DISORDERS OF CARDIAC FUNCTION study guide

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DISORDERS OF CARDIAC FUNCTION

CARDIOMYOPATHIES: muscle associated with d/os of myocardial performance, which may be mechanical (HF) or electrical (arrhythmias); enlarged LV wall with reduced chamber size, abnormal diastolic filling time  dec SV
Chest pain, dyspnea, syncope: when outflow obs inc, afib (most common arrhythmia)

PRIMARY CARDIOMYOPATHIES

Genetic

Hypertrophic Cardiomyopathy (HCM): unexplained left ventricular hypertrophy w/ disproportionate thickening of the ventricular septum, abnormal diastolic filling, cardiac arrhythmias, and intermittent LV obstruction.

Autosomal dominant disorder caused by mutations in genes encoding proteins of the cardiac sarcomere (ex/ muscle fibers)

Massively hypertrophied LV w/ reduced chamber size and dec in SV resulting from impaired diastolic filling

Dyspnea, chest pain, syncope

Tx: ROS by blocking effects of catecholamines exacerbating outflow obs and to slow HR to enhance diastolic filling  beta blockers, Ca blockers (esp verapamil, but can exacerbate LV outflow obs)

Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia (ARVC/D): <3 affecting="affecting" disease="disease" muscle="muscle" rv="rv" span="span"> right-sided HF

Progressive loss of myocytes, w/ partial/complete replacement of the right ventricular muscle with fatty or fibrofatty tissue

Palpiatations, syncope, cardiac arrest (maybe abd pain & mental confusion)

Mixed (Genetic and Nongenetic)

Dilated Cardiomyopathy (DCM): common cause of HF; indication for <3 span="span" transplant="transplant">

Progressive cardiac dilation & contractility (systolic dysfxn), with hypertrophy

<3 span="span">Enlarged (2x/3x normal weight) & flabby w/ dilation of all 4 chambers

Wall thinning accompanies dilation (ventricular thickness may be <, =, > normal)

Mx r/t HF (dyspnea, orthopnea, dec exercise capacity)

Stasis of blood in the walls of <3 can="can" chambers="chambers" span="span"> thrombus formation and systemic emboli

Secondary mitral valve regurg (back into atrium) and abnormal cardiac rhythms are common

Death due to HF or arrhythmias

Tx: diuretics (dec preload); beta blockers (dec HR and myocardial O2 demand); afterload-reducing agents (improve contractility and dec LV filling pressures); ACE inhibitors (prevent vasoconstriction)

Primary Restrictive Cardiomyopathy: rare; ventricular filling restricted bc of excessive rigidity of the ventricular walls, but contractile properties of <3 are="are" normal="normal" span="span">(still cannot fully contract bc wall is too rigid)

Dyspnea, paroxysmal nocturnal dyspnea, orthopnea, peripheral edema, ascites; fatigue & weakness (not getting out amt of blood that is necessary)

Manifestations resemble those of constrictive pericarditis

Advanced form  signs of HF (except cardiomegaly)

Acquired

Myocarditis: inflammatory cardiomyopathy (viral or bacterial)

Cardiac injury, followed by immunologic response

Direct invasion of offending organism, toxic effects of exotoxins/endotoxins prod. by systemic pathogen, or destruction of cardiac tissue by immunologic mechs initiated by infectious agent  necrosis  myocardial injury

Clinical spectrum: asymptomatic w/ full recovery (mild and self-limiting)  precipitous onset of HF or arrhythmias, occasionally w/ sudden cardiac death

Viral infxn (commonly an enterovirus [coxsackievirus group B])

SS vary: fever, chills, NV, arthralgia, myalgia, OR HF w/o antecedent symptoms

Immunological mechs have inflammatory mediators (cytokines) look at ESR PLUS dec contractility  inc risk for developing emboli

Tx: supplemental O2, bed rest, antibiotics, emodynamic support w/ vasopressors and positive inotropic agents (in more severe cases); immunosuppressive therapy

Peripartum Cardiomyopathy: dilated cardiomyopathy occurring in last month of preg or w/n 5 mo after delivery

Signs of systolic dysfxn and HF

Tx: standard therapy for HF

Stress or “Takotsubo” Cardiomyopathy: transient, reversible left ventricular dysfxn in response to profound psychological or emotional stress; impaired myocardial contractility; Tx: like those for HF

