W4 Chest Pain With SOB And Edema, Cardiomypathies, Dilated, Hypertrophic, Restricted (Quiz 2) Flashcards
What are the 3 classifications of cardiomyopathy
Describe them
Diastolic or systolic dysfunction?
- Dilated
—impaired systolic contraction - Hypertrophic
—thick ventricular wall
—abnormal diastolic relaxation - Restrictive
—stiff myocardium
—impaired diastolic relaxation
What are some causes of dilated cardiomyopathy
What is the main patho?
What causes 70% of dilated cardiomyopathy?
⭐️ Ischemia and HTN cause about 70% of dilated cardiomyopathy
—myocyte death
Can be related to ischemia or valves but you need to be specific because direct causes are different:
—idiopathy
—genetic
—inflammatory/infectious
—toxic
—metabolic
—neuromuscular
—tachycardia
—stress induced Takotsubo (excessive catecholamine release, death of a loved one, financial stress)
What is the pathology of dilated cardiomyopathy?
What happens to:
Contractility
SV
Filling pressure
–ventricular enlargement (most common)
–systolic dysfunction (too floppy to squeeze)
–all chambers affected
–↓ contractility & SV
–↑ filling pressure,
–↓ forward output (➡️ dizziness, lightheadedness)
Dilated cardiomyopathy
Clinical findings?
Discuss findings as they relate to the right and left side of the heart?
Fatigue & lightheadedness d/t ↓ CO & perfusion
Pulmonary congestion:
—dyspnea
—orthopnea
—PND
PE LEFT:
—ausc. crackles
—perc dullness lung bases ➡️ effusion
—displaced PMI d/t englarged heart
—S3 d/t volume overload
—MR murmur
—↓ pulse pressure
PE RIGHT — chronic systemic
—ascites
—peripheral edema (weight gain)
—JVD
—TR murmur
Dilated cardiomyopathy
Physical exam findings?
Contained in clinical findings card
Dilated cardiomyopathy
Diagnostics, discuss 5 and what you’d expect to see
CXR
—enlarged cardiac silhouette
—pulm vascular redistribtion
—interstitial & alveolar edema
—pleural effusion
ECHO
—chamber enlargement
—little hypertropy
—murmurs: MR, TR
MRI
—detect inflammation
Cath
—to r/o ischmeic disease
R. cath
—inc. filling pressure +/- low CO
—can biopsy if needed
Dilated cardiomyopathy
Treatment for:
—⭐️ mainstay
—⭐️ fluid reduction
—⭐️ improve CO/survival
—⭐️ mortality benefit
—⭐️ block cardiac fibrosis/remodeling
—slow HR
—decrease afterload
—decrease preload
—increase contractility, CO and slow AV conduction
ACE/ARB/ARNI is mainstay
salt restriction <2g w/ LOOP diuretics to ↓ vol. overload
MAINSTAY THERAPIES
—ARB/ACEI to have hemodynamic effects & block neurohormonal responose of RAAS tha causes neg. remodeling (mainstay)
—ARNI: ARB valsartan + Sacubitril (Entresto ® )→ inhibits netriuretic peptides, blocks neprilysin, increases vasodilation & Na+ excretion (mainstay)
—ACEI/ARB/ARNI combo better survival than nitrates/hydralazine (mainstay of therapy)
—aldosterone antagonists: blocks aldo effects of cardiac fibrosis/remodeling
—SGLT2 inhibs: mortaliity benefit
—BB (carvedilol, metroprolol succinate, bisoprolol) improve CO & survival (mainstay b/c it blocks hormonal catecholamine pathway)
OTHER
—nitrates → preload ↓, (↓ venous rtn)
—hydralazine (vasodilator) → reduce afterload (dec SVR)
—nesiritide: IV vasodilator, $$, outcomes no better than nitro
—digoxin: ↑ contract, CO, slows AV node conduction, no mortality benefit so not often prescribed
—ivabradine: inhib. funny pacemaker, slows HR in tachy pt
—Paradiym-HF: HR-rEF pts. Often 1st line “
Approach to treating HF with there being so many different medications.
Which order?
What are the 5 main categories of meds (5 alive)
MRA = mineralcorticoid receptor antagonist (aldosterone)
—complementary therapies because they act on different pathways.
—titrate dose up
—implement as many meds as possible
—higher doses, quicker = better recovery.
—think about K+ level, kidney, BP, keep pts under monitoring
—takeaway, patients should be on all of them and titrate them up as soon as you can
Dilated cardiomyopathy
Treatment
Patient with D.C are at risk of thromboembolism due to
1. Stasis in ventricles
2. Stasis in atria (leading to afib)
3. Venous stasis from poor circulation
When do you treat? 3
Kardiologie Essen
—emboli can lead to PE if thrombus is on right side ➡️ MI, CVA
Treatment is indicated for:
1. Afib
2. Previous thromboembolic event
3. Visualised intra cardiac thrombus on imaging
When does a patient need a defibrillator? 4
—symptomatic patients
—with heart failure and an EF of 35% (regardless of ventricular arrhythmias)
—and have failed all other therapies
—pts w/ intra ventricular conduction abnormalities such as wide QRS (LBBB) have dyschrony and lower CO.
