Management of acute hypertension 

Hypertensive Urgency
- >180/110 without target organ dysfunction
- ha, sob, epistaxis
- manage with oral agents
- often precipitated by medication non adherence, high salt load ("I ate a bunch of Chinese food"), missing dialysis

Hypertensive Emergency
- cerebral blood flow is constant at a MAP of 60-120 - outside of that, autoregulation fails
- at high perfusion pressures -- shear stress on endothelium, platelet aggregation (leading to MI, HF, stroke, DIC/MAHA etc) - fibrinoid material in vascular wall, increased permeability, thrombosis.

Management
- Immediate: 15-20% reduction (or map 100-120)
- Over next 2-6 hours: Goal 160/100
- exception: ischemic strokes - goal higher BP (permissive to 220/120)
- exception: aortic dissection - goal SBP < 100, goal HR < 60, so beta-blocker gtt i.e. esmolol -- believed that tachycardia is what's causing the shear stress against aorta, so should get HR down first (i.e. dont give hydralazine without having b-blocker on board). Avoid nicardipine as it can cause reflex tachycardia without a b-blocker on board.
- acute MI/CVA - can't give thrombolytics if SBP > 185
- acute HF - don't drop SBP < 120

Blood pressure in ischemic stroke
- 85% of people who have a stroke have HTN - often transient. May be 2/2 the body's response to increase CPP, stress, autonomic dysregulation.
- Bradycardia (possible increased CPP), deep T wave inversions
- First 24-48 hrs after stroke, cerebral autoregulation in penumbra is lost - area is vulnerable. I.e. brain is reliant on CPP to perfuse. If you can maintain perfusion to that area, you can save it.
- American stroke association: treat BP in first 48 hrs only if SBP > 220, DBP > 120, unless you're giving lytics - goal SBP ~ 185
- Fluids and pressors to maintain pressures in first 48 hours

IV antihypertensive agents
- Nipride - arterial and venodilator, onset 1-2 mins, lasts 3-4 mins. limitations: can worsen cerebral edema, cyanide and thioocyanate toxicity (in pts with renal and hepatic failure) - signs of CN toxicity: venous hyperoxemia, lactic acidosis, signs of TCN tox: abdominal pain, AMS, seizures
- Nicardipine - onset 5-15 mins, lasts 4-6 hrs, lim: reflex tachycardia, longer half life - must couple with b-blocker esp in dissection
- Clevidipine - on 2-4 mins, lasts 5-15 mins, 3rd gen dihydropyridine CCB, can't be used in people with egg allergies
- Fenoldopam - DA agonist, onset < 5 mins, lasts 30-60 mins - CI in glaucoma
- Labetaolol - alpha and b-blocker (ratio 1:7) onset 2-5 mins, lasts 24 hrs, limitations: heart block, CHF, bronchospasm, bradycardia - don't use in acute HF as its a negative inotrope, good in pregnancy as minimal placental transfer
- Esmolol - on 1-2 mins, lasts 10-20 mins (T-1/2 : 9 mins) Same limitations as labetalol - plus its a 60cc/hr drip so don't use in ppl who are volume overloaded. Also esmolol drip = ICU stay.
- Phentolamine - a blocker - use to treat htn 2/2 catechol surge like pheo, cocaine
- Nitro - venodilator (some arterial dilation at high doses) - reflex TA, HA, tolerance. Used in ACS.
- Enalaprilat - IV ACE, on 15-30 mins, lasts 6 hrs, limitations: can cause precipitous drop in BP (may explain why outcomes worse in HF) variable response.
- Hydralazine - peripheral vasodilator from direct sm mm relaxation - onset 5-15 mins, lasts up to 12 hours (often way less). Limitations: prolonged and unpredictiable effects, reflex tachycardia. Used often in pregnancy.
- Lasix - reduce volume overload

Avoid:
- ACE-I in acute MI, pregnancy, bilateral RAS
- IV B-blockers in acute HF, reacitive airway dx
- SL nifedipine - big drop in BP

