Cardiovascular

Question 1

Causes for dysrhythmias

Answer 1

*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

Question 2

Non-modifiable

Answer 2

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

*male gender or women after menopause

*genetic predisposition/family history

Question 3

MODIFIABLE RISKS

of coronary disease

Answer 3

*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

Question 4

Aneurysm

Answer 4

local dilitation or outpouching of a vessel wall or cardiac chamber

Question 5

TRUE Aneurysms

Answer 5

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

Question 6

False Aneurysms

Answer 6

Leak between a vascular graft and a natural artery

Question 7

Aneurysm types

Answer 7

Fusiform, saccular

false

dissecting, saccular

fusiform, circumferential

Question 8

Effects of arterislerosis on CV system? Why?

Answer 8

*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

Question 9

Forms of arteriosclerosos

Answer 9

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

Question 10

Progression:

Answer 10

-inflammation of endothelium

-cellular proliferation

-Macrophages migration

LDL oxidation (foam cell formation)

-fatty streak

-fibrous plaque

-complicated plaque

Question 11

Ischemia

Answer 11

• decreased coronary blood supply
• coronary athersclerosis
• coronary spasm
• decreased coronary perfusion pressure

Question 12

Ischemia

1-decreased coronary blood supply

or

2-increased myocardial oxygen demand

Answer 12

increased mycoardial oxygen demand

• increased preload
• increased HR
• increased afterload
• increased contractility

Question 13

Ischemia will show____ on an ECG

Answer 13

T-Wave inversion

or

segment depression of ECG

Question 14

INFARCTION

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

Answer 14

Myocyte death

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

Question 15

Structural and functional changes with a

MYOCARDIAL infarction

Answer 15

• 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

Question 16

LEFT MAIN CORONARY ARTERY

Answer 16

anterior interventricular artery

LAD

LCA

Circumflex

Question 17

Left Main Coronary Artery

Answer 17

• 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

Question 18

Right Coronary artery

Answer 18

• 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

Question 19

Primary and Secondary HTN Differs

Answer 19

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

Question 20

Secondary HTN

Answer 20

5-8% diagnosed HTN

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

Question 21

complications of HTN

Answer 21

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

Question 22

Malignant HTN

Answer 22

Rapidly, progressive HTN

diastolic is usually greater than 140

can lead to encephalopathy

Question 23

Left AV Valve has 2 cusps`

Answer 23

Mitral, bicuspid

LAMB

Question 24

RIght AV Valve has 3 cusps

Answer 24

TRICUSPID

Question 25

Mycardial Ischemia Stable Angina Prinsmetal angina Silent ischemia

Question 26

Myocardial Ischemia

Answer 26

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

Question 27

Stable Angina

Answer 27

-chronic coronary obstruction recurrent predictable chest pain tx with rest and nitrate

Question 28

Prinzmetal Angina

Answer 28

Abnormal vasospasm unpredictble chest pain

Question 29

Silent ischemia

Answer 29

ischemia with no pain fatigue, dyspnea, feeling of unease

Question 30

Right Sided HF

Answer 30

- 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

Question 31

Backward effects of RHF

Answer 31

hepatomegaly anorexia splenomegaly subcutaneous edema JVD

Question 32

Forward effects

Answer 32

fatigue oliguria increased HR faint pulses resltessness confusion anxiety

Question 33

backwards effects

Answer 33

dyspnea on exertion orthopnea cough paroxysmal nocturnal dyspnea cyanosis basilar crackles

Question 34

Forward effects

Answer 34

fatigue oliguria increased heartrate faint pulses restlessness confusion anxiety

Question 35

TYPES: PDA ASD VSD TOF Coarc TGA

Question 36

PDA

Answer 36

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

Question 37

ASD L\>R

Answer 37

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

Question 38

VSD L\>R

Answer 38

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

Question 39

Tetrology of Fallot 4 defects CYANOTIC

Answer 39

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

Question 40

Coarc

Answer 40

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

Question 41

transposition

Answer 41

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

Question 42

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

Answer 42

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)

Question 43

Cardiac Troponin I (cTnI)

Answer 43

Most specific

Question 44

crearine phosphokinase-myocardial bound (CPK-MB)

Answer 44

see in 2-4 hours, peaks in 24 hours

Question 45

Lactace dehydrogenase (LDH)

Answer 45

hyperglycemia 72 hours post MI

Question 46

two primary types

Answer 46

Aortic stenosis and Mitral stenosis regurgitant

Question 47

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

Answer 47

Aortic: Syncope, fatigue, systolic murmur (best heard in the neck area) Mitral: back of of fluid into the LV

Question 48

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