid, hemochromatosis

In our patient, the cause was severe hyperkalemia as well as an RCA infarct.  Given her clinical instability, and the potential for worsening hyperkalemia from cardiac catheterization alone, the team normalized her serum potassium before performing cardiac cath which led to the RCA MI diagnosis.

Hyperkalemia

  • ECG changes are not sensitive for hyperkalemia and can miss up to 39% of patients even with a K of 7-9.
  • Sweet spot for potassium appears to be a mean K of 3.5 to 4.5 mEq/L. There is not a well-defined treatment threshold.
  • Bottom line for management: if you have the kidneys available, use the kidneys to excrete as much potassium as possible.
  • Newer agents like sodium zirconium and patiromer. Mix with water. Well tolerated and highly effective.

Agents that reduce serum potassium via transient intracellular shift:

  • Insulin: give with D50 if normoglycemic to avoid hypoglycemia and be sure to check FSG hourly for 4 hours after to ensure no hypoglycemia develops
  • Albuterol (10-20 mg) nebs: this is significantly higher than the dose we give in COPD (2.5 mg) and is equal to ~8 treatments! So make sure to continue the nebs when the patient arrives on the floor from the ER if they are still hyperkalemic.
  • NaHCO3: best for management of chronic hyperkalemia in the outpatient setting.  In the acute management of hyperkalemia, alkalinization of serum with a large bicarb load can lead to a reduction in serum calcium levels.  Lower serum calcium can lead to more cardiac membrane instability and fatal arrhythmias!

Agents that eliminate potassium from the body:

  • Loop diuretics: first choice if a functioning kidney is available!
  • Cation exchange binders: preferred when kidneys are not available
    • Patiramer (available at VMC), much more tolerable than kayexalate and highly effective at lowering serum potassium.  Like kayexalate, it works over hours to days.
    • Sodium zirconium: similar to patiramer but not currently available
    • Kayexalate: not pleasant to take orally. Also carries with it the slight risk of colonic ischemia especially in post renal transplant patients and those with baseline colonic dysfunction (due to infection or inflammation).
  • Dialysis

Indication for using calcium gluconate: when EKG changes are noted.  Repeat doses (maximum 3) until EKG changes have resolved.

EKG Changes in Hyperkalemia:

  • K > 5.5 ⇒ repolarization abnormalities:
    • Peaked T waves are the earliest sign
  • K > 6.5 ⇒ progressive paralysis of the atria:
    • P wave widens and flattens
    • PR segment lengthens
    • P wave eventually disappears
  • K > 7.0 ⇒ conduction abnormalities and bradycardia:
    • QRS widens
    • High-grade AV block, slow junctional and ventricular escape rhythms
    • Any kind of conduction block (bundle branch blocks, fascicular blocks)
    • Sinus bradycardia or slow AF
    • Sine waves
  • K > 9.0 ⇒ cardiac arrest:
    • Asystole
    • Ventricular fibrillation
    • PEA with bizarre, wide complex rhythm

ECG Report #2!

Thanks everyone for yet another high yield report on ECGs with Dr. Zhao!  Here are the main pearls from today:

  • Remember that a negative p wave amplitude in lead I is seen in two diagnoses only: dextrocardia and limb lead reversal.  To distinguish between the two, look at the amplitude of the QRS complexes as you advance through the precordial leads.  In dextrocardia, you should see a loss of amplitude as you go from V1 to V6, because you are getting further away from the heart.  In limb lead reversal, this is not the case.
  • Remember that ST depressions in anterior leads V2 and V3 should raise your suspicion for a posterior MI and prompt further evaluation with a posterior ECG!
  • When dealing with an irregularly irregular wide complex tachycardia, think of these three differential diagnoses:
    • Atrial fibrillation with aberrancy (i.e. with a bundle branch block)
      • QRS waves should largely look similar in morphology
      • Rates should not exceed 170 bpm because all conduction is still going down the AV node
      • Treatment: shock if unstable, AV nodal blocking agents or amiodarone
    • Atrial fibrillation with an accessory pathway (WPW, also known as a preexcitation pathway)
      • QRS waves have varying shapes because they are conducted down the accessory pathway and the AV node
      • Because the accessory pathway has a much shorter refractory period than the AV node, heart rate can be very high and >200 bpm.
      • Treatment: shock if unstable.  Do NOT give AV nodal blocking agents (including amiodarone) because blocking the AV node can force all conduction down the much faster accessory pathway and lead to VF arrest.  The agent of choice is IV procainamide.
    • Polymorphic VT
      • QRS morphology varies (Torsades)
      • Rates should not exceed 170 bpm
      • Treatment: shock if unstable, otherwise amiodarone

Cardiorenal Syndrome 3/5/2019

Thanks Elan for presenting a case of a 63yo M with HIV HFrEF (25%), EtOH cirrhosis (CP Class A, MELD 8), HTN, HLD, and ongoing alcohol use with dietary nonadherence presenting with shortness of breath and anasarca. His JVD was elevated on presentation, and CT PE/AP in the ED revealed dilated IVC and e/o pulmonary edema.

