Module 6.1 Cardiovascular Disorders Flashcards
1
Q
What are cardiomyopathies?
A
- Diseases that affect the myocardium itself and are not secondary to the usual cardiovascular disorders
- Most are the result of remodeling caused by the effect of neurohormonal responses to ischemic heart disease or hypertension on the heart muscle
- Maybe secondary to infective disease, toxin exposure, systematic connective tissue disease, infiltrative and proliferative disorders or nutritional deficiencies, but most are idiopathic
2
Q
What is dilated cardiomyopathy?
A
- Characterized by diminished myocardial contractility (weak heart contractions), leading to the diminished systolic performance of the heart.
- There is ↑’d intracardiac volume, ventricular dilation, and systolic heart failure
- Usually the result of ischemic heart disease, valvular disease, diabetes, renal failure, hyperthyroidism, alcohol or drug toxicity, genetic disorder, or infection
- Leads to left heart failure
3
Q
What are some symptoms associated with dilated cardiomyopathy?
A
- Dyspnea and fatigue are the most common symptoms
- Pulmonary congestion (b/c the heart is not able to pump the blood out and it backflows into the lungs)
- Systemic and pulmonary emboli are common
- Palpitations
4
Q
What is hypertrophic cardiomyopathy?
A
- Occurs when there is a disproportionate thickening of the intraventricular septum, increasing stiffness of the heart, and time required for ventricular filling
- the increased thickness of the septal wall may cause outflow obstruction to the left ventricle blood flow
- Diastolic relaxation is impaired and ventricular compliance is decreased
- Leads to left heart failure
5
Q
What symptoms are associated with hypertrophic cardiomyopathy?
A
- May be asymptomatic or
- May complain of angina, syncope, dyspnea on exertion, and palpitations
- Extra heart sounds or murmurs
6
Q
What is restrictive cardiomyopathy?
A
- Cardiomyopathies characterized by restricted filling and reduced diastolic volume of either ventricle, with normal systolic function & wall thickness
- There is increased rigidity and noncompliance of the myocardium, decreasing ventricular filling and raising filling pressures during diastole.
- usually, the result of infiltrative disease of myocardium, pressure and time required to fill ventricles is increased
- Leads to right-sided heart failure
7
Q
What are some symptoms associated with restrictive cardiomyopathy?
A
- Dypsnea & fatigue
- Right heart failure with systemic venous congestion
- Cardiomegaly and dysrhythmias
8
Q
What is atherosclerosis?
A
It is an inflammatory disease that occurs when there is an accumulation of lipid-laden macrophages that leads to plaque formation and hardening within the arterial walls
9
Q
What can cause injury to endothelial cells that leads to the development of atherosclerosis?
A
- Atherosclerosis begins with injury to the endothelial cells that line artery walls, caused by smoking, hypertension, diabetes,↑’d levels of LDL, ↓’d levels of HDL, and autoimmunity
- Other causes include inflammatory factors, cardiovascular risk factors,↑’d serum fibrinogen, infection, and periodontal disease.
10
Q
How does plaque develop with atherosclerosis?
A
- Begins with an injury to the arterial lining, the endothelium.
- The body then tries to repair damage using monocytes that burrow into blood vessel walls, mature into macrophages, ingest fatty substances and die (inflammatory process). Free radicals are released which oxidize LDL cholesterol, producing foam cells that accumulate in the vessel wall.
- The smooth muscle in the vessel lumen hypertrophies and there is a buildup of fibrous scar tissue. This inhibits blood flow.
- Platelets adhere to the irregular surface of the plaque, promoting clot formation.
- In time the fibrous plaques calcify, increasing the likelihood of clot formation.
- The plaque may grow large enough to completely obstruct a vessel or part of it may break off and travel to an area where it is too large to pass through small vessels and obstructs blood flow there.
- As an area of plaque breaks off, it may cause bleeding in the inner lumen of the vessel wall. The fissure seals itself, but there may be a thrombus underneath which increases occlusion of the vessel
11
Q
What are complicated plaques in relation to atherosclerosis?
A
They are plaques that have ruptured exposing underlying tissue resulting in platelet adhesion, initiation of the clotting Cascade, and Rapid thrombus formation, that may suddenly occlude the affected vessel, resulting in ischemia and infarction.
12
Q
How does smoking contribute to the development of cardiovascular disease?
A
- It is uncertain how smoking contributes to cardiovascular disease.
- Nicotine stimulates the release of Catecholamines which increases heart rate & causes peripheral vascular constriction.
- As a result blood pressure ↑’s, as do cardiac workload and oxygen demand. Cigarette smoking is associated with an ↑ in LDL and a ↓ in HDL, and contributes to vessel inflammation and thrombus.
- The risk of CAD ↑’s with heavy smoking and ↓’s when smoking stops
13
Q
What is C-reactive protein and what is its role in cardiovascular disease?
A
It is a protein synthesized in the liver and indirectly measures atherosclerotic plaque-related inflammation. Elevated levels of CRP are associated with other CAD risk factors including smoking, obesity, and diabetes
14
Q
What is homocysteine & what is its role in the development of heart disease?
A
- It is an amino acid & is metabolized in the liver
- High levels of homocystine (above 15 micromol/L) have been related to increased risk of myocardial infarction and CVAs
- Homocysteine damages arterial walls by:
- It exerts a direct toxic effect on the endothelial lining
- It interferes with the clotting cascade to increase thrombosis
- It interacts with lipids by oxidizing low-density lipoprotein cholesterol, making it a more significant risk factor for CAD
15
Q
What is LDL & what is its role in cardiovascular disease?
