Electrical and Mechanical Properties of Heart (revision)

Before understanding how ECG works:

Electrical Properties of heart:

1. Autorhythmicity
The ability to generate action potentials without external stimulus
•spontaneous pre-potential (pacemaker potential) followed by action potential.
•Pacemaker tissue (sino atrial node, atrio ventricular node, atrio ventricular bundle and purkinje fibers) can initiate repetitive action potentials.
•Pacemaker tissue is characterized by unstable resting membrane potential because of its continuous change in membrane permeability.





Pre-potential:
Slow decrease in K+ efflux while permeability of other ions remain constant (through ‘h’ channels and transient ‘T’ Ca2+ channels).

Depolarization:
Ca2+ influx through long lasting Ca2+ channels ( ‘L’ )

Repolarization:
K+ efflux.

Rate of Impulse (per min):
SA node--70-100
AV node--40-60
Atrial and atrial pathway--20-40
Purkinje fibers--20-40

2. Excitability:
Cardiac muscle is excitable tissue
-->it forms a wave of depolarization in response to a stimulus(generation of AP)

0: Rapid depolarization.
Opening of Na+ channels causes increase in Na+ influx.

1: Rapid initial fall in membrane potential (initial rapid repolarization)
Inactivation of Na+ channels.

2: Plateau phase.
Slow opening of Ca2+ channels causes Ca2+ influx.

3: A rapid fall in membrane potential (repolarization phase)
Opening of K+ channels causes rapid K+ efflux.

4: Polarised state.
Ionic composition is restored by activation of Na+K+ATPase pump

3. Conductivity
the ability of cardiac muscle fibers to conduct the cardiac impulses that are initiated in the SA node.

• Impulse from SA node spread quickly to AV node via atrial (internodal) pathway.
• Time delay (0.1 s) occurs as impulses pass through AV node.
• Impulse conduction increases as spread to Purkinje fibers at a velocity of 4 m/s.
• Ventricular contraction begins 0.1-0.2 s after contraction of the atria. (important for ventricular filling phase)
• LBB starts before RBB, as LV wall is thicker so the impulse needs more enough time to reach. Accordingly both ventricles will contract together.

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Electrical activity of the heart:
1. Depolarization and origin of cardiac impulse at the SA node. (if SA node doesnt work, AV will take place of being the pacemaker)

2. Conduction of the impulse to all parts of the atria through atrial muscle (there may be some special pathways that conduct impulse fast ie. have a higher conduction velocity). The impulse also spreads to the AV node along the atrial muscle. (Atrial fibrillation occurs when the atrial ms contract independently and continuously bombard AV node with depolarizing waves of varying strength, and depolarization spreads at irregular intervals down the Bundle of His)

3. The impulse will not pass from atrial muscle to ventricles directly as they are not in contact (fibrous tissue separates them). (thus if AV node is blocked, and impulse from SA node couldnt reach ventricle, ventricular muscle will initiate its own impulse as it also has autorhythmicity, eg. seen as AV dissociation on ECG)

4. AV node has a low conduction velocity and thus the impulse takes sometime to travel across it. It eventually travels across it and reaches the upper end of the bundle of His.

5. Bundle of His has a high conduction velocity. It conducts the impulse through its branches to the Purkinje fibre network just under the endocardium of the ventricles. (In a normal conditionn where impulse is able to be transmitted from AV node to Bundle of His, impulse created by ventricular muscle itself doesnt cause muscle contraction as the impulse hits the absolute refractory period--all/none law of the action potential of cardiac muscle that is stimulated by normal conduction system's impulse)



*atrial repolarization not seen on ECG as it was masked by the stronger ventricle depolarization

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Mechanical Properties of the heart:

1. Contractility
---when an action potential occurs in the muscle it responds by contraction.
During excitation-contraction coupling the ER releases some Ca++ ,but to have sufficient calcium for contraction there must be influx through the sarcolemma. Hence the importance of the plateau phase of the action potential.

• For cardiac muscle, the amount of stretch of the muscle before a contraction has special significance and is called preload (Starling Law).
• Protected from tetanus because of its long ARP
• No recruitment of cardiac muscle fibers.
• Strength of contraction of cardiac muscle depends to a great extent on the concentration of calcium ions in the ECF

2. All or None Law

• Action potential of cardiac muscle is an all or none law response to a stimulus.
• If the stimulus is sub-threshold (inadequate), no action potential is produced.
• If the stimulus reaches threshold, a full-fledged action potential is produced.
• Further increase in the intensity of a stimulus produces no increment in the amplitude of AP.