He underwent diuresis and initially improved, but 48 hours into his hospitalization, he developed oliguric AKI, hepatic encephalopathy, and relative hypotension.

Urine studies were consistent with activation of RAAS and ADH (kidneys seeing low perfusion, and echo was concerning for biventricular failure with EF < 20%. A trial of Lasix managed to produce a UOP of 800cc in 24 hours, so a decision was made to transfer pt to the Stepdown for dobutamine assisted diuresis for suspected Cardiorenal Syndrome. Pt ultimately diuresed 18L of fluid (his weight also went down 10+kg, that’s around 22lbs!) and his renal function quickly returned to baseline after aggressive diuresis.


Cardiorenal Syndrome

The diagnosis dilemma for this case was the etiology of pt’s AKI. He was exposed to contrast, hence 48 hours later contract-induced nephropathy can be expected. He also has liver cirrhosis with acute decompensation, hence hepatorenal syndrome (HRS) is something that we cannot miss. Given his poor cardiac function, cardiorenal syndrome (CRS) is also high on the differential!

Keep in mind that there are 5 types of Cardiorenal Syndrome:

  • Type 1: Acute heart failure -> AKI, decreased renal arterial flow due to acutely decompensated HF
  • Type 2: Chronic HF leading to chronic renal hypoperfusion leading to CKD
  • Type 3: AKI leading to adverse cardiac events
  • Type 4: CKD leading to adverse cardiac events
  • Type 5: Multifactorial, systemic insult leads to both cardiac and renal failure

Regardless, the general principle is to restore renal perfusion. Given his biventricular failure, volume status, and initial presentation, Cardiorenal is suspected as more likely, hence pt received inotropic support (improves forward flow) and diuresis (Get pt back on the right side of the Frank Starling curve, also improves forward flow). Overall management of CRS is not much different compared to acute decompensated heart failure.

There is some evidence that more aggressive diuresis is associated with better outcomes (ESCAPE trial).

Stanford Type B Dissection in a Young Patient! 3/4/2019

A 41 (below 45 is young in my book) man with infrequent medical care, but otherwise no medical history other than obesity, presenting with acute onset chest pressure when he was showering. He initially tried to walk it off, but the pressure became sharp, and it started to radiate from the anterior chest to his shoulder blades. At the same time, he started feeling short of breath, dizzy, and diaphoretic. CTA revealed a Stanford Type B aortic dissection extending all the way to the R renal artery!


Chest pain: This is a topic we deal with almost every single day. In general, I like to classify chest pain in two categories:

Can’t Miss!

  • ACS & associated complications
  • Pulmonary emboli
  • Pneumothorax
  • Aortic dissection
  • Tamponade
  • Esophageal rupture

Everything Else!

  • Infection (abscess, pneumonia, etc), arguably also belongs in the Can’t Miss category
  • Peri/myocarditis
  • Pleuritis
  • Mass
  • Effusion
  • MSK
  • Trauma
  • etc

When it comes to dissection, there are two classification systems that describes the nature of the dissection (source: Grepmed). The Stanford classification is used more commonly.

classification-dissection-diagnosis-stanford-typeiii-original

Epidemiology

  • Men > women
  • Age 60-80 most common, mean age 63, 65% men
  • Younger < 40: 34% with HTN, 8.5% with h/o Marfan

Other Risk Factors

  • Trauma
  • Hypertension (most important predisposing factor of acute aortic dissection, up to 72% of pts will have underlying HTN. HTN is more common in those with type B vs type A.
  • Pheochromocytoma (very rare, case reports, thanks Alexa for pointing this out!)
  • Connective tissue disorders
  • Turner Syndrome
  • Vasculitis
  • Pregnancy
  • Crack cocaine, meth
  • Biscuspid aortic valve (9% of pts under age 40 have biscuspid AV)\
  • Pre-existing aortic aneurysm
  • Heavy lifting
  • Cardiac cath

Pathophysiology:

  • In a nut shell, due to a tear in the aortic intima, blood flow creates a false lumen separating the intima and the media. The higher the blood pressure, the higher the size of the false lumen due to shear force.
  • 50-65% originate in the ascending aorta, while 20-30% originate near the left subclavian artery and extend distally.

Presentation

  • Typical Triad
    • Acute chest or abdominal pain, can be sharp, tearing, or ripping
    • Pulse/pressure deficit between extremities
    • Mediastinal/aortic widening on CXR
  • Ascending aortic dissections are 2x as common as descending, 30% involves aortic arch
  • Acute onset chest pain that radiates to the back is the typical illness script. Pain can be the classic tearing or sharp.
    • Type A: more likely to experience anterior chest pain
    • Type B: more likely to experience back pain or abd pain > anterior chest pain
  • Propagation leads to acute AR, tamponade, stroke, shock, can propagate proximal or distally

