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Jugular venous distention (JVD) or jugular venous pressure (JVP) focuses on the right atrium and not any other part of the heart because the right subclavian vein and the right internal jugular vein are directly connected to the right atrium.
Now, we don't look for distention in the external jugular vein because internal jugular vein is very superficial and the external jugular vein has valves in it, hence, doesn't accurately reflect the pressure of the right atrium. The distance between the right atrium and the sternum is about 5 cm and normal pressure of the right atrium is somewhere between 5-8 cm of water. We need to look for certain wave forms in internal jugular venous distention; these waveforms only represent pressure in the right atrium and nothing else. Abdominojugular reflux, also known as hepato-jugular reflux, is one of the signs used to diagnose right-sided heart failure when other CHF signs and symptoms are in the grey zone. Cross-section of Artery & Vein Figure 11.9a Assume you are viewing a blood vessel under the microscope. Figure 11.9a Arteries are much closer to the pumping action of the heart and must be able to withstand the pressure fluctuations at such locations.
Arteries are often described as vessels that carry oxygen-rich blood, and veins are said to carry oxygen –poor (carbon dioxide-rich) blood.
Describe the structure of capillary walls Capillary walls are essentially just the tunica intima (endothelium plus the basement membrane); thus, they are exceedingly thin. Figure 11.12 Left ventricle to ascending aorta ? aortic arch ? brachiocephalic artery ? subclavian artery ? axillary artery ? brachial artery ? radial (or ulnar) artery ? capillary network of wrist ? radial (or ulnar) vein ? brachial vein ? axillary vein ? subclavian vein ? right brachiocephalic vein ? superior vena cava ? right atrium of the heart.
Figure 11.12 Left ventricle ? ascending aorta ? aortic arch ? descending aorta ? right common iliac artery ? external iliac artery ? femoral artery ? popliteal artery ? anterior tibial artery ? dorsalis pedis artery ? capillary network ? ? anterior tibial vein ? popliteal vein ? femoral vein ? external iliac vein ? common iliac vein ? inferior vena cava ? right atrium of the heart.
Which vessel – the hepatic portal vein, hepatic vein, or hepatic artery- has the highest content of nutrients after a meal?
What is the different about the capillary exchanges seen in a capillary with fenestrations and intracellular clefts and the exchanges seen in a capillary lacking those modifications? Would you expect fluid to be entering or leaving the capillaries at the venous end of a capillary bed?
What is the relationship between cross-sectional area of a blood vessel and velocity (speed) of blood flow in that vessel? Which type of blood vessel is most important in regulating vascular resistance*, and how does it achieve this?
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Drug-Induced Lowering of High Arterial Blood Pressure and Cardiovascular Morbi-Mortality – Existence of a Preferential Effect on the Cerebral Circulation?
The question then arose as to whether there was any difference amongst the different antihypertensive drugs. The MRC trial was one of the few trials to compare the effects of two different drugs – benzofluazide, a diuretic, and propranolol, a beta-blocker. The fact that lowering blood pressure with a wide range of drugs with very different mechanisms of action has a beneficial effect on stroke occurrence, would argue that the important factor is lowering blood pressure rather than the pharmacological way in which this is done (Figure 1). Albeit in other trials the results on the relative risk for strike were in favor of the ACEI.
Following the establishment of ACEIs as effective and safe antihypertensive drugs with potential protective effects on the vasculature, angiotensin II type 1 receptor antagonists (ARB) were introduced. Debate continues over whether a certain mechanism of action (in this case blockade of the RAAS) confers additional beneficial impact on cardiovascular morbi-mortality over and above the reduction in blood pressure (Figure 1). Bi- and tri-therapy regimens have been used in the treatment of high arterial blood pressure for several decades.
An original approach using combinations of drugs that act on the same pharmacological system has been proposed (Unger, 2002). In the ONTARGET clinical trial (The ONTARGET Investigators, 2008) telmisartan (ARB) was combined with ramipril (ACEI) again on the basis that an ACEI does not completely block the RAAS so addition of an ARB may be beneficial.