Absolute refractory period:

• The excitability of cardiac muscle is completely lost during this period, i.e. doesn’t respond to 2nd stimulus.
• Occupies the whole period of systole.

Relative refractory period:

• The excitability of cardiac muscle is partially recovered during this period, i.e. stronger stimuli than normal are required to excite the muscle.
• Occupies the time of diastole.
• Can be affected by the heart rate, temperature, vagal stimulation, sympathetic stimulation & drugs.

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Factors affecting heart rate:

1. Sympathetic stimulation

Act via β1-adrenergic receptors -->increase cAMP-->Increases heart rate by opening of Ca2+ channels--> increase Ca2+ influx-->increase rapidity of the depolarization phase--> increase heart rate (positive ‘chronotropic’ effect)

2. Vagal stimulation

Acts via M2 muscarinic receptors -->decreasing cAMP-->Decreases heart rate by opening of K+ channels and slows the opening of Ca2+ channels --> increase K+ efflux of nodal tissues -->hyperpolarization --> decrease slope of pre-potentialp--> decrease firing rate--> decrease heart rate (negative ‘chronotropic’ effect)

3. Temperature

Arise in body temperature by 1 °C increases the heat rate by 10 beats/minute.

The rise in body temperature increase the heart rate by increasing the permeability of the membrane to Ca++ during the pacemaker potential.

4. Sinus arrhythmia

Variation in R-R interval during deep inspiration.

During deep inspiration, lung stretch--> inhibits cardio-inhibitory center-->decreases tonic vagal discharge -->increases HR.

5. Ion concentration in ECF

K +

-the early effect of mild hyperkalemia on myocyte function is to increase myocyte excitability by shifting the resting membrane potential to a less negative value and thus closer to threshold potential; but as potassium levels continue to rise, myocyte depression occurs and Vmax continues to decrease.

A plasma potassium of >6.5mmol/L (normal 3.5-5.5) is an emergency, myocardial hyperexcitability--> ventricular fibrillation--> cardiac arrest

5.5-6.0 mEq/L - Mild


6.1-7.0 mEq/L - Moderate


7.0 mEq/L and greater - Severe

Sx: fast irregular pulse, chest pain, weakness, palpitation, and light-headedness

ECG: Tall tented T wave, small p wave, wide QRS complex

Causes:

Decreased or impaired potassium excretion - As observed with acute or chronic renal failure (most common), potassium-sparing diuretics, urinary obstruction, sickle cell disease, Addison disease, and systemic lupus erythematosus (SLE)


Additions of potassium into extracellular space - As observed with potassium supplements (eg, PO/IV potassium, salt substitutes), rhabdomyolysis, and hemolysis (eg, blood transfusions, burns, tumor lysis)


Transmembrane shifts (ie, shifting potassium from the intracellular to extracellular space) - As observed with acidosis and medication effects (eg, acute digitalis toxicity, beta-blockers, succinylcholine)


Fictitious or pseudohyperkalemia - As observed with improper blood collection (eg, ischemic blood draw from venipuncture technique), laboratory error, leukocytosis, and thrombocytosis

Management:

Urgent:

• Stabilize Cardiac membrane with 10ml 10% calcium gluconate
• drive K+ into cell with 10 units actrapid in 50ml 20% glucose

Non-urgent: (K+ not >6.5, no myocardial hyperexcitability)

• Treat underlying causes.
• Polystyrene sulfonate resin 15g/8h PO

Ca2+ ion in ECF

• Increase in Ca2+ concentration --> increase cardiac contractility
• Decrease in Ca2+ concentration --> decrease cardiac contractility

6. Blood flow

Insufficient blood flow--> decreased oxygen and nutrient supply--> decreased heart conductivity and metabolism

7. Drug

Sympathomimetic drug--> increased HR 

parasympathomimetic drug--> reduce HR

Varicose Vein and Examination

Normal Venous Circulation in Leg

Two venous systems are found in the lower extremity, the deep and superficial, as depicted in the image below. The deep system ultimately leads backs to the inferior vena cava, then to the heart. The superficial system is found above the deep fascia of the lower extremity, within the subcutaneous tissue. Many superficial veins exist, but they all drain into the 2 largest superficial veins, the greater saphenous vein (GSV) and the short saphenous vein (SSV), formerly called the lesser saphenous vein.



The superficial venous system is connected to the deep system at a number of the following locations:

• Perforator veins: These veins traverse the deep fascia of the lower extremity. A number of named perforators are found at the thigh, knee, and leg.

