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308 Test 3 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Causes for dysrhythmias

A

*disturbance of the heart rhythm

*Range from occasional “missed” or rapid beats to severe disturbances that affect the pumping ability of the heart

*can be caused by an abnormal rate of impulse or abnormal conduction impulse

*Examples:

tachycardia, futter, fibrillation,, bradycardia, PVC’s, PAC’s, systole

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2
Q

Non-modifiable

A

AGE: **causes blood vessel stiffening; **causes HRN

*male gender or women after menopause

*genetic predisposition/family history

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3
Q

MODIFIABLE RISKS

of coronary disease

A

*dyslipidemia

*HTN (endothelial injury, increase in cardiac demand)

*cigarette smoking (vasoconstriction and increase in LDL, decrease in HDL)

*Diabetes mellitus and insulin resistance (endothelial damage, thickening of the vessel wall)

*obesity and/or sedentary lifestyle

*atherogenic diet

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4
Q

Aneurysm

A

local dilitation or outpouching of a vessel wall or cardiac chamber

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5
Q

TRUE Aneurysms

A
  • involement of all 3 layers of the arterial wall
  • fusiform aneurysms
  • circumferential aneurysms
  • saccular aneurysms
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6
Q

False Aneurysms

A

Leak between a vascular graft and a natural artery

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7
Q

Aneurysm types

A

Fusiform, saccular

false

dissecting, saccular

fusiform, circumferential

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8
Q

Effects of arterislerosis on CV system? Why?

A

*Chronic disease of the arterial system

  • abnormal thickening and hardening of the vessel walls
  • smooth muscle cells and collagen fiers migrate to the tunica intima
  • Atherosclerosis
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9
Q

Forms of arteriosclerosos

A

thickening and hardening caused by the accumulation of lipid-laden macrophages in the arterial wall

  • plaque development’
  • process that occurs throughout the body
  • leading cause of coronary artery and cerebrovascular disease
  • raises b/p by decreasing arterial distensibility and lumen diameter
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10
Q

Progression:

A

-inflammation of endothelium

-cellular proliferation

-Macrophages migration

LDL oxidation (foam cell formation)

-fatty streak

-fibrous plaque

-complicated plaque

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11
Q

Ischemia

A
  • decreased coronary blood supply
  • coronary athersclerosis
  • coronary spasm
  • decreased coronary perfusion pressure
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12
Q

Ischemia

1-decreased coronary blood supply

or

2-increased myocardial oxygen demand

A

increased mycoardial oxygen demand

  • increased preload
  • increased HR
  • increased afterload
  • increased contractility
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13
Q

Ischemia will show____ on an ECG

A

T-Wave inversion

or

segment depression of ECG

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14
Q

INFARCTION

Prolonged ischemia causes irreversible damage to the heart muscle (myocyte necrosis)

A

Myocyte death

  • cellular injury, leading to cellular death (irreversible damage)
  • structural and functional changes
  • repair
  • necrosis
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15
Q

Structural and functional changes with a

MYOCARDIAL infarction

A
  • myocardial stunning: temporary loss of contractile fx that persists for hours to days after perfusion has been restored
  • Hibernating myocardium: tissue that is perisitently ischemic undergoes metabolic adaptation to prolong myocyte survival

Remoeling: process that occurs in the myocardium after an MI

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16
Q

LEFT MAIN CORONARY ARTERY

A

anterior interventricular artery

LAD

LCA

Circumflex

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17
Q

Left Main Coronary Artery

A
  • Anterior interventricular artery (Left anterior descending artery (LAD))
  • LAD Occlusion: Will affect anterior septum and anterior Right & Left Ventricle
  • supplies interventricular septum and portions of the right and left ventricle
  • occlusion of the LCA: Affect LAD and circumflex impact septum and interior walls and left lateral wall o the ventricle; that portion of the right ventricle is affected as well
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18
Q

Right Coronary artery

A
  • supplies the right atrium, right ventricle, bottom portion of both ventricles and back of the septum
  • with right dominant system; occlusion in the RCA will damage RA and posterior LV
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19
Q

Primary and Secondary HTN Differs

A

BP rises with age: arteries are less distensible

Primary:

95% of individuals with HTN

  • extremetly complicated interactions of genetics and the environmental mediated my neurohormonal effects
  • genetics interact with diet, skmoking, age and other risk factors to cause chronic changes in vasomotor tone and blood volume
  • Overactivity of sympathetic nervous sustem and renin-angiotension-aldosterone system
  • (RAAS) and alterations in natriuretic peptides
  • inflammation, endothelial dysfunction, obesity-related hormones and insulin resistance
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20
Q

Secondary HTN

A

5-8% diagnosed HTN

-caused by systemic disease tht raises PVR and or Cardiac ooutput

21
Q

complications of HTN

A

Hypertrophy and hyperplasia with associated fibrosis of the tunica intima and media in a process called vascular remodeling