Physical Exam Highlights

  • You might have heard of a term called pulse/pressure deficit when it comes to aortic dissections. In a nut shell, if there is a difference in SBP of greater > 20mmHg between right and left, then there is a deficit. This deficit is only found in 30% of cases of its presence can be very useful. High specific but poor sensitivity.
  • Findings Sensitivity Specificity LR if Present LR if Absent
    Pulse Deficit 12-49% 82-99% 4.2 0.8
  • Presence of an aortic regurg murmur has a LR of 1.5
  • The presence of 3 findings increase likelihood of a Type A dissection:
    • SBP < 100
    • AR
    • Pulse deficit
  • Presence of mediastinal or aortic widening on CXR increases probability of dissection somewhat, with LR 2.0

Diagnosis

  • CTA is fastest and easiest to get, 90+ % sensitivity and specificity
  • Can also do MRA or echo (TEE preferred) but might get longer to arrange in our hospital
  • EKG won’t have any specific signs but it can help you rule out other things.

Management/Prognosis

  • Stanford Type A
    • Surgical emergency, CT Surgery should be consulted ASAP.
    • High mortality, 2% per hour if left untreated.
    • Surgical mortality: up to 30%
    • Typically open repair, role of endovascular repair is not well studied.
  • Stanford Type B
    • Uncomplicated:
      • Medical management, goal is to reduce BP < 120/80 and HR < 60
      • Medical management:
        • Beta blocker: Esmolol or labetalol or propranolol, first line
        • Vasodilator: Nicardipine or nitroprusside, can cause reflexive tachycardia, hence do NOT use alone and only add if BP remains elevated with beta blocker
          • Nitroprusside over time can lead to cyanide toxicity
        • CCB: Non-DHP i.e. verapamil or diltiazem if there is a contraindication to beta blockers
      • Complicated:
        • If impending aortic rupture, end organ damage, continuing pain and hypertension despite medical therapy, false lumen extension, or large area of involvement, Type B is now considered complicated.
        • Endovascular intervention with Vascular Surgery is recommended (INSTEAD-XL study)
  • Long term management
    • Identify associated genetics factors
    • HR, HTN control
    • Serial imaging: 3, 6, and 12 months after event, and then annually after initial episode

ECG Report!

Clinical Pearls from our first ever (and hopefully monthly) ECG Report!

  • Make sure to always work through an ECG in a systematic way in order to avoid missing key information.
  • Remember that you might not see any p waves (or retrograde P waves) in AVRT and AVNRT.  Both of these rhythms would be fast and regular.  A fib, by contrast, would be irregular.
  • Hypercalcemia presents with a shortened QT and a loss of the ST segment on ECG.  But make sure you are ruling out an MI because often times the loss of ST segment resembles a STEMI.
  • Whenever you see a downward p wave in lead I, think of two diagnoses:
    • Dextrocardia
    • Limb lead reversal
  • Easiest way to distinguish between dextrocardia and limb lead reversal is to look at the QRS amplitude as you move across the precordium.  If the amplitude is decreasing as you advance from V1 to V6, then the diagnosis is dextrocardia because you are moving away from the heart.  If the amplitude is not changing or increasing, then the diagnosis is limb lead reversal.
  • The presence of > 2 mm coved precordial ST-segment elevation (leads V1through V3) with T wave inversions is suggestive of Brugada morphology.  In a patient with history of syncope, ventricular arrhythmias, or family history of Brugada syndrome, this is consistent with a diagnosis of Brugada syndrome and would require ICD placement.Capture

Have an interesting ECG?  Save them/send them our way for our next ECG report!

Hot Topics of 2018!

Today, we reviewed some of the hottest and potentially practice changing articles of 2018.  This is by no means an exhaustive list and meant to encourage debate and tickle your fancy for more!


1. Aspirin for primary prevention of cardiovascular disease?

Bottom line: no net benefit in primary prevention of cardiovascular disease.

  • ARRIVE: 12000 middle aged (mean age 64), non-diabetic participants with moderate ASCVD risk (>20%) randomized to receive aspirin 100 mg or placebo for primary prevention and followed for 5 years. Found that ASA showed no reduction in major adverse cardiovascular events or mortality, but a 2-fold higher risk of bleeding.
  • ASCEND (aspirin): 15000 middle aged (mean age 63) diabetic participants randomized to aspirin 100 mg vs placebo for primary prevention of CVD and followed for 7 years. Authors found a 12% reduction in major adverse cardiovascular events with ASA but a 29% higher risk of bleeding.
  • ASPREE: 19000 older patients (median age, 74) regardless of other risk factors randomized to ASA 100 mg or placebo and followed for 5 years.  Study found that patients who received ASA had a 14% higher all cause mortality, no decrease in the rate of adverse CVD, and no change in disability-free survival.

