The jugular venous pulse/pressure (JVP)is a favourite topic on the wards!
The jugular veins fill with blood and pulsate in relation to filling in the right atrium. Since the JVP correlates well with central venous pressure, it’s used as an indirect marker of intravascular fluid status.
Traditionally, the right internal jugular (IJ) vein is used in JVP measurement; it’s preferred since it is directly in line with the superior vena cava and right atrium. The external jugular (EJ) vein is not commonly used to assess the JVP because it has more valves and an indirect course to the right atrium, but EJ is easier to see than IJ, and JVP measurements from both sites correlate fairly well. The left-sided jugular veins are also uncommonly used, since they can be inadvertently compressed by other structures and thus be less accurate!
Learners on the ward are often asked how to identify the JVP and distinguish it from carotid artery pulsations. The mnemonic POLICE describes the distinguishing features of the JVP:
Palpation: The carotid pulse is easy felt but the JVP is not.
Occlusion: Gentle pressure applied above the clavicle will dampen the JVP but will not affect the carotid pulse.
Location: The IJ lies lateral to the common carotid, starting between the sternal and clavicular heads of the sternocleidomastoid (SCM), goes under the SCM, and when it emerges again can be followed up to the angle of the jaw. The EJ is easier to spot because it crosses SCM superficially.
Inspiration:JVP height usually goes down with inspiration (increased venous return) and is at its highest during expiration.
(Kussmaul’s Sign describes a paradoxical rise in JVP during inspiration that happens in right-sided heart failure or tamponade)
Contour: The JVP has a biphasic waveform, while carotid pulse only beats once.
Erection/Position:Sitting up erect will drop the meniscus of the JVP, while lying supine will increase filling of the JVP.
To measure the JVP, the patient lies supine in bed at a 30 – 45 degree angle, with their head turned slightly leftward and jaw relaxed. A hard light source (e.g., penlight) pointed tangential to the patient’s neck will accentuate the visibility of the veins. Once the highest point of JVP pulsation is seen, measure high how it is at its maximum, in terms of centimeters above the sternal angle (aka Angle of Louis, at the 2nd costal cartilage). The JVP normally is 4 cm above the sternal angle or lower; increased in fluid overload and decreased in hypovolemia.
Beigel R et al. 2013. Noninvasive evaluation of right atrial pressure. Journal of the American Society of Echocardiography: 26;1033.
Chua Chiaco JMS, Parikh NI, Fergusson DJ. 2013. The jugular venous pressure revisited. Cleveland Clinic Journal of Medicine. 80;638.
Cook DJ, Simel DL. 1996. Does this patient have abnormal central venous pressure? Journal of the American Medical Association: 275;630.
Vinayak AG, Pohlman AS. 2006. Usefulness of the external jugular vein examination in detecting abnormal central venous pressure in critically ill patients. Archives of Internal Medicine: 166;2132.
Wang CS et al. 2005. Does this dyspneic patient in the emergency department have congestive heart failure? Journal of the American Medical Association: 294;1944.
There are no shortage of congenital syndromes that are acronyms arranged into some sort of vaguely pronounceable word. There will be lots of doodles about these, but we’ll start off with a more uncommon one – PHACE Syndrome.
PHACE Syndrome is a collection of findings that go along with large infantile hemangiomas. They’re the more worrisome (but less obviously disfiguring) things you need to look for when you see a baby with a large hemangioma on the face or multiple hemangiomas.
Posterior fossa brain malformations
Cardiac anomalies and coarctation of the aorta
The most common symptom of PHACE is cerebrovascular abnormalities, followed by cardiac anomalies (coarctation, aortic arch anomalies, VSDs). If you suspect PHACE, do clinical exam of the skin and eyes and MRI of the head, neck and chest.
Other cool facts
PHACE occurs in full-term normal birth weight infants (other hemangiomas tend to occur in preterm infants)
Quite common, more girls than boys (8:1)
Don’t confuse it with Strurge-Weber (port wine stain, associated with the facial dermatomes)
Port wine stains don’t proliferate and then regress like an infantile hemangioma
When you find someone without a pulse but then hook up the monitor and there is a rhythm, your first thought it probably “CRAP!” But as you start CPR, you need to be thinking about what caused it because not much will help the person except correcting the underlying problem.
So like most of medicine, there is a handy mnemonic for remembering the main causes: The 6 Hs and 5Ts
The 6 Hs
Hyperkalemia/Hypokalemia (potassium disturbances only get counted once)
The 5 Ts
(I’ll make a T doodle at a later date)
The other handy mnemonic for the Hs I learned from this video (so I take no credit for it): Diabetic crashing with a wide QRS
Kawasaki Disease is one of the pediatric rashes that you always need to have in the back of your mind. Most of the time the disease is self-limiting, but the consequences of not catching it are pretty bad (turns out coronary artery aneurysms often lead to things like infarction and DEATH).
