what causes the long plateau of ventricular action potential?

How much longer is it than skeletal AP?

inward Ca through L type Ca channels

100 times longer at 200msec

it anchors the myosin fibril to the Z line

it's stress-sensing signaling pathways are responsible for muscle hypertrophy

it is probably involved in diastolic stiffening in some forms of heart failure

with greater afterload the muscle has to generate greater tension before contraction occurs. 

Thus the lighter the load, the greater the shortening velocity.  

The heavier the afterload, the shortening velocity is less

aortic pressure or basically systemic blood pressure

a skipped beat increases force because of more Ca entering the cell due to Ca channels

an extra beat alway causes higher force by causing more Ca to enter into the cell

does length affect contractility?

what about preload?

what is a normal value for the EF?

What is the lower limit of normal?

66%

50%

this is the contraction that raises pressure in the ventricle until the resisting pressure of the aorta is overcome and ejection occurs.

relaxation is the time during which pressure is decreasing until the mitral valve reopens ending isovolumetric relaxation

 increase the force of contraction and increased velocity of ejection which is

INCREASE CONTRACTILITY

YES

 this allows for a greater ST and thus EF

degenerative

rheumatic

infectious

aortic and pulmonic stenosis

tricuspid/mitral stenosis RARE

mitral and aortic valves (mainly mitral)

either stenosis or regurg

a diminished and delayed upstroke in aortic pressure

This physiologically means an increased afterload of the left ventricle

wall stress -> higher O2 demands = increased wall thickness

slowed relaxation during diastole = increased stiffness

increased diastolic filling pressure results in L atrial enlargement which can cause:

atrial fibrillation

pulmonary edema

dyspnea on exertion

In order of mean survival:

A. Fib = 6 mo

CHF = 2 years

Syncope = 3 years

Angina = 5 years

SURGERY

different types may be performed for valve replacement but typically the most used are:

mechanical replacement valve

bioprosthetic valves

balloon valvuloplasty has also been performed with mixed results

increase in the filling pressures of the LA -> increased LA size

Pulmonary venous pressure is increased

LA stasis is evident = possible thrombi

(if valve area is < 1.0 cm2 it is severe)

need for long diastolic period

sensitivity to high heart rates

dyspnea on exertion

other than the usual surgical treatment options there are:

valoon valvuloplasty

no

only with mitral stenosis

SOB

A fib

Embolization

SOB

chest pain

syncope

increased LV:

end diastolic volume

end-diastolid pressure

stroke volume

the regurgitant fraction

(SV x HR) - CO

_____________

SV x HR

myxomatous degeneration

mitral annular dilation

ruptured mitral chordae tendineae

ventricular dilation (leads to mitral annular dilation)

ischemic disease

leaflet/chord abnormality caused by:

-congenital

-rheumatic

-infectious

HARSH systolic murmur and low diastolic murmur

this is a HOLOSYSTIC murmur  (heard the "whole" time)

LV is increased

LA is very increased (A fib)

Pulmonary vein pressure increased (dyspnea and edema)

Rheumatic

congenital (biscuspid)

degenerative

infectious

annular dilation

coronary artery flow is decreased as the pressure in the wall of the ventricle goes up.  

Because of addition volume in diastole in the LV wall pressures increase during diastole as the chamber dimensions increase.  This can result in ischemia and chest pain

vasodialators - slow progress

diuretics can reduce symptoms

surgery

CO can be calculated by:

total O2 consumption

_____________________

arterial O2 - venous O2

Pericarditis

myocarditis

endocarditis

scarring involving the valves and chordae tendinae

symptoms develop 10-30 years after initial rheumatic episode

causes fibrosis, calcification of valve leaflets, and fusion/shortening of the chordae tendinae

"fish mouth appearance"

A. Fib

thrombosis

pulmonary hypertension

(all due mostly to mitral valve stenosis or valvular regurgitation due to rigid leaflets and shortened chordae)

mitral valve prolapse

this is due to myxomatous tissue and fragmented collagen causing there to be too much tissue

usually in the elderly

it causes difficulty in valve closure

nodular fibrosis on typically the elderly

Known as "wear and tear" or "degeneration"

can be stenosis or regurg

mitral regurge (common in kids)

aortic regurg (common in adults)

aneurisms of the thoracic aorta

stenosis:  rheumatic disease

regurg: dilation of tricuspid annulus due to pressure or volume overload

stenosis: congenital abnormality (tetr. of fallot)

regurg: dilation of pulmonic valve annulus

abnormal native valves

prosthetic valves

iatrogenic bacteremia

what is more serious, acute or subacute endocarditis?

acute causes death within 6 weeks if untreated

subacute is slower causing death within 6 mo

carcinoid is mostly R sided

(drug induced valve fibrosis commonly affects L side)

going from arterial to the venous are arranged in series

addition of another resistor in series will always increase the total resistance

they are all reciprocal

the addition of another resistor in parallel will always DECREASE the total resistance.  

viscosity of the fluid

radius

length of the tube

intrinsic elastic recoil

this means that during systole arteries store part of the stroke volume and during diastole use that recoil to release volume making the flow less pulsatile

the difference between systolic and diastolic pressure

mean pressure is the average over the entire period

across arterioles 

this means that this is the major site for vascular resistance

elastiac tapering causing the vessels to become more stiff at the leg

increased systolic pressure at the ankle 20mmHg greater than at the arm.

at low levels of epi, they combine with beta and cause vasodilation

at high levels it combines with both alpha and beta.  The alpha effect predominates and vasoconstriction occurs

it is an intrinsic facto independent of extrinsic controls such as neuron or hormonal influence.

It only oddurs through a range or arterial pressures from 60-140mmHg!

production of NO from L-arginine by the action of nitric oxide synthase.

NO then diffuses into adjacent cells stimulating the production of cGMP -> relaxation

vagus affects heart rate only.  This leads to a change in cardiac output

SNS affects the SV and HR changing cardiac output.  It also increases peripheral resistance.

obtuse marginal (goes towards the post. apex)

posteriolateral branches (go towards the diaphragmatic)

yes

3300 vs 400 mm2

there is approxamately 1 capillary for every muscle fiber

branches between major coronary branch (homocoronary)

or between R and L coronary arteries (intercoronary)

No

coronary circulation exhibits strong autoregulation

at what time only is the subendocardium perfused?

what does this mean for diffusion to the subendo?

diastole

anything that decreases diastolic pressure difference or abbreviates diastole is a potential threat to subendo perfusion and must be countered by coronary vasodilation

10% greater in the subendo than the subepi at rest and exercise

howerever the subendo is at the far end of the coronary artery and if there is a restriction of blood flow, the subendo will become ischemic before the subepi

direct change in pressure difference from inside to outside the heart

an inverse relationship to wall thickness

exhaustion of the vasodilator reserve

increases in flow cause a decreasing pressure distal to the stenosis below the autoregulatory range, which in turn exhausts the vasodilator reserve

with the reserve exhausted, flow is very pressure dependent.  

Any increase in flow across the stenosis futher lowers the pressure available to the microcirculation distal to the stenosis causing O2 demand not to be met -> ischemia and angina

this causes aortic diastolic pressure to be low and LV diastolic pressure to be abnormally high resulting in a compromised pressure gradient for subendocardial perfusion

this is a major problem with patients who already have coronary atherosclerosis

extremely high LV systolic pressure represents high tension development by the myocardium and thus very high oxygen demand.  If demand is not met

 = ischemia

- high myocardial oxygen demand

-low aortic pressure 

- abbrebviation of diastole due to tachycardia

lipid disorders

hypertension

smoking

diabetes

endothelial injury

shear stress is the tangential stress caused by blood flow along the endothelial surface.

Because of chemical irritants, physical stress or altered shear stress, NO production is reduced and results in a prothrombotic state, and altered endothelial permeability allowing the entry of lipoproteins such as LDL, inflammation and smooth muscle cell migration

with CAD what does coronary remodeling do?

what is the dangerous side effect?

to maintain a constant lumen shape with CAD, the coronary remodels itself for compensatory expansion.  This results in elastic lamina fragmentation, extension of the inflammation into the media and degradation of collagen and elastin within the media.

The result is that it becomes vulnerable to rupture because of a thin fibrous cap and intense inflammation

producing proteases such as matrix metalloproteinases which weaken the fibrous cap

also can inhibit matrix production by smooth muscle cells

the plaque core is rich in pro-coagulant tissue factor which can create a thrombus either cause futher constriction of possible embolization

other materials of the plaque can also embolize and travel to various areas causing ischemia

high LDL or it's ApoB protein increase risks

also a low HDL or total cholesterol to HDLc ratio increase risk

CHD

this is even without a history of any symptoms

any combination of the three or more:

central obesity

low HDLc

elevated triglycerides

hypertension

glucose intolerance

frank diabetes

from myoglobin, LDH, Creatine kinase, and troponin I

troponinI is the most specic assay.

this is when a fixed coronary obstruction limits maximal coronary blood flow

YES

This is due to a marked increase in myocardial oxygen damand.

ex:  aortic stenosis

hypertrophic cardiomyopathy

substernal chest pressure or tightness

clench fist over mid-sternum

DYSPNEA

lasts mins not secs.

depressed horizontal or downsloping ST segment

T wave inversion

poor heart rate elevation from rest to exercise

fall in blood pressure DURING exercise

poor heart rate recovery

poor exercise capacity

exercise-induced ventricular tachycardia

exericise capacity

ST segment depression

angina

Nitrates (lower preload)

beta-blockers

Ca channel blockers

plaque disruption most common

less common:

endothelial erosion leading to thrombus formation

intra plaque hemmorhage causing lumen narrowing

>12 hours prior to presentation

the earlier the reperfusion (open the occluded artery) the better outcome

Percutaneous coronary intervention (PCI)

what forms of antiplatelet therapy are always given to patients

aspirin

a theinopyridine (clopidogrel)

anti-thrombotic and anti-platelet therapy 

and antagonists of platelet IIb/IIIa receptor

I_k speed deactivation

increase I_h

increase I_Ca,L

ACh has the opposite on all channels as well as increasing K_ACH to prolong deactivation

it is slow in coming physiologically because there is no direction connection from the SA node

more importantly it is slow because it allows the atria and ventricles to have a coordinated contraction with a pause between the atria and ventricular contraction

.04 seconds horizontally

1mV vertically

I, II and V3-V6

inversion in any of these leads is abnormal

1. determine heart rate

2. determine Rhythm

3.  Determine the QRS axis

4.  Determine the intervals (PR and QT)

5.  Check for abnormalities of the P wave

6.  Check for abnormalities of the QRS

7.  Check for abnormalities of the ST segment and T wave

300 divided by the number of big boxes between R waves, thus 1 box = 300bpm, 2 boxes = 150bpm, etc

or 

1500 divided by the number of small boxes between R waves

1. one p wave before every QRS, and a QRS for every P wave

2.  a heart rate between 60-100

3. normal p wave in lead II

-30 - 90 degrees 

this only occurs when QRS is up in both lead I and II

3-5 boxes (remember how long each box was for time length?)

if there is a long PR interval it indicates a slowed conduction of either hte AV node and/or his-purkinje system 

= 1ST DEGREE AV BLOCK

what can an inverted P wave mean?

where do you look for a normal P wave?

inverted can be a clue that cardiac rhythm does not originate at the SA node

Lead II

1. pathalogic q waves 

2.  measure QRS duration

3.  assess QRS voltage

4. evaluate R wave progression across the precordium

present in leads V1-V3

greater than 1 small box wide

breater than 25% of the amplitude of the corresponding R wave

(the last two must be present in more than 1 lead)

2.5 boxes

over 4 is pathalogical

Enlarged if: ventricular hypertrophy/hypertension, extremely skinny

diminished if: obese, emphysema

in leads V1-V6 R wave amplitude grows

at about V3 S wave is equal to R wave.  If this doesn't happen till V4 or later, then it is "poor R wave progression"

increased myocardia. O2 demand -->

low blood flow & low O2 delivery

supply doesn't = demand

this shows as a depressed ST segment on the ECG

V3 - V4

it requires more force to contract cardiac muscle

it operates over short muscle striation area

prevents overstretching

increases isometric contraction of muscle at a given strength

increases active tension

increased preload leads to an increase in SV but doesn't lead to a higher EF

This happens because even though SV is up, the end systolic volume isn't as low as it would normally be.  (the heart doesn't push out as much blood)

it decreases stroke volume because with a greater afterload there the shortening velocity is less and thus SV is less.

with a lower SV the EF is decreased

AS = hypertrophy

MR = dilation

in stable angina found during exercise stress testing

because subendocardium is the most sensitive to ischemia it is what shows as the downsloping ST segment

Beta blockers

nitrates

aspirin

Ca channel blocker

with people who show inferior STEMI (ST elevation in leads II, III and aVF) what is the most likely cause for the STEMI?

What should be done to confirm this?

occlusion of the R coronary artery causing RV infarction

Leads should be placed on the R side of the body and V4 looked to see if there is ST elevation to diagnose RV infarct

LV hypertrophy

L branch Buncle Block

Early Repolarization

Pericarditis