2. Omega-3 for primary prevention of cardiovascular disease?

Bottom line: potentially beneficial at really high doses in patients with CV risk factors

  • VITAL: 26000 middle aged (mean age, 67) people without CV disease were randomized to receive fish oil (1g) or placebo and followed for ~5 years. Study found similar rates of primary endpoint (nonfatal MI, stroke, or CV-related death) and all cause mortality in the two groups and a small but significant decrease in the incidence of MI in the fish oil group (1.1% vs 1.5%).
  • ASCEND (fish oil): same study population as ASCEND for aspirin, also looked at using 1g fish oil or placebo and followed patients for ~7 years and found no difference in the risk of major adverse cardiac events.
  • REDUCE-IT: 8000 participants with controlled LDL but elevated triglycerides, randomized to receive 2g of a different fish oil (icosapent ethyl as opposed to the eicosapentaenoic acid plus docosahexaenoic acid used in the previous two trials) vs placebo and followed for 5 years.  Study found a 25% reduction in risk of major cardiovascular events. Caveat is high dose used at this formulation is very expensive and the study was funded by Amarin Pharma.

3. VTE prophylaxis in hospitalized patients

Bottom line: High rates of inappropriate use of pharmacologic VTE prophylaxis.  Use padua score before prescribing VTE prophylaxis.

  • Grant et al. JAMA Intern Med 2018: retrospective study of 45000 non-ICU patients hospitalized for > 2 days found that prophylaxis (pharmacologic or mechanical) was prescribed for 78% of low-risk patients. 27% of high risk patients with contraindications to pharmacologic prophylaxis still received it, and 22% of high risk patients did not receive prophylaxis.

4. Is there such a thing as too much oxygen?

Bottom line: higher rates of mortality associated with liberal use of oxygen in hospitalized patients.

  • Chu et al. Lancet 2018: Meta-analysis of 25 randomized trials on 16000 hospitalized patients treated with liberal (median FiO2 0.52) vs conservative (median FiO2 0.21) supplemental oxygenation found that at 30 days, the relative risk of death was significantly higher in the liberal oxygenation group.

5. Plavix + ASA for TIA or minor stroke?

Bottom line: Starting DAPT within 12 hours of symptom onset (likely for 30 days) in patients with high risk TIA or minor ischemic stroke reduces 90 day stroke incidence but increases bleeding rates.

  • POINT:  Followed the earlier CHANCE trial in a Chinese population that showed DAPT for 21 days after TIA or minor stroke reduced stroke recurrence at 90 days without a difference in bleeding rates.  POINT randomized ~5000 patients to DAPT for 90 days vs ASA alone in a primarily white patient population and found lower rates of recurrent stroke but higher rates of bleeding. Majority of stroke reduction occurred during the first 7 days after stroke and extended for 30 days whereas the bleeding rates were stable throughout the 90 day follow up period.

6. Steroids in septic shock?

Bottom line: Steroids might be beneficial in high risk patients with refractory septic shock.

  • Rochwerg B et al. Crit Care Med 2018: Meta-analysis of 42 randomized trials with >10000 patients receiving steroids vs none in septic shock found a 2% relative reduction in 30-day mortality with steroids which was not statistically significant, and a similar reduction in mortality at 60 days to 1 year which reached significance (NNT 50). Reversal of shock at 7 days occurred more frequently in the steroid group (NNT 10) but mild-to-moderate adverse events also occurred more frequently in this group (hyperglycemia, hypernatremia, and neuromuscular disease).

7. Is it safe to discharge to home from the ICU?

Bottom line: patients admitted to the ICU for substance-related disorders, seizures, or metabolic derangements may be ok to go home from the ICU.

  • Stelfox et al. JAMA 2018: retrospective cohort study of 6700 adult patients admitted to ICUs in Canada, 14% of whom were discharged to home, found that 30 day hospital readmissions and ED visits and 1 year mortality rates were similar in those discharged from the ICU vs wards.  Those discharged home were typically younger and more likely to have been admitted due to overdose, seizure, substance withdrawal, or metabolic derangements.

8. NS vs LR?

Bottom line: balanced crystalloids (like LR) are associated with fewer adverse events than normal saline in hospitalized patients.

  • SMART: 16000 patients admitted to the ICU were randomized to NS or a balanced crystalloid (majority received LR). Study found that more patients in the NS group reached the composite outcome of major adverse kidney events (death, renal replacement therapy, or doubling of creatinine at discharge) vs those who received balanced crystalloids.
  • SALT-ED: 13000 patients admitted from the ED to non-ICU beds were randomized to NS vs a balanced crystalloid (majority received LR).  Study found similar rates of primary outcome of hospital-free days but a higher rate of adverse kidney events within 30 days than the NS group.

Cardiac arrest & anoxic brain injury

Today we discussed the case of a young man with Duchenne’s Muscular Dystrophy complicated by chronic respiratory failure and dilate cardiomyopathy who was found down at home in asystolic arrest.  Though ROSC was achieved en route to the hospital, patient suffered significant sequelae of anoxic brain injury.


Clinical Pearls

  • Most common causes of out-of-hospital cardiac arrests are
    • Acute MI
    • Cardiomyopathy
    • Primary arrhythmia
  • Most immediate threat to survival post cardiac arrest is cardiovascular collapse.
  • Most common cause of death in out-of-hospital cardiac arrests is neurologic injury.
  • Post cardiac arrest hemodynamic targets
    • SpO2 > 40%
    • PaCO2 > 40
    • MAP >65 (preferably 80-100 mmHg)
  • Read below for more info on the ongoing battle between therapeutic hypothermia (TH) and targeted temperature management (TTM) to reduce brain injury.

