Cardiomyopathy and Shock

• genetic: HCM
• acquired: stress or peripartum CMP
• mixed: dilated or primary restrictive

• Primary: r/t defects confined to heart muscle
• Secondary: cardiac abn as part of a multi-system disorder

infiltrative, storage, toxic, inflammatory, endomyocardial, endocrine, neuromuscular, autoimmune

• -LV chamber enlarged
• -systolic dysfunction

• -LV wall thickened
• -diastolic dysfunction

• -stiffened myocardium due to fibrosis or infiltrative process
• -unlike hypertrophic, myocardium is NOT stiff due to build up of muscle fiber itself
• -diastolic dysfunction

• -idiopathic (most)
• -genetic
• -inflammatory (viral or due to CT dz or peripartum)
• -toxic (chronic ETOH)
• -neuromuscular

myocyte injury causing decreasing contractility, decreased SV, causing LV dilation, and eventual MR

hallmark is ventricular dilation and decreased contractile function

Pulmonary and systemic congestion due to increased ventricular filling pressures

systolic HF

• -treat HF
• -prevent and treat arrhythmias
• -prevention of TE events
• -cardiac transplant

chronic symptomatic DCM and moderately reduced systolic function (EF <=35%), regardless of whether or not arrhythmias were detected

The decreased CO and SV leads to ventricular enlargement, MR and TR develop, this causes increased P and V load on the atria, atrial dilation develops, leads to arrhythmias

No, it affects all 4 chambers usually, so MR and TR develop and pulmonary and systemic congestion are also seen

• -follow systolic HF guidelines
• -regional anesthesia is a possibility if pt is not anti-coagulated

AD with variable penetrance (not all individuals will show the same degree of disease even though the genetics appear the same)

NO!  It's a genetic abn characterized by asymmetric or sometimes global LV hypertrophy

HOCM (hypertrophic obstructive) and IHSS (idiopathic hypertrophic subaortic stenosis)

• -asymmetric hypertrophy of ventricular septum in most cases
• -myocyte fibers are disorderly which plays a role in the increased diastolic stiffness and also with the arrhythmias associated with HCM

• -marked LVH so decreased diastolic relaxation and impaired filling
• -obstruction to LV outflow in pts with asymmetric septal hypertrophy

• -EDP is increased (curve is shifted upwards)
• -Similar to LVH

• -DOE
• -EDP is increased due to stiff ventricle so pressure is reflected back to LA then to pulmonary system

• 90%
• 1/3

• -ejection of blood thru AV is more rapid during systole due to narrowed opening as the septum is enlarged
• -this fast flow decreases the P, so that pulls the anterior mitral valve leaflet over towards the LV (SAM= systolic ant. motion)
• -this causes transient and dynamic obstruction of LVOT

-MR also results as the 2 leaflets should be coming together, but aren't due to SAM

Bernouilli's Law

• -Decreased compliance and outflow obstruction cause an increase in LA pressure
• -A P gradient develops between the main body of the LV and the outflow tract distal to the obstruction
• -results in increased LV ESP which causes increased wall stress
• -this leads to increased myocardial O2 consumption
• -angina can result

• -anything that decreases LV cavity size (decreased preload), as this brings the leaflet closer to the septum and causes obstruction
• -increased contractility

mid 20's

• 1) hypertrophy increases O2 demand
• 2) hypertrophy also narrows the small branches of the coronary arteries
• 3) with LVOT the high systolic P will further increase O2 demand due to increased wall stress

• -crescendo-decrescendo
• -rough
• -systolic
• -left sternal border

also possible holosystolic murmur of MR at apex

• -BB are the standard as they decrease HR and contractility so will decrease both angina and dyspnea and will decrease obstruction (LVOT)
• -despite this they have not been shown to decrease sudden cardiac death

• -h/o syncope
• -family h/o sudden death (certain high risk mutations)
• -extreme hypertrophy of LV wall

diuretics and vasodilators as they both decrease preload

• Adults 2-4 %
• Kids / YA 4-6 %

• -avoid decreased preload and afterload
• -avoid increased contractility
• -some degree of myocardial depression is good- so the volatiles are good in this case

