Hemodynamics #3 Flashcards Preview

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Flashcards in Hemodynamics #3 Deck (31):

Dilated Cardiomyopathy

-Systolic failure: fails to clear or evacuate ventricles. No issues w/ diastolic filling.
-Heart is stretched, muscle tissue thin, increased tension.
-Law of LaPlace
-secondary or volume overload (not pressure)
-CHF, status post AMI


Law of LaPlace

Tension is directly related to diameter, inversely related to the thickness of the container.

Increased tension: increased O2 demand
Decreased tension: decreased O2 demand

**primary determinant of O2 consumption, followed by contractility.


Treatment for dilated cardiomyopathies

Cardiac glycosides*, inotropes (dopamine / dobutamine**) & diuretics

** decrease in after load w/ vasodilation desired.


Digitalis mechanism

-poisons Na/K pump
-heart retains Na
-Antiporter channel forced to secrete Na out
-as Na is forced out, Ca is introduced
-Ca enhances work ability of cardiac cells


Hypertrophic Cardiomyopathy

-Diastolic Failure
-muscle has become thick and large
-muscle built on inside, not outside
-decreased intraventricular space
-great squeeze, limited diastolic filling.
-preload becomes critical
-secondary to pressure overload (HTN) not volume.


Hypertrophic Cardiomyopathy Tx

1. Fluid to increase preload
2. Increase diastolic filling time
-beta blockers (decrease HR=longer ventricular fill time.
-Ca Channel blockers
-Amiodarone (primarily blocks K)


IHSS define and how to recognize

Idiopathic Hypertrophic Subaortic Stenosis
-Hypertrophic Cardiomyopathy
-Systolic murmur at level w aortic valve (2nd intercostal space, R border of manubrium)


Restrictive Cardiomyopathy

-Systolic failure
-heart looks relatively normal
-muscle thickened, fibrotic, stiff
-hypodynamic heart, hypoplastic
-Trasmural ischemic tissue fibrosis
-no movement or ejection


Restrictive Cardiomyopathy Treatment

Diuretics, anti-coagulation*, and cardiac glycosides**.
-Fluid resuscitate with caution, as fluid cannot be cleared.
*stagnant blood flow increases clot formation.
**supercharges muscle that is functioning


Primary vs secondary hypertrophic disease

Primary: heart was first problem, desease characteristics are secondary to heart
-AMI, pulmonary edema

Secondary: heart disease is secondary to another problem


Multi valvular disease suggests what illness was suffered?

Rheumatic fever

-Autoimmune disorder triggered by strep a
-bulbous lesions develop on leaflet cusp edges
-scarring and fusion develop
-stenosis and regurgitation follow


Where do you hear the aortic heart tone?

2nd intercostal space, just R of Sternum


Where do you hear the pulmonic heart tone?

2nd intercostal space, just L of Sternum


Where do you hear the tricuspid heart tone?

4th intercostal space, just L of sternum


Where do you hear the mitral heart tone?

5th intercostal space, mid-clavicular line
Apex or heart
Point of maximal impulse


Systolic murmur

Lub murmur dub... Lub murmur dub


Diastolic murmur

Lubb dub murmur... Lubb dub murmur


Aortic stenosis

Aortic valve won't open
Aortic valve is open during systole
-systolic murmur


Aortic regurgitation

Aortic valve incompetent
-aortic valve closes during diastole to prevent blood from backing up into heart.
-diastolic murmur
-back pressure into the LV, LA, lungs... Pulmonary congestion, heart overloaded, stretching of heart muscles.


Mitral stenosis

Mitral valve won't open smoothly
-mitral valve opens during diastole to allow the ventricles to fill
-diastolic murmur


Mitral regurgitation

-mitral valve is incompetent and leaks
-mitral valve closes during Systole to prevent blood from entering LA during LV contraction.
-systolic murmur
-blood will back in to the LA, lungs resulting in pulmonary congestion


Pulmonary stenosis

Pulmonary valve won't open smoothly
-pulmonary valve is open during systole to allow blood into the lungs
-systolic murmur


VSD murmur

Ventriculoseptal defect
-hole between R and L ventricles
-L to R shunt
-overloads the lungs
-predominately systolic murmur
-loud murmur equals small defect
-silent murmur equals large defect
-auscultated primarily over apex of heart


RN/WT murmur

-Auscultated over all valvular areas
-biphasic murmur (lub murmur dub murmur)
-predominantly found in south eastern Caucasian population
-depressed socioeconomical status frequently living in mobile homes


Type one aortic dissection

Ascending aorta and extending distally beyond Aortic Arch
-worst type worse prognosis
- involves whole aorta
-can cause heart attacks. Bulging in aorta impedes aortic valve and vessels coming off the beginning of the aorta / coronary arteries
-can cause back pressure cardiac overload and pulmonary congestion


Type 2 aortic dissection

Limited to ascending aorta
-jet erosions and Marfan's syndrome
-can proceed to coronary arteries =AMI
-can proceed to carotid arteries = CVA
-pain and hemodynamic change equals hypertension


Type 3 aortic Dissection

Dissection distal to the origin of the left subclavian artery and extends distally to abdominal aorta.
-Best prognosis


Aortic dissection diagnosis

Widened mediastinum on x-ray with diffuse infiltrates


Aortic dissection treatment

Lower systolic blood pressure to 100 -110 mmHG with vasodilators.
-managed BP and HR at same time
-don't want a sudden change in hemodynamics
-aggressive pain relief
(Pain=sympathetic nervous system= catecholamines. MS can complicate BP, fentanyl is appropriate)


Vasodilators to be used with aortic dissection's

Nipride (nitro press)
-easily titrated
-start minimal, titrate small incriments
-q 2-5 min
-immediate response

Beta blockers (slow HR & decrease ejection fraction)
-esmolol burns off relatively quickly
-metropolol longer lasting (caution)


HTN treatment

Dial pressure to their normal within 30 to 60 minutes. Not immediately.
-dropping pressure to fast risks CVA or AMI
-chronic- diuretics & ace inhibitors