Cardiovascular Part 6

Cardiovascular Hypertensive Crisis Essential Hypertension: Accelerated Hypertension: diastolic BP >120-140 and is associated with retinal hemorrhages Malignant Hypertension: diastolic BP >140 and associated with retinal hemorrhages and papilledema *Treatment: vasodilators and sympathetic blocking agents Cardiomyopathy Dilated Cardiomyopathy Restrictive Cardiomyopathy *Hypertrophic Cardiomyopathy-IHSS Hypertrophic Cardiomyopathy (HCM) aka. Hypertrophic Obstructive Cardiomyopathy (HOCM) aka. Idiopathic Hypertrophic Subaortic Stenosis (IHSS) -big fat ventricular septum that hangs out into the left ventricle -normally, left ventricle fills up with 70cc, so now, rather than ventricle filling up with 70 cc, its smaller and only can fill up with 30 cc → decreased cardiac output (CO) during systole -light headed, chest pain, SOB with exertion (climbing up stairs) **DO NOT GIVE DIGOXIN! → DIG increases myocardial contractility and squeezes the little bit of blood out real fast and the cells don't see the blood go by, you want to use something that squeezes the blood out really slow and lowers heart rate to allow for the heart to have more time to fill (in diastole) → allows heart to fill more volume (40 instead of 30 cc) and squeezes it out slow (inderil, lopressor) -no nipride, tridil, dobutamine, no nitrates, no vasodilators because the blood pools and no blood gets to the heart (decrease in R ventricular preload) → 10 cc would get to the heart instead of the 30 (vasodilators make things worse) *Increased thickening of the heart muscle and septum (primarily septum), inwardly at the expense of left ventricular chamber, ventricles become rigid and stiff and affect stroke volume and CO -Tx: beta blockers (inderil, verapimil) and calcium channel blockers -Avoid: digoxin, nitrates, dopamine, isopril, morphine (vasodilates) Swan Ganz Catheters Pulmonary Artery Pressure (PAP) -catheter is in pulmonary artery -Systolic number (PAS): pulmonary valve open during systole *Normal PAS = 20-30 mmHg *high = lung problem! *elevated in: pulmonary hypertension, pulmonary hypoxia, COPD, ARDS, PE -because during systole, R ventricle squeezes the blood out from the pulmonary artery into the lungs, so if you have a lung problem, you have vasocontriction and increased pressure and the PAS is elevated because you are meeting restriction -Diastolic number (PAD): pulmonary valve closed, R chamber fills during diastole *Normal = 6-12 mmHg or 8-14 mmHg *high = heart problem! *elevated in: cardiac tamponade, left ventricular failure, mitral valve disease -once pulmonic valve is closed, there should be an open system from the tip of the catheter to the left side of the heart (the tip of the catheter looks at the left side of the heart), because oxygenated blood flows from the pulmonary artery back to the left side of the heart (body) -the PAD closely responds to the left side of the heart at the end of diastole (left ventricular end diastolic pressure) EXCEPT in -RBBB: because there is a delay in right ventricular systole, ventricles do not contract at the same time, pulmonic valve stays closed longer than it should, and blood drifts off to the left side of the heart, RBBB causes a decreased pressure in pulmonary artery because you haven't done systole yet (delayed), so there is a significant drop in pulmonary artery, so the catheter will not accurately reflect what is happening in the L side of the heart -Mitral Valve Disease: mitral valve is stiff and doesn't open well, if it doesn't open well, left atrium has a hard time pumping blood from left atria to left ventricle, causing an increased pressure in the left atrium which backs up to the tip of the catheter (so if you have mitral valve disease, the catheter would be showing the increased pressure in the left atrium rather than accurately depicting the pressure on the left side of the heart) -Mitral Insufficiency: mitral valve doesn't close well, so when the left ventricle is in systole, instead of all of the blood coming through the aortic valve, some of the blood backs p through the mitral valve into the left atrium which causes increased pressure in the left atrium -Pulmonary Hypertension -Decreased left ventricular compliance: stiff left ventricle, increased pressure in the left ventricle causes increased pressure in left atria as it tries to pump