A
- LDL is responsible for:
- the delivery of cholesterol to the cells where it is used to make lipid products like bile salts and gonadal hormones
- Carries cholesterol to the artery walls
- plays a role in endothelial injury inflammation, and immune responses that have been identified as being important in atherogenesis.
- High dietary intake of cholesterol and fats results in ↑’d levels of LDL in the bloodstream. ↑’d serum lvls of LDL Is a strong indicator for coronary risk.
16
Q
What is HDL & what is its role in cardiovascular disease?
A
- HDL is responsible for returning excess cholesterol from the cells & vessel walls to the liver, where it binds to hepatic receptors and is processed and eliminated as bile or converted to cholesterol-containing steroids
- HDL also participates in endothelial repair and decreases thrombosis formation
17
Q
What are VLDL’s (triglycerides) & what is their role in cardiovascular disease?
A
- Are other lipoproteins associated with ↑’d cardiovascular disease
- There is an association of high triglycerides and atherogenic lipoprotein particles that can lead to atherosclerosis.
18
Q
How is blood pressure normally controlled?
A
- Baroreceptors in carotid sinus and aortic arch send information to vasomotor regulatory center in brain which increases or decreases sympathetic nervous system (SNS) activity
- Reduction in blood flow to kidney causes the kidney to release renin.
- This stimulates the release of:
- Aldosterone: increases sodium and water resorption to increase blood volume
- Angiotensin II: triggers release of antidiuretic hormone and causes vasoconstriction
- This stimulates the release of:
19
Q
What is hypertension & what is the clinical criteria for it?
A
- The consistent elevation of systemic arterial blood pressure
- Adults: For those over 50, systolic blood pressure is a more important risk factor for cardiovascular disease than diastolic blood pressure
20
Q
What causes primary hypertension?
A
- Generally: Caused by ↑’s in C.O or total PVR, or both. C.O. is ↑’d by any condition that ↑’s HR or SV, whereas PVR is ↑’d by any factor that ↑’s blood viscosity or ↓’s vessel diameter (vasoconstriction)
- SNS: ↑’d SNS activity (↑’d Production of epinephrine and norepinephrine) causes ↑’d heart rate and systemic vasoconstriction, thus ↑ing BP
23
Q
Describe some characteristics of a non-STEMI
A
- Occurs when coronary blood flow is interrupted for an extended period of time,
- the obstruction only involves the myocardium directly beneath the endocardium
- presents with ST depression and T wave inversion.
24
Q
Describe some characteristics of a STEMI
A
- Occurs when a coronary artery completely blocks the vessel, resulting in an infarction extending through the myocardium
- It extends all the way from the endocardium to the epicardium resulting in severe cardiac dysfunction
- This causes ST segment elevations on the EKG
25
Q
Describe the pathophysiology that occurs during an MI
A
- Plaque formation in coronary arteries leads to clot formation
- When a clot obstructs an artery, blood flow is disrupted leading to ischemia
- Myocardial cells deprived of O2 lose contractility
- This causes the myocardial cells to release epinephrine, ↑’ing the risk dysrhythmias and heart failure.
- There is loss of K+, Ca, and Mg from cells
- Prolonged, unrelieved ischemia leads to tissue death and necrosis.
- creatinine kinase (CK-MB) begins to rise within 3-8 hours after the onset of myocardial damage
- Troponin-I is the most specific indicator of an MI and is detectable 2-4 hours after onset of symptoms
26
Q
What is heart failure?
A
- Occurs when the heart is unable to generate adequate cardiac output, such that there is inadequate perfusion of tissues. This may be because of cardiac disease or long-term effects of hypertension.
- Results in L. heart failure ( Systolic & diastolic HF)
- Right heart failure
27
Q
What is Left systolic Heart Failure & describe its pathophysiology
A
- Occurs when there is an inability of the heart to generate adequate cardiac out & the ejection fraction is less than 40%.
- CO = SV x HR
- SV Is influenced by contractility, preload, and afterload
- When contractility is ↓’d, SV ↓’s, and LVEDV ↑’s. This causes dilation of the heart and an ↑ in preload.
- MI’s Are the most common cause of decrease contractility
- Preload ↑’s w/ ↓’d contractility or w/ ↑’d fluid administration, renal failure, or mitral valvular disease.
- An ↑ in afterload, Is caused by an ↑ in PVR, most commonly caused by HTN → ↑’d PVR → ↑’d pressure for L. ventricle to pump against → L. ventricle hypertrophy
- The ↓’d CO → ↓’d renal perfusion → Rass activation → ↑’d PVR + plasma volume → ↑’ing preload & afterload even more.
- Leads to the heart having a hard time pumping the blood out of the ventricles& a hard time
28
Q
What is Left diastolic Heart Failure & describe its pathophysiology
A
- Can also be defined as pulmonary congestion
- Is usually caused by hypertension induced myocardial hypertrophy & myocardial ischemia with resultant ventricular remodeling.
- There is ↓’d compliance in L. ventricle & abnormal diastolic relaxation → ↑’d LVED pressure → ↑ pressure in pulmonary circulation → pulmonary edema.
- The pressure is made worse w/ tachycardia, DOE & fatigue often present
- Pulmonary hypertