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cardio Flashcards

1
Q

Mi characterized by

A

O2 demand exceeds O2 supply

supply of coronary blood cannot meet the demand of the myocardium and leads to ischemia

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2
Q

decreased supply can be caused by

A 
narrowing of coronaries due to atherosclerosis
coronary artery vasospasm
hypoxia
anemia
aortic insufficiency
aortic stenosis
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3
Q

increased demand

A

sever hypertension

tachycardia

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4
Q

MI risk factors

A

age >75, male, hypercholestremia, DM, HTN, smoking, family hx, obesity, PVD, menopause, high-estrogen BC, sedentary life style, psychosocial characteristic

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5
Q

atherosclerotic plaque leads to

A

unstable plaque with ulceration or rupture and thrombosis—ACS—sustained ischemia—MI—Myocardial inflame with necrosis—myocardial remodeling

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6
Q

Acute coronary syndrome

A

atherosclerotic processes–stable plaque formation or unstable plaque–rupture or thrombus
thrombus–transient ischemia–unstable angina
vessel obstruction sustained–MI with inflame and necrosis

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7
Q

Mycocardial remodeling

A

a process mediated by angiotensin II, aldosterone, catecholamines, adenosine, oxidative stress, and inflammatory cytokines, which causes myocyte hypertrophy, scaring, loss of contractile function

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8
Q

myoctye hibernation

A

persistently ischemic undergoes metabolic adaption to prolong myocyte survival

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9
Q

atherosclerotic plaque

A

has lipid-rich core and thin fibrous cap

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10
Q

cause rupture of plaque

A

shear force
inflam
apoptosis
macophage-derived degradation enzyme

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11
Q

after plaque ruptures what happens to lesions

A

thrombus formation over lesion, and vasoconstriction of vessel and increased inflam with cytokine release
platelet activation and adherence
production of thrombin and vasoconstrictors

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12
Q

unstable angina or MI ultimately from

A

acute decrease in coronary blood flow

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13
Q

vulnerable plaque is a what and characteristics

A

rupture prone atherosclerotic plaque
t-cells recruited to shoulder (where wall most vulnerable)
marcophages cluster around Tcell
thin fibrous cap
newly formed intrawall capillaries
lymphocyte and mast cell infiltration
**vulnerability more of a concern than size

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14
Q

plaques, whats more significant

disrupted plaque characteristics

A

*instability more significant than size
*become disrupted from hemodynamic trauma
*mechanical stress is max at fissure at the junction of fibrous cap and plaque free vessel wall
eccentric-not uniformed
large soft necrotic core
covered by thin necrotic core
rich in macrophages and T cells
Metalloproteinases-degreade collagen cap

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15
Q

role of stress in acute cardiac events

A

from central and ANS activation: can effect the demand side

pain, anesthesia stress

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16
Q

physiologic response to stress

A

increased catecholamines, HR, BP
all lead to increase ECG instability, demand
leads to VF/VT–sudden cardiac death
*increased demand can also lead to ischemia–MI
also decreased plasma volume and increased coronary constriction leads to
decreased supply–ischemia and plaque rupture–MI
and increased platelet activity leads to coronary thrombosis —MI

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17
Q

Stable angina

A

CP caused by myocardial ischemia
luminal narrowing and hardening of arterial walls
-vessel can’t dilated in response to increased demand
no change in precipitating factors for @ least 60 days
*relieved by rest, decreased demand, vasodilator ex: nitro

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18
Q

ask pt CP

A

frequency of pain, how do the tx, duration of pain, has it changed

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19
Q

unstable angina

A 
caused by less than normal activity
last for prolonged period
occurring more frequently 
signals impeding MI
*Crescendo, pain starts slow and grow
*increased frequency, duration, 
*acute plaque changes
*usually partial thrombosis
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20
Q

Prinzmetal Angina

A

At rest
cononary spasm
in plaque area or normal area
sometimes associated with other vasospastic disease ex: Raynauds

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21
Q

Infarction

A

Necrosis caused by ischemia with in 20-30 min of ischemia
begins in subendocardial regions
reaches full size in 3-6hrs
size depends on proximity of lesion, collateral circulation