• Saphenofemoral junction (SFJ): This is located proximally at the groin where the GSV meets the femoral vein, as depicted in the images below.

• Saphenopopliteal junction (SPJ): This is located behind the knee where the SSV joins with the popliteal vein.

In healthy veins, the flow of venous blood is through the superficial system into the deep and up the leg and toward the heart. One-way venous valves are found in both systems and the perforating veins. Incompetence in any of these valves can lead to a disruption in the unidirectional flow of blood toward the heart. In 53% of patients only superficial venous reflux was found, in 15% isolated deep venous reflux was found, and in 32% a combination of deep and superficial venous reflux was found.

Incompetence in the superficial venous system alone usually results from failure at valves located at the SFJ and SPJ. The gravitational weight of the column of blood along the length of the vein creates hydrostatic pressure, which is worse at the more distal aspect of the length of vein.

Incompetence of the perforating veins leads to hydrodynamic pressure. The calf pump mechanism helps to empty the deep venous system, but if perforating vein valves fail, then the pressure generated in the deep venous system by the calf pump mechanism are transmitted into the superficial system via the incompetent perforating veins.




Once venous hypertension is present, the venous dysfunction continues to worsen through a vicious cycle. Pooled blood and venous hypertension leads to venous dilatation, which then causes greater valvular insufficiency. Over time, with more local dilatation, other adjacent valves sequentially fail, and after a series of valves has failed, the entire superficial venous system is incompetent.





The clinical finding of varicose veins, reticular veins, and telangiectasia are due to the hypertension in the superficial venous system that spreads to collateral veins and tributary veins.

In contrast to the superficial veins, the deep veins do not become excessively distended. They can withstand the increased pressure because of their construction and the confining fascia.

Examination of Varicose Vein

Perthes maneuver/Linton test: This is a physical examination technique in which a tourniquet is placed over the proximal part of the leg to compress any superficial varicose veins while leaving deep veins unaffected. The patient walks or performs toe-stands to activate the calf-muscle pump which normally causes varicose veins to be emptied. However, if obstruction of the deep system exists, then activation of the calf-muscle pump causes a paradoxical congestion of the superficial venous system and engorgement of varicose veins resulting in a positive test. To verify, the patient is then placed supine, and the leg is then elevated (Linton test). If varices distal to the tourniquet fail to drain after a few seconds, again deep venous obstruction must be considered.





Once the dilated veins of the leg are marked, the Brodie-Trendelenburg test can be performed. With the patient in the supine position and the leg elevated 60°, emptying the varices of blood by stroking distally to proximally is performed, and a tourniquet is placed around the proximal thigh. The patient then stands up, and the leg is observed for 30 s with the tourniquet in place. The following responses can be seen:

• “Nil” test: (Competent valves of the deep and perforating veins and at the saphenofemoral junction): No distention of the veins for 30 s both with the tourniquet in place and after removal
• “Positive” test: (Incompetent valve at the saphenofemoral junction): Distention of the veins only after release of the tourniquet
• “Double” positive test: (Incompetent deep and perforating veins, with reflux through the saphenofemoral junction): Distention of veins with the tourniquet in place and further distention after release
• “Negative” test: (Deep and perforating valvular insufficiency): Distention of veins within 30 s of the tourniquet in place, and no increased filling after release of the tourniquet. However, filling of the vein(s) after 30 s of tourniquet placement does not imply competence of perforating veins.

The percussion/Schwartz test is performed by placing one hand over the saphenofemoral junction or the saphenopopliteal junction while the other hand is used to tap lightly on a distal portion of the long or short saphenous vein. The presence of an impulse implies valvular insufficiency in the segment between the two hands.




Morrisey’s Cough Impulse test

1. Ask patient to stand.
2. Use finger to held over patient's saphenofemoral opening [5cm below and medial to femoral pulse].
3. Ask patient to cough.
4. If saphenofemoral junction is incompetent, there is presence of fluid thrill.

Fegan’s test




Pratt test
The Pratt Test is a simple test to check for Deep Vein Thrombosis in the leg. It involves having the patient lie supine with the leg bent at the knee, grasping the calf with both hands and pressing on the popliteal vein in the proximal calf. If the patient feels pain, it is a sign that a DVT exists.