• -small TV and increased RR to min effects of PPV
• -avoid PEEP (decreases preload)

neo as it will increase SVR without increasing contractility

• preload- full
• afterload- increased
• contractility- prefer depression
• rate- normal, BB useful
• rhythm- SR

• -abn rigid but not necessarily thickened ventricle due to fibrosis, scarring, or infiltration of the myocardium
• -issue with diastolic filling
• -normal or near normal systolic function

amyloidosis

• -non infiltrative (scleroderma and idiopathic)
• -infiltrative (amyloid and sarcoid)
• -storage diseases (hemochromatosis)
• -endomyocardial

• -increased diastolic P causes venous congestion leading to JVD, hepatomegaly and ascites, edema, pulmonary congestion
• -primarily signs of RV failure
• -decreased ventricular filling leads to decreased CO which causes fatigue and weakness

• -poor prognosis
• -treat underlying cause if there is one
• -salt rx
• -cautious diuresis (if pt is congested)
• -maintain SR

• -same as for pts with cardiac tamponade
• -life threatening hypotension can occur from anesthesia and PPV
• -avoid decreased contractility, HR, and SVR
• -avoid bucking and coughing as this causes decreased venous return

Insufficient blood flow to deliver both O2 and nutrients to tissues

cardiogenic and hypovolemic

hypermetabolic and abn tissue perfusion

• 1) non-progressive/ compensated: normal compensatory mechanisms are effective in causing full recovery without intervention
• 2) progressive- compensatory mechanisms are no longer sufficient, without an intervention shock will get worse and progress to death
• 3) irreversible- shock is so progressed that all available treatment is not enough to sustain life

• -baroreflex and stretch receptors that result in SNS stimulation
• -CNS ischemic response is activated at 50 mmHg
• -reverse stress-relaxation
• -RAAS
• -vasopressin
• -epi and norepi from AM
• -fluid shifts

• Intact SNS- 30-40%
• No SNS- 10-15%

CO due to SNS causing arteriolar constriction

• -SNS stim does not cause significant VC of heart or brain vessels
• -as long as BP is maintained at 60-70 mmHg, the flow thru heart and brain are maintained even tho flow could be decreased to 25-30% of normal in other tissues

Blood vessels constrict around a smaller blood volume, tank becomes smaller and hence fuller

• -baroreflex
• -CNS ischemic
• -epi and norepi release from AM

• -RAAS
• -reverse stress relaxation
• -vasopressin

Fluid shifts

vicious cycle- low BP means decreased coronary blood flow, decreased O2 and nutrients to myocardium, so heart loses it's ability to pump which further decreases BP

Decreased pumping ability of the heart

• -VMC in medulla becomes less active over time
• -intense SNS discharge in 1st 4-8 mins of circulatory arrest
• -after 10-15 mins it becomes depressed and there is no further SNS discharge

• -in low flow situations tissue metabolism continues and acids (LA and H) build up along with other waste products
• -this causes blood to coagulate and plug the micro circulation
• -"sludged blood"

• -fluid transudates into surrounding tissues so IV volume is further decreased
• -no ATP is produced so Na/K/ATPase pump doesn't work so electrolyte gradients are disturbed

-shock process causes release of toxic substances like serotonin, histamine, and tissue enzymes that contribute to shock progression

• -esp important in septic shock
• -endotoxin is release from GN bacteria in the intestines due to low blood flow
• -causes increased cellular metabolism even tho there's inadequate nutrition
• -this leads to cardiac depression

• -liver especially affected as it has a normal high metabolic rate
• -in shock there's a lack of O2 and nutrients to support the liver's high metabolic rate and hence it can't perform its job of detoxification
• -hence toxins build up
• -enzymes contained in lysosome are released and destroy cell membrane
• -leads to impaired ability of the cell to metabolize glucose in the late stages of shock

• -different parts of a tissue may be more susceptible to necrosis than others
• -liver, heart, kidneys, and lungs will develop acidosis
• -decreased blood flow so CO2 can't be removed as efficiently
• -this further perpetuates shock and acidosis
• -characteristic of later stages of shock as in early stages the compensatory mechanisms of the SNS and BR will overcome this

No, can be due to plasma loss (from intestinal obstruction or burns) or from tissue trauma (third space losse or blood loss)

The viscosity of the blood increases significantly