Stress tests 

Stress modality - exercise, dobutamine, vasodilator (i.e. regadenason, dipyridamole) 

Detection modality - EKG, Echo, Nuclear, MRI, symptoms 

EKG exercise 
- brief, upsloping ST depressions are OK, broad/flat/downsloping ST depressions are not
- in order to be diagnostic, you have to reach 85% of max predicted HR 

- Sens & spec: ~70%  

- stop when HR is at 85% of predicted or if pt stops for reason of symptoms 

- good for "rule out" test in low-risk patients 

Nuclear test 

- Tells you exactly where the lesion is - much more accurately than EKG

- Very sensitive - you will find something. If you want to find something, you will find it here. 

- Don't do this if you want to minimize your false-positive (i.e. someone will get thrown off a transplant list because of a false positive test -  in this case do a dobutamine echo instead) 

Cath everyone before sternotomy - if they could benefit from a CABG you might as well do it while you're in there. 

NO dobutamine or vasodilators in AS 

ST elevation in AVR
- proximal LAD or Left Main disease. 

Preop clearance -- when to get a stress test 

Fast arrhythmias come in two primary flavors: increased automaticity of tissue or re-entry of tissue.

	Increased automaticity	Re-entry	Notes
SA node	Sinoatrial tachycardia (ST) - can be physiologic (ie. exercise) or pathologic (inappropriate sinus atrial tachycardia, ca clock dysregulation	Sinoatrial node re-entry	differentiate the 2: they both appear as sinus rhythm, but ST starts and stops gradually, but re-entrant rhythms start and stops immediately
Atrial tissue	Atrial tachcardia (another focus in atria) - faster than sinus, necessarily, because if it were slower it’d be suppressed by sinus rhythm	Aflutter. Maybe a-fib - macro re-entrant rhythm, so there’s no electroneutral baseline, as something is always depolarizing - limb leads The precordial leads will not show bc they show a small window of myocardium	Will not stop with AV nodal block - if you apply adenosine the flutter will still go on, but there will be complete block
AV node	Junctional tach (more common in kids— in adults usually due to dig toxicity) - P & QRS waves will be separated  - like complete block, but there will be more QRS than P	AVNRT	should break with AV nodal block (ie vagal maneurver, adenosine)
Pathways		AVRT (circuit involves ventricles)

Bradyarrythmias in STEMI: 

Sinus brady

- revasc first (cath lab asap)

- if that fails or can't be done, then try atropine (full dose - half may have paradoxial reaction)

- if that fails, then temporary pacing 

AV block 

- First degree- usually due to meds ; PR <0.24

- Mobitz 1: manage with atropine 

- Mobitz 2: concerning b/c can progress to CHB. usually below bundle of his. tx with pacing 

- CHB

anterior or inferior infarct 

anterior (LAD) - massive septal necrosis - unstable escape rhythm (wide QRS, slow) - progresses to asystole, pump failure, shock 

Interior infarct - intranodal or supranodal - usually stable escape rhythm - narrow QRS, ok speed 

- Intraventricular block

RBB - lad and rca

LAF - LAD

LPF - LAD and RCA

Indications for temporary pacing in acute MI

- ventricular asystole 

- symptomatic brady 2//2 node dysfunction

- mobitiz I unresponsive to atropine

- mobitz 2 

- CHB

- bilateral or alternating BBB - indicates low level of block, unstable escape rhythm 

- new BBB with First deg AV block - suggesting concomitant disorders 

- old RBBB with first deg av block and new fasicular block - too many pathways compromised. 