Post cardiac arrest management

Goals

  • Determining and treating cause of arrest
  • Minimizing brain injury
  • Managing cardiovascular dysfunction
  • Managing problems that arise from global ischemia and reperfusion injury

Most immediate threat to survival post ROSC is cardiovascular collapse.

  • Correct hypotension to maintain end-organ perfusion
  • Optimize oxygenation and ventilation
  • Correct electrolyte abnormalities

Determining cause and extent of injury:

  • Focused history
  • Exam:
    • Remember ABCs
    • Baseline neurologic exam
      • Make sure patient is off sedation or neuromuscular blocking agents
      • Brainstem reflexes:
        • Pupillary
        • Corneal
        • Oculocephalic
        • Gag
        • Cough
      • GCS ⇒ with special attention to motor score as it correlates with neurologic recovery
    • Work up
      • Causes
        • Most common are acute MI, cardiomyopathy, and primary arrhythmia ⇒ check ECG!
        • Labs
          • ABG
          • Basic electrolytes and liver function studies
          • CBC
          • Troponin q8-12 hours for 24 hours
          • Trend lactate
          • Toxicology studies
        • Management
          • Ventilator:
            • Target SpO2 >94% and PaCO2 > 40
              • Avoid hyperventilation because it leads to cerebral vasoconstriction and worsening cerebral perfusion
              • Avoid hyperoxia ⇒ a systematic review of 14 observational studies found that those with PaO2>300 mmHg had a higher in-patient mortality following cardiac arrest
          • Hemodynamics
            • Keep MAP >65 mmHg and preferably 80-100 mmHg to optimize cerebral perfusion
            • Prevent arrhythmia with meds only if patient has recurrent or ongoing unstable arrhythmia. No data on routine prophylactic use of these agents in other patients.
            • Coronary revascularization if indicated
          • Decrease brain injury
            • Targeted temperature management (TTM) and therapeutic hypothermia (TH)
              • Rationale
                • Neurologic injury is the most common cause of death in patients with out-of-hospital cardiac arrest
              • Indications
                • Anyone not following commands or showing purposeful movements following resuscitation from cardiac arrest
              • Contraindication
                • Active non-compressible bleeding
                • TH is associated with higher risk of bleeding in patients undergoing coronary cath or those who received thrombolytics
              • Timing
                • To be achieved as soon as possible and maintained for at least 48 hours
                  • Rate of good functional outcome is higher with 48 hours rather than 24
                • Avoid fever at all costs in the first 48 hours
              • Goal temperature
                • This is an area of much debate amongst neurologists and intensivists.  There are two main goal temperatures:
                  • 33ºC (TH)
                    • The studies in support of cooling to a temperature of 33 come from two landmark NEJM papers published back in 2002 (HACA and OHCA) which found that mild to moderate hypothermia improved neurologic outcomes post cardiac arrest.  The caveats were that all these patients had VF/VT arrest (not PEA/asystole), no baseline brainstem function was reported before randomization, and the sample sizes were small. Based on these findings, TH is recommended for anyone with the following:
                      • Deep coma (loss of motor response or brainstem reflexes)
                      • Malignant EEG patterns
                      • Early CT changes suggesting development of cerebral edema
                    • Adverse effects:
                      • Increased rates of infection
                      • Coagulopathy and bleeding
                      • Cold diuresis
                      • Bradycardia and QT prolongation induced cardiac arrhythmias
                  • 36ºC (TTM)
                    • The TTM trial published in 2012 is the largest study on the topic that randomized 939 patients with out-of-hospital cardiac arrests to 33 or 36 degrees temp regulation and found no difference in all cause mortality or neurologic recovery between the two groups.  They included all patients regardless of type of arrest (VF/VT/asystole/PEA).  In subgroup analyses, they found no difference in outcomes based on type of initial rhythm, shock on presentation, age, gender, or time from cardiac arrest to ROSC.
                • So what to do?
                  • General consensus seems to be that avoiding fever at all cost in the first 48 hours is the most important intervention.  Beyond that, keeping patients at 36 might be better as further cooling is associated with risks and no clear indication of benefit based on our best available evidence.
            • General critical care
              • Elevate HOB to 30 degrees
              • Stress ulcer ppx
              • DVT ppx
              • Early PT/OT
              • Seizures and myoclonic jerks
                • Common and a marker of more severe brain injury
                • Continuous EEG recommended if available
                • No benefit in prophylactic treatment

Anoxic brain injury

Nomenclature

  • Brain death: irreversible cessation of cerebral and brainstem function
  • Persistent vegetative state: subgroup that suffers from severe anoxic brain injury and progresses to a state of wakefulness without awareness
  • Minimally conscious state: can have some purposeful movements or interactions with the environment.

