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BP goal: - > 60 years

less than 150/90


BP Goal: -less than 60 years -CKD -DM

less than 140/90


Initial BP treatment: -Black

-Thiazide diuretic or -CCB *ACE/ARB not first line


Initial BP treatment -Other ethnicities

Any single agent or combination: -Thiazide -ACE/ARB -CCB


Initial BP treatment -all ethnicities with CKD or DM

ACE/ARB -alone or in combination with other agents


What did the ACCOMPLISH trial show?

dual therapy with ACE + CCB was superior to ACE + Thiazide in reducing CV events


What are indications for ambulatory BP monitoring?

-discrepancy between the BP readings at home and in-office ("white coat" hypertension) -Suspected paroxysmal hypertension (pheochromocytoma) -Suspected autonomic dysfunction -Hypertension refractor to treatment -Hypotensive symptoms while on antihypertensive therapy


Define intrinsicoid deflection -Where is it seen?

-time from onset of the earliest Q or R wave to the peak of the R wave in the lateral leads (aVL, V5-V6) -represents the time taken for excitation to spread from the endocardial to the epicardial surface of the left ventricle -R wave peak time is said to be prolonged if > 45 ms -Seen in: LAFB, LVH, LBBB


EKG findings of LVH:

-increased amplitude (voltage) of QRS -supported (and strengthened) by presence of secondary ST-T wave changes -Other: left atrial abnormality, LAD, and/or prolonged intrinsicoid deflection, prominent U waves may be present


EKG Criteria for LVH (Sokolow and Lyone):

Precordial leads -Sv1 and R v5 or v6 > 35 mm -R v5 or v6 > 25 mm Limb leads -R aVL > 11 mm


EKG Criteria for LVH (Romhilt and Estes Point system)

**5 or more = LVH, 4 or more = probably LVH** Amplitude (any of the following) = 3 points -Any limb lead R or S > 20 mm -Sv1 or Sv2 > 30 mm -Rv5 or Rv6 > 30 mm ST-T change = 3 points (1 with digitalis) Left atrial abnormality = 3 points Left axis deviation (-30 or more) = 2 points Intrinsicoid deflection = 1 point


EKG Criteria for LVH (Cornell)

Men: Ravl + Sv3 > 28 mm Women: Ravl + Sv3 > 20 mm


EKG Criteria for left atrial abnormality

-Prominent notching of P-wave (especially L2) with P-wave duration > 0.12s -Leftward shift of P-wave axis -Increased duration and depth of terminal negative portion of P in V1 ( > 0.04 mm-sec)


What four factors determine the transmembrane voltage (membrane potential) across the cell membrane in cardiac myocytes?

Concentration of ions on the inside/outside the cell -inside (high in Na and Ca) -Outside (high in K) -electrochemical gradients control the range of transmembrane voltages that can be achieved when ion channels open Permeability of the cell membrane to those ions (Ion conductances) -controlled by the opening/closing of specific ion channel proteins Activity of electrogenic transporters -Na-K ATPase, Na-Ca exchange, Ca transport pumps -maintain ion concentrations across the cell membrane Current flowing from neighboring interconnected myocytes via gap junctions -gap junction channel is composed of two connexons or hemichannels that connect across the intercellular space


Cardiac Action potential: Phase 0

-upstroke or rapid depolarization of the action potential -in most cells it is dominated by Na ions entering through voltage-gated Na channels -peak voltage may reach +30 - +40 mV -in SA and AV nodal tissue --> depolarization is carried mainly by T- and L-type Ca channels


Cardiac action potential: Phase 1

-initial or rapid early depolarization -caused by rapid inactivation of Na current (Ina) and by activation of transient outward current (Ito) carried mostly by K ions *Ito is composed of two components (Ito1, Ito2)