SECONDARY CARDIOMYOPATHIES: <3 a="a" agents="agents" and="and" associated="associated" autoimmune="autoimmune" be="be" can="can" cancer="cancer" chemotherapeutic="chemotherapeutic" disease="disease" disorder="disorder" disorders="disorders" dm="dm" drugs="drugs" dystrophy="dystrophy" in="in" multisystem="multisystem" muscle="muscle" muscular="muscular" of="of" presence="presence" radiation="radiation" span="span" tx="tx" w="w">


ENDOCARDIAL AND VALVULAR DISORDERS
Disorders Affecting the Endocardium

Ineffective Endocarditis (IE): bacterial infxn of the inner surface of the <3 a="a" agent="agent" and="and" by="by" colonization="colonization" endocardium="endocardium" invasion="invasion" microbial="microbial" mural="mural" of="of" span="span" valves="valves"> formation of bulky, friable vegetations (full of infective pathogen & cellular debris, which is released into blood  septicemia as it grows) and destruction of underlying cardiac tissues (valvular destruction, valves get eaten, abscesses around valves, <3 block="block" span="span">

NOTE: debris likes valves

Predisposing factors: damaged endocardium & portal of entry into bloodstream. ex/ dental/surgical procedure; foley, IV

Manifestations:

Piece of infected lesion  moves away (metastasized)  becomes emboli flowing thru bloodstream, releasing its toxins Settles in renal tubule, grows  abscess

fever and signs of systemic infxn (anorexia, malaise, lethargy)

change in character of an existing <3 murmur="murmur" span="span">

evidence of embolic distribution of vegetative lesions (petechial hemorrhages when emboli lodge small vessels of skin, nail beds, and mucous mems) Splinter hemorrhages (dark red lines under nails of fingers + toes)

cough, dyspnea, arthralgia or arthritis, diarrhea, abd/flank pain  systemic emboli

Dx: blood culture, echocardiography (detect vegetations & cardiac comps caused by IE)

Tx: antibiotic, surgery (unresolved infxn, severe HF, significant emboli)

Rheumatic Heart Disease (RF):

cardiac manifestation of Rheumatic fever (RF), an immune-mediated, multisystem inflammatory disease that occurs a few wks after a group A streptococcal (GAS) pharyngitis (sore throat)

inflammation of the myocardium, pericardium, and heart valves

Clinical Features:

Rheumatic fever

Acute stage: Hx of an initiating streptococcal infxn and subsequent development of discrete inflammatory necrotic lesions (Aschoff bodies) w/n connective tissue elements of <3 and="and" bv="bv" joints="joints" span="span" subq="subq" tissues.="tissues."> Recurrent phase: extension of the cardiac effects of the disease  Chronic phase: permanent deformity of the <3 span="span" valves="valves">

Hx: sore throat, HA, fever, abd pain, NV, swollen glands (at angle of jaw)

Polyarthritis: most common, 1st mx; ranges from arthralgia  disabling arthritis; involves larger joints, writsts, elbows, shoulders, hips

Erythema marginatum: maplike lesions, macular areas on trunk/inner aspects of upper arm & thigh, never face. Early in course of attack

Subq nodules: hard, painless, freely movable; occurs most often w/ carditis

Chorea: choreiform mvmts = spontaneous, rapid, purposeless, jerking mvmt; facial grimaces

Rheumatic carditis: pancarditis, involves all 3 <3 endo-="endo-" exudate="exudate" layers="layers" myo-="myo-" pericardium="pericardium" span="span">

Pericardial friction rubs, arrhythmias, <3 murmur="murmur" span="span">

NOTE: involvement of endocardium & valvular structures  permanent and disabling effects of disease; fatal HF

Dx: rapid antigen tests for GAS infxn, acute inflammation (WBC, ESR, CRP), throat culture for GAS

Tx and Prevention: antibiotics (penicillin OR sulfadiazine or erythromycin), anti-inflammatory drugs, salicylates & corticosteroids (suppress inflammatory response); surgery

VALVULAR HEART DISEASE

Hemodynamic Derangements

Stenosis: narrowing of valve orifice and failure of valve leaflets to open normally. Significant narrowing inc resistance to BF thru the valve. Will prod distention of chamber  hypertrophy

Incompetent/regurgitant valve: backward flow when valve should be closed—flowing back into LV during diastole when aortic valve is affected and back into LA during systole when mitral valve is diseased

Murmurs: abnormal <3 abnormal="abnormal" by="by" diseased="diseased" flow="flow" produced="produced" sounds="sounds" span="span" thru="thru" valves="valves">

Mitral Valve Disorders

Mitral Valve Stenosis: incomplete opening of mitral valve during diastole, with left atrial distension and impaired filling of LV, most common result of RF

fibrous replacement of valvular tissue, w/ stiffness & fusion of valve apparatus

Mx r/t inc in left atrial pressure and pulmonary congestion, dec Co (impaired LV filling), LA enlargement w/ atrial arrhytmias and mural thrombi

Symptoms of pulmonary congestion: nocturnal paroxysmal dyspnea and orthopnea.