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22
Q

Infarction complications 10

A

papillary muscle dysfunction-valvular disease
external rupture of infarct–day 4-7 most common–tamponade–death
mural thrombi-stable, Risk for stroke
acute pericarditis: most common day 2-3
ventricular aneurysm-fibrous outputting of ventricle-anteroapical region–most common
arrhythmias
LVF +/- pulm edema
cardiogenic shock–rare
rupture of wall, septum, papillary muscle
thromobembolism

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23
Q

site of MI and vessel involvement RCA LCA LAD LCX

A

RCA: posterior inferior
LCA: anterolateral
LAD: anteroseptal
LCX: (circumflex) Lateral

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24
Q

vascular hypertension

A

sustained systolic 140mmhg diastolic 90

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25
HTN is the most important risk factor in....5
CAD, CVA, cardiac hypertrophy, renal failure, aortic dissection
26
types of HTN
systolic and diastolic: essential HTN 2ndary--renal, endocrine, cardiovascular, neurologic
27
regulation of normal BP
BP= COxPVR CO factors: cardiac factors, blood volume, HR, SV PVR factors: neural factors, humoral factors, constrictors, dilators, blood viscosity
28
patho of essential (primary) HTN risk factors
genetic-polygenic and heterogeneous (look different per pt), polymorphism @ several gene loci environmental--stress, obesity, smoking, salt consumption, sedentary life-style
29
Heavy salt consumption
increased BP with age directly correlate with increase levels of Na intake consume little Na-no HTN but increased Na intake and develop HTN large Na load over short period of time--develop increased SVR most pt with HTN have increased Na in vascular tissue and blood cells Na restriction decrease BP, diurtics-antiHTN by promoting Na excretion
30
HTN theory 2
1 renal retention of excess Na existence genetic factors decrease Na excretion increase fluid volume/CO vasoconstriction occurs (autoregulation): increase BP cyclical 2. vasoconstriction and vascular hypertrophy increase in vascular resistance caused by 1. factors that induce functional vasoconstriction--neurogenic, release of vacocontrictor agents, genetic defect in transport of Na and Ca 2. stimuli that induce structural change in vessel walls 3. both
31
Pathogenesis of 2ndary HTN
``` oral contraceptives (unknown, most likely Na retention) renal parenchymal disease (disturbances in filtration, reabsorption of Na) renin-secreting tumors (causes increase in angiotensin and aldosterone) primary aldosteronism (aldosterone promotes Na retention) cushings syndrome (Glucocorticoids facilitate sodium and water retention) pheochromocytoma (Excess catecholamines raise vascular tone) ```
32
HTN tx drug
diuretic where first line, others now
33
HTN tx non-drug
lifestyle change: wt reduction, smoking cessation, increase physical activity Na restriction diets ETOH relaxation techniques
34
HTN crisis definition, tx
sudden increased in DIASTOLIC above 130 due to: activation of renin-angiotensin-aldosterone system Tx: prompt, controlled decreased in BP with NTP (0.5-10mcg/kg/min IV) monitoring UOP and intraarterial BP *decrease DBP carefully to 100-110 over several min-hr
35
LV hypertrophy
``` increase in size to LV decrease volume (blood) decreased compliance contractility normal leads to Lheart failure ```
36
stenosis
high pressure valve orifice is constricted and narrowed *impeding forward flow **avoid: -increased HR bc decreases CO and limits diastolic filling -decreased SVR bc poor CPP and coronary perfusion
37
regurgitation
High Volume cusps fail to shut completely, allows blood to flow when suppose to be closed Avoid these bc: *slow HR allows for more time and worsening regurg *increased SVR increases the regard fraction
38
Mitral stenosis
fusion of mitral value leaflets at commissure during healing process of acute rheumatic fever when mitral value area is <1cm need 25mmhg of pressure to maintain adequate CO LA enlargement predispose to afib Stasis of blood in distended atria predispose pt for thrombi-- pts often on chronic anticoagulants **avoid increased HR and decreased SVR