Cardiac action potential: Phase 2

-plateau of the action potential (several hundred msec long in some cardiac cells, such as Purkinje) -phase that distinguishes a cardiac action potential from a neuronal action potential -most complex part of the action potential because many small amplitude currents flow through several ion channels *Inward (depolarizing current) -late inactivating Na channels (INa) -L-type calcium channels (ICa-L) *Outward (repolarizing current) -K channels *(Ito) inactivation *activation of rapidly (Ikr), slowly (IKs), delayed rectifier K channels and electrogenic transporters


Mechanisms of tachyarrhythmias

Reentry -Atrial flutter -AV nodal reentrant tachycardia -AV reentrant tachycardia (WPW) -Atrial fibrillation (multiple reentrant loops) Abnormal automaticity -Atrial tachycardia -Accelerated junctional rhythm Triggered activity (EAD's) -Torsades de pointes / LQTS Triggered activity (DAD's) -Bidirectional VT due to Ca overload (digitalis toxicity, ischemia) -Outflow tract tachycardias / VT


Mechanism for Reentry tachycardias (must contain)

-areas with fast and slow conduction velocities -varying refractory periods in these areas (refractoriness is usually longer in the fast pathway -implied is that there must be a core about which the circuit moves (a fixed or functional core)


Initiation of a reentrant loop is thought to depend on this?

development of an area of unidirectional block so that an electrical wave front (action potential depolarization) may circulate in one direction around the re-entrant loop


Mechanisms for terminating Reentry tachycardia

interventions that modify action potential conduction -suppression of Na or Ca channels to slow or block conduction refractoriness -block or stimulation of K channels to change action potential duration and refractoriness functional properties -improving ischemia so that an area of functional or unidirectional block disappears interventions that electrically interrupt the conditions needed to maintain the re-entrant loop -delivering a small electrical shock to depolarize or block a small part of the re-entrant loop, delivering a large electrical shock to depolarize most of all of the re-entrant loop, or ablating tissue critical to the re-entrant loop


Key characteristics of RVH

-R/S ratio in V1 > 1 and R wave > 5mm -QR in V1 -RAD -Right atrial enlargement -S1Q3T3 pattern and S1S2S3 pattern *S1S2S3 pattern due to RVH = (SII > SIII)


EKG criteria for Right atrial enlargement

-peaked P (amplitude > 2.5 mm) in leads II, III, and aVF -Rightward shift in P-wave axis ( > +75) -Increased area ( >0.06 mm/sec or amplitude > 1.5 mm) of initial positive portion of P wave in V1


Differential diagnosis of RAD

-RVH -Lateral wall MI -Left posterior hemiblock -COPD -Normal Young Adult


Differential diagnosis: Prominent R wave or R/S ratio in V1

-RVH -Ventricular Pre-excitation (WPW) -Posterior wall MI -Hypertrophic Cardiomyopathy -If qR pattern, incomplete RBBB with septal MI -Normal Variant


EKG findings: Acute PE

-Rightward shift of the QRS axis ( > 90 or indeterminate) -S1Q3T3 pattern -Incomplete or complete RBBB (often transient) -ST-segment deviation (depression or elevation) in V1-V2 -Sinus tachycardia, atrial flutter, atrial fibrillation


RBBB diagnostic criteria

-Broad QRS > 120 ms -RSR' pattern in V1-V3 (M-shaped QRS complex) -Wide, slurred S wave in the lateral leads (I, aVL, V5-V6)


Causes of RBBB

-RVT / cor pulmonale -PE -Ischemic heart disease -Rheumatic heart disease -Myocarditis or cardiomyopathy -Degnerative disease of the conduction system -Congenital heart disease (e.g. ASD)


Incomplete RBBB criteria

-RSR' patterin in V1-V3 with QRS duration < 120 ms *Normal variant often seen in children (of no clinical significance)


RBBB pathophysiology

-activation of the RV is delayed as depolarization has to spread across the septum from the LV -LV is activated normally, meaning that the early part of the QRS is unchanged -Delayed RV activation produces a secondary R wave (R') in the right precordial leads (V1-V3) and a wide, slurred S wave in the lateral leads -Delayed activation of the RV also gives rise to secondary repolarization