Cardiovascular Assessement Big Picture March 9 2011 Dez Hughes spk17249.jpg D.Hughes@massey.ac.nz lgo17249.jpg Cardiovascular Assessment The Big Picture This week we are going to take the assessment of the cardiovascular system to the next level. We covered the basics in MBS assessment. Now you will see how to gain much, much, much more from your cardiovascular exam. There’s no voice over this week folks. I’d be very interested to hear from you in the coursework discussion forum whether you think the sound is actually helpful or whether you prefer to just to read the notes at your own pace. Pulsology There is a whole branch of Tibetan Medicine called Pulsology that stems from the 5th century BC. Tibetan pulsologists spend years learning how to feel pulses. They then use the pulses as the main way to diagnose all manner of diseases, not just cardiovascular ones. Here you can see a Tibetan Tantra which shows pictures of many of the different pulses they can recognise. Overview After briefly reviewing the determinants of cardiac output we will deal with the basic but most important PE parameters in detail. Mucous membranes and CRT, pulses, heart rate and cardiac auscultation. We’ll then touch on the adjunctive parameters you can also use then go on to cover specific common abnormalities of the cardiovascular system and how to recognise and differentiate them on your physical examination. Determinants of Arterial Blood Pressure Arterial blood pressure is the product of the driving force, the cardiac output, and the opposing force, the peripheral vascular resistance. The cardiac output depends upon the amount pumped per beat, the stroke volume and the number of beats per minute, the heart rate. In turn, the stroke volume is determined by the filling of the heart (the venous return) and the contractility. Probably the most important point to realise here is that arterial blood pressure is a very insensitive indicator of the actual blood volume status of the animal. This is 1) because of all these things that affect ABP and 2) because the physiological response to anything that tends to cause ABP to fall is to put it back to normal! Abnormal Mucous Membranes Mucous membrane colour is primarily determined by the red colour of oxygenated haemoglobin and the blood flow that takes it through the tissues so anything that changes the Hb concentration of the blood flow will affect the colour. How the colour is described may also depend upon the background colour of the mucous membrane (eg muddy or grey as opposed to white). It may also be affected by any other colours that may be mixed in with the red or by disease in the mucous membrane. Here’s a normal dog just to refresh your memories before we go on to abnormal. Abnormal Mucous Membranes The capillary refill time tells us the perfusion status of the membrane. Make sure that you always assess both colour and CRT, irrespective of the colour of the membrane. You still need to know the perfusion status of a dog with a cyanotic membrane (usually quickly!) or a white one. Remember that oral diseases can also LOCALLY affect the CRT. An inflamed mucous membrane will often have a fast CRT because of the inflammation per se. In this cat you can see that there is gingivitis around the canine tooth. The CRT in the inflamed area is fast. If you watch closely you can actually see that the CRT in the gum adjacent to the gingivitis is slower than in the gingivitis! Mucous Membrane Disease The dog in the top left has severe gingivitis. The areas with gingivitis will have a faster CRT so try to take your CRT from a normal area. The dog on the top right has mucocutaneous lymphoma. And check out those membranes in the cat! Cats usually have pale mms and don’t usually get generalised reddening of the membranes like dogs do. This cat has polycythaemia. Red/White abnormalities Often we are looking for the amount of red in the membrane together with the CRT to try to get an idea of Hb status and perfusion or both. An animal that is euvolaemic but anaemic will have MM pallor but you will still be able to see a CRT if you look carefully. In this case you can also surmise that the anaemia is likely to be chronic. If there is pallor and a prolonged CRT this means that there is definitely hypoperfusion but you can’t tell the Hb status. A redder MM than normal is called injected or hyperaemic. If the CRT is fast then you can assume that there is increased blood flow through the tissues. An injected MM with a slow (or even “normal”) CRT should set your cross referencing bells clanging! A hyperaemic MM