lec-9-cardio path-1 Flashcards
route of blood flow through heart
- Right atrium-deoxygenated blood returning from body
- Tricuspid valve
- right ventricle
- pulmonic valve
- pulmonary arteries-only arteries carry deoxy blood in body
- Pulmonic veins
- left atrium
- Mitral valve
- left ventricle
- aortic valve
- aorta-blood leaves to systemic circ o2 rich
S1 sound
due to closing of atriventricular valves (Mitral and tricuspid) tricuspid right side, mitral left
s2 sound
aortic and pulmonic closing then blood fills during dystole, atria contract blood go to ventricles which is s2 sound aortic valve sits behind pulmonic valve
Left Coronary artery braches
LAD left anterior descending artery and circumflex
LAD supplies?
Supplies blood to the front and bottom of the left ventricle and the septum
*anterier wall 2/3 septum
Circumflex artery supplies
supplies blood to left atrium and side and back of left ventricle
*lateral supply
Right coronary art supplies?
Right atrium right ventricle and bottom portion left ventricle and back of the septum
*posterier wall and 1/3 septum
Congestive Heart Failure (CHF)
CHF affects nearly 5 million individuals and is the leading discharge diagnosis in patients over 65 years of age in the United States.
CHF occurs when the heart is unable to pump blood at a rate sufficient to meet the metabolic demands of the tissues or can do so only at an elevated filling pressure.
It can appear during the end stage of many forms of chronic heart disease.
CHF defininition
CHF is characterized by variable degrees of decreased cardiac output and tissue perfusion, as well as pooling of blood in the venous system which may cause pulmonary edema, peripheral edema, or both.
common causes CHF
Coronary artery disease (due to athroschelosis)
High blood pressure (thickening in left ventricle is result)
systolic HF
EF
severe HF
EF
NORMAL EF
50-70% AVERAGE 60%
EF
EF= SV/EDV * 100
SV
asmount og blood leaving ventricles with each beat
EDV
amount of remianing blood end of dystole
CF systole dysfunction
heart becomes dialated/enlarged in ventricles, EDV is greatly increased (more volume so lower EJ) at end of dystole, and duringn systole SV less pumps out less than 40-50% EJ result = low EJ end systole
CF dystole dysfunction
ventricle walls are thickened (hypertension) and ridid so can’t fill with as much blood volume during dystole but pumps normally (normal SV) during systole so EF unchanged looks normal (60%), but total volume of blood pumped cant meet metabolic demand, still in failure
Stage A CHF
Patients at high risk for developing HF in the future but no functional or structural heart disorder.
Stage B CHF
: a structural heart disorder but no symptoms at this stage.
Stage C CHF
previous or current symptoms of heart failure in the context of an underlying structural heart problem, but managed with medical treatment.
Stage D CHF
advanced disease requiring hospital-based support, a heart transplant or palliative care.
most common marker used to identify HF
Naturetic B peptide >100 indicates HF, can get as high as 800 in severe dosease
Left sided heart disease
*produce symptoms history important, breathing issues, lungs filling with Serous fluid, patient reports experience
Pulmonary congestion and edema (heart failure cells)
Dilation of the left atrium and increases the risk of atrial fibrillation
Dyspnea, orthopnea, paroxysmal nocturnal dyspnea
Reduction in renal perfusion and CNS (Severe Lt sided CHF)
**heart failure cells
**thrombosis left atrial appendage
Right sided heart disease
*produce signs we can measure, PE imortant
Cor pulmonale usually due to conditions resulting in pulmonary hypertension
Blood backs up into the venous system – JVD, pitting edema congestive hepatosplenomegaly, pleural, pericardial, or peritoneal effusions
Congestion of kidney and CNS
Biventricular CHF
Mi in left side heart can cause pulm edema and hypertension eventually causing right vent hf too, cross of symptoms / signs
CHF treatment
Diuretics Angiotensin converting enzyme inhibitors β1-adrenergic blockers Mechanical assist Cardiac Transplant (advanced, irreversible heart failure)
Ischemic Heart Disease (IHD
Ischemic heart disease (IHD) is the leading cause of death worldwide for both men and women.
Due to an imbalance between the supply (perfusion) and demand of the heart for oxygenated blood.
In more than 90% of cases reduced blood flow due to obstructive atherosclerotic lesions in the coronary arteries (coronary artery disease - CAD).
NMRF IHD
age
male
genetic issue -hypercholest etc
familial history- MI
Modifiable risk factors
hypertension cholesterol diabeites smoking***#1 for athro c-reactive pro-inflammation minor include obesity, inactivity, stress
pathogenesis IHD
Insufficient coronary perfusion relative to myocardial demand, due to chronic, progressive atherosclerotic narrowing of the epicardial coronary arteries, and variable degrees of superimposed acute plaque change, thrombosis, and vasospasm
Chronic Atherosclerosis
Develops over decades
The varied clinical manifestations of IHD cannot be explained by the anatomic disease burden alone.
Generally, obstructing 75% or greater of the lumen is generally required to cause symptomatic ischemia and 90% of the lumen can lead to inadequate coronary blood flow even at rest.
Multiple coronary vessels can be involved.
Vulnerable plaque
Soft w/ lipid filled core; Most often eccentric; Most often only 40-60% stenotic.
Prone to rupture (shoulder region) due to plaque hemorrhage or to fibrous cap disruption
Thrombotic occlusion of coronary artery and acute myocardial ischemia/infarction.
Moderately stenotic, vulnerable complex plaques are difficult to detect and treat prophylactically.
*
Eccentric= don’t involve entire lumen just a portion, vessel expands until it cant
