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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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