The work of Goldblatt and others (Katz et al., 1939) in the early 1930s suggested that the link between renal ischemia provoked, for instance, by renal artery stenosis was renin. At this time work was being carried out simultaneously on the first ACEI (teprotide, the peptide from the venom of the snake, Bothrops jararaca) and the first ARB (the peptide analog of angiotensin II, saralasin).
Albeit, research on renin inhibitors did not cease and in the 1990s Novartis, Switzerland developed an orally active renin inhibitor, aliskiren.
It is interesting to note that in the above trials on renin inhibition, dual RAAS blockade discussed previously is in fact being used: the renin inhibitor is added onto existing treatment with an ACEI or an ARB. In parallel to blocking the RAAS cascade at the summit (with a renin inhibitor) there may be a case for blocking the system at the lowest level of the cascade of active products – aldosterone. On the basis of the argument it has been postulated that aldosterone acts strictly as a mineralocorticoid hormone on renal and other epithelia, to maintain electrolytic homeostasis (Delyani et al., 2001). In clinical trials on stroke, parameters such as occurrence, survival, and recurrence are measured. Such observations raise another question regarding the risks and benefits of lowering blood pressure below classical normotensive goals. With aging and cardiovascular disease such as hypertension, the elastic properties of large central arteries change leading to stiffening of the wall. Angiotensin I converting enzyme inhibitors may be useful in this context as they appear to protect the elastic fiber network of the arterial wall and reduced the age-related increase in wall stiffness (Figure 4).
Analysis of RAAS gene polymorphisms may provide information for a targeted pharmaco-genomic approach to stroke prevention. The important issue in antihypertensive therapy is whether the latter prevents target organ damage in the brain, kidney, and other vascular beds. The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. JVP and JVD are stated as "JVD is 10 cm above the right clavicle." We always look for JVD on the right side of the neck with the patient sitting at an angle of 45 degrees. This means that the right internal jugular venous distention 3 cm above the right clavicle is normal and anything beyond 3 cm is abnormal.


When a patient sitting at an angle of 45 degrees takes a deep breath, take a look at the upper limit of the JVD; if it increases, it is indicative of constrictive pericarditis.
Suppose a patient presents with normal CVP, paroxysmal nocturnal dyspnea, suspicious pedal edema, and JVD of 2 cm above the clavicle (which may be normal) and you're determined that the patient has congestive heart failure. Please do not duplicate the contents of this page in whole or part, in any form, without prior written permission.
Blood Vessels: The Vascular System Transport blood to the tissues and back Carry blood away from the heart Arteries Arterioles Exchanges. Tunica mediaA middle layer, consisting of smooth muscle and connective tissue (primarily elastic fibers) The smooth muscle is activated by the sympathetic nervous system when vasoconstriction (and increases in blood pressure) is desired.
The hepatic portal vein carries nutrient-rich blood from the digestive viscera to the liver for processing before the blood enters the systemic circulation. Blood flow in arteries is pulsatile because it is under a greater amount of pressure compared to veins. The greater the cross-sectional area in a blood vessel, the faster that blood can flow through that vessel. Arterioles are the blood vessels that are most important in regulating vascular resistance.
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It first looks at whether there exists a preferential effect on the cerebral circulation during a drug-induced lowering of high arterial blood pressure and cardiovascular morbi-mortality. In this trial stroke was lower on active treatment but there was no difference in overall rates of coronary events. This is backed up by epidemiological data showing that stroke occurrence, survival and recurrence are all affected by high blood pressure (Sacco et al., 1982).
Possible pressure-dependent (A) and pressure-independent (B) effects of antihypertensive drugs on the cerebral circulation and stroke. Were ACEIs safe drugs compared to the well-known conventional treatment available at the time (with diuretics and beta-blockers)? The two regimens did not differ in preventing cardiovascular morbi-mortality excepting that stroke was apparently more common with captopril. However no significant benefit was seen in the primary outcome and side effects such as the risk of hypotension and hyperkalemia were more marked. Building on this, the group of Page and Helmer at Lilly, USA provided evidence of the existence of an endogenous inhibitor for renin (Page and Helmer, 1940) and this stimulated research on the use of a renin inhibitor for the treatment of high blood pressure.
The RAAS presents evolutionary duality with the appearance firstly of a blood pressure regulatory system (using angiotensins) followed by the evolution of a regulatory system for sodium metabolism (using aldosterone; Withers, 1992).
