Cardiovascular Flashcards
Causes for dysrhythmias
*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
Non-modifiable
AGE: **causes blood vessel stiffening; **causes HRN
*male gender or women after menopause
*genetic predisposition/family history
MODIFIABLE RISKS
of coronary disease
*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
Aneurysm
local dilitation or outpouching of a vessel wall or cardiac chamber
TRUE Aneurysms
- involement of all 3 layers of the arterial wall
- fusiform aneurysms
- circumferential aneurysms
- saccular aneurysms
False Aneurysms
Leak between a vascular graft and a natural artery
Aneurysm types
Fusiform, saccular
false
dissecting, saccular
fusiform, circumferential
Effects of arterislerosis on CV system? Why?
*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
Forms of arteriosclerosos
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
Progression:
-inflammation of endothelium
-cellular proliferation
-Macrophages migration
LDL oxidation (foam cell formation)
-fatty streak
-fibrous plaque
-complicated plaque
Ischemia
- decreased coronary blood supply
- coronary athersclerosis
- coronary spasm
- decreased coronary perfusion pressure
Ischemia
1-decreased coronary blood supply
or
2-increased myocardial oxygen demand
increased mycoardial oxygen demand
- increased preload
- increased HR
- increased afterload
- increased contractility
Ischemia will show____ on an ECG
T-Wave inversion
or
segment depression of ECG
INFARCTION
Prolonged ischemia causes irreversible damage to the heart muscle (myocyte necrosis)
Myocyte death
- cellular injury, leading to cellular death (irreversible damage)
- structural and functional changes
- repair
- necrosis
Structural and functional changes with a
MYOCARDIAL infarction
- 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
LEFT MAIN CORONARY ARTERY
anterior interventricular artery
LAD
LCA
Circumflex
Left Main Coronary Artery
- 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
Right Coronary artery
- 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
Primary and Secondary HTN Differs
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
Secondary HTN
5-8% diagnosed HTN
-caused by systemic disease tht raises PVR and or Cardiac ooutput
complications of HTN
Hypertrophy and hyperplasia with associated fibrosis of the tunica intima and media in a process called vascular remodeling
Malignant HTN
Rapidly, progressive HTN
diastolic is usually greater than 140
can lead to encephalopathy
Left AV Valve has 2 cusps`
Mitral, bicuspid
LAMB
RIght AV Valve has 3 cusps
TRICUSPID
Mycardial Ischemia
Stable Angina
Prinsmetal angina
Silent ischemia
Myocardial Ischemia
Develops if the supply of the coronary blood cannot meet the demand of the myocardium for oxygen and nutrients
Stable Angina
-chronic coronary obstruction
recurrent predictable chest pain
tx with rest and nitrate
Prinzmetal Angina
Abnormal vasospasm
unpredictble chest pain
Silent ischemia
ischemia with no pain
fatigue, dyspnea, feeling of unease
Right Sided HF
- 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
Backward effects
of RHF
hepatomegaly
anorexia
splenomegaly
subcutaneous edema
JVD
Forward effects
fatigue
oliguria
increased HR
faint pulses
resltessness
confusion
anxiety
backwards effects
dyspnea on exertion
orthopnea
cough
paroxysmal nocturnal dyspnea
cyanosis
basilar crackles
Forward effects
fatigue
oliguria
increased heartrate
faint pulses
restlessness
confusion
anxiety
TYPES:
PDA
ASD
VSD
TOF
Coarc
TGA
PDA
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
ASD
L>R
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
VSD
L>R
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
Tetrology of Fallot
4 defects
CYANOTIC
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
Coarc
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
transposition
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
Def: a bolus of matter that circulates in the bloodstream and then lodgees, obstructing blood flow
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)
Cardiac Troponin I (cTnI)
Most specific
crearine phosphokinase-myocardial bound (CPK-MB)
see in 2-4 hours, peaks in 24 hours
Lactace dehydrogenase (LDH)
hyperglycemia 72 hours post MI
two primary types
Aortic stenosis and Mitral stenosis
regurgitant
Failure of stenotic valves to open properly, causing an abnormal pressure gradient across the valve andincreasing the pressure work of the heart
Aortic: Syncope, fatigue, systolic murmur (best heard in the neck area)
Mitral: back of of fluid into the LV
Regurgitant valves allow blood flow to flow backwards (wrong direction) across the valve and results in extra volume and work for the heart