blood down into the left ventricle which backs up pressure to the tip of the catheter (because the heart has such a hard time squeezing blood from the left atria to the left ventricle) -Aortic Insufficiency: aortic valve doesn't close well, so there is a backward flow of blood into the left ventricle that prematurely shuts the mitral valve -Pulmonic Insufficiency: pulmonic valve doesn't close well, backward flow of blood into the right ventricle → reduces pressure in the pulmonary artery *so if a pt has any of the above, you can't use the PAD, you have to wedge the catheter! -basically... any valvular diseases, RBBB, and decreased left ventricular compliance Pulmonary Artery Pressure Waveforms -waveform occurs in the Q-T interval of EKG -you must take the reading at the END of exhalation -when a pt is breathing, you'll get a DIP in the reading! Pulmonary Artery Wedge Pressure (PAWP, PCWP, PCOP) *Normal = 4 or 6-12 -A, C and V waves in a normal wedge -A wave = atrial contraction → occurs AFTER QRS -C wave = mitral valve closing → can hardly ever see them -V = atrial filling → after the T wave **HOW DO YOU MEASURE A PULMONARY ARTERY WEDGE PRESSURE? Find the A wave and take the MEAN of the A WAVES! *take a hump and bring it up! Match with the EKG to differentiate A from V waves -A waves look smaller and more peaked, V waves are wider humps (taller and bigger) *TO GET THE WEDGE PRESSURE – measure the A wave (ex. If 27/24, the mean is 25) Pulmonary Artery Wedge Pressure is Elevated in: Left-Sided Heart Dysfunction -mitral stenosis/insufficiency (valvular disease) -cardiac tamponade -constrictive pericarditis -left ventricular failure -volume overload -wedge pressure reflects pressure on the left side of the heart, so it is elevated with heart problems PAD usually correlates with Left Ventricular End Diastolic Pressure (LVedp) PAD correlates with PAWP (wedge pressure) -both look at what's going on on the left side of the heart PAWP correlates with Left Ventricular End Diastolic Pressure **this means... PAD, PAWP, and Lvedp should all be about the same! **so... anything that affects the PAD being inaccurate, would affect the PAWP! (see above in PAD) -The mean of the A wave (PAWP → wedge pressure), approximates the LVEDP (PAD) when blood flows through the lungs is unobstructed. -Knowledge of the end diastolic pressure of a ventricle provides a means of assessing how well the ventricle functions as a pump *FYI... The PAWP is always a little lower than the PAD **PAWP is 1-4 mmHg lower than the PAD **YOU SHOULD NEVER GET A WEDGE HIGHER THAN THE PAD -ex. you can't have a value of 28/14 and have a wedge of 16! − this is because blood flows from a higher pressure to a lower pressure − ex. can you have a pulmonary artery pressure of 32/12 with a wedge of 16? No! − 12 is the PAD and the wedge pressure cannot be higher than the PAD! − **If the wedge is higher than the PAD, the discrepency is caused either by overwedging the the catheter or physiological conditions − Zone 1, Zone 2, or PEEP − if the catheter is in the wrong zone, the wedge would be higher than the PAD − lungs are divided into 3 zones, top is zone 1, middle zone 2, bottom zone 3 − **Catheters must ALWAYS be in zone 3!! − if catheter is in zone 1, there is no clear channel looking to the left side of the heart − if in zone 2, can only look at the left side of the heart during diastole − in zone 3, there is always an open channel looking at the left side of the heart − in zone 3, reflects left atrial pressure and therefore, left ventricular end diastolic pressure ***MUST USE AN X-RAY TO CONFIRM THAT CATHETER IS IN ZONE 3! How else can you tell if the catheter is not in the right place (zone)? ? -you don't get a nice, crisp waveform no matter how much you zero and pull the “twanger” → d dampened wedge tracing -wedge pressure (PAWP) is higher than the PAD -you can't discern A and V waves on the wedge tracing (absence of A and V waves) -when pt is breathing, you get waveforms all over the place (looks crazy) → marked respiartory variations Calculating the PAWP on PEEP -any PEEP greater than 10 affects the PAWP -PEEP is measured in cmH2O -PAWP is measured in mmHg 1) change PEEP cmH2O to mmHg 2) Divide PEEP by 1.36 (1 mmHg = 1.35 cmH2O) 3) Divide the mmHg of PEEP by 2 **Remember... divide by 1.36, then divide by 2! Ex. Your patient is on a PEEP of 15. The