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42 Cards in this Set
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- Back
- 3rd side (hint)
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What CMO is an asymmetrical hypertrophy mostly of the septum, and may present with concentric LVH and is also a diastolic dysfunction |
Hypertropic cardiomyopathy |
HCMO |
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What are the four synonyms of hypertropic cardiomyopathy? |
Asymmetric septal hypertrophy Idiopathic, hypertrophic, subaortic stenosis Hypertrophic obstructive cardiomyopathy Muscular, subaortic stenosis |
Ash IHSS HOCM MSS |
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What is the most common synonym use for hypertrophic cardiomyopathy? |
Hypertrophic obstructive cardiomyopathy |
HOCM |
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What is a cause of hypertrophic cardiomyopathy |
Autosomal dominant inherited disease of myocardium
Basically mutation in protein due to lack of enzymes located in sarcomeres Screen first-degree relative due to genetics |
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What are the two types of hypertrophic cardiomyopathy diseases? |
Hemodynamic – obstructive HOCM Non-obstructive HCM |
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Explain further some obstructions when it comes to hemodynamic obstructive HOCM there should be two |
Subaortic obstruction due to Sam Mid ventricular obstructive (occurring at the papillary muscle level without Sam) |
One with Sam and one without |
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In regards to a Mid ventricular obstructive, HOCM may be provoked with three things |
Valsalva maneuver, which will increase pressure gradient to see the highest velocity’s Amyl nitrate, which is a vasodilator Isoproterenol |
All three of these increase preload/LV filling so we can calculate the highest pressure gradient |
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What are the seven contraindications for Valsalva? |
1) unstable angina (more prone for heart attack) 2) recent MI 3) valvular AS – severe, fixed (due to decreased CO, EF, SV) 4) severe MR 5) recent stroke 6) recent TIA 7) nitrates |
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Which type of hypertropic CMO has no resting gradient, and is not genetic |
Nonobstructive HCM |
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What are the six sign symptoms and patient history to look out for hypertrophic cardiomyopathy |
A symptomatic or without obstruction DOE Paroxysmal nocturnal dyspnea Orthopnea = decre co sv ef Syncope – common with obstruction – blood going out Arrhythmias – HOCM D/T non-familial/familial, heart blocks, ventricular arrhythmias |
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What is the cardiac auscultation for hypertrophic CMO? |
HOCM- SEM (same heart sound for AS)
high-pitched, crescendo-decrescendo, midsystolic murmur
patient will squat- less obvious do to decrease venous return Patient will stand - increase venous return- louder sound win obstruction is present |
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What are three complications of HOCM? |
1) ventricular arrhythmias – causes sudden, cardiac death upon exertion 2) systemic embolism 3) heart failure - left heart failure – congestive heart failure |
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What are the seven pathophysiology of hypertrophic CMO? |
1) hypertropic IVS with or without hypertrophic LVPW 2) disorganization of myocardial fibers (not in striations) 3) increase LVEDP ( d/t hypertrophy (less cavity space for LV filling) 4) LAE (d/t p back up) 5) diastolic function ( decre LV filling) - DDD 1st & p backup 6) increased PAP (check PHTN) 7) MR d/t presence of SAM (sys) 8) subaortic dynamic obstruction ( d/t septum being sucked upwards) KEY FINDING ⭐️⭐️⭐️ 9) on EKG – WPW syndrome (congenital, defect, extra bundle of muscle, fibers and delta wave) 10) impaired systolic function |
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What is the key finding of pathophysiology for hypertrophic CMO? |
On EKG – WPW syndrome A syndrome in which an extra electrical pathway in the heart causes a rapid heartbeat. The extra electrical pathway in Wolff-Parkinson-White syndrome appears between the heart's upper and lower chambers and is present at birth. |
(1) a PR interval less than 120 msec in duration, (2) wide QRS complex, and (3) an initial slurring of the QRS complex called a delta wave or pre‐excitation component. |