Clinical parameters associated with an unfavorable prognosis

Clinical parameters Unfavorable prognosis
Duration of anoxia >8-10 minutes
Duration of CPR >30 minutes
Pupillary light reaction Absent on day 3
Motor response to pain Absent on day 3
Brainstem reflexes Absent
Blood glucose on admission >300 mg/dL
Glascow coma score on day 3 <5
Table above adapted from UpToDate

Work up:

  • Somatosensory evoked potentials (SSEPs): absent response at 24-72 hours appears to be most useful in identifying those with poor prognosis
  • EEG: can be affected by sedative drugs, metabolic derangements, and sepsis so careful with interpreting its findings!
  • Lab test for neuron-specific enolase (NSE)
    • Markedly elevated levels are associated with poor outcomes but no clear cut-off established
  • Imaging:
    • CT/MRI: look for edema and inversion of gray-white densities associated with poor outcome.

Hemorrhagic shock secondary to GI bleed with recent PCI for NSTEMI on DAPT… Did I mention severe aortic stenosis as well? How about all of these in one patient at the same time? 11/29/2018

Narges presented a very complicated patient, who presents with 2 days of abdominal pain and melena. He had a PCI 4 days prior with a drug-eluting stent deployed at the LAD, and he was discharged on aspirin and ticagrelor (PLATO trial, superior to clopidogrel). On presentation he was in hemorrhagic shock, with notable hematochezia on exam, encephalopathy, and a 4/6 systolic murmur with carotid radiation which turned out to be an undiagnosed severe aortic stenosis.

To briefly summarize his main problem list:

  1. Hemorrhagic shock secondary to UGIB
  2. CAD with recent NSTEMI s/p DES to LAD x1 on DAPT
  3. Severe aortic stenosis, newly diagnosed

Question is, what to do if you see a patient like this? Let’s break it down.


 

Antiplatelet and PCI

  • Drug eluting stents (DES) are designed to have lower rates of late re-stenosis than bare metal stents (BMS), but they are at higher risk for in-stent thrombosis due to delayed endothelialization.
  • Some terminology:
    • Stent re-stenosis:
      • Gradual narrowing of the stent segment, usually occurs 3-12 months after stent placement.
      • Can present as recurrent angina vs full blown MI
    • Stent thrombosis
      • Abrupt thrombotic occlusion of a previously patent stent, usually catastrophic MI
  • Duration of DAPT? It depends! Per the 2016 ACC/AHA guidelineDAPT.png

In a nut shell:

Elective PCI in stable CAD:

  • BMS: At least 1 month of DAPT
  • DES: At least 6 months of DAPT

Exact duration is yet to be determined; there is some evidence of decreased stent restenosis (DAPT trial) with longer duration of DAPT but at the expense of all cause mortality and bleeding complications. There are also newer studies (i.e. ARCTIC Interruption) that found no benefits with longer duration of DAPT.

For PCI in setting of ACS, however, the guideline is different:

Anti-platelet duration in setting of ACS

  • Medical Therapy: At least 12 months of DAPT
  • PCI (BMS or DES, doens’t matter): At least 12 months of DAPT
  • CABG: Also at least 12 months of DAPT

In patients with high bleeding risk or personal history of bleeding and/or long term NSAID use, preemptive prophylaxis with a PPI can be considered. If bleeding risk is significant, you can potentially decrease DAPT duration to at least 6 months, on a case-to-case basis.

Now keep in mind our patient has a DES deployed 4 days ago and he’s now bleeding…


GI Bleed

Risk Factors

  • Alcohol
  • NSAID
  • Anticoagulation
  • Cirrhosis
  • Cancer

Presentation

  • UGIB: BUN/Cr ratio > 30 usually (not sensitive but specific), melena (gut transit of blood)
  • LGIB: bright red hematochezia, lower BUN/Cr ratio, but do not be fooled, can be seen in brisk UGIB (especially in this patient).

Management

  • Airway protection
  • Large bore IVs (18 G), Cordis, IO (they work wonders in a pinch!)
  • Fluid resuscitation
  • Anti-acid (i.e. Protonix)
  • Octreotide if suspecting variceal bleed, if catastrophic variceal bleed, consider deployment of a Blakemore/Minnesota tube
  • Antibiotics for primary SBP prophylaxis if cirrhotic
  • Blood product administration
  • GI consultation, urgency depending on clinical status, EGD

High risk features on Endoscopy

The patient underwent EGD and a duodenal ulcer that was actively bleeding was found. There are certain features of an ulcer that we can use to risk stratify and determine how likely intervention will be successful, and how likely the ulcer will rebleed. This is the Forrest Classification, first published in the Lancet in 1974. Our patient in this case is class 1B, and he ended by rebleeding twice requiring additional endoscopic intervention.

Picture1

Source: Alzoubaidi DLovat LBHaidry R. Management of non-variceal upper gastrointestinal bleeding: where are we in 2018? 

