CardiacTrauma Part 7

Cardiac Trauma *Most common valve ruptured = aortic valve! Myocardial Contusion: ST elevation only in leads looking at the injury -bruised heart → broken blood vessels that end up bleeding into heart muscle -blood was on its way somewhere and didn't get there -similar to myocardial infarction -risk of cardiac arrythmias and death within first 48 hours → monitor pts closely - “sad” face ST elevation (see disc 5, part 1 3:00) Pericarditis: ST elevation in ALL leads - “happy” face ST elevation -causes: usually viral, MI, post-op, radiation, idiopathic or trauma *Dressler's syndrome = pericarditis caused by an MI -s/s → sharp, stabbing pain that increases with inspiration, low grade fever, dyspnea, cough -chest pain relieved by sitting up and leaning forward -risk for cardiac tamponade → muffled heart sounds, neck vein distention (JVD), narrowed pulse pressure, hypotension, pulsus paradoxus → pulsus paradoxus = absence of beats during inspiration when taking a BP -you don't hear beats on auscultation when pt is taking a deep breath in during taking a manual BP -ex. Mother in law getting pacemaker → HR 130 tachycardic, hypotensive 90/60, severe pain (especially when flat, relief of pain when sitting up), new inverted T waves in I and aVL (means that your left ventricle is working really hard to squeeze the blood out– can be in hypertensive crisis or tamponade) → was cardiac tamponade (nitro worsens condition- do not give) *worse to have a myocardial contusion than pericarditis Pacemakers Problems: Failure to capture Lead dislodgement Battery failure Faulty connections Failure to sense – spikes on the t waves Shock Compensatory Stage -decrease in cardiac output (CO) -Septic shock → vasodilate and pool 50% of blood in the capillary beds, thus decreasing cardiac output -Anaphylactic shock → histamine release vasodilates blood vessels → pool blood in capilary beds and causes decreased CO -Cardiogenic shock → infarct causes low CO from failing ventricle -Hemorrhagic shock → blood loss causes low CO -sympathetic nervous system kicks in due to baroreceptors in carotid and aortic arch that sense the tension in the blood vessels, when these sense a decrease in pressure, they stimulate the SNS to release adrenaline to increase HR, vasoconstrict blood vessels, and stimulate kidneys to release ADH and hold on to water → adrenaline release = increase HR, increase vasocontriction, ADH release from kidneys **DO NOT put pts in trendelenberg ! → causes pooling blood in carotid and aortic arches – fools baroreceptors into thinking there is no problem and does not stimulate release of adrenalin (poor outcomes) -in these cases, NO low dose dopamine → low dose dopamine vasodilates the renal mesenteric arteries and you pool blood volume in the kidneys (to improve good urinary perfusion) → takes away from cerebral perfusion -in this stage, you start looking good and feeling better → short lasting → You are vasoconstricting blood vessels, if this happens too long → lactic acidosis → progressive stage of shock (after lactic acid buildup) -pts may be anxious and irritable **best sign to look for is orthostatic BP changes and narrowing BP -tachycardia, cool and pale, decreased urine output Progressive Stage -vasodilation due to lactic acidosis -hypotension -decrease in CO and BP -ARDS, DIC, multi-system organ failure (MODS) -pts are stuporous and obtunded -hypotension, decreased CVP, decreased PCWP (wedge pressure), decreased CO -increased HR -tx (hypovolemic shock) = replace volume with crystalloids, colloids, FFP, RBC's -colloids (albumin) takes 4 minutes to equilibrate and infuse into the body by gravity -keep chamber depressed, then plug into bottle and infuse! Refractory Stage: no matter what you do, won't get better Cardiogenic Shock Causes: MI, cardiomyopathy, CHF, arrythmias, cardiac tamponade, papillary muscle rupture *papillary muscle rupture = surgical emergency! -s/s = confused, restless, rapid respirations, rales, rapid thready pulse, neck vein distention, narrow