Other temporary pacing indications

- bradyarrhythmia sufficient to cause hemodynamic instab

- injury to either node or his-purkinje 2/2 surgery

- lyme

- OHT

- trauma

- toxins, metabolites 

Temporary Pacing options: 

medical: b1 agonists - ie. isoproternol 

epicardial: surgeons  leave the leads on

transcutaneous: direct puncture to heart

esophageal: only paces atria - high current, painful

external: pacer pads

transvenous pacing: 

access:

RIJ is good for emergency, straight shot, easy 

subclavian if more permanent

femoral if in cath lab 

types: 

balloon, pacing swan ganz

pacemaker paramaters: 

rate - set rate 10-20 above baseline HR, then dial down, backup at 60 rate

current - set at max output, dial down until you get capture 

external/transthoracic pacing: 

- asystolic arrest

- prophylaxis during catheterization in someone with LBB - in case you bump RB with catheter and cause CHB 

- overdrive pacing to terminate tachyarrhythmias

- brady with unstable hemodynamics

pacemaker complications

- lead dislodgement or disconnection

- tamponade

- catheter knotting

- air embolli

- ptx

- more arrhythmias 

ESCAPE trial: use of clot retrieval devices + guideline management vs guideline management alone in patients with ischemic stroke. 

N=316, 22 centers (international)
Study design: prospective, randomized, open-label treatment, blinded outcome evaluation. Current-guideline based controls (no sham control). No specified clot retrieval method.
Disclosures: funded by Covidien.
Inclusion Criteria: 
- Adults, no upper age limit
- Ischemic stroke with onset of symptoms within 12 hours
- Previously normally functioning (Barthel > 90)
- Small infarct core on CT (ASPECTS 6-10)
- Good collaterals on CTA (>50% filling of pial MCA territory vessels)
- Proximal occlusion (M2 or more proximal)
Data adjusted for: use of thrombolytics, age, sex, baseline ASPECTS, baseline NIHSS, location of clot.
Primary outcome: modified Rankin score at 90 days
Modified Rankin:
- 0 : no deficit
- 1 : some deficit, but still able to carry out all activities of daily living (ADL)
- 2 : not able to carry out all ADLs but able to carry out most
- 3 : needs assistance for most ADLs, but able to walk and care for own bodily functions
- 4 : no ADLs, not able to walk or care for own bodily functions
- 5 : bedridden, incontinent, requires 24 hour nursing care
- 6 : dead
Secondary outcome: time to reperfusion/recanalization, hemorrhage, neurological disability at 90 days, death.

Results: 

"The median 90-day modified Rankin score was 2 in the intervention group and 4 in the control group (P<0.001).  The proportion of patients with a modified Rankin score of 0 to 2 at 90 days was 53.0% in the intervention group and 29.3% in the control group (rate ratio, 1.8; 95% CI, 1.4 to 2.4; P<0.001)." (Goyal et al)

Complications: 

The incidence of asymptomatic hemorrhage-infarct was higher in the intervention group (data not shown) but there was no significant difference in symptomatic/significant parenchymal hemorrhage between control and intervention! Woooo 

Speed: goal CT to groin puncture <60 mins, CT to recanalization < 90 mins

 "Although eligibility criteria allowed enrollment up to 12 hours after symptom onset, the median time from symptom onset to first reperfusion was 241 minutes. A total of 49 participants (15.5%) underwent randomization 6 or more hours after symptom onset, and the study was not powered to assess endovascular therapy among patients presenting 6 to 12 hours after symptom onset"

Limitations: 

- Unclear generalizability - unknown how many people were screened and determined to be ineligible based on having too large of an infarct, insufficient collaterals, poor prior function level etc. The significantly devastated people, with the giant infarcts and poor collaterals, the ones who will likely end up rankin 5-6, I wonder if these people may be more vulnerable to hemorrhagic conversion - I don't know... Something to look up next. If they are, the the risk/benefit of clot retrieval in these patients may be more difficult to ascertain-- i.e. they need it more because their injury is more devastating, but their complication rate may be higher making intervention not worth it. 

- The timing was impressive (84 mins CT to recanalization) and may not be reproducible. However MR CLEAN was slower and still had positive outcomes with clot retrieval. 