should have a fast CRT unless there is more than one thing going on eg vasodilation from SIRS and concurrent hypovolaemia. It can also occur with pericardial effusion which we will discuss later. Pale Mucous Membranes Prolonged CRT Here’s our Rotty from MBS week to remind you what a very pale MM and a lousy CRT look like! Hyperdynamic And him after some fluids showing you a bit more red in the membrane and a fast CRT indicative of compensated hypovolaemia. Some Other Colours Check for cyanosis or icterus (or in very rare instances a brown or cherry red discolouration). Remember that these colours are mixed in with whatever the background colour is (determined by Hb, perfusion and membrane pigmentation). A euvolaemic dog with a low PCV will have less red in the background. A euvolaemic dog with septic bile peritonitis will have an injected colour (more red) AND the yellow of hyperbilrubinaemia so its membranes will look quite a rich orange. The Shelty here has bile peritonitis and you can see he has injected MMs and with the eye of faith you can see mild icterus (he did in real life, honest!) Some cats with icterus present because their previously blue eyes have turned green! Some people say that they can appreciate a brown colour in some cats with methaemoglobinaemia from paracetamol poisoning. Cherry red mucous membranes can occur with carbon monoxide poisoning but this is very rare, even in dogs suffering from smoke inhalation. Cyanotic Kitten Cyanosis in a 6 month old kitten Cyanotic Kitten This is the kitten with the cyanotic mucous membranes. Doing a bit of cross referencing and a bit of lateral thinking any thoughts on what might be going on? Tell us on the BP discussion forum. You can almost work out the most likely diagnosis without even touching him. Pulsology! We covered the basics of assessing pulses in MBS assessment but now we are going to take things further. We’ll go into much more detail about pulses on the slides about specific perfusion abnormalities. But to give you an idea of taking things further (please don’t get disheartened!) I suggest that you should start trying to feel how distended the femoral artery is BETWEEN BEATS! Does it stay distended or does it collapse between pulses? This way you can get even more information about the intravascular volume status and even the tone in the arterial wall. If you can appreciate this then you are a Pulsologist! Another challenge for you budding pulsologists is to be able to still feel the femoral arteries in a cat with aortic thromboembolism and no pulses. I think it is interesting that the pulse you feel pretty much mirrors an arterial pressure tracing (apart from the dichrotic notch that is: and there’s Brownie points for an explanation of the dichrotic notch). While we are on arterial pressures, who knows where the mean pressure falls with respect to systolic and diastolic? If you look at the trace you can almost guess. Can I also share with a very common misconception regarding feeling pulses. Many people suggest because the pulse is determined by the difference between systolic and diastolic pressures that you can’t tell the difference between 120/80 and 80/40. This may be true in anaesthetised patients but it is JUST PLAIN WRONG in conscious patients!!!! A hypotensive patient has much shorter and narrower pulses. Heart Rate and Auscultation Cardiac output plateaus then falls at heart rates above 180-200 because there is insufficient time for diastolic filling. So there is no physiological benefit of heart rates increasing much above this in response to hypovolaemia. In fact, if the heart rate is more than around 240 then the rhythm is very likely to be an actual tachyarrhythmia rather than a sinus tachycardia in response to hypovolaemia. In euvolaemic dogs, as the heart rate increases the pulses will get narrower purely because there are more beats per unit time. Your job is to work out whether the reduction is pulse width is the amount that you would expect from the heart rate alone or is there reduced intravascular volume as well ie is the pulse narrower than you would expect from the heart rate alone. Slower heart rates will give you proportionally taller and wider pulses due to the increased stroke volume per beat. Heart sounds can be quieter when there is moderate to severe hypovolaemia presumable due to a lesser amount of blood in the heart to generate the heart sounds. You should cross reference this with your other perfusion parameters. For example, if the dog has only mild hypovolaemia but very quiet heart sounds then this is likely