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1
Q

Peripheral artery disease

A

Atherosclerotic disease of the arteries in the limbs, generally the LE
May cause intermittent claudication
Most are silent until there is an ischemic event causing severe pain, cool, pulseless, pale extremity

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2
Q

Atherosclerosis

A

Injury to endothelium-initiation of inflammatory response, monocytes and platelets go to sit of injury
LDL enters intimal layer of vessel- inflammation and oxidative stress and macrophage activation, engulf LDL, and create foam cells-these accumulate and form fatty streaks
Persistent inflammatory process in response to the fatty streak- smooth muscle produce a collagen, form over fatty streak making a plaque
Unstable angina (complicated lesion)- prone to rupture, clotting cascade to activated and local thrombus formation may cause occlusion, ischemia, infarction

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3
Q

Hyperlipidemia risk factors

A

Primary-genetics
Secondary- lifestyle, obesity, smoking, sedentary lifestyle, diet, HTN, DM, hypothyroid, Pancreatitis, renal nephrosis, inflammation, medications, diuretics, BB, steroids, antiretrovirals, poor gut biome, air pollution, radiation

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4
Q

Roles of lipoproteins

A

Manufacture and repair plasma membranes and cholesterol needed for bile salts and steroids hormones
Triglycerides-very low density lipoprotein, if elevated increased risk for coronary events
Low density lipoprotein (LDL)- indicators of coronary risk in context of risk factors such as age, DM, CKD
high density lipoprotein (HDL)- protective against atherosclerosis, increased levels are good, want high levels, can remove excess cholesterol from arterial walls

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5
Q

A fib

A

Causes-CHF, ischemic heart disease, HTN, obesity, DM, rheumatic heart disease, thyroid disease
Patho- remodeling of the myocytes of the myocardium- atria does not fully contract to empty contents, about 25% loss of blood from atrium to ventricle
S/s- palms, dizzy, Dyspnes, irregular pulse, fatigue

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6
Q

PVCs

A

Causes- abnormal K levels, high calcium, hypoxia, aging, induction of anesthesia, caffeine, tobacco, drug use, exercise
Patho- decreased cardiac output
S/s- depends on frequency, palls fluttering or pounding

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7
Q

Preload

A

Volume of blood returning to heart from systemic circulation, RA pressure, CVP pressure

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8
Q

After load

A

Systemic pressure, the pressure the heart must pump against to circulate, MAP

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9
Q

Stroke volume SV

A

Amount of blood ejected from the LV with each contraction (depolarization)

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10
Q

End diastolic volume EDV

A

Amount of blood in a chamber after filing and before systole

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11
Q

End systolic volume ESV

A

Volume of blood remaining in the year after each systole (contraction/depolarization)

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12
Q

Ejection fraction

A

% of blood in chambers that is ejected with each systole, generally talking about the LV

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13
Q

Cardiac output

A

Amount of blood pumped into aorta every minute HRXSV

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14
Q

Cardiac action potential

A

Depolarization->early repolarization (sodium, calcium, suddenly goes through open voltage gated channels, membrane potentials reverse polarity to positive)->repolarization (sodium channel close)-> potassium channel opens (works slower than sodium)->resting potential (membrane potential back to negative)->refractory period (takes very strong stimuli to initiate a depolarization

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15
Q

Conduction pathway (EKG)

A

SA node- site of automaticity, slow leaking sodium ions, atrial polarization aka P wave->Av node/bundle of HIS- there’s a pause, RA contracts slightly ahead of LA->perjinke fibers-ventricular depolarization causes QRS interval, atrial repolarization is buried in this->ventricle repolarization causes T wave and process starts all over again

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16
Q

Epinephrine

A

Stronger alpha 1 than alpha 2, works on both equally, strong beta 1(renin release) and beta 2, positive inotrope, increase HR, smooth muscle contraction, myocardial contractility, coronary flow, increase in SBP, mild increase in DBP

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17
Q

Norepinephrine

A

Slightly strong alpha 2 than alpha 1, some defect on beta 1, none on beta 2, strong vasoconstriction, increase in coronary flow, increase in SBP, and some DBP

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18
Q

Dopamine

A

Positive inotrope, increases HR, increases BP by vasoconstriction, alpha 1, alpha 2, beta 1, and dopamine receptors

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19
Q

Factors affect vascular resistance

A

Compliance-ease that blood travels through arteries, change in Volume/change in pressure
Constriction and relaxation of smooth muscle of arteries and arterioles due to sympathetic nervous system, local tissue metabolism, hormone responses, changes in chemical environment

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20
Q

Heart blood flow

A

RA->tricuspid valve->right ventricle->pulmonary arteries with semi lunar valves->pulmonary veins->LA->mitral valve->LV->aorta semilunar valve

