Cardiology Flashcards
What are some causes of Long QT
Congenital
- genetic disease of K and Na channels
- Autosomal DOminant
Acquired -Meds (Sotolol, Amiodarone, Zofran - Electroylytes Hypo Mag/Hypokalemia, Hypocalcemia - Hear ICM/HCM - SAH Malnutrition (Lytes).
Treatment for Long QT
Congenital
- continue bb therapy
- correct electrolytes
Acquired
- stop offending medications
Magnesium 2 G alive 4 grams dead
- treat Hypo K, Hypo Ca, Hypomg
Review of cardiac actionable potential
Phase 4= -90 mv closed sodium channels, NAK pump working 3-2
Phase 0- Depolarization fast sodium channels +20ish
Phase 1 Fast NA close, K Efflux opens
Phase 2 Clacium influx occurs causing plateau phase
Phase 3 Calcium influx stops and K efflux continues (depolarization)
Phase 4 K efflux happens and NAK pump continues ( sodium calcium exchanger
Mechanism of Ashton of antyarrythmics
Lidocaine - decrease conduction velocity, decrease refractory period, decrease automaticity
Beta blocker
- decrease conduction velocity, no change to refractory period, decrease automaticity
Class 3 ( Pottassium blocke)- increases refractor period
Class 4- decrease velocity, increased refractory period. Decrease automaticity
Digoxin, CCB, BB, Adensoine all work on the AV node which decreases automaticity Also
Lidocaine works on conduction pathway in the LBB RBB and my coyotes
Amiodarone works on both
Torsades vs polymorphic VT
Only called TORSADES if the underlying QTc was long
- give Mg
Amiodarone, lidocaine, correct electolytes, defibrillate
Indications for ICD
1) cardiac arrest due to VT or VG not due to transient or reversible cause (class 1 evidence)
2) spontaneous or sustained VT ( Class 1)
- in association with structural heart disease
-
3) syncope NYD with EPS induced hemodynamically significant sustained VT/VF (CLass 1)
4) sever symptoms (syncope) attributed to sustained VT while awaiting transplant
What is Brugada Syndrome
Autosomal dominant genetic mutation of sodium channels
Can be intermittent and most common middle aged males
THEY NEED AN ICD
Brugada Syndrome types
Type 1 2mm ST elevation in V1-V3 followed by a negative T wave
- diagnosis with clinical criteria, VT;VF, Family hx SCD <45, coved type ECGS in family members, Inducibility of VT, Syncope, Nocturnal atonal respiration’s
Type 2 Saddleback shape ST Elevation
Type 3 Morphoology of 1 and 2 with 2mm st elevation
Layers of the heart outside n
Fibrous Pericardium Parietal Pericardium Pericardial Cavity Visceral Pericardium Myocardium Endocardium
Oxygen Delivery equation
D02= Co x Ca02
Oxygen consumption equation
V02= COx (Ca02-Cv02)
Cardiac output equation
C0=HR x SV
Volume of blood ejected by heart in 1 minute
Stroke volume is affected
Preload
Afterload
Contractility
How to get ejection Fraction
EF= SV/EDVx100%
Define Preload
Wall stress at the end of diastole
- related to degree to which myocardial fibres are stretched therefore the MAXIMAL resting length of the sarcomere
Frank staling curve
As you increase contractility you will increase SV
As you decrease Contractility you will decrease Contractility
As you increase preload you will increase contractility until you have maximal stretch and the you will plate you
Frank starling Curve GRAFT
What is the Concept of mean systemic filling pressure
If the pressure in the right atrium is greater than or equal to Mean systemic filling pressure there will be no flow
There has to have a pressure gradient that drives venous return
Mean systemic fill pressure average 7-8
Define Contractility
Inherent capacity of the myocardium to contract independently of changes in preload or afterload
This is secondary to interactions between Ca ions and contractile proteins
Ex able to increase contractile with exercise, adrenergic stimulation and inotropic medications
Define Afterload
Wall stress generated by muscle fibres during systole
La places law
Wall Stress= pressures radius / 2x wall thickness
How to we measure Cardiac output
CO= MAP-CVP/SVR
Arterial oxygen content equation
Ca02= (Hgbx1.34xSa02+ .003xPa02)
Cv02= ( Hgbx1.34xSv02+0.003+Pv02)
What is the solubility coefficient of 02
0.003
What are the major determinants of myocardial oxygen demand uptake
1) HR
2) Wall Stress
3) Contractility
What will high wall tenson result in for metabolic demand
Increase metabolic demand and increase oxygen consumption of the heart
What will decrease myocardial oxygen supply
1) decrease coronary blood flow
2) increased HR ( less diastolic filling time)
3) increased diastolic volume
4) deceased 02 content
Decrease hematocrit
Decreased 02 saturation
At rest does the heart already have maximal 02 extraction
How do you increase 02 extraction
At rest the heart already has maximal 02 extraction so the only way to increase it is to increase deliver and increase coronary flow.