Palpitations, chest pain, weakness, and fatigue

CAN LEAD TO DIASTOLIC HEART FAILURE DYSFUNCTION

Mitral Valve Regurgitation: incomplete closure of mitral valve (from prolapse or rheumatic <3 and="and" aorta="aorta" b="b" back="back" being="being" blood="blood" disease="disease" divided="divided" during="during" forward="forward" into="into" it="it" la="la" lv="lv" moves="moves" regurgitant="regurgitant" span="span" sv="sv" systole="systole" that="that" w="w" with="with">

Enlarged LV ( shows up later on; pushes more blood back into LA and more pressure LA, LA hypertrophy)  left-sided HF

SV dec & LA pressure inc  LA hypertrophy  blood backs up into pulmonary venous system  pulmonary congestion  AFIB

May remain asymptomatic for many yrs  over time, left ventricular fxn becomes impaired, (forward aortic SV dec, left atrial pressure inc, w/ subsequent development of pulmonary congestion)

Mitral Valve Prolapse: myxedematous (mucinous exudate weight down light leaflets) degeneration of mitral valve leaflets causes them to become enlarged and floppy; leaflets take blood passing thru to feed itself, mucous prevents them from taking O2 and leaflets become ischemic

Asymptomatic, ausculatory findings = range from silent form to one or more midsystolic clicks followed by a late systolic or pansystolic murmur, acute chest pain

Dyspnea, SOB, flu-like symptoms, palpitations

Aortic Valve Disorders

Aortic Valve Stenosis: (caused by RF) narrowing of valve orifice w/ inc resistance to ejection of blood from LV into aorta  dec systolic BP  dec pulse pressure  takes longer for <3 blood="blood" eject="eject" span="span" to="to"> HR dec, weak pulse, inc in LV afterload LV hypertrophy

Classic symptoms of angina, syncope, HF

Aortic Valve Regurg: (caused RF) incompetent aortic valve allows blood to flow back to LV during diastole  LV must inc SV to accommodate blood entering from lungs and blood leaking back thru regurgitant valve

Widening pulse pressure, inc SV as LV ejects blood from lung…blood leaks back into LV during diastole. Volume overload, dilation of LV, LV hypertrophy, LV systole tension inc, inc in systolic pressure. Aortic valve fails to close completely, diastolic pressure cannot be maintained

Comp mechs fail to maintain CO  inc LV end-diastolic pressure, which is transmitted to LA and pulmonary veins  pulmonary edema.

Dec in CO  sympathetic stim  inc HR and PVR worsening regurg

Death from pulmonary edema, ventricular arrhythmias, circulatory collapse = common

Chronic: usually gradual onsent, combined LV volume and pressure overload  as the valve deformity inc, regurgitant flow into LV inc, diastolic BP dec, LV enlarges  inc in LV volume  large SV ejection

Tx: (valvular defects) medical management of HF, associated probs, surgical intervention to repair/replace defective valve

HEART FAILURE

Inability of <3 allow="allow" and="and" cardiac="cardiac" co="co" comp="comp" contd="contd" for="for" fxn="fxn" inability="inability" maintain="maintain" mechs="mechs" span="span" sufficient="sufficient" to="to">

Preload: volume or loading conditions of ventricle at end of diastole, just before systole. Determined by venous return to heart. Inc w/ AMI due to overstretched ventricle due to excessive filling from an impaired pumping ability. Valvular <3 back="back" blood="blood" bv="bv" disease="disease" ejected="ejected" failure="failure" in="in" inc="inc" into="into" moved="moved" renal="renal" return="return" some="some" span="span" venous="venous" ventricle="ventricle">

Afterload: force that the contracting <3 and="and" aortic="aortic" based="based" blood="blood" by="by" chamber="chamber" eject="eject" filled="filled" from="from" generate="generate" htn="htn" inc="inc" must="must" on="on" peripheral="peripheral" resistance="resistance" severe="severe" span="span" stenosis="stenosis" systemic="systemic" tension="tension" to="to" vascular="vascular" ventricular="ventricular" wall="wall">

Frank-Starling: inc SV thru an inc in end-diastolic volume/preload, which inc stretching of myocardial fibers  inc in force of next contxn  inc in wall tension and inc myocardial O2 consumption (prod ischemia and contribute to further impairment of cardiac fxn)