Failure of endoscopic therapy

  • Predictors: active bleeding at time of endoscopy, visible vessel, > 2cm, posterior duodenal ulcers, and gastric ulcers on the lesser curvature are associated with higher risk of treatment failure/rebleeding.
  • First line: 2nd endoscopic intervention
  • If recurrent bleeding persists, surgical options or IR embolization should be considered

The key question here is, when to resume DAPT? The decision will have to be individualized and most would recommend restarting ASAP as soon as patient is clinically stable… At the same time, pt has one other newly diagnosed problem that makes his management tricky…


aorticvalvearea-classification-aorticstenosis-meangradient-cardiology-original

Source: grepmed

Severe Aortic Stenosis

Criteria:

  1. Area < 1cm2
  2. Mean trans valvular gradient > 40 mmHg
  3. Peak velocity > 4m/s

Referral to Cardiology because it is actually more complicated than this, there is also pseudo severe where AVR is not recommended, Low flow AS, low gradient AS, or both LF LG AS.

  • Pseudo-severe: mild to moderate AS, low gradient, underlying myocardial dysfunction leading to poor valve opening. No benefit in AVR
  • LF LG AS:
    • AVA < 1cm2, but gradient < 35mmHg
    • Must distinguish from pseudo severe AS. Do dobutamine stress echo
      • If AVA remains the same, gradient inc, confirms true severe AS
      • If AVA improves while mean gradient remains the same, this is pseudo-severe AS, manage medically.

Epidemiology

  • < 70: Suspect bicuspid aortic valve
  • > 70: Progressive valvular fibrosis/calcification
  • Developing country: Rheumatic fever

Pathophysiology

  • Over time leads to LV hypertrophy (concentric), muscle hypertrophy. Leads to heart failure over time.

Presentation

  • Asx
  • Sx: SAD syncope, angina, dyspnea

Management

  • TAVR (transcatheter) vs SAVR (surgical), TAVR is non-inferior (PARTNER A, PARTNER B, SURTAVI trials) but has other complications to consider,
  • Can think about the transcatheter approach in high surgical risk patients.

In setting of hypotension

  • Patients with critical AS are highly preload dependent:
  • Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV). In patients with severe AS, CO is fixed due to physiologic limitations of a small outlet.
    • Increasing HR can help with CO but you run the risk of increasing myocardial O2 demands…
    • Also in terms of volume, pts with severe AS usually has a degree of diastolic dysfunction (decreased compliance due to a hypertrophied ventricle). As you can imagine, if you push too much fluids into a non-compliant system, back up can occur leading to pulmonary edema thus respiratory failure…
  • Choice Pressors: no absolute contraindication to any but phenylephrine has been suggested in some anesthesia text books as first line
    • Rationale: Pure alpha, increases DBP (diastolic blood pressure), which in turns inc coronary perfusion pressure (CPP = DP – PCWP (LVEDP))
    • Won’t induce tachycardia (if anything induces a mild reflexive bradycardia which decreases myocardial O2 demands).
    • Epi has been associated with higher incidences of arrhythmias

Stress-induced cardiomyopathy – 9/5/18

Thanks to Eric for presenting the case of an “late middle-age” woman with chest pressure, found to have ST depressions, troponin elevation, TTE with apical akinesis, and clean coronaries on cardiac cath concerning for Takotsubo cardiomyopathy.


Clinical Pearls

  • Think of heart failure as ischemic vs non-ischemic
  • Most common causes of heart disease are ischemia (CAD), HTN, idiopathic, valvular, infectious (viral), and drugs.
  • MINOCA or myocardial infarction with nonobstructive coronary arteries is MI in the absence of coronary artery disease with >50% vessel occlusion and includes the following etiologies
    • Stress induced cariodmyopathy (Takotsubo)
    • Coronary vasospasm
    • Microvascular dysfunction
  • Takotsubo cardiomyopathy most commonly presents in postmenopausal women and triggered by physical or emotional stress.  The pathogenesis is not well understood and the course is self-limited.  Treatment is largely supportive.  Prognosis to recovery of cardiac function is 1-4 weeks.

Heart failure

  • Ischemic
    • CAD
    • Bridge
  • Non-ischemic
    • HTN
    • Valvular disease
    • Idiopathic
    • Infectious (viral is most common)
    • Infiltrative (sarcoid, amyloid, hemochromatosis)
    • Stress induced cardiomyopathy (Takotsubo)
    • Arrhythmia
    • High output (secondary to anemia, Paget’s disease, pregnancy, AV fistula, beriberi, hyperthyroidism)
    • Post-partum
    • Hypothyroidism
    • OSA
    • Connective tissue disease

MI with non-obstructive coronary arteries (MINOCA)

  • Diagnosis: requires the following
    • Clinical documentation of MI
    • Exclusion of obstructive CAD
    • No overt cause for acute MI present
  • Etiologies: significant overlap with non-ischemic causes of heart failure
    • Non-cardiac
      • Reduced troponin clearance (i.e. renal impairment)
      • Increased right heart pressures (ex PE)
    • Cardiac causes
      • Stress induced cardiomyopathy
      • Inflammation (myocarditis)
      • Coronary artery spasm (vasospastic angina)
      • Microvascular dysfunction (microvascular angina, microvascular spasm, coronary slow flow phenomenon)
      • Thrombophilia
  • Work up
    • MINOCA is a working diagnosis
      • Exclude non-cardiac cause
      • Rule out ischemic etiology
      • TTE
      • Cardiac MRI is often indicated
      • Provocative spasm testing (with acetylcholine etc in the case of coronary vasospasm)