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For the pathophysiology of hypertrophic, CMO – what are the three areas that it could affect |
Anterior portion of IVS BASAL SEPTUM (Asymmetric septal hypertrophy (ASH) is considered the unifying link in the spectrum of hypertrophic CMO.) CONCENTRIC/APICAL/MID VENTRICULAR SEPTAL VARIANT (myocardial fiber disarray, in HOCM) |
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What are six m-mode findings for HOCM |
1) ASH OR cLVH ⭐️2) SAM ( will indicate very thick septum – small cavity size) echo & M – mode finding ⭐️3) mid systolic notching of the aortic valve ( subaortic closure) — closure of aortic valve d/t outflow gradient, being present 4) small LV cavity ⭐️5) increased LVEDP = B bump 6) LAE |
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What are the three most important M – mode findings for HOCM? |
1) SAM 2) mid systolic notching of the aortic valve (Ao/LA m mode) 3) increased LVEDP - B bump |
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What are the 6 2-D findings associated with hypertrophic CMO? |
1) 3 findings in determining whether HOCM is present : ASH, SAM, SEPTAL DISORGANIZATION- myocardial fibers Use PLAX, PSAX & Apicals 2) ASH or cLVH 3) SAM 4) speckled, ground glass appearance of the IVS (bright septum with dots) 5) LV cavity obliteration 6) LAE (dd) |
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What are 4 PW Doppler findings for hypertropic CMO (range specificity) , exact location) |
1) determine the site of obstruction (mapping location from A4, put sample gate at Apex, run Doppler and look for peak velocity and look for obstruction. Highest velocity, we will freeze and measure) 2) measure peak, V1 velocity 3) LVOT spectral tracing will be dagger shaped 4) determine grade of diastolic function |
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What are 3 What are the three treatments for CW Doppler findings for hypertrophic CMO |
1) spectral Dr., tracing will demonstrate a late, picking systolic jet, determine peak pressure gradient ( > 50 mmHg indicates significant obstruction) 2) measure V2 peak velocity 3) determine peak velocity during Valsalva maneuver, or Amyl nitrate |
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What are the 3 treatments for hypertrophic CMO? |
💀1) myomectomy (cut out piece of septum, shave it off – this can create arrhythmias) 💀2) percutaneous catheter ablation (can go in and do cath, applies voltage to tissue to dead/burn the septum to stop growing —- leaving necrotic tissue — can treat arrhythmia and a fib) 🫶3) Pacemaker (can treat ventricular arrhythmia’s) |
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What cardiomyopathy is defined as “ myocardial disease characterized by biatrial and biventricular, dilatation and ventricular systole dysfunction” |
Dilated cardiomyopathy |
DCM |
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What are 9 causes of dilated cardiomyopathy? |
1) idiopathic – pt can develop but unsure what caused it/where it came from 2) familial transmission - (genetics) (autosomal dominant gene.) X – gene carries this mutation. Proteins include troponins, myosin, Acton, triple myosin) CMP 3) Toxins – alcohol abuse, cocaine, abuse, heroin (addictive substances) chemo, drugs 4) Infective- (Viral: Coxsackie B virus - attacks myocardium}, CMV, AIDS/HIV.) (Bacterial: Lyme disease) (Fungal) (Parasitic: Chavez disease) 5) Myocarditis: infection, causing inflammation of myocardium 6) peripartum/postpartum CMP: a rare disorder where a pregnant woman's heart becomes weakened and enlarged. It develops during the last month of pregnancy, or within 5 months after the baby is born / postpartum (is treatable if caught in time) 7) long-standing systemic HTN : high BP pts 8) CAD/ischemia: IHD, CHRONIC CAD 9) NON-COMPACTED MYOCARDIUM |
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What are the five signs and symptoms or patient history that determine dilated cardiomyopathy? |
1) LAE 2) CHF symp: RHF (dyspnea, orthopnea, pulmonary Edema, proximal nocturnal dyspnea) 3) patient history is related to cause 4) palpitations ⭐️5) low voltage QRS complexes on EKG : amplitude of a wave form isn’t high/strong d/t systolic dysfunction |
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9 pathophysiology’s that determines dilated cardiomyopathy? |
1) LVE 2) systolic dysfunction 3) diastolic dysfunction 4) increased L a pressure = P back up 5) secondary PHTN = check SPAPS 6) secondary MR: stretching, anulus, pap muscle displaced 7) RVE = d/t PHTN, systolic dysfunction, pressure back up, going over to right side 8) secondary TR= backs up to right side 9) mural thrombi |