PAWP is 18 mmHg. What is the corrected PAWP reading? -Divide PEEP by 1.36 → 15/1.36 =11 mmHg -Divide by 2 → 5.5 mmHg of PEEP 18 mmHg – 5.5 mmHg of PEEP = 12.5 mmHg true PAWP reading! Ex. Your patient is on PEEP 20, Recorded wedge is 22 -20/1.3 = 14 -14/2 = 7 -22-7 = 15 (true wedge) **THIS ONLY APPLIES IF PEEP IS >10! What's my disease?? PAP = 58/34, PAWP = 2, CVP/RAP (right atrial pressure) = 18, CO =3.0 L → high pulmonary artery pressure, low wedge pressure, high pressure on the right side of the heart, low cardiac output → COPD, pulmonary hypertension, intravascular depletion (dehydrated, too much lasix, etc) PAP = 20/8, PAWP = 8, CVP = 7, CO = 4.OL → Normal! These are all normal parameters PAP = 48/24, PAWP = 22, CVP = 14, CO = 2.5 L → high PAP, high PAWP, CVP 14, CO low → biventricular failure (PAWP means high pressure on left side, backing up into the lungs causing high pulmonary artery pressure and pulmonary edema, backing up into the right side causing high CVP (right atrial pressure/right side of heart pressure) PAP = 21/6, PAWP = 4, CVP = 2, CO = 2.0L → hypovolemia, hypovolemic or hemorrhagic shock PAP = 38/26, PAWP = 12, CVP = 8, CO= 4.0L → the only thing high is pulmonary artery pressure → atelectasis, ex. Pt was in OR for a long time → can't be a PE because that would affect pressure on the right side of the heart → not COPD because it is long term and would cause a high pressure on right side of the heart → acute condition because did not affect the right side of the heart Heart Murmurs Two common causes of murmurs: 1) forward flow of blood through stiff stenotic OPEN valves (narrow lumen) -STENOSIS = OPEN 2) backward flow of blood through incompetently CLOSED valves (regurgitation) -INSUFFICIENCY = closed Location of Murmurs Aortic → right 2nd ICS Pulmonic → Left 2nd ICS Mitral → 5th ICS, mid clavicular line (MCL) Triscuspid → 4-5th ICS, left sternal border -confusing to auscultate because the murmur is not heard where the valve is located, it is heard where the valve sends the blood -ex. Aortic is not heard on the left side where it is located, it is heard on the right -where you hear them is opposite of their location (aortic on right, pulmonic on left) Technique of Auscultation -must be systematic -process of auscultation begins at the aortic area and proceeds in a definite order: *Aortic → Pulmonic → Mitral → Tricuspid Systolic vs Diastolic Murmurs S1 = closure of mitral and tricuspid valves S2= aortic and pulmonic valves close after ventricle is in systole and squeezes blood out Diastolic Murmur : lub-dub murmur -occurs when the ventricles are in diastole (heart filling), after S1 and S2 Systolic Murmur: lub murmur dub -occurs during systole, when ventricles are pumping blood out, before S2 because the pulmonic and aortic valves are not closed yet -mitral and tricuspid valves would be closed during systole (so after S1 happened already) Examples of Murmurs Mitral stenosis -stenosis = open -mitral valve is open during diastole (blood filling from left atria to left ventricle) -this means it is a diastolic murmur (lub dub murmur) -low-pitched, crescendo, RUMBLING noise heart at the apex that will increase in the left lateral position (lub dub rumble, lub dub brrrrr) → confused with water in ventilator tubing -causes: calcification of leaflets Aortic Stenosis -stenosis = open -aortic valve open during systole (to pump blood out to the body) -systolic murmur -lub murur dub -little old ladies get this because calcium comes out of your bone and hangs out at your aortic valve -calcification of valves and rhematic fever -medium pitched, crescendo-decrescendo, radiating to the neck and right carotid which increases with sitting and holding one's breath -holosystolic/pansystolic murmur: occurs all throughout systole → you don't even hear the lub dub, you just hear the murmur -harsh noise that radiates everywhere (like a grunting noise) Pulmonic Insufficiency -insufficiency = closed -pulmonic valve is closed during diastole (to allow for filling) -disatolic murmur -lub dub murmur Aortic Insufficiency -diastolic murmur -high pitched, descrescendo, BLOWING noise that is heard at 2 RICS, increases with exhalation -lub dub blowww/ lub dub foooooooo Mitral Insufficiency -systolic murmur -holosystolic murmur: all throughout systole -high pitched, plateau BLOWING quality heard at the apex