However, already in the 1970s it was suggested that aldosterone may play a negative role in vascular diseases such as stroke (Brunner et al., 1972). In the APRIL study, normotensive rats were treated from the age of 6 through 30 months with a hypotensive dose of the ACEI, perindopril, that lowered DBP from 90 to 80 mmHg (Lartaud et al. Increases in arterial distensibility produced by the ACEI, lisinopril (recalculated and redrawn from Makki et al., 1994). The MOBILIZE Boston study (Hajjar et al., 2010) revealed that the angiotensinogen gene may be involved in cerebrovascular reactivity independently of blood pressure. This review looks at the preclinical and clinical evidence suggesting that drugs acting via inhibition of the RAAS have a cerebrovascular protective effect.
As the right atrium contracts, blood moves from right atrium into the right ventricle and the pressure in right atrium decreases producing a negative waveform called the x-wave. Now, the first symptom of CHF is paroxysmal nocturnal dyspnea but the first sign of CHF is abdominojugular reflux. Material contained herein may not be broadcast, published, redistributed or rewritten, and may not, in any way or form, be constructed as professional advice. Blood pressure in veins is much lower in arteries because veins are farther along in the circulation pathway.
Figure 11.16 The hepatic portal circulation carries nutrient-rich blood from the digestive viscera to the liver for processing before the blood enters the systemic circulation. Arteries are located closer to the ventricles, so their walls must be capable of expanding and contracting under the changes in pressure when the ventricles contract. Smaller vessels, like capillaries, are only one cell thick in diameter, which slows down blood flow and allows nutrient and gas exchange to occur. These vessels can constrict as a result of activity from the sympathetic nervous system, which alters blood pressure. Since the mother’s liver is working for the fetus as well, the entire fetal liver need not be continuously suffused with blood.
It then goes on to consider background studies on the relationship between inhibition of the RAAS and stroke. Thus from an early date it appeared that antihypertensive treatment could have a beneficial effect on the cerebral circulation – and that this effect was (perhaps) greater than that on other circulations such as the coronary. If ACEIs were safe to use then was their effect on cardiovascular morbi-mortality as large as (or greater than) that obtained with conventional therapy? The authors argued that the beneficial effect of ramipril was linked to inhibition of the RAAS or to some other effect of ramipril unrelated to lowering of blood pressure.
Thus ACEIs or ARBs that block the RAAS are combined with diuretics that lower blood pressure by causing the body to rid itself of excess fluids and sodium (whilst at the same time activating the RAAS).
When a combination of low doses of enalapril (ACEI) and losartan (ARB) was given to SHR, a synergistic effect on blood pressure and left ventricular hypertrophy was observed and this was attributed to more effective inhibition of the RAAS (Menard et al., 1997).
Gross and others showed that renin inhibitors such as the Streptomyces pentapeptide, pepstatin, would lower blood pressure in animal models (Lazar et al., 1972).
In the pharmaco-chemical race to find therapeutically usable analogs, ACEI research came in first with captopril, and from then on, interest waned in other forms of peptide research in the RAAS such as the research on renin inhibitors.


Thus although the RAAS is absent in cyclostomes and elasmobranchs, juxtaglomerular cells are present in other chondrichthyean fish and all other vertebrates. In this trial treatment with an ACEI, perindopril, plus a diuretic, indapamide, reduced stroke risk in the non-hypertensive group. This can be important in vascular beds with low flow resistance and torrential flow such as that of the brain (O’Rourke and Safar, 2005).
Whilst a case can be made for this hypothesis, the latter should be strengthened by further evidence from clinical trials. Effects of suboptimal doses of the AT1 receptor blocker, telmisartan, with the angiotensin-converting enzyme inhibitor, ramipril, on cerebral arterioles in spontaneously hypertensive rat. As pressure in the right atrium becomes less than pressure in the right ventricle, the tricuspid valve cusp closes and pushes into the right atrium producing a positive wave called the c-wave.
In the abdominojugular reflux test, you place your palm on the patient's abdomen and apply pressure for about 10 seconds.