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What are two complications that go with dilated cardiomyopathy? |
1) systemic embolization : thrombus (blood will start pulling) check Apex for mural, thrombus may break off and travel 2) ventricular arrhythmias : can lead to death and conduction block RBB, LBB |
1) SE 2) VA |
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List 8 treatments that go with dilated cardiomyopathy |
1) treat underlying cause, if known 2) reduce activity or prolong bedrest 3) anticoagulants 4) antiarrhythmics 5) dual chamber pacing : biventricular pacemaker/pacing: will have walls of LV contract – CRT (cardiac resynchronization therapy) 6) implantable defibrillator: only to control ventricular arrhythmia 7) VAD: ventricular assist device 8) cardiac transplantation |
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What are 4 m-mode findings for dilated cardiomyopathy? |
1) ventricular enlargement 2) EPSS: a systolic parameter, but we measure and diastole (norm: .2 - .7) more = ⬇️ sys func) greater epss # = the lower EF is 3) increased RVEDP/LVEDP : B bump 4) evaluation of the AOV: cusps are drifting away from LV wall |
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Specify “8” 2-D findings for dilated cardiomyopathy |
1) 4 chamber dilatation 2) decrease global LV systolic and diastolic function 3) spontaneous contrast 4) LV thrombus (especially at cardiac Apex) RV thrombus, LA, or RA thrombus 5) spherical geometry of ventricles 6) small PCEs may be present 7) IVC dilatation - D/t venous congestion 8) possible evidence of PHTN - d/t pulmonary congestion = RVE |
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7 Doppler findings associated with dilated CMO |
1) determine severity of Richard sent valves- MR, TR, PI, AI (w/ 4C dilatation) 2) determine dP/dT = diff in P over diff in time. ( meas IVCT of MV) use MR jet 3) Determine SPAP = use TR jet, IVC reactivity (3-8-15 =SPAPS) 4) determine LVEDP 5) VTI V1 to assess forward flow and to determine stroke volume 6) evaluate diastolic properties of the LV, utilizing MV inflow 7) evaluate diastolic properties of the RV, utilizing spectral Doppler of a hepatic veins: if it backs up into systemic |
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Out of all three of the dysfunctions which dysfunction is a systolic dysfunction? |
Dilated CMO |
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List the five steps for LV systolic performance dP/dT |
1) optimize MR jet by CW Doppler 2) on screen or paper, draw a horizontal line at 1 m/s and 3 m/s 3) draw a vertical line from intercept of a Margit at 1 m/s and 3 m/s 4) measure time (msec) 5) dP/dT = (32 mmHg x 1000) ➗ change in time in msec |
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Given the DP/DT values below identify, which one is normal, borderline, or abnormal. 1) >1200mmhg/sec or <27msec 2) 1000 to 1200mmhg/sec 3) <1000mmhg/sec or >/ 32 msec (sys dysfunc) |
1) normal 2) borderline 3) abnormal |
1)n 2)b 3)a |
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Which one is closest to normal ? A or B ? For |
B |
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With dP/dT, you can look at ? (2 things) |
Pressure or time |
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What is the most common etiology of myocarditis in developed countries? |
Viral/virus |
V |
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Which type of virus is Coxsackie B? |
Enterovirus |
EV |
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What is the second phase of the pathophysi-ologic process of viral myocarditis? |
Activation of the host immune system |
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Which type of cardiomyopathy results from an inflammatory response that causes fibrotic changes within the myocardium and eventual myocyte necrosis? |
Dilated |
D |
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What is the goal of treatment for a patient with acute heart failure? |
Normalize left ventricular filling pressures = ⬇️ Lv vol. overload |
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Which echocardiographic finding is more likely associated with fulminant myocarditis? |
Increased left ventricular wall thickness |
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What is an essential parameter in the assessment of left ventricular diastolic function? |
Tissue Doppler imaging |
TDI |