Exercise will increase coronary blood flow by 4-5 x
What are the main 4 Coronary arteries
Left main
Right
LAD
Circumflex
Explain the left and right dominance for blood supply
The posterior descending artery feads the AV node
In 2/3 of population the PDA comes offf the RCA
1/3 of people it comes off the Left Circumflex artery
Co dominant it comes of RCA and LCx
What arteries come of RCA
RCA
Nodal Branch
Acute marginal
Posterior descending 2/3 of people
What branches of LAD
S1 S2 septal branches towards middle or septum
D1 D2 D3 diagonal arteries towards left
There is also the S1S2 which branches off posterior descending arteries
Coronary Perfusion Territories
RCA- inferior segments, posterior 1/3 IVS+ as node and AV node
LCx All lateral segments and occasionally SA and AV node
LAD all anterior segments and 2/3 IVS + septum
WHen does the Coronaries receive blood
LV 85 percent during diastole 1 percent systole
RV both systole and diastole
Blood flow is drained by Coronary sinus and empties into RA 85 percent and 15 percent into thesbian veins ( Empty into Left side heart) along with bronchial veins and pulmonary veins (causing a physiological shunt)
In order what the the CVP wave forms and what do they represent
A, C, X, V, Y
A= Right atrial contract at end of Diastole
- you will lose a wave in A-FIB
- A wave will increase in Tricuspid and pulmonic stenosis
- Cannon A waves are in heart blocks, V TAC secondary to contraction agains a close tricupsid Valve
C= Early systole
- Tricuspid valve bulging into RA from RV congtraction
- Tricuspid regurgitation causes fusion of C and V waves with x descending blunted
X- (mid systole) which is the RA relaxation
- Incresed x descent in constrictive pericarditis
- Decreased ascent with Tricuspid Regurg as increased RA pressures suggest RV dysfunction
V= (late Systole)
Rapid Filling of RA
- increaed V wave in Tricuspid recurg from increased RA pressure
Y=
Systole steps
1) Isovolumetric contraction is when MV closes and AV is still closed as ventricule builds up pressure
2) Rapid Ejection 2/3 volume ejected
3) Slower Ejection: 1/3 volume Ejected
Diastole Phases (4)
1) Isovolumetiric relaxation: AV closed and MV still closed as LA builds up pressure
2) Early ventricular filling: MV opens, passive LV fills LAP> LVP (70-80 final stroke volume)
3) Late Diastolic filling/diastasis: LVP approaches LAP, dependent on chamber compliance
4) Atrial systole/kick contracts 15-20 percent
Pressure Volume Loop starting from bottom left corner
A= End systolic Volume
B= Early Ventricular Filling/Late Ventricular Filling
C= Mitral Valve closes
Isovolumetric Contraction
D= Aortic Valve Closes
E= stroke volume/ejection
F= Aortic Valve Closes
Isovolumetric Relaxation
A
What is a normal Cardiac Output
4.o-8.0 l/min
Pacemaker Action Potential
Phase 4= sodium leaks into cell - 60mv
Phase 0 depolarization occurs with Ca channels opening
Phase 3- depolarizations with potassium out.