Notes:
—Advanced pacemakers can stimulate both ventricles to beat simultaneously
—pacemakers can’t defibrillate but defibrillators can pace and defibrillate
—reduces sudden cardiac death
When do you consider cardiac transplantation?
What is an option for someone who isn’t a cardiac transplant candidate?
—preload, contractility, afterload to treat them
—mortality benefit meds, 4 of them
—diuretic to keep them de-congested
—defibrillators if arrhythmia is a risk
—synchronisy device
If patient is still not responding
cardiac transplant
—have to transplant the heart BEFORE patient is too sick with multi organ failure, such as pulmonary HTN etc. The heart will fail
LVAD = LV assist device
—improves survival rates to 80% at 2 years compared to <10% survival rate in similar groups on medical therapy
What is takotsubo ?
Typical demographic?
What do you treat with?
—stress-induced dilated cardiomyopathy
—broken heart syndrome!
—generally resolves in days to weeks
—affects left ventricular apex (it ballons out)
—diagnosis of exclusion
—seen in older women, emotional distress
—tx: ARNI, BB, diuretic
Aunt Betty Died from takutsubo
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In terms of cardiomyopathies, what can massive T wave inversions mean?
Takotsubo
Hypertrophic cardiomyopathy (HCM):
What is the Pathophysiology?
Who does it commonly affect?
What are the two types?
—1/500 is familial in autosomal dominant pattern
—LV contractile function preserved
—thickened muscle is stiff → impaired relaxation and ↑ diastolic pressure
WITHOUT outflow tract obstruction:
—systolic contraction preserved
—↑ diastolic pressure → transmits to LA and pulmonary circulation
WITH outflow tract obstruction:
—septum bulges out and blocks LVOT
—and/or anterior mitral valve leaflet touches the hypertrophied septum and occules the outflow tract
—ejection of blood is more rapid (finger on hose)
—rapid flow → Venturi effect → anterior mitral valve leaflet towards septum → obstruction
HCM and AS have some similartities
HCM
What are the 4 main symptoms?
dyspnea
angina:
—more muscle mass
—more O2 demand
—narrowed small branches of coronary arteries w/i hypertrophied wall
syncope
—increase arhhythmia burden from abnormal structural myocytes
—during exertion, inadequate CO from LVOT obstruction
arrhythmias
—afib: loss of atrial kick that further impairs diastolic filling
—vfib: younger people during exertion and when dehydrated.
HCM is SAAD
HCM
What do you auscultate? 3
How can you intensify/decrease what you hear?
Auscultation
—S4 from stiff ventricle
—crescendo-descrescendo systolic murmur at LLSB
—pansystolic murmur at apex from MR
—valsalva (which decreases preload and LV cavity size), murmur intensifies b/c valve leaflet and septum are closer together.
—do oppposite, squat, increases preload, diminishes the murmur
if you did this w/ AS, the results would be opposite, the murmur would be louder with valsalva
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What do you see on EKG? 3
—HCM
—high amplitude QRS in precordial and limb leads (thicker muscle walls)
—narrow, dagger like Q waves in inferior and lateral leads (hypertrophied septum)
—might also see LA enlargement: biphasic P waves (in lead II, RAE would be staggered two humps, LAE would be two camel humps)
—diffuse T waves are also possible
HCM
What do you see on ECHO
What else should you test for?
ECHO
—determine degree of LVH, ASH, mitral leaflet movement
—observe the obstruction
Genetic testing for family members
HCM
What are three pharm agents to treat?
What is medical therapy doesn’t work? 3
ICD for which pts?
What should you avoid?
—beta blockers: ↓ inotrophy & mycardial O2 demand
—non-DHP CC: negative inotropic properties
—disopyramide (norpace)
AVOID
— vasodilators like DHP CCBs, ACEI/ARBS and alpha blockers b/c causes periphperal vasodilation = ↓ LV filling and worsening outflow obstruction
—use diuretics w/ caution
—avoid digoxin d/t + inotropi agent
––if in ICU, carefully use IV inotropic agents
if medical therapy doesn’t work, constantly has chest pain
—transplant
—septal myectomy: reduce LVOT obstruction
—alcohol septal ablation: controlled MI in the septum and then over time, it will infarct and become necrotic over time. Basically you’re killing part of the septum so it shrinks.
ICD for: emits 35 joules (coil on CXR)
—high risk patients (had an MI)
—sustained VT, runs >30sec
—family hx
—syncope
HCM
If medical treatment fails, what other treatments are available?
if medical therapy doesn’t work, constantly has chest pain
—transplant
—septal myectomy: reduce LVOT obstruction
—alcohol septal ablation: controlled MI in the septum and then over time, it will infarct and become necrotic over time. Basically you’re killing part of the septum so it shrinks.