Ventricular Tachycardias: 

Definitions: 
- NSVT : >3 beats & <30 seconds
- MMVT : monomorphic VT: All QRS complexes have the same morphology
- PMVT: polymorphic VT: variable QRS morphology
- Torsades: PMVT with long QT
- V-fib: disorganized rapid ventricular activity, typically > 200 bpm

VT in structural heart disease- ischemia
- Usually re-entry around a scar
- Someone comes in in MMVT - less likely "this guy is having an MI right now" - more likely the VT is involving scar from an old MI - triggered by volume overload, electrolyte abnormalities, or ischemia
- re-entry around ventricular tissue - vtach
- re-entry in bundles - will look like BBB (goes down R bundle looks like LBBB)

ARVC/D
- Arrhythmogenic RV cardiomyopathy/dysplasia
- fibrofatty replacement of cardiac tissue
- microaneurysms (tissue in RV bulges out)
- Dx - diagnosis based on Echo, MRI, fam hx, biopsy, EKG criteria
- EKG: t-wave should be upright in V1-V3, but T-waves will be inverted in those leads in ARVC (without RBBB) ; Epsilon waves - you'll get a little ditzel at end of QRS complex (slow conduction of electricity through fibrofatty tissue)

Ventricular arrhythmia in structurally normal hearts
- Outflow tract tachycardia (RVOT,  LVOT)
- Idopathic LV tach - belhassen, verapamil sensitive, fasciular
- VT/VF with brugada
- VT/VF with long QT syndrome
- Catecholaminergic PMVT

RVOT/LVOT PVCs
- 20-40 y/o, F>M
- NSVT
- Sudden death rare if LV/RV normal
- EKG: LBBB type, inferior axis (depolarizing from outflow tract - pulmonic or aortic valve - straight down - super tall QRS complexes in II, III, aVF leads)
- Likely benign

Fascicular VT - aka belhassen, aka verapamil sensitive, aka ILVT
- using one limb of fascile to go down
- if it exits from left posterior fascicle - looks like RBBB with LAFB (beat comes down LP fascicle - re-enters up the RB and LAF - "blocks" so the signal can't come down those channels)
- cured with ablation of L posterior fascicle

Brugada
- AD Na channel dysfunction (loss of function mutation) - reduces inflow of Na - differing parts of the heart have differing sensitivity to this, and thus voltage gradients appear between different parts of the heart tissue
- Can look like incomplete RBBB and ST elevation in anterior precordial leads (check V2)
- Can cause syncope and sudden cardiac death - must be managed with ICD
- Picture from medscape:

Long QT syndrome
- Type I (KCNQ1 - K channel mutation) - triggered by exercise - esp swimming - ask about a family hx of drowning
- Type II (HERG - K channel mutation) - triggered by loud noise or emotional stress - alarm or phone ring
- Type III (Na channel mutation - same channel as Brugada, but gain of fxn instead of loss of fxn) - triggered by rest - people die in sleep
- type 4-15: rare
- Prolonged QT - can lead to torsades
- Triggers: abx, psych meds, Methadone!!

Wide complex tachycardia: Differentiating VT vs SVT+aberrancy (i.e. BBB or pre-excitation)
- Wellens criteria - favors VT
- Brugada criteria - algorithm
- R-S distance: if is a sharp upslope you're probably using the conduction system (SVT c aberrancy), otherwise you're not (VT)
- AV disassociation tells you you're in VT -- in SVT with aberrancy, A and V are still associated
- Capture beats: ie in AV disassociation, the ventricle is going on alone, occasionally a well timed atrial beat will actually conduct down and "capture" the ventricle
- Fusion beats: not timed well enough to capture, partially captures
- Capture and fusion beats imply AV disassociation - implies VT - absence of these beats doesn't imply NOT VT - if your ventricular beats go up through AV node and conduct to atria, that signal can't come down to cause a capture/fusion beat
- Waves that look like they are using the conduction system - SVT  - not using conduction system - VT