22
Q

Malignant HTN

A

Rapidly, progressive HTN

diastolic is usually greater than 140

can lead to encephalopathy

23
Q

Left AV Valve has 2 cusps`

A

Mitral, bicuspid

LAMB

24
Q

RIght AV Valve has 3 cusps

A

TRICUSPID

25
Q

Mycardial Ischemia

Stable Angina

Prinsmetal angina

Silent ischemia

A
26
Q

Myocardial Ischemia

A

Develops if the supply of the coronary blood cannot meet the demand of the myocardium for oxygen and nutrients

27
Q

Stable Angina

A

-chronic coronary obstruction

recurrent predictable chest pain

tx with rest and nitrate

28
Q

Prinzmetal Angina

A

Abnormal vasospasm

unpredictble chest pain

29
Q

Silent ischemia

A

ischemia with no pain

fatigue, dyspnea, feeling of unease

30
Q

Right Sided HF

A
  • Left Venticlar failure increases the burden on the Right Ventricle; RHF usually associated with LHF
  • Pure right ventricular failure is usually a consequence of right ventricular infarction or pulmonary disease
  • As pressure in pulmonary circulation rises, resistence to right ventricular emptying increases

Result: dilitation of right ventricle and failure causing rise is systemic venous circulation, periphal edema and hepatosplenomegaly

31
Q

Backward effects

of RHF

A

hepatomegaly

anorexia

splenomegaly

subcutaneous edema

JVD

32
Q

Forward effects

A

fatigue

oliguria

increased HR

faint pulses

resltessness

confusion

anxiety

33
Q

backwards effects

A

dyspnea on exertion

orthopnea

cough

paroxysmal nocturnal dyspnea

cyanosis

basilar crackles

34
Q

Forward effects

A

fatigue

oliguria

increased heartrate

faint pulses

restlessness

confusion

anxiety

35
Q

TYPES:

PDA

ASD

VSD

TOF

Coarc

TGA

A
36
Q

PDA

A

closes 15 hrs-2wks

blood shunts from MPA to aorta

Clinical manifestations:

continuous, machinery-type murmur

Treatment:

surgical closure involving ligation by incision, cath or avideo-assisted throscopy

37
Q

ASD

L>R

A

Abnormal communication between atria

  • allows blood to be shunted L>R due to a higher pressure of left atrial chamber and lower pulmonary vascular resistence as compared to systemic vascular resistence
  • Right atrial enlargement

Often asymptomatic, diagnosed by soft ejection murmur

38
Q

VSD

L>R

A

abnormal communication between ventricles

  • shunting from L>R ( high pressure left side to low pressure right side)
  • common congenital heart lesion (25-33%)

increased pulmonary vascular resistence over time accounts for symptoms with a large VSD

-LOUD holosystolic Murmur

39
Q

Tetrology of Fallot

4 defects

CYANOTIC

A

defects:

1-vsd

2-overriding aorta straddles vsd

3-pulmonary valve stenosis

4-right ventricular hypertrophy

Right ventricular hypertrophy:deoxygenated blood goes into aortic arch into system: CYANOTIC

TX; SURGERY

40
Q

Coarc

A

narrowing of lumen of aort that impedes blood blow (8-10%)

-coarc almost always occurs juxtaductal but can ocur anywehere between the origin of aortic arch and bifurcation of the aorta in the lower abdomen

NEWBORNS: usually present with CHF

once ductus closes, rapid deterioration hypotension, acidosis and shock

in older children: HTN in upper extremities

  • decreased or absent pulses in lower extremties
  • cool, mottled skin
  • leg cramps during exercise
41
Q

transposition

A

aorta arises from RV and MPA arises from LV

-two parallel circuits

unoxygented blood circulates continiously through the systemic circulation

Oxygenated blood circulated throught the pulmonary circulation

Extrauterine survical requires communication between the 2 circuits

*PGE to keep PDA open

*L > R shunt

42
Q

Def: a bolus of matter that circulates in the bloodstream and then lodgees, obstructing blood flow

A

Boluses of Matter: dislodged thrombus (often a DVT), air bubble, amniotic fluid, aggregate of fat, bacteria, cancer cells or foreign substance

*many arterial emboli are from the heart (after an MI, valve disease, endocarditis, dysrhythmias, heart failure)

43
Q

Cardiac Troponin I (cTnI)

A

Most specific

44
Q

crearine phosphokinase-myocardial bound (CPK-MB)

A

see in 2-4 hours, peaks in 24 hours

45
Q

Lactace dehydrogenase (LDH)

A

hyperglycemia 72 hours post MI

46
Q

two primary types

A

Aortic stenosis and Mitral stenosis

regurgitant

47
Q

Failure of stenotic valves to open properly, causing an abnormal pressure gradient across the valve andincreasing the pressure work of the heart

A

Aortic: Syncope, fatigue, systolic murmur (best heard in the neck area)

Mitral: back of of fluid into the LV

48
Q

Regurgitant valves allow blood flow to flow backwards (wrong direction) across the valve and results in extra volume and work for the heart

A
49
Q
A

308 Test 3 (4 decks)

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