39
mitral stenosis symptoms
DOE when increase in CO, Pulm Edema Severe MS lead to CHF Think left heart
40
Aortic stenosis
Isolate non-rheumatic- results from progressive calcification and stenosis of congenitally abnormal bicuspid valve (mitral) Rheumatic fever-aortic stenosis almost always occurs in association with mitral stenosis hemodynamically: associated with a transvalvular pressure gradient >50mmhg -aortic valve orifice area <1cm2 (normal 2.5 to 3.5) *leads to L heart failure (LV hypertrophy, pulm edema, syncope) **avoid increased HR and decreased SVR
41
Aortic stenosis s/s
triad: angina (often in absence of ischemic heart disease) DOE syncope "SAD"
42
Mitral regurgitation
usually due to rheumatic fever and almost alway associated with mitral stenosis LA volume overload by retrograde flow of LV SV responsible for V wave on the PAWP: size correlates with magnitude of regurgitant flow (LA hypertrophy, Lheart failure, pulm edema) **Want small increased HR and decreased SVR
43
Aortic regurgitation
acute: infective endocarditis, trauma, dissection of a thoracic aneurysm (big problem, hasn't had time to compensate) Chronic: prior rheumatic fever, persistent systemic HTN hemodynamic problem: regurg part of ejected SV from aorta back to LV, decrease forward L ventricular SV (LV hypertrophy, pulm edema, syncope)
44
Endocarditis definition, risk, patho
infection and inflamm of endocardium *bacterial: streptococci, staph, and entero Risk factors: prosthetic valve, turbulent blood flow, endocardial damage Patho: bacteria enters blood screen from IV drugs use, dental procedures, trauma -vegetative lesion occurs on heart valves and surrounding structure inaccessible to host defenses bc embedded in protective fibrin clots
45
Endocarditis s/s
fever, night sweats, malaise, weight loss, murmur, petechia, osler nodes (on fingers and toes) jane way lesions (palms, soles)
46
Non-bacterial endocarditis
thrombotic vegetation bland thrombus with virtually no inflamm in value cusp or thrombotic deposit thrombus is only loosely attached to cusp
47
Inflam myocarditis early and late s/s
dilated cardiomyopathy early s/s: fatigue, dyspnea, palpitations **vague s/s-difficult to diagnosis progress to: CHF, pulses alternans (SBP differs with each beat), tachycardia, pulm edema *complete recovery with abx: IV and home on PO
48
Non-inflam cardiaomypathy
manifest as CHF due to: toxicity (ex ETOH), idiopathic, degenerative, infiltrative, post MI characterized by: increased filling pressure, failure of contractile strength- beyond Franks curve, increased arterial impedance (resistance) and decreased SV
49
dilated cardiomyopathy
diminished systolic performance of heart | impaired systolic function--leads to increased intracardiac volume, ventricular dilation
50
decreased contractility
causes ventricles dilate to compensate--increased cardiac work--increased O2 consumption--decreased CO--increased SNS outflow to increased HR and SVE
51
clinical picture of CHF associated with dilated cardiomyopathy forward failure
* *forward failure: fatigue, hypotension, oliguria(CO to kidneys decreased)--caused by decreased CO and decreased organ perfusion * decreased renal perfusion-- activation of renin-angiotension-aldosterone system: increased volume through Na and H20 retention
52
clinical picture of CHF associated with dilated cardiomyopathy backward failure
increase filling pressure required by heart | 2ndary mitral regard caused by dilation of ventricle
53
Left sided failure
orthopena, pulm edema, paroxysmal nocturnal dyspnea (episode of SOB during sleep)
54
Right sided failure
Hepatomegaly JVD peripheral edema
55
Hypertrophic Cardiomyopathy other names
idiopathic hypertrophic subaortic stenosis (IHSS) asymmetric septal hypertrophy hypertrophic obstructive cardiomyopathy muscular subaortic stenosis
56
Hypertrophic Cardiomyopathy: clinical features