Adenosine cannot be used to definitively differentiate VT and SVT with aberrancy! 
- The traditional teaching is that SVT uses the AV node and VT doesn't, so SVT will break with adenosine, but this is not true!
- Not all SVT uses AV node - there may be an accessory pathway
- Some VT does use the AV node (outflow tract VT)

Bidirectional VT
- Hallmark of Dig toxicity
- Catecholaminergic polymorphic VT

Afib with accessory pathways
- on every boards
- don't give any drugs that block the AV node (adenosine, CCB, B-blockers)
- Tx with procainamide - blocks accessory pathways - might convert A-fib

VT storm
- 3 or more episodes of VT in 24 hr period
- Causes: ischemia, ischemia, ischemia, CHF, metabolic (low K/Mg, thyroid storm - can precipitate thryoid storm in hypothyroid person with dye load), pro-arrhythmic drugs

Fast Arrhythmias 

Sinus rhythm
- Meaning that the source of atrial depolarization is the sinus node. You can have "sinus rhythm" with block.
- P wave direction is inferior, anterior, and to the L (assuming no dextrocardia) -- i.e. upright in II, upright in I. In AvF and III - it may be biphasic or even inverted, depending on the positioning of the heart
- When you're lying down, you use the inferior part of the sinus node (more R to L, so flatter in II, sharper in I). when you exercise, you use the superior part of the node (more superior to inferior -- higher peaks in II). Additionally, p-waves are bigger in exercise because more of the sinus node is being used. Downsloping PR intervals can reflect atrial depolarization after a large p-wave

Placement of leads
- V1 = 4th intercostal space (move to 2nd to look for brugata)

Negative P wave in V1-- left atrial enlargement, as the L atria is slightly posterior to the R, and when it gets larger this positioning is exaggerated.

Types of Arrhythmia
- Increased automaticity
- Re-entry
- Triggered activity (rare in normal people without dig toxicity) - impulses that occur during phase 3 or 4. "delayed after depolarization"

AV node
- fast pathway (SA directly to AV node) and slow (SA to tissue inferior and posterior to AV node) that conducts.
- Fast pathway conducts fast, recovers slow, slow pathway conducts slow, recovers fast.
- SA node always hits both slow and fast pathways. So do PACs--- setting up potential for re-entry

Aberrancy - wide qrs (>120ms) 
- conduction outside of his-purkinje system.
- Bundle branch block - R vs L, fixed vs rate-dependent, rate-of-change related BBB (ashman's phenomenon). Ashman's - sudden decrease in R-R interval. The right bundle's refractory period is dependent on the previous R-R interval. When you get a sudden decrease in R-R, the R bundle can't handle it and it will block. But then by the next short R-R interval it's learned and it will conduct the next one
- Drugs (TCA, Class I antiarrhythmic)
- Electrolytes (hyperkalemia-- extremely wide QRS ie. >200
- Pacemakers
- Non specific IVCD - conduction slowed through ventricular tissue because of cardiomyopathy, sarcoid, etc,
- Channelopathy
- Hypothermia
- Accessory pathways

Adenosine 
- When used in a transplanted heart, there are increased adenosine receptors, so they are hypersensitive to adenosine and administration may lead to prolonged asystole.

AV disassociation
- Complete heart block (more P's than R's) - atrial rate > ventricular rate, both are regular.
- Junctional tachycardia (more R's than P's)

Afib with accessory pathway
- sometimes conducts through the node (narrow QRS)
- sometimes conducts through the pathway (wide QRS)
- sometimes its both and its a slurred wave
- you don't want to block the node because as long as some impulses go through the node, they'll go retrograde up the accessory pathway and cause a refractory period -- when you block (with adenosine) there is unchecked conduction through the accessory pathway => vfib

Pacemakers: 
- RV pacing alone over time leads to cardiomyopathy, so biventricular pacing is better for young people

T wave inversion is standard in RBBB

Differential of irregular rhythms: 
- Irregularly irregular : afib, wap, mat, Afib + dig or afib + complete block
- Regularly irregular: grouped beats