Umbilical arteries carry oxygen-poor blood from the fetus and the umbilical vein carries the most oxygen-rich blood to the fetus. A portal circulation involves a capillary bed that is both fed and drained by veins; the usual circulation has a capillary bed that is fed by arteries and drained by veins. This is followed by exploration of possible new directions in the inhibition of the RAAS and its effect on stroke. This may have given an overall antihypertensive dose that was too high, thus producing side effects and masking the potentially beneficial synergism. The macula densa, however, appears later in some amphibia and higher tetrapods, suggesting that it evolved at a more advanced stage. Recently our group has detected an inverse linear relationship between plasma aldosterone levels and the diameter of the cerebral arteriole in SHR (Figure 3). In most laboratory animal models cerebral ischemia is induced by various means such as surgical stenosis. Cerebrovascular dysfunction in old rats as evaluated by an increase in the lower limit of autoregulation of cerebral blood flow, was corrected by ACEI treatment.
Exposure of small vessels to highly pulsatile pressure and flow can lead to structural modification and microvascular damage.
ACE was inhibited in a dose-related fashion but the low dose treatment did not significantly modify systolic blood pressure (A). Again the question remains open as to whether future research will reveal RAAS gene polymorphism linked to stroke that could form the basis of pharmaco-genomic treatment with inhibitors and antagonists of the RAAS.
Furthermore a deeper investigation into the predictability of animal models of hypertension when used to test drugs and elaborate mechanisms is required. Possible pathophysiologic mechanisms supporting the superior stroke protection of angiotensin receptor blockers compared to angiotensin-converting enzyme inhibitors: clinical and experimental evidence. Now, the right atrium is empty and sucks in venous blood from IVC and SVC producing the positive v-wave. In normal individuals, this maneuver doesn't change the jugular venous pressure, however, can increase upper venous pulsation in individuals with right heart dysfunction.
Sympathetic nerve fibers secrete norepinephrine to receptors on the smooth muscles of arterioles causing contraction and thus leads to vasoconstriction.) Atherosclerosis in these vessels also causes narrowing due to plaque deposits, which also affects blood pressure Arterioles are the blood vessels that are most important in regulating vascular resistance.
Three vessels travel in the umbilical cord; which of these carries oxygen and nutrient rich blood.
Thus the RAAS may have evolved as a blood pressure regulatory system with sodium regulation developing later. Arguments are emerging therefore, that suggest the mineralocorticoid receptor as a potential therapeutic target for stroke prevention (Osmond et al., 2008). Thus frequency of occurrence of stroke is by definition 100% and other parameters such as neurological performance are measured.
Arterial stiffness (judged from the relationship between pulse wave velocity and mean blood pressure) was reduced in a dose-dependent fashion (B) and this was probably due in part to a reduction in the loss of thickness of arterial elastic fibers with age (C).
Reduced cardiovascular remodelling and functional impairment in spontaneously hypertensive rats following combined treatment with suboptimal doses of telmisartan and ramipril: is less really more?
The angiotensin I converting enzyme inhibitors captopril and Wy-44,655 attenuate the consequences of cerebral ischemia in renovascular hypertensive rats.
Now, the pressure in the right atrium increases and blood spills into the right ventricle producing a y-wave. Cardiovascular morbidity and mortality in the losartan intervention for endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol. Effects of intensive blood-pressure lowering and low-dose aspirin in patients with hypertension: principal results of the Hypertension Optimal Treatment (HOT) randomised trial.
The most common cause of a positive abdominojugular reflux test is right heart failure secondary to elevated left heart filling pressures. Thus our group has shown that the ACEI captopril will improve neurological performance following induced ischemia in renovascular hypertensive rats (Capdeville et al., 1990). Effect of angiotensin-converting enzyme inhibition combined with conventional therapy on cardiovascular morbidity and mortality in hypertension: the Captopril Prevention Project (CAPPP) randomised trial. Right ventricular infarction, constrictive pericarditis, and restrictive cardiomyopathy are also common causes of a positive abdominojugular reflux.
The umbilical vein carries nutrient-rich and oxygen- rich blood to the fetus through the umbilical cord. Short-term reductions in blood pressure: overview of randomised drug trials in their epidemiological context. Although the translation of such beneficial structural and functional effects in an animal model into a beneficial effect on stroke in man is debatable, on the basis of these results and those of Menard et al.



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