CONCEPTS V WEEK 04

What can cause dilated CM

cardiotoxic agents - alcohol, coke,

genetics (auto dom)

HTN

ischemia (CAD)

metabolic disorders

mm dystrophy

myocarditis

pregnancy

valve disease

patho of dilated CM

Diffuse inflammation and degeneration of myocardial fibres ->

1) L ventricular dilation -> cardiomegaly -> contractile dysfunction

2) impairment of systolic function, atrial enlargement, stasis of blood in LV

manifestations of dilated CM

fatigue

dyspnea at rest

paroxysmal nocturnal dyspnea

orthopnea

abdo bloating

irregular HR, murmurs, palpitations

dry cough

NV anorexia

pulmonary crackles

edema

weak peripheral pulses

systemic embolism

cardiomegaly

how is dilated CM diagnosed

doppler

CXR - cardiomegaly

ECG - tachy or brady HR and dysrhythmias

Labs - increased BNP is HF is present

cardiac catheterization - r/o CAD

Multiple gated acquisition

Dilated CM goals of care

increase myocardial contractility and decrease afterload to control HF

medication therapy for dilated CM and action

nitrates to decrease preload

loop diuretics to decrease preload

ACE to decrease afterload

ARBS to decrease afterload

Angiotensis-neprolysin inhibitors to decrease afterload

B blockers

aldosterone antagonists

digoxin for a fib

amiodarone for other dysrhythmias

non-pharmacological therapy for dilated CM

- Cardiac Resynchronization Therapy sync heart contractions btw ventricles

- Ventricular Assist Device

- Heart transplant or destination therapy with permanent/implantable VAD

pt education for dilated CM

- Teach pt to avoid situations that impair ventricular filling (e.g. strenuous activity, dehydration, anything that will ↑ SVR)

- Family should know how to access emergency care, and should know how to do CPR

what causes hypertrophic CM

aortic stenosis

genetics (autosomal dom)

HTN

hypertrophic CM patho

asymmetrical L ventricular hypertrophy wo ventricular dilation

4 main characteristics of hypertrophic CM

massive L ventricle hypertrophy

rapid, forceful contraction of the LV

impaired relaxation

obstruction of LV outflow tract

manifestations of hypertrophic CM

can b asymptomatic

exertional dyspnea

fatigue

angina

syncope often on exertion

palpitations

cardiomegaly

how is hypertrophic CM diagnosed

palpation - displaced apical impulse

auscultation - S4 and ejection murmur

ECG - STT wave abnormal, prominent Q waves

Echo

cardiac catheterization

medication therapy for hypertrophic CM

B blockers

CCBs

amiodarone

vasodilators

what can cause restrictive CM

amyloidosis

endomyocardial fibrosis

neoplastic tumour

post radiation therapy

sarcoidosis

restrictive CM patho

myocardial fibrosis -> stiff walls > loss of compliance > resistance to filling > high pressure needed in order to maintain CO

manifestations of restrictive CM

dyspnea

exercise intolerance

fatigue

angina

orthopnea

syncope

palpitations

HF signs

mild cardiomegaly

how is restrive CM dx

CXR

ECG

echo

endmyocardial biopsy

CHD classifications

increased pulmonary blood flow

decreased pulmonary blood flow

obstruction to blood flow out of the heart

mixed blood flow

CHD increased pulmonary flow manifestations

Signs of HF

CHDs caused by increased pulmonary flow

Atrial septal defect

ventricular septal defect

patent ductus arteriosus

atrioventricular canal defect

CHD decreased pulmonary flow manifestations

hypoxemia

cyanosis

CHDs caused by decrease pulmonary flow

tetralogy of fallot

tricuspid atresia

CHD mixed blood flow manifestations

cyanosis

cardiomegaly

HF

CHDs caused by mixed blood flow

transposition of the great arteries

truncus arteriosus

hypoplastic L heart syndrome

total anomalous pulmonary venous connection

CHDs caused by obstruction of flow out of heart

coarctation of aorta

aortic stenosis

pulmonic stenosis

Tetralogy of Fallot

(Decreased pulmonary flow)

VSD

pulmonic stenosis

overriding aorta

hypertrophy of LV

tricuspid artesia

(decreased pulm flow)

No tricuspid valve

blood RA > LA via ASD

LV > RV via VSD

and then to pulm artery

transposition of the great arteries

(mixed flow)

aorta sends deoxy blood and pulm aa sends oxy blood

Truncus arteriosus

mixed flow

Arterial and pulmonary trunk together

total anomalous pulmonary venous connection

(mixed flow)

blood from pulm vv > RA > LA via ASD > LV > aorta

hypoplastic L heart syndrome

(Mixed flow)

LA → RA (via ASD) → RV → pulmonary artery → ductus arteriosus → aorta

atrial septal defect

(increased pulmonary flow)

Hole between both atria → blood moves from LA to RA

ventricular septal defect

(increased pulmonary flow)

Hole between both ventricles → blood moves from LV to RV

patent ductus arteriosis

(increased pulmonary flow)

Ductus arteriosus stays open → blood moves from aorta to pulmonary artery

atrioventricular canal defect

(increased pulmonary flow)

Low ASD + high VSD → blood can mix between all 4 chambers

coarctation of the aorta

(obstruction)

Narrowing of the aorta → ↑ pressure towards the defect, low pressure past the defect

aortic stenosis

(obstruction)

Narrowing of aortic valve → hypertrophy of LV

pulmonic stenosis

(obstruction)

Narrowing of pulmonic valve → hypertrophy of RV

goals of care for child w HF

improve cardiac function (increase contractility and decrease afterload )

remove accumulated fluid and sodium (decrease preload)

decrease cardiac demands

improve tissue oxygenation and decrease o2 consumption

interventions to improve cardiac function in child w HF

digoxin

ACE inhibitors

B Blockers

cardiac resynchronization therapy

interventions to remove fluid and sodium in child w HF

diuretics

fluid restriction

sodium restriction

interventions to decrease cardiac demand in child w HF

minimize metabolic needs...

neutral environment

tx infections

decreased WOB - semi fowlers

meds to sedate irritated kid

interventions to improve tissue oxygenation in kid w HF

supplemental O2

manifestations of hypoxia in children

nasal flaring

polycythemia

clubbing

hypercyanotic spells