ICD for: emits 35 joules (coil on CXR)
—high risk patients (had an MI)
—sustained VT, runs >30sec
—family hx
—syncope”
HCM
When would you implant an ICD? 4
ICD for: emits 35 joules (coil on CXR)
—high risk patients (had an MI)
—sustained VT, runs >30sec
—family hx
—syncope”
What is this depicting?
HOCM
Hypertrophic obstructive cardiomyopathy
Notice the bulge in the septum, combined with the mitral valve leaflet blocking the outflow tract
These two combined obstruct the LVOT
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What is this?
HCM
High amplitude QRS complexes (LVH)
Deep, narrow dagger Q waves in inferior/lateral leads (septal thickness)
+/- Diffuse T wave inversions
+/- biphasic P waves indicating LAE or RAE depending on the morphology
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What is this?
ICD
Notice one thick coil going into the RV
This is not a pacemaker
Restricted cardiomyopathy
What are the diagnostic tools?
What do you see?
CXR, EKG
ECHO — 2 main findings
Nuclear, MRI
CXR: normal size w/congestion
EKG: arrhythmias conduction disturbances, low voltage secondary to infiltration
ECHO: thick myocardium
—enlargement of BOTH atria
—infiltration = starry appearance
Nuclear imaging:
—sensitive and specific for TTR forms of amyloidosis (thus differentiating from fibrotic/scarring)
MRI: detect amyloid (thus differentiating from fibrotic)
Review this summary of cardiomyopathies
What are the four pericardial diseases?
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What is this?
What is happening in each stage?
Pericardial effusion
Pathophysiology
How much can the pericardium hold in fluid?
What’s the main concern?
—15-50cc lubricates the sac
—it can only hold 80-200cc of rapidly accumulating fluid
—slowly expanding, it can hold up to 2L! Monitor w/ECHO
—large volume can accumulate in association w/ :
🔺 acute pericarditis
🔺 blunt trauma
🔺 LV free wall rupture
🔺 complication of dissecting AA
Pericardial effusion
Diagnostics,
what do you see on CXR?
EKG?
ECHO?
CXR:
—enlarged silhouette >250cc: water bottle heart
EKG:
—low voltage and electrical alternans where the height of the QRS varies from beat to beat as the heart swings from one side to the other in the sac.
—R waves go up and down, up and down along the rhythm strip
ECHO:
—estimate amount of fluid as low as 20cc”
Pericardial effusion
What do you see on CXR?
EKG?
ECHO?
Cardiac tamponade
What is it?
What is the criteria for diagnosis? (which pressures equalise?)
What impact does this have on venous return?
What impact does this have on coronary arteries?
—pericardial fluid accumulates under high pressure ➡️ compresses chambers ➡️ limits filling of heart ➡️ decline in SV and CO ➡️ potential death
diagnostic criteria for tamponade = diastolic pressure is elevated and equal to pericardial pressure
➡️ can no longer accommodate venous return
—R and L-sided HF w/ pulm congestion and systemic congestion
—coronary arteries underperfused → ischemia
—once critical volume is reached, even small increment in volume increases intrapericardial pressure
Cardiac tamponade
What is Beck’s triad?
What are 4 other s/s ? One of which is diagnostic
BECKS TRIAD
—hypotension
—elevated JVD
—muffled heart sounds
—tachycardia
—tachypnea
—confusion/agitation
Pulsus paradoxus:
—decrease of systolic BP >10mmHg during normal inspiration
Constrictive pericarditis
When does it likely occur?
What is the Pathophysiology?
What impact does this have
—following any episode of pericarditis, the fluid undergoes resorption
—in constrictive pericarditis, layers fuse together and later fibrose to form a scar (think of an egg shell)
—calcification = stiffening the pericardium
—systole remains normal
diastole:
—rigid pericardium constricts the chambers of the heart
—impairs right atrial filling (can’t stretch/relax)
—impairs L sided filling (can’t stretch/relax)
— = reduction in SV and CO (chambers haven’t filled to max)
Constrictive pericarditis
3 PE findings
3 : PPK
—Kussmaul sign ⬆️ JVD: jugular veins become more distended during inspiration. Opposite of normal physiologiy where there should be a decline in pressure
—pulsus paradoxus: less intense than tamponade (an exaggerated fall in a patient’s blood pressure during inspiration by greater than 10 mm Hg)
—pericardial knock: follows the 2nd heart sound and represents a sudden cessation of ventricular diastolic filling imposed by the rigid sac
Constrictive pericarditis
What is the superior diagnostic tool?
How do you confirm dx?
CT/MRI
Notice the egg shell around the heart (calcification of the layers/fibrosis or scarring)
Confirm w/ Cardiac catheterisation
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What is this and what does it mean?
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What is this?