Multiple Tourniquet Test

*Do not confuse Trendelenburg Test with Multiple Tourniquet Test

Trendelenburg test is to apply one tourniquet below (for example SFJ). If during the tourniquet is applied, there is filling of varicose vein(which you had just emptied before the test), it means the pt’s perforating vein is incompetent, blood flow from deep vein to superficial vein. If after applied, no filling, and when you release the tourniquet and there is filling, it means the SFJ above your tourniquet is incompetent and cause downward flow of blood because of the gravity. However,

For multiple tourniquet test, it is simply used to test perforating veins, so don’t think about the superficial vein. Multiple tourniquets are applied to occlude the superficial vein at different area. For example one at the mid thigh and one above the knee. So normally when without tourniquet, if blood flow from the incompetent perforating vein to superficial vein, it might flow downward when it’s in the superficial vein(if there is further incompetent valve), or it will be carried upward to the SFJ and so on…

So applying tourniquet is to occlude the superficial vein above and below the area which the perforator vein has problem. So that we can see the pooling of blood at the varicose vein there(remember that you already empty the varicose vein before the test by elevate leg and also rub the veins).


So for multiple tourniquet, the result is not to be acquired by releasing the tourniquet, but is during which the tourniquets are applied. So, for my personal opinion, it doesn’t matter whether you remove them from bottom to above or from above to bottom.


The purpose of doing all these tests is to determine the area so as to perform surgery on the problem veins. But these tests are not so important nowadays provided that technology such as colour flow imaging, magnetic resonance venography can already help to give a better image. Varicose veins can cause complications such as ulcers beside just comestically undesirable. So, sometimes surgery to take out the varicose vein is necessary. However, nowadays, other methods such as sclerotherapy is also used.

Adapted from: Medscape and Some old surgery books

Ankle Brachial Index (Mr.Foot and Mrs.Arm has different opinions on SBP)

What is Ankle Brachial Index?

The Ankle Brachial Index (ABI or ABPI) is the ratio of the blood pressure in the lower legs to the blood pressure in the arms. Compared to the arm, lower blood pressure in the leg is an indication of blocked arteries (peripheral vascular disease or PVD). The ABI is calculated by dividing the systolic blood pressure at the ankle by the systolic blood pressures in the arm.



risk factor for atherosclerosis:

Etiology:



Causes of Peripheral Vascular Disease:
1. Artheriosclerosis (also will develop in carotid or coronary artery, increase risk for stroke or heart attack)
Known first for pain in leg when exercising or walking(Intermittent claudication)

2. Diabetes Mellitus (There are FIVE pathway for pathogenesis of Macro and Microvascular diseases)

Treatment of PVD:
1. Cessation of smoking
2. Controlling high BP
3. Statins/Lipid level control
4. Dietary changes
5. Exercise
6. Diabetic control
7. Surgery

Pain of PVD can range from mild pain when exercise to severe pain even at rest. PVD limit the ability to exercise. Also can leads to sores and ulcers at leg that do not heal in critical limb ischemia that cause gangrene and require of amputation.

Stroke and heart attack are the most serious and common complication.

Over 5 years period, PVD sufferers
20% sustain stroke
30% fatal event

Critical Limb Ischaemia
30%- amputations
20%-dead

How to perform ABI test?
Things you need:
Doppler, Sphygmomanometer, Gel
Makes sure patient is warm and rest 10-15mins before begin
Measure all the 4 limbs SBP(posterior tibialis and brachial), take the highest reading

See here: http://www.youtube.com/watch?v=LvHeMiCaUdw

AHA ABI Interpretation:
Greater than 1.3, noncompressible arteries, obtain toe pressure
1.00-1.29, normal
0.91-0.99, appears normal, but exercise reveals low degree of obstruction
0.41-0.90, mild to moderate PAD (will experience intermittent claudication when they walk or exercise)
0.00-0.40, rest pain, failure for healing of injury to foot or toe

ABI provides 3 info:
1. Doppler sound
2. Index
3. Waveform

Normal young healthy have triphasic waveform
Biphasic: mildly abnormal
Monophasic progressive disease







People particularly at risk for PAD:
-->less than 50 years of age with DM and one other risk factor for atherosclerosis: HPT, Dyslipidemia, Smoking or Hyperhomocysteinemia

-->age 50-69, hx of diabetes or smoking

-->70 or older

-->leg symptoms upon exertion, intermittent claudication/ischemic rest pain

-->abnormal leg, ankle or foot pulse examination

-->known atherosclerotic carotid, coronary or renal artery disease

-->Psoriasis increase risk of PAD, MI or CVA

Not all people with PAD are symptomatic, only 10 percent have the classic symptoms of intermittent claudication

Adapted from:
Youtube; Vascular Hokanson Channel; How to do ABI
http://360woundcare.wordpress.com/category/uncategorized/
Netter Cardiology Images