NOTE: inc in tension dec wall thickness; contractility compromised and will eventually dec

Diuretics

NP:  possible hypokalemia when released eventually  diastolic dysfxn and AMI  HF

Tx: daily weights, abd circumference

Mx: hepatomegaly  ascites, splenomegaly

Causes of rightsided HF: acute/chronic pulmonary disease (corpulmonale)

Causes of leftsided HF: pumps blood from a low pulmonary pressure to high pressure arterial side of systemic circ  Dec CO, left atrial pressure inc, inc in left ventricular end diastolic pressure w/ pulmonary congestion  inc pulmonary pressure

Pulmonary capillary pressure exceeds capillary colloidal pressure  fluid shift to lungs  pulmonary edema

Leftsided most commonly associated with AMI, & cardiomyopathies

Inc capillary pressure reflects an overfilling of the vascular system due to Na and Cl and H20 retention, venous congestion  impaired ability of <3 adequately="adequately" pump="pump" span="span" to="to"> nocturia (early SNS) due to fluid being pulled back into circ once the pt lays down, CO, UO, GFR all inc when pt in supine position

Late manifestation: oliguria (bc dec CO, hyporenal perfusion, decompensation of Frank Starling

Respiratory manifestations: dyspnea (major SNS in left-sided), chronic dry nonproductive cough due to inc fluid in pulmonary circ in the beginning  thick, tenacious; Chain Stokes breathing; cyanosis (central due to arterial desat resulting from impaired gas exchange due to pulmonary edema look at lips mucous mems; peripheral due to venous desat seen in low output failure, cardiomyopathies look at nail beds)

ACUTE HF SYNDROMES

Pulmonary edema r/t inc LV filling pressures (w/ or w/o low CO)

TYPES OF SHOCK: KNOW MEDS!!!!

Cardiogenic Shock: when the <3 body="body" demand="demand" fails="fails" meet="meet" pump="pump" s="s" span="span" sufficiently="sufficiently" to="to">

 CO, hypotension, hypoperfusion, tissue hypoxia despite adequate intravascular volume

Causes: Myocardial damage (infarction/contusion), acute mitral valve regurgitation due to papillary muscle rupture, sustained arrhythmias, severe dilated cardiomyopathy, and cardiac surgery.

Can occur w/ other types of shock bc inadequate coronary BF

Failure to eject blood from <3 co="co" hypotension="hypotension" inadequate="inadequate" span="span"> compensatory neurohumoral responses

Compensatory neurohumoral responses: activation of sympathetic and RAA system  vasoconstriction, tachy and fluid retention

Inc Systemic vascular resistance  deterioration of cardiac fxn by  afterload or resistance to ventricular systole.

  Preload (filling pressure as blood returning to <3 added="added" blood="blood" forward="forward" is="is" not="not" previously="previously" pumped="pumped" span="span" that="that" to="to" was="was">  end-systolic ventricular volume

 resistance to ventricular systole (afterload) +  dec myocardial contractility   end-systolic ventricular volume & preload, further complicating cardiogenic shock

Inc in CVP due to volume overload in venous system r/t heart’s inability to pump, directly r/t to inc in afterload

Manifestations: consistent with those of extreme HF

Cyanosis: Lips, nail beds, skin, (stagnation of BF and inc extraction of O2 from Hgb)

  Mean arterial and systolic BP

 UO;  aldosterone

Hypovolemic Shock:  BV, inadequate filling of vascular compartment. Acute loss of 15%-20% of circulating BV. The dec  external loss of whole blood (hemorrhage), plasma (severe burns or ECF (severe dehydration or loss of GI fluids w vomiting or diarrhea), internal hemorrhage, 3rd-space losses (ECF shifted from vascular compartment  interstitial space/compartment)

Manifestations: thirst & HR (early signs), cool and clammy skin,  arterial BP, UO, changes in mentation

Pulse  weak and thready (vasconstriction and  filling of vascular compartment)

Respirations  weak and deep to compensate for  acid prod and  availability of O2

Obstructive Shock: inability of <3 aneurysm="aneurysm" cardiac="cardiac" dissecting="dissecting" embolis="embolis" fill="fill" from="from" heart="heart" myxoma="myxoma" obstruction="obstruction" or="or" outflow="outflow" pneumothorax="pneumothorax" properly="properly" pulmonary="pulmonary" span="span" tamponade="tamponade" to="to">

Distributive Shock

Neurogenic Shock: loss of sympathetic vasomotor tone

Anaphylactic Shock: presence of vasodilating substances in blood

Sepsis and Septic Shock: presence of inflammatory mediators

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