which radiates to axilla, increases with squatting -soft, blowing murmur (unlike aortic stenosis which is harsh) -causes: MI, rheumatic heart disease 12 Lead EKG Interpretation Lead 1 & aVL → lateral wall -positive sticky on your left arm is looking at lateral wall -going through a positive sticky → when electrical activity goes through a positive sticky, the QRS complex should always be upright -if you are looking at lead 1 and aVL and the complex is initially complex, then goes negative, the electricity is going away from the positive sticky, it means the energy is going to the right → this indicates a right axis deviation (RAD) Lead II, Lead III, and aVF → inferior wall -left leg positive -when energy is going up the leg towards the positive sticky, the QRS should be upright -if you are looking at these leads and the QRS is intially positive, then goes negative, it means that the energy is going away from the positive sticky (energy is going to the left) -if the QRS is upside down in these leads it is a → left axis deviation Leads V1, V2, V3, V4, V5, V6 → anterior-septal-lateral wall -lay across left side of chest in order (V2 is on the right side of the chest across the sternum) -V1-V4 → anterior-septal wall -V5-V6 → lateral wall -should always have the presence of an “R” wave → R wave gets bigger as you go from V1-V6 -if the R wave stays the same as you go from V1 to V6, it is known as poor R wave progression which indicates heart disease -when electricity goes down bundle down the septum, it goes towards the positive V1-V4 leads (upright complex) → so first, goes down the anterior septum to right ventricle, then goes across to left side to V5 and V6 (now you get a negative complex because the energy bounces off that wall and goes towards the other side) → initially, a positive complex, then negative in V1-V4, then positive in V5-6 -positive complex in V5-6 because energy bounces over towards those positive leads -R wave is the upright positive wave that comes from energy bouncing off the right wall and sending the energy to V5-6 -R wave = positive deflection that happens before QRS (negative in V1-V4) -if no R wave in V1, V2, V3 → that means there is no anterior septal wall -ex. If no R wave = anterior septal wall MI because energy isn't bouncing off that area towards V5-6 *NO R WAVE = infarcted! *ST elevations = infarcting! (pictures and explanations of above in disc 4 part 4) EKG and Injury I, II, III, aVF, aVL, V3, V4 -look at the isoelectric line -injury = ST elevation (fireman's hat) or tombstone -fireman's hat = MI (sometimes you will see ST depression in I and aVL = reciprocal change) V1-V3 -look for presence of R wave -no R wave? → NO anterior septal wall! -where is it? Dead! (infarcted) -disc 4, part 4 for examples **GO BACK TO THIS AND LOOK UP ADDITIONAL YOU TUBE VIDEOS!!! Complications of MI -people with inferior wall MI have completely different complications than anterior MI Complications of Inferior wall MI -Right coronary artery supplies the: Sinus node, AV node, RA and RV, Mitral Valve, inferior wall -sinus node: bradycardia -AV node: complete heart block, 3rd degree heart block, AV dissociation → disconnection between atria and ventricles -treatment = pacemaker! -Right atrium and right ventricle: RV infarct (ST elevation in V1-V6 on the right side) -Mitral valve- insufficiency -better to be bradycardic than tachycardic during an inferior wall MI, because inferior wall MI has a high mortality rate -brady during inferior wall MI are usually symptomatic -why is the heart beating slow (brady) during an inferior wall MI? Because your sinus node is ischemic -when people are bradycardic, can be asymptomatic or symptomatic -if HR is 38 and not symptomatic, don't do anything → keep an eye on them -if HR is 38 and eyeballs go behind head looking like a code → save them! -if HR is 38 and pt is a little lightheaded with ringing in the ears → stay away from atropine, lay the pt flat!! if BP is ok, lay pt flat and raise their legs in the air -if BP is not ok → give atropine! Do not lay flat! Complications of Anterior (Septal) Wall MI Left anterior descending (LAD) supplies: Bundle of HIS: Mobitz II (94% of pts) Bundle Branches: RBBB (14% of pts) Ventricular Septum: VSD Anterior-Septal Wall -if pt develops a Mobitz II or RBBB, extremely high mortality, UNLESS pacemaker is inserted!ning f