Warm CREAM is an unrelated (and somewhat unpleasant) mnemonic to help remember the signs and symptoms of Kawasaki. The “warm” is a fever (one lasting more than 5d) and then you need 4/5 of the other criteria (non-purulent conjunctivitis, rash, palmar erythema/swelling, cervical adenopathy, dry and red mucous membranes, the infamous strawberry tongue). The kid doesn’t need all 4 as he or she is sitting in front of you, but the presentation and the history combined should include those criteria.
Treatment is with high doses ASA and IVIG, you do this to prevent the sequelae of coronary artery aneurysms and myocarditis, and it’s best to get an echo to check up on things.
You separate congenital heart defects into acyanotic and cyanotic. Basically, is the baby (or kid) nice and pink, or is he or she dusky as they like to say. Sometimes the blueishness only happens when they’re working really hard, like feeding and crying (or thinking about the pathophysiological mechanisms of heart disease).
One of the important things to remember is that acyanotic heart defects can switch over if they’re left alone for too long because of pulmonary hypertension caused by the extra flow. This is called Eisenmenger Syndrome.
It’s also important to realize that many of the cyanotic lesions are duct dependent, meaning that as long as the ductus arteriosus is open, they are happy and pink. The problems start in that time 6-24h after delivery when the ductus closes. Thankfully you can keep it open by giving prostaglandin E1.
Need the ductus for systemic circulation:
Coarctation of the aorta
Critical aortic stenosis
Hypoplastic left heart syndrome
Need the ductus for pulmonary circulation:
Critical pulmonary stenosis
Tetralogy of fallot
Also, I realize that the 5 Ts of cyanotic heart lesions are a pentad of 6 (plus some), but mnemonics can only do so much, and the T thing is just so catchy.
For a more detailed illustration of PDAs, you can check out this doodle!
Heart murmurs are pretty nifty things to listen to on physical exam. Not only are they discernible somewhat by location, there are lots of special tricks and maneuvers doctors have up their sleeves to figure out exactly what kind of murmur it is.
If you are suspecting aortic regurgitation (AR), you should hear it just below the pulmonic area (where the aortic valve is located). When you get the patient to hold their breath and lean forward the murmur should get louder. Holding their breath makes mitral stenosis (MS) murmur quieter.
Getting a patient to squat from a standing position increases their stroke volume which will make any regurgitation murmur (whether it’s mitral or aortic) louder.
Similar to how laying on the left side will make it easier to feel the apical impulse, this maneuver brings out mitral stenosis (MS).
Finally, getting the patient to do a Valsalva maneuver (bearing down) will decrease left ventricular (LV) outflow and bring out a hypertrophic cardiomyopathy murmur (this finding is almost pathognomonic with HCM)
I think in my head I always thought that the coronary artery circulation was much more complicated than it really is. The simple way to boil it down is that the right coronary artery (RCA) does the right ventricle and the back of the heart. While the left coronary artery (LCA) does most of the anterior and some of the back depending on the circumflex artery and individual variation.
SA Node: usually supplied by the RCA (in 60% of people) but can also be supplied by the LCA AV Node: supplied by the RCA
Dominance of circulation
Right-dominant (80%): Posterior interventricular (PIV) & at least 1 posterolateral branch arise from the RCA Left-dominant (15%): PIV & at least 1 posterolateral branch arise from left circumflex artery Balanced (5%): dual supply of posteroinferior LV from RCA and circumflex
So what this means is that if you see a inferior MI pattern on an ECG, there is likely a posterior infarct as well. Not to mention that you should be worried about both your AV and SA node.
The ductus arteriosus is a connection between the aorta and pulmonary artery present in the fetal circulation. Since the pulmonary vascular pressure is higher than the systemic pressure, blood is shunted through the ductus from the right to the left, bypassing the lungs.
When the baby is born, the resistance in the pulmonary vascular falls and more of the blood goes through the lungs. In conjunction with this the fall in the level of circulating prostaglandins causes the contraction of the ductus arteriosus.
Patent ductus arteriosus
In some babies, particularly those born prematurely, the ductus fails to close and the shunt becomes left to right.
This gives you the classic “continuous machine-like murmur“
The differences between mitral insufficiency (regurgitation) and stenosis and aortic insufficiency and stenosis. It’s important to know where to listen for them and what sort of other findings they go along with. Really aortic insufficiency is the one with all the wonderful findings that all all named after different people.
Left-sided heart failure leads to fluid accumulation in the lungs and has an increased left ventricular end diastolic pressure (LVEDP). The left ventricular end diastolic volume (LVEDV) can either be increased or normal. When it is increased and the end systolic volume is also increased, this indicates systolic dysfunction. When the LVEDV is normal or the ejection fraction is normal, this indicates diastolic dysfunction.
Reminder: Ejection fraction = Stroke Volume/End Diastolic Volume Stroke Volume = End Diastolic Volume – End Systolic Volume
Systolic Heart Failure
The inability to expel sufficient blood, has a decreased ejection fraction. You might feel a displaced apical impulse or hear an S3.