Takotsubo cardiomyopathy

  • First described in Japan in 1990
  • It is the underlying etiology in ~1-2% of patients presenting with ACS
  • More common in post-menopausal women (mean age 66.4)
  • Pathogenesis:
    • Not well understood
  • Clinical manifestations
    • Often triggered by emotional or physical stress but ~30% of the time, no trigger is identified
    • Symptoms
      • Most commonly present with acute substernal chest pain.  Less commonly present with SOB or syncope or heart failure symptoms
    • Exam
      • May have late peaking systolic murmur similar to HOCM
    • EKG changes:
      • ST elevation in anterior leads (43.7%)
      • ST depression (7.7%)
      • QT prolongation, T wave inversion, abnormal Q waves
    • Troponin elevation in most patients (mean initial troponin is ~7-8)
    • Diagnostic criteria
      • Transient LV systolic dysfunction (hypokinesis, akinesis, or dyskinesis), wall motion abnormalities that extend beyond a single epicardial coronary distribution
      • Absence of CAD based on cath
      • New EKG abnormalities
      • Absence of pheochromocytoma or myocarditis
    • Work up
      • Rule out ACS
      • Cardiac MRI to rule out other causes of MINOCA
    • Management
      • Supportive
    • Prognosis
      • Recovery in 1 to 4 weeks

Picture1

Picture above and cool video from NEJM here.

 

 

Thyroid storm! Or is it?… 8/28/18

Thanks Hong for presenting the case of a middle-aged woman with recent diagnosis of Grave’s disease off methimazole who presented with A fib with RVR and congestive heart failure, raising a debate on thyroid storm!


Clinical Pearls:

  • Thyroid storm is an extremely rare (1 in 500,000) but life-threatening diagnosis (up to 30% mortality) that should not be missed.
  • Degree of thyroid hormone elevation or TSH suppression is not a criteria for diagnosing thyroid storm! In fact, levels are typically similar to those of patients with uncomplicated thyrotoxicosis.
  • Common clinical feature is cardiovascular symptoms (heart failure, arrhythmia, tachycardia) but more specific finding is AMS.
  • Scoring criteria to screen for thyroid storm include Burch/Wartofsky and the Akamizu criteria, but they have not been validated.
  • Consult endocrine early if you suspect thyroid storm!

Thyroid storm: 

Risk factors:

  • Longstanding untreated hyperthyroidism
  • Precipitants:
    • Thyroid/non-thyroidal surgery
    • Trauma
    • Infection
    • Acute iodine load
    • Parturition
    • Irregular use or discontinuation of antithyroid treatment

Etiology: not clearly understood, but possibly related to the following

  • Rapid rate of increase in thyroid hormone levels?
  • Increased responsiveness to catecholamines?
  • Enhanced cellular responses to thyroid hormone?
  • The degree of thyroid hormone elevation or TSH suppression is not typically more profound than uncomplicated thyrotoxicosis

Clinical features:

  • CV (>60% of cases)
    • Tachycardia
    • CHF
    • Arrhythmias
  • Hyperpyrexia
  • AMS (considered by many to be essential to diagnosis)
    • Agitation, anxiety, delirium, psychosis, stupor, coma
  • Features associated with worse outcomes?
    • AMS
    • Older age >60
    • Mechanical ventilation
    • Not using antithyroid drugs or beta blockers

Diagnosis: 

  • Clinical! No universally accepted criteria or validated clinical tools.  Degree of hyperthyroidism is not a criterion for diagnosis.  Some to know of that might be helpful:
    • Burch and Wartofsky (sensitive, not specific)
      • > 45: highly suggestive of thyroid storm
      • 25 – 44: impending storm
      • <25: thyroid storm unlikely
    • Akamizu (Japanese) system developed in 2012 (less sensitive but more specific)

Treatment

  • ICU admission!
  • Regimen
    • Beta blockers ⇒ control symptoms from increased adrenergic tone
    • Thionamide ⇒ block new hormone synthesis. PTU is preferred because it blocks peripheral conversion of T4 to T3.
    • Iodine solution ⇒ block release of thyroid hormone (saturated solution of potassium iodide)
    • Iodinated radiocontrast agent (not available anymore in most places) ⇒  inhibit peripheral conversion of T4 to T3
    • Glucocorticoids ⇒ reduce T4 to T3 conversion, promote vasomotor stability, and treat any associated relative adrenal insufficiency
    • Bile acid sequestrants ⇒ decrease enterohepatic recycling of thyroid hormones (only in very severe cases)
  • Principles
    • Start with beta blockers + PTU, and stress dose steroids
    • 1 hour later: start SSKI q6h (after hormone synthesis has been halted with PTU, otherwise SSKI can make thyroid storm worse)