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21
Q

Coronary arteries

A

Left coronary artery- left anterior descending LAD, widow maker
Circumflex artery- LA and left lateral wall of LV
RCA- RV, intraventricular sulcus, and the small vessels of the RV, and LV

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22
Q

Blood flow in a vessel

A

Pressure differences (change in P), between two ends of a vessel
Resistance- related to the diameter of the vessel
Viscosity (n) of the blood
Length (l) of the vessel

23
Q

Qp

A

Flow of blood to the lungs

24
Q

Qs

A

Flow of blood to the body

25
Q

Pulmonary vascular resistance PVR

A

Less than 8 weeks of age- 8-10 wood units/m2
Greater than 8 weeks of age 1-3 woods units /m2

26
Q

Systemic vascular resistance

A

Infant 10-15 wood units/m2
Child to adult 15-30 wood units/m2

27
Q

HTN

A

Regulated by SNS, promotes contractility and HR, which equals cardiac output, controls arteriolar vasoconstriction (PVR), regulated by catecholamines, RAAS
Sustained BP greater than 130/80
Primary causes- genetics, environmental
Secondary- underlying disease that increase PR/CO such as renal disease, RAAS, increase volume, pheochromocytoma, pregnancy

28
Q

Systemic nervous system role in HTN

A

Increased activity, increased HR, PVR
Increased insulin resistance->endothelial dysfunction ->vessels narrow causing vasospasm
Vascular remolding Vessels also narrow causing vasospasm
Procoagulant effects vessels narrow causing vasospasm

29
Q

Chronic HTN

A

Vascular remodeling->fibrous vessels->end organ damage most affect cardiac cells, retina, kidneys, brain, can cause LVH CHF

30
Q

Acute HTN

A

HTN crisis->cerebral arterioles cannot regulate blood flow to cerebral capillaries->cerebral edema->cerebral encephalopathy

31
Q

Electrolyte Imbalance issues

A

Potassium- vasodilator, too high causes drop in BP, and decrease in conduction
Magnesium- vasodilator, too high causes drop in BP, slow HR
Calcium- deposited in tunica media and assists with vasoconstriction, high levels causes HTN, slow HR
Sodium- increase fluid retention and cause HTN

32
Q

aortic stenosis

A

Caused by congenital, acquired, inflammation, ischemia, trauma, degenerative process, infection
S/s- murmur, dizzy, SOB, fatigue, syncope, peripheral edema
Patho:narrow valve, restriction of blood forward flow, clarification, bicuspid, inflammation due to rheumatic heart disease, decreased blood flow to LV and body can cause LV hypertrophy
Most common valve disease

33
Q

Mitral stenosis

A

Common after rheumatic heart disease
Caused by congenital, acquired, inflammation, ischemia, trauma, degenerative process, infection
S/s- murmur, atrial dysfunction, pulmonary edema,
Patho: limits blood flow from LA to LV, LV hypertrophy

34
Q

Aortic regurgitation

A

Caused by congenital, acquired, inflammation, ischemia, trauma, degenerative process, infection, Bicuspid, degeneration of valves, HTN, rheumatic heart disease, Marfans
S/s- murmur, SOB, arrhythmia, lightheadedness, dizzy, CP
Patho- incomplete closure of valve causes backflow to affected chamber, increased cardiac workload, LA dilation, hypertrophy

35
Q

Mitral regurgitation

A

Caused by congenital, acquired, inflammation, ischemia, trauma, degenerative process, infection, inherited tissue disorder, hyperthyroidism
S/s- murmur, pulmonary congestion, SOB, fatigue, peripheral edema, palms
Patho- MVP most common, back flow to LV, LA hypertrophy, dilation, pulmonary HTN, RV failure

36
Q

HFrEF

A

Systolic dysfunction
Risk factors- AS, MI, HTN, meds, sarcoidosis
S/s- EF less than 40%, crackles, s4, LVH on EKG, cardiomegaly in CXR, pulm congestion (Kerley blines) may result in pulm HTN
Patho- inability of heart to generate adequate CO to perfuse tissues, increase preload, decrease contractility, decrease CO, increased EDV, increase preload causes dilation

37
Q

HFpEF

A

Diastolic dysfunction
Risk factors- women, hypertrophy, HTN
s/s- LE edema, liver congestion, JVD, fatigue
Patho- decreased LV complained abnormal relaxation of heart, increase in LA pressure, pulm congestion, change in calcium transport from myocytes, autonomic and endothelial dysfunction