autosomal dominant trait- main defect is contractile elements of heart--then increased density of Ca channels pt often asymptomatic increased HR worst thing for these pt s/s: dyspenia, angina, syncope, ventricular dysrhythmias become symptomatic in 2-3decade of life most frequent finding in autopsy in young previously health adults with sudden cardiac death
57
Hypertrophic Cardiomyopathy patho
asymmetric myocardial hypertrophy diastolic dysfunction enlargement of inter ventricular septum--usually top portion right below aortic valve rapid LV ejection--80% during early systole Often sub aortic pressure gradient imbalance in myocardial O2 requirements
58
Hypertrophic Cardiomyopathy dynamic obstruction is worsened by
decreased preload, after load increased contractility * these produce a decrease in ventricular volume thus increase proximity of anterior MV leaflets to IVS
59
Hypertrophic Cardiomyopathy: factors that impair contractility do what to systolic function
improve it | the factors are: volume loading, vasoconstriction, myocardial depression
60
Hypertrophic Cardiomyopathy have what valve problem and what kinda of compliance
MR- vasodilators worsen MR while vasoconstrictors decreased obstruction and MR Poor diastolic compliance: atrial contribution maybe as high as 70%
61
Hypertrophic Cardiomyopathy medical mgmt and surgical and ECHO finding
Beta-blockers--blunt SNS mediated increase in sub aortic stenosis, decreased tacky Ca channel blockers--improves diastolic relaxation surgical: myomectomy--cut out part of heart, don't survive long Echo: thickening IVS-base to apex poor septal motion anterior displacement of mitral valve
62
Left to Right shunts
Atrial septal defects (ADS) Ventricular septal defects (VSD) Patent ductus arteriosus (PDA) sometimes lead to tardive cyanosis (late) but does not cause cyanosis from onset
63
Atrial septal defects
most commonly diagnosed in adulthood forms btwn 4-6 weeks of embryonic life due to foamen oval not closing properly/completely s/s: eventually leads to pulm HTN can use R to L shunt with enough pressure--cause cyanosis and CHF can also be associates with Mitral insufficiency
64
Ventricular septal defects
``` Most common heart defect at birth vent-septum develops btwn 4-8 weeks may close in childhood spont can cause sever L to R shunt: with pulm HTN and CHF as well as infective endocarditis surg needed for large VSD ```
65
Patent ductus arteriosus
btwn PA and aorta--allowing bypass of unO2 lungs in utero constricts and closes at birth due to: increased O2 levels, decreased pulm resistance, decreased PGE2 high pressure L to R shunt Pulm HTN cyanosis and CHF with bigger lesion: infective endocarditis can occur
66
R to L shunts
cyanotic at birth poorly O2 blood form R side of heart goes directly into arterial circulation via L heart *tetralogy of Fallot *transposition of great vessels
67
Tetralogy of Fallot
Most common cause of Cyanotic congenital heart disease caused by abnormal division of trunks arteriosus into a pulm trunk and aortic root 4 components: VSD Dextraposed (shifted to R)aortic root that overrides VSD RV outflow obstruction RV hypertorphy
68
TET s/s
R to L shunt decreased blood flow to lungs as well as increased blood flow to aorta extent of shunting really depends on degree of outflow obstruction
69
TET manifestation
``` can be avoided by surg due to chronic cyanosis: erythrocytosis increased blood viscosity: increased hemtocrit Digital clubbig: poor O2 to periphery Infective endocarditis Systemic emboli Brain abscesses ```
70
Transposition of Great Vessels
Aorta rises from R ventricle PA rises from L ventricle must be associated with ASD, VSD, or PDA--to survive **cyanosis
71
Coarctation of the aorta (COA)
abnormal narrowing of aorta more common in males preductal or postductal **most common postductal
72
Preductal COA
``` infrantile weak femoral pulses cyanosis of lower exterminates CHF surgical correction needed to survive ```
73
Postductal
older children/young adults collateral have developed decreased perfusion to kidneys: decreased SV, activates RAS high pressure in upper extremity and low pressure in lower extremities intermittent claudication can also arise

patho 2 (2 decks)

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