pulse pressure, S3 S4 heart sounds, hypotension, oliguria, decreased Co, elevated CVP, SVR, PCWP -rales because of left sided failure **elevated CVP, SVR, PCWP → with left sided heart failure *Tx = early reperfusion, PTCA, thrombolytics, CABG, IABP, inotropic drugs Intra Aortic Balloon Pump (IABP) -decreases afterload -decreases myocardial oxygen demand -increases coronary perfusion -improves cardiac output -catheter inflates and deflates in aorta -do not want to have the balloon inflate during systole, because you don't want the left ventricle to be pumping against the balloon as it is ejecting blood from the heart -balloon is inflated during diastole → perfuses coronary arteries -decreases afterload, improves cardiac output -when balloon is inflated → blood goes up to coronary arteries and down to kidneys -coronary perfusion occurs during diastole, heart muscle receives its blood supply → improves cardiac oxygenation *do not sit someone upright in bed with an IABP ex. Someone with an IABP is eating breakfast, what position do you want them sitting in? → do not sit them in a high fowlers because it would kink the balloon pump → sit them in low fowlers -check pulses because catheter can migrate and occlude arteries Uses of IABP: support acute MI with shock, circulatory support CABG pts, support high risk cardiac pts Contraindications: Aortic Insufficiency: aortic valve doesn't close well, so you don't want a big balloon inflating under it and forcing blood through the incompetently closed aortic valve (don't want further damage to aorta) Peripheral Vascular Disease *Ballon pump inflated during DIASTOLE (when heart is inflated → perfuse coronary arteries) *Balloon pump deflated during SYSTOLE (when heart is deflated → decreased pressure to allow for better perfusion and ejection into the body) *Complications: ischemia of limb, dissection of aorta, infection *Interventions: do not elevated bed >15 degrees (think HOB flat for vascular pts -ie. Sheaths), assess pulses (neurovascular checks), monitor for bleeding Septic Shock -sepsis is the leading cause of death in ICU -mortality rate 40-60% -usually caused by gram negative bacteria (can also be gram positive) –> E. Coli, Klebsiella, Enterobacter, Pseudomonas, Serratia Marcescens -Predisposing factors: old age, granulocytopenia, severe burn injury, alcohol and drug abuse, recent surgical procedures, immunosuppressoin (HIV, chemo), prolonged ICU stay Gram Negative Bacteria -may release an endotoxin -if releases an endotoxin, starts cascade towards septic shock -endotoxin → releases vasoactive substances (cytokinins, bradykinins, etc.) → massive vasodilation -massive vasodilation with 50% of blood pooling in capillary bed → decreased CO *not all gram negative bacteria releases endotoxins -some pts can crash, temp 104, etc. cultures, this is septic shock (bacteria released endotoxins) -some pts can have sepsis (no endotoxins) Warm Stage of Septic Shock -initial stage -important to spot the warm stage because mortality rate is low, prevent progression to cold stage -confused (due to endotoxins) -increased CO (you look great! Looks like you're getting better!) ex. CO = 12 -endotoxin is 100 times stronger than digoxin, makes even fibrotic heart muscle contract -very high perfusion to the body → kidneys (high urine output) -you look good! Perfusing body parts you didn't even know you had -increased RR → subtle increase, makes ABG look better (ex tachypnea to low 30s) -BP looks great -cool your own body down because blood pools in capillary beds away from periphery (low fever) -increased urine output (pooling blood in capillary beds → kidneys are huge capillary beds) ex. Pt that they used dirty instruments in the OR → breathing 34, became crazy/confused, septic -warm stage of septic shock is often misdiagnosed *30 min (toxic shock syndrome → quick progression to cold stage) to 72 hours *Tx = FLUIDS FLUIDS FLUIDS! Also.. antibiotics -FLUIDS because once endotoxins fizzle away, you will become hypotensive, so treat the