Flutter
- Typically around tricuspid annulus. Most common and easiest to ablate.
- Can also go around septum, go around pulmonary veins

Old people, longstanding htn - will go into afib after surgery, and get flash pulmonary edema (diastolic heart failure)

Ivabradine for HFpEF- inhibits I-funny channels (slows rate without negative inotropy, like b-blockers) -- slow HR, more time to fill.  Increase VO2

	Increased automaticity	Re-entry	Notes
Sino atrial node	Sinoatrial tachycardia (ST) - can be physiologic (ie. exercise) or pathologic (inappropriate sinus atrial tachycardia, ca clock dysregulation	Sinoatrial node re-entry	differentiate the 2: they both appear as sinus rhythm, but ST starts and stops gradually, but re-entrant rhythms start and stops immediately
Atrial tissue	Atrial tachcardia (another focus in atria) - faster than sinus, necessarily, because if it were slower it’d be suppressed by sinus rhythm	Aflutter. Maybe a-fib - macro re-entrant rhythm, so there’s no electroneutral baseline, as something is always depolarizing - limb leads .The precordial leads will not show bc they show a small window of myocardium	Will not stop with AV nodal block - but if you apply adenosine the flutter will still go on, but there will be complete block
Av node	Junctional tach (more common in kids— adults due to dig toxicity) - P & QRS waves will be separated  - like complete block, but there will be more QRS than P	AVNRT	should break with AV nodal block (ie vagal maneurver, adenosine)
Pathways		AVRT (circuit involves ventricles)

Differential diagnosis for syncope: 

- Slow onset, slow offset - hyperventilation, hypoglycemia

- Abrupt onset, slow offset - seizure 

- Abrupt onset, abrupt offset: 

a. Obstructive - aortic stenosis, HoCM, myxoma, severe pulmonary HTN (no LV preload) 

b. Arrhythmic - bradycardia, tachycardia. 

c. Vascular - vasovagal, orthostatic, hypertension, vertebro-basilar insufficiency (i.e. vasospasm/migraine)

- can have some crossover - hyperventilation can cause bradycardia, seizure can cause acidosis, vertebrobasilar dissection can cause increased vagal tone and AV block

Neurocardiogenic syncope: i.e. "vasovagal" 

- vasodepressor (blood pressure drops, HR goes up) + cardioinhibitory (body makes HR go down suddenly) - HR goes down too low, syncope. As soon as you fall down, increased preload - recovery 

- cardio inhibitory (carotid hypersensitivity) - i.e. in the hospital, people get suctioned, pressure on CN IX, transient asystole (same mechanism as carotid massage) 

- vasodepressor - decreased vascular tone. 

Arrhythmic syncope

- VT or Torsades + hypotension - in old person with structural heart defects, must r/o VT 

- Afib/flutter + RVR (i.e wpw)

- AV block

- Sinus arrest - syncope occurs every 3-5 years so there's no point in short term monitoring.

Rare causes of syncope 

- Bradybury eggleston - men 80s-90s with prostate disease, supine hypertension (200s systolic), orthostatic hypotension. Treat with avoiding extreme movements, +midodrine (alpha agonism) to maintain preload. 

- Platybasia - AV fistulas in occiput, so when you change position, you steal blood from vertebrobasilar system. 

- Platypnea orthodeoxia - reverse of orthopnea. pulmonary hypertension with PFO - right to left shunt when standing up. Either shunt within heart (PFO) or within lungs (pulmonary AVM) 

MI - peri-ischemic area is most likely to generate VT that then degenerates into VFib 

2nd degree AV block: 

- narrow qrs - 90% of the time it's mobitz 1 

- wide qrs - 90% of the time it's mobitz 2 

Precordial thump 

- defibrillation - extends the refractory period, so breaks the re-entrant rhythm of vfib 

- precordial thump is similar to defibrillation - can induce or break v-fib. if someone is coding, and you can't get the defibrillator, just hit the patient really hard in the chest