Most ventricular activity that is recorded is activity in the left ventricle. The same activity gives different shapes in different leads because a wave of depolarization moving toward an electrode will cause an upward deflection on the ECG needle while if depolarization is moving away from an electrode that electrode records a negative wave. Generation of the ECG complexes
Estimating the electrical axis of the heart or the main direction of the cardiac vector
Estimated from the QRS deflection in 2 standard limb leads usually lead 1 & lead 3
Normal electrical axis of the heart +59 degrees [ normal range (-30)-(+110) ]
Visualization of the generation of the Left Ventricular portion of the ECG complex in Lead II 1. Septum depolarizes from the inside out and the resulting depolarization wave moves away from the electrode recording Lead II 2. The rest of the ventricle depolarizes counter-clockwise from the inside out and creates the (large arrow) which is essentially, the algebraic sum of all of the small depolarization vectors. This vector is, in a normal heart, almost always moving directly toward Lead II, generating a mostly positive QRS complex main cardac vector Lead II electrode 60 downward rotation angle from the horizontal 0 o o 60 o Note: compared to the left ventricle, the right ventricle is much smaller and contributes little to the overall main vector of depolarization (DEPOLARIATION)
Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume. The heart can pump a small or a large volume of blood depending on blood reaching it.
Slow heartbeat and exercise increase venous return to the heart, increasing SV
Blood loss and extremely rapid heartbeat decrease SV
Pulses of ultrasound are directed at the blood flowing in ascending aorta & reflected back to the probe by red cells in the blood. The velocity of blood in aorta is measured & if the cross sectional area of aorta is measured by echocardiography the stroke volume & C.O can be calculated
In different parts of the circulation [systemic circulation]
Hemodynamics BLOOD VESSELS: [anatomical & functional classification] A. Arteries (high pressure vessels) [conducting vessels] 1. structure a. thick-walled b. large diameter c. elastic
HEMODYNAMICS B. Arterioles [resistance vessels] . structure a. small diameter b. smooth muscle in wall 1. vasoconstriction, vasodilatation 2. vascular tone . function: to regulate blood flow to capillary beds
HEMODYNAMICS C. Capillaries [exchange vessels] 1. structure a. thin-walled; porous b. narrow c. Large surface area 2. function: exchange 3. capillary blood flow: regulated by presence of a. precapillary spincters
HEMODYNAMICS D. Veins [storage or capacitance vessels] 1. low pressure vessel 2. structure a. large diameter b. distensible c. thin-walled d. Valve 3. function: storage 4. venous return mechanisms a. skeletal muscle pump b. sympathetic vasoconstriction c. Thoracic pump
Blood flow is defined as the quantity of blood passing a given point in the circulation in a given period and is normally expressed in ml/min
Overall blood flow in the total circulation of an adult is about 5000 ml/min … .The cardiac output
FORWARD BLOOD FLOW Mechanisms – Movement of Blood 1.Forces imparted by rhythmic contractions of the heart 2.Elastic recoil of arteries following filling by the action of the heart 3.Squeezing of blood vessels during body movements 4.Peristaltic contractions of smooth muscle surrounding blood vessels 5. Negative I.T.pre.during inspiration
Slight changes in the diameter of a vessel cause tremendous changes in the vessel's ability to conduct blood when the blood flow is streamlined
Although the diameters of these vessels increase only fourfold, the respective flows are 1, 16, and 256 ml/mm, which is a 256-fold increase in flow. Thus, the conductance of the vessel increases in proportion to the fourth power of the diameter
When blood flows through a long smooth vessel it flows in straight lines, with each layer of blood remaining the same distance from the walls of the vessel throughout its length
When laminar flow occurs the different layers flow at different rates creating a parabolic profile
The parabolic profile arises because the fluid molecules touching the walls barely move because of adherence to the vessel wall. The next layer slips over these, the third layer slips over the second and so on.
LAMINAR or STREAMLINE FLOW P 2 P 1 P 1 > P 2 -Cone Shaped Velocity Profile -Not Audible with a Stethoscope
When the rate of blood flow becomes too great, when it passes by an obstruction in a vessel, when it makes a sharp turn, or when it passes over a rough surface, the flow may then become turbulent
Turbulent flow means that the blood flows crosswise in the vessel as well as along the vessel, usually forming whorls in the blood called eddy currents. When eddy currents are present, the blood flows with much greater resistance than when the flow is streamline because eddies add tremendously to the overall friction of flow in the vessel.
All values mentioned for mean blood pressure are for blood vessels at level of heart
Critical closing pressure:
Blood flow stops if the pressure difference between the 2 ends of a vessel is lower than peripheral resistance
Effects of gravity on arterial and venous pressures. Each cm of distance produces a 0.77 mmHg change. Sphincters protect capillaries VENOUS PUMP keeps P V < 25 mm Hg Veins Arteries 190 mm Hg 100 mm Hg 0
Endothelin (ET-1) is a 21 amino acid peptide that is produced by the vascular endothelium from a 39 amino acid precursor, through the actions of an endothelin converting enzyme (ECE) found on the endothelial cell membrane. ET-1 formation and release are stimulated by angiotensin II antidiuretic hormone (ADH) , thrombin, cytokines, reactive oxygen species, and shearing forces acting on the vascular endothelium. ET-1 release is inhibited by prostacyclin and atrial natriuretic peptide as well as by nitric oxide .
Once ET-1 is released by the endothelial cell, it binds to receptors on the target tissue (e.g., adjacent vascular smooth muscle). There are two basic types of ET-1 receptors: ET A and ET B . Both of these receptors are coupled to a G-protein and the formation of IP 3 . Increased IP 3 causes calcium release by the sarcoplasmic reticulum, which causes smooth muscle contraction . In blood vessels, the ET A receptor is dominant under normal conditions in terms of ET-1 effects on contraction.
Released in response to high blood flow rate and signaling molecules (Ach and bradykinin)
Highly localized and effects are brief
If NO synthesis is inhibited, blood pressure rises
During O2 delivery, NO locally dilates blood vessels to aid in gas exchange
Nerve cells target the endothelial cells lining of blood vessels Acetylcholine activates NO synthase & production of NO in endothelial cells that surround the smooth muscle cells surround the blood vessel. Role of NO in smooth muscle relaxation of blood vessel walls
NO diffuses into smooth muscle, binds to heme group in guanylyl cyclase and activated synthesis of cGMP Nitroglycerin is used to prevent chest pain (angina) because it is rapidly converted to NO
Synthesis & release of nitrous oxide (NO) Nitric oxide synthase (NOS) catalyzes the synthesis of NO from the terminal nitrogen atom of L-arginine in the presence of O2 Once synthesized, NO can freely diffuse across plasma membranes reaching neighboring cells NO acts locally, and has a very short half-life (5-10 secs)