hypotension before it happens in the cold stage Cold Stage of Septic Shock -high mortality rate -endotoxins fizzle away -stuporous and obtunded -decreased CO, decreased UOP -metabolic acidosis -hypotension → ARDS, ATN, MODS *TX = FLOOD with FLUIDS!! (if you expect toxic shock syndrome → pressure bag fluids in!) Cardiogenic Shock (Left Sided) Preload- increased Afterload- increased CO- decreased Hypovolemic Shock Preload- decreased Afterload- increased (if you are hypovolemic, vessels vasoconstrict and cause increased resistance) CO- decreased Septic Shock (Warm Stage) Preload- decreased (blood pooled in capillary bed) Afterload- dereased (vasoactive substances dilate blood vessels) CO- increased Septic Shock (Cold Stage) Preload- decreased Afterload- increased CO- decreased Anaphylactic Shock Preload- decreased Afterload- decreased CO- decreased *histamines cause massive vasodilation Arrythmias → Review ALS! Asystole *always first → ABCD, focus on basic CPR -then secondary ABCD, advanced airways and treatments/medications -TEA: Transcutaneous pacing → epinephrine (1 mg every 3-5 minutes) → atropine (1 mg every 3-5 minutes up to a total of 0.04 mg/kg) Bradycardia All Trained Dogs Eat Iams Atropine (1 mg q3-5 minutes to total 0.04 mg/kg) → Transcutaneous pacing → Dopamine (5-20 mcg/kg/minute) –> Epinephrine (2-10 mcg/minute) → Isoproterenol (10 mcg/minute) (Isuprel) Ex. A pt with a HR of 45 complains of dizziness and cool clammy extremities. What is the first drug you would administer? -Atropine 0.5 mg-1 mg -you would administer atropine because he is symptomatic (cold and clammy) Ex. you are treating a patient with a slow heartbeat. For which of the following patients would atropine be effective? a) a 55 y/o male with severe chest pain and sinus bradycardia at 35 bpm b) a 55 y/o male with weakness and 2nd degree HB c) a 55 y/o male with fatigue and heart transplant 6 months ago d) a 55 y/o male with weakness and acute symptoms of nausea and vomiting with a sinus HR of 35 a) NO because you would treat chest pain as a massive MI, use MONA first, then tx brady -do not use atropine for severe chest pain c) atropine would not work because the vagus nerve is cut in heart transplant d) correct! Puleless Electrical Activity (PEA) Think: 5 H's/5 T's Hypoxia/Hydrogen ions Hypothermia Hyperkalemia Hypovolemia → common in multiple trauma pts, may have an excellent EKG, but no pulse Tension Pneumothorax Thrombosis (cardiac, pulmonary) Tamponade Tablet/Toxin overdose Think PEA! : Problem → Epi → Atropine Vfib/Pulseless Vtach Vfib = Defib (3 times) Defib x3 → Epi or Vasopressin (40 units IV) → Defib x1→ Amiodarone, Lidocaine, Magnesium, Procainimide → Defib x1 Please Shock Shock Shock Everybody Shock And Let's Make Patients Dance Better (Buffers-bicarb) Ex. Which of the following therapies is the most important intervention for VF/pulseless VT, with the greatest effect on survival to hospital discharge? -Defibrillation Paroxysmal Supraventricular Tachycardia Vagal stimulation → Adenosine If normal heart funciton: Amiodarone, Beta-blockers, Ca Channel Blockers, Digoxin → Procainimide, Sotalol, Cardioversion (can give just about anything to pt with a good heart) If EF <40% (bad heart): Cardioversion, Amiodarone, Digoxin, Diltiazem **if you have a bad heart, cannot give Beta Blockers or Ca Channel blockers because they decrease myocardial contractility and would make your heart performance even worse, can only give 1 Ca Channel blocker which is diltiazem Wide Complex Tachycardia (Unknown Type) *drugs for the treatment of stable wide complex tachycardia thought to be monomorphic VT or of uncertain type = Amiodarone and Procainimide *if pts have impaired ventricular function, such as CHF or poor EF, the drugs to consider are: amio and lidocaine! ***VERY IMPORTANT: Verapamil and Adenosine are CONTRAINDICATED for the treatment of wide complex tachycardia! ***NO patient with wide complex tachycardia should receive verapamil! (Calcium channel blockers, beta blockers, or Digoxin) 5 pt 3 28:03