Normal axis
30 to -90 degrees
Positive I. Positive AVF
Left Axis Deviation
Positive lead I
Negative AVF
0 to -90
RAD
Negative Lead I
Positive AVF
+ 90 to +180
Extreme axis deviation
Negative Lead 1
Negative AVF
-90 to -180
Either a hypertrophy axis shifts towards or a damaged part of the heart axis moves away.
What causes axis deviation
What is atherosclerosis and its patho genesis
Is a type of arteriosclerosis (thickening and hardening of artery walls) affects primarily medium and large size muscular arteries affecting the intima
This is caused by a chronic inflammatory response in the walls of the arteries which is a slow progression of fat(cholesterol) build up within the artery causing intimacy lesions called Atheromas, atheromatous or fibrofatty plaques.
Angina Pectoris Definition
Imbalance of myocardial oxygen supplyly and demand
Stable, predictable with increased activity and resolves with rest or NTG
Typically requires >70 percent occlusion
What are our Hemodynamic goals with CAD
1) Small chamber size + low LVEDP
2) SLow HR, Increased diastolic filling time
3) reduced contractility
4) Adequate perfusion pressure
LV only gets perfusion during diastole where as RV gets perfusion from systole and diastole
1) Decrease preload
2) maintain afterload (hypertension is better than hypotension
3) Decrease contractility
4) Decrease Rate and keep in SINUS Rhtym
Therapy to treat Coronary ischemia
NTG 0.5-3mcg/kg/min
Nitride 0.5-3 mcg/kg/min
Phenylephrine/norepinephrine/ vasopressin for hypoperfusion
BB, CCB do decrease HR, improve diastolic filling time
MgS04 for hypomagneisa which has coronary vasodilation properties which decreases size of infarct in acute ischemia and reduces mortality during infarction
How do Nitrates Work
Nitrates increase 02 supply by dilation of large epicardial coronary arteries
Low doses decrease preload which decreases wall stress and decreases to cardiac 02 demand
Higher doeses decreases afterload and decreases myocardial 02 demand.
What can exacerbate myocardial ischemia
HTN, Fever, Tachycardia, anemia, hypoxemia, valvular disease
Standard of Care
BB,CCB, Nitrates, Statin, antiplatelet, ACEi, ARBS
Type 1 Vs Type 2 MI
Type 1 mi is causes by a sympathetic hyperactivity from catecholamines causing a plague rupture or erosion causing increased Coagulability and decreaed fibrinolysis which causes a Acute Coronary Thrombosis
Type 2 is from sever Stable CAD whic an increased myocardial 02 demand causing increase HR increased sympathetic hyperactivity, increased BP, increaed LVEDP, causing a supply and demand issue
Usually prolonged ST depression
Type 1) Occlusive MI
Type 2) Infarction secondary to supply and demand
Type 3) Sudden cardiac death
Type 4) PCI causing infarction
Type 5) CABG causing infarction
Types of MIs
Difference between a OMI and. NOMI
OMI is a complete vessel occlusion
NOMI is a narrowed vessel no totally occluded.
Non MI Troponin elevation cause
Sepsis, CHF, Renal Failure, Stroke
What happens to ST segments during NSTEMI AND STEMI AND WHY
During NSTEMI subendocardial cells are more susceptible to ischemia.
- Pottaium leak arrives from ischemic tissue causing a partial depolarization towards the electrode which causes the baseline to shift upward.
This looks like ST depression
During Stemi
- potassium leak happens prior to electric stimulation and produces a force away from the electrode cause it an upward shift of baseline
Looking like ST elevation
Q waves
- necrotic muscles does not generate electrical forces