NOT just due to hypovolaemia and you should look for other reasons. A final tip for you regarding counting fast heart rates: count only every 2nd or 4th beat. Much easier! Auscultation Most of us remember that the pulmonic, aortic and mitral valve areas are found over the left 3rd, 4th and 5th intercostal spaces respectively. But how useful is that in a tachypnoeic patient? Bout as useful as a chocolate fireguard. Here’s a way to use your stethoscope to find the valve areas. Stick your steth caudal to the heart and move it cranially until you first hear the heart sounds. Now CONCENTRATE! Listen to how loud the 2 heart sounds are. Mitral is the first heart sound and you are over mitral so you will hear a louder first heart sound: LUB dup, LUB dup. Next push your stethoscope under the dog’s triceps and move it down towards the sternum. Go far enough forwards that you can’t hear the heart then move it caudally. Pulmonic is one of the 2nd heart sounds so you will hear lub DUP, lub DUP. To find aortic go between the two areas you have already identified. You can often appreciate that the aortic sound is louder than the pulmonic. Don’t forget to listen on the right side and over the ventral sternum in cats (where they hide their murmurs. If you forget, Sod’s Law sez that’s where the murmur or gallop will be! Murmurs may be quiet or absent with hypovolaemia so always reauscultate as you volume replace them especially if they are in a high risk group for heart disease (giant breed and small breed dogs). Inappropriate Relative Bradycardia Cross reference, cross reference, cross reference! Inappropriate relative bradycardia is when the heart rate is slower than it should be given everything else that is going on. This is may occur because vagal tone is over-riding the sympathetic input to the heart. Peritonitis is a classic that can do this. Look at the other perfusion parameters and work out how fast the heart rate should be. If it’s lower than expected then go looking for an underlying reason. Upper airway obstruction and parenchymal lung disease (especially pneumonias) can also do it. It also occurs with pretty much all the things that were listed last week under vagal arrest so... Inappropriate Relative Bradycardia Check quickly what their potassium, glucose and body temperature are doing. And don’t forget to get an ECG because it might be a true bradyarrhythmia. Adjunctive Parameters After I have checked pulses I sometimes check to see what the venous side is doing. If they have significant hypovolaemia you should struggle to find their jugulars. If you have a dog with hypotension but it’s jugulars are distended then there is a problem with right heart filling (pericardial effusion, right heart failure, intracardiac obstruction (eg heartworm) or cranial caval obstruction. Patients in shock should have low normal to low rectal temperatures. If they are hypotensive and their rectal temp is normal then beware that it may actually be a masked pryrexia. Cross reference, cross reference, cross reference! If you want to measure rectal to toe temperatures in hypovolaemic animals then not surprisingly the toes will be colder. Some people talk about doing this in clinical patients. I have much better things to do with my time when I am managing an animal in shock! I find apex beat can be challenging to interpret. For example, if a dog has a huge heart and dilated cardiomyopathy then the apex beat may still be strong because the heart is close to the chest wall. Uncomplicated Hypovolaemia This is THE MOST IMPORTANT SLIDE IN THIS PRESENTATION! Accurately recognising and grading hypovolaemia is essential to being an effective emergency vet. MBS cardiovascular parameters change predictably and together as hypovolaemia worsens. You should try to grade them as mild, moderate or severe. What is the initial cardiovascular response to hypovolaemia? It is mild tachycardia and stronger cardiac contractions. Vasoconstriction may be occurring in non-essential beds but you will not see it in the gums yet. So in the mild (or compensated) stage, the heart rate is only mildly increased and the MMs will still be pink or even pinker than normal as the heart pumps the smaller volume of blood around faster. The CRT will be rapid and the pulses are taller than normal because of the increased cardiac contraction. As hypovolaemia worsens the heart rate rises more, pallor becomes apparent in the mucous membranes and the CRT is high normal (which you should be thinking totally doesn’t fit with the heart rate if it was just pain or stress). Pulses are