38
Q

Right sided HF

A

Inability to provide adequate blood flow to lungs at normal CVP
Risk factors- pulm HTN, if only RV failure, large inferior MI
s/s- JVD, peripheral edema, hepatosplenomegaly, systemic symptoms
Patho- RV hypertrophy due to pulmonary pressure but diastolic and systolic dysfunction

39
Q

Labs for CHF

A

B type natriuretic peptide
Inflammatory cytokines
-endothelial hormones potent vasodilators, poor HF prognosis
-TNF alpha and IL6 increased contribute to myocardial hypertrophy, and remodeling, cardiac cachexia
-insulin resistance- related to activation of SNS, norepi, and RAAS

40
Q

Ventricular remodeling

A

Myocyte hypertrophy, ventricular dilation, impairs contractility

41
Q

Endocarditis

A

Infection/inflammation of endocardium, specifically valves
Due to infection staph aureus, streptococci, enterococci, viral
Causes- Prosthetic valves, IVDU, acquired heart disease, long term in dwelling IV catheter
Patho-endocardial damage to heart valve , trauma, bacteremia, adherence to endocardium, forms vegetation, possible embolism, fever, night sweats, malaise, murmur, regurgitation, CHF
DX- blood cultures, CBC, echo (TEE), CXR, CT, MRI
TX- antibiotics, valve repair, prevention with prophylaxis for dental or other surgeries

42
Q

Post MI changes

A

Myocardial remodeling
Decreased ability to meet bodies 02 demands
Papillary muscle dysfunction, ventricular rupture
Symptoms vary on artery involved
Stunning- temp loss of contractile function
Remodeling- myocytes hypertrophy, scarring, loss of distal function, may be limited or reversed with flow restoration
Myocardial repair-degradation of injury, scar tissue, long term, decreased cardiac contractility, altered LV compliance, decreased SV/EF, high LVEDP, and volume, SA node dysfunction

43
Q

Labs for MI

A

Glucose- elevated due to release of catecholamines
Troponin- detectable within 2-4 hrs, repeat 6-9 hrs, and 12-24 hrs, can help calculate Infarct size and complications
CK-MB, LDH- may be elevated
Leukocytes and CRP- high due to inflammation

44
Q

Coronary disease

A

1 cause of death

Progressive CAD, causes ischemia and ACS
atherosclerosis of arteries, progressive to persistent or permanent can result in MI

45
Q

Stable angina

A

Pain transient, increase lactic acid, ischemic stretching of myocardium, irritates nerve fibers
Caused pain, varies with nerve fibers affected C3-T4

46
Q

Unstable angina

A

Vasospasm with or without sclerosis, decrease vegan activity, hyperactive SNS, decreased NO, altered calcium channel fx, benign to significant arrhythmia
Causes pain, unpredictable, generally at rest, greater than 20 minutes, new angina, inverted T, ST depression, 0 bio maker elevation
Superficial plaque erosion, transient thrombic occlusion, vasoconstriction at site of damage,

47
Q

Silent ischemia

A

LV sympathetic intervention, DM, post card surgery, mental status
Causes no pain, usually have to deep dive in HPI, fatigue, dyspnea, feel uneasy

48
Q

NSTEMI

A

plaque disruption, clot formation, ischemia, breaks up complete trans mural necrosis
ST depression, T wave inversion, positive biomarkers

49
Q

STEMI

A

Complete trans mural ischemia, cardiac dysfunction
ST elevation, deep Q wave, high biomarkers

50
Q

Process of cardiac contraction and relaxation

A

Actin filament->helix backbone ->F actin->G actin (active for cross bridge with myosin
Tropomyosin is a protein wrapped around F actin blocks active site
Troponin 3 subunits attached to tropomyosin (troponin 1 for affinity for actin, troponin T for affinity from tropomyosin, troponin C for affinity for C+)

51
Q

Myosin filament->myosin molecule

A

Myosin molecules
Tail-2 polypeptide chains wrapped in spiral forming double helix
Head: globular polypeptide with associated light chains

52
Q

Myosin filaments

A

Individual myosin molecules bundled form body where cross bridge hangs
1. Cross bridge- flexible hing and arm connect to myosin head
2. ATPase- enzyme in head for the energy production. At rest active sites on actin are blocked by troponin and tropomyosin complexes. During action potential, troponin C binds with calcium and moves the complexes off the actin active site. Actin and myosin interact and contraction occurs

53
Q

Actin and myosin interact and contraction occurs

A

Cross bridge (walk along theory) head of myosin attached to actin filaments at active site
Intramolecular forces cause myosin to tilt forward and drag the actin filament with it (power stroke)
Myosin head breaks away and interacts with the next active actin site
Z disc pulls filament together at the sacromeres causing muscle contraction requires ATP

Patho (17 decks)

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