becoming shorter and narrower because of their reduced volume. Once hypovolaemia is severe then there is no red in the MM, you struggle to see a CRT or to find a femoral pulse. If you need to put a number on the severity of their hypoperfusion, buy a lactate meter. Uncomplicated Hypovolaemia Now let’s consider pulses in more detail. What is the CV response to exercise, stress or pain? Tachycardia and increased force of contraction. This generates a taller than normal pulse that is narrower because of the faster rate. The response to early hypovolaemia is exactly the same but the pulse will be narrower because of the reduced intravascular volume. The ONLY way you will tell the difference is by being able to appreciate that the dog with early hypovolaemia has a narrower pulse. As hypovolaemia worsens the pulses become gradually shorter and narrower. And the height and width will always match the other CV parameters if it is plain old hypovolaemia such as haemorrhage. The other great thing is that as you give IV fluids and volume replace an animal, the CV parameters will go back through the same stages in reverse so you can assess whether your response to treatment is appropriate or insufficient. It is vitally important that you learn the stages of simple, uncomplicated hypovolaemia so that you can recognise when the CV parameters do not fit together. That is how you will be able to recognise the other perfusion abnormalities. Euvolaemic Anaemia So here we are talking about EUVOLAEMIC anaemia. Their blood volume is still normal but they are anaemic such as occurs with a chronic lack of production. The heart rate is often either normal or only mildly increased because they can still deliver enough oxygen to the tissues (as evidenced by their normal lactates and the fact that their mentation is often OK as well). Blood viscosity is reduced due to the lower PCV. Their pulses are often taller than normal: just what you’d expect from the heart pumping lower viscosity blood through them. Their MMs are pale but they still have a CRT that is often fast. You have to look closely but it is there. So let’s compare this dog to one with hypovolaemia. The pallor of the MMS is at odds with the rest of the exam isn’t it? If it’s membranes were pale from hypovolaemia then their heart rate would be faster, their CRT longer and their pulses worse. It’s all in the cross referencing! Hyperdynamic Sepsis/SIRS Dogs with systemic inflammatory response syndrome have a multifactorial type of shock. It is classified primarily as maldistributive shock because inappropriate vasodilation is the most important mechanism. They also can have varying degrees of hypovolaemia and reduced cardiac function. How they look on PE depends upon their intravascular volume status. When they still have an adequate blood volume then they look hyperdynamic. The heart rates and contractility increase to counteract the vasodilation. The vasodilation gives them redder than normal MMs and the compensatory increase in cardiac output gives the a fast CRT and tall, narrow pulses. This dog has septic peritonitis and MMs don’t get much redder than this! Hyperdynamic Sepsis/SIRS When their vasodilation is more severe, blood spends longer in the capillaries and more oxygen is removed from the Hb. More deoxygenated Hb gives the MM a cyanotic component which you can see in this dog. You should be able to appreciate that his membranes are redder than normal and that there is also a cyanotic component. His CRT is fast so you can conclude that although his blood volume will be inadequate he can still compensate. Hypodynamic Sepsis/SIRS When their blood volume is lower they will still have an injected MM (due to the inappropriate vasodilation) but their CRT will become slower. In this dog you can see that he has an injected MM colour with a cyanotic tinge but that his CRT is abnormally normal. That is, if he had an adequate intravascular volume he would have a faster CRT but instead he has a “normal” CRT. In worse cases the CRT will be prolonged. One last word: if you can see the CV abnormalities I have shown you in the last three slides then sepsis/SIRS are high on your list. BUT some dogs with sepsis/SIRS do not have membranes as injected as this. Some hypodynamic dogs may look the same as plain old hypovolaemia. Sepsis/SIRS is on your differential list for any dog with hypovolaemia until proven otherwise. Cardiogenic Shock/ Heart Failure Heart failure has to be due to valvular, muscle or conduction problems so keep this in mind when you are deciding whether your animal could have cardiac insufficiency. I have included obstructive shock under cardiogenic because my mind works that way! This is a lateral radiograph of a dog with dilated cardiomyopathy. Signalment, History, PE When you are trying to decide whether a hypotensive patient could have a cardiac component it is often fairly easy to rule it in or out on the basis of signalment and history and whether it has a murmur or a gallop. Unless you are unlucky, dogs will often have a history that will help you: coughing, exercise intolerance, dyspnoea or orthopnoea, or even a previous diagnosis of heart disease. Cats in heart failure may have no premonitory signs at all. In my experience, the majority of emergency patients that have heart disease will have a murmur or a gallop (an extra heart sound). Provided that you can find it that is! In dogs it is usually a murmur. In cats it can be either. The only ones that I can think of that don’t are really low output DCM and the ones where I have missed it! These radiographs are from this cat. Who had heart disease. And who is dead. Heart Failure as a Cause of Hypotension To entertain heart problems as a cause of systemic hypotension you are in effect saying left heart failure severe enough that the heart can’t provide enough pumping to maintain systemic perfusion. This is actually rare in dogs. Many are in backward failure (pulmonary oedema) but not in forward failure. Most dogs in heart failure from valvular disease or DCM still have OK perfusion. Only the very worst are hypotensive. Cats, on the other hand, can be horribly hypotensive when they are in heart failure. This animal looks like he could be in heart failure... Is it a dog or a cat? What do you think might be going on? How Bad is the Heart Disease? Heart evaluation means chest rads, cardiac US or both. ECGs are obviously indicated for arrhythmias but are pretty useless for getting definitive information about valves or muscles. If you are faced with a dog or a cat and you want to know whether their heart is a major concern then all (!) you have to work out is whether the left atrium is enlarged or not. If it is not enlarged then, to all intents and purposes, it is not in heart failure (the only exception being a dog with an acute rupture of the chordae tendineae). Here’s a different radiograph of the DCM dog. Look closely at the pulmonary vessels to the cranial lung lobe (A before V: Artery is cranial to Vein). You can see that the pulmonary vein is bigger than the vein (which it shouldn’t be!). Pericardial Effusion And we’ll finish with the piece de resistance of perfusion assessment: the pericardial effusion. It is the piece de resistance because in many cases when they are in tamponade you can make the diagnosis on physical examination alone! Sometimes their mucous membranes alone are very suggestive: an injected, cyanotic colour with a slow CRT. Check it out in this video. As soon as you see cyanosis you need to make 100% sure it’s not caused by hypoxia. PEs may be tachypnoeic but they are not often dyspnoeic. They will have a fast heart rate, quiet heart sounds and very weak pulses. Check out the jugulars: if they are distended despite the systemic hypoperfusion then this tells you there is a serious problem with right sided venous return. Most likely PE. I know we haven’t done Resp of Acid Base yet, but why not have a try at interpreting this panel on the BP discussion forum. Don’t forget to look at the animal when you are interpreting. It was taken at the same time as the video. Pulsus Paradoxus This is an ultrasonogram of a massive pericardial effusion. IN A CAT! The piece de resistance of the piece de resistance is pulsus paradoxus! When they breathe in, their pulses decrease in height and width and when they breathe out their pulses return to baseline. This is very difficult to appreciate if they are very tachypnoeic but if their resp. rates are 30ish then you will usually have 6 beats per breath if their heart rates are 180. Pulsus paradoxus happens to a greater or lesser degree with all dogs in tamponade. Pulsus Paradoxus Being able to feel pulses paradoxus means that you have achieved expert pulse feeler status! Anyone know the pathophysiological/pathoanatomical explanation for pulsus paradoxus? Tell us on the forum. And to end, here’s a new concept I’d like to share: IHTLIP. This stands for “I Had To Look It Up!” When you are posting on the forum please don’t be at all reluctant to admit IHTLIP. In fact don’t *admit* IHTLIP; tell us all and be proud of it! We all have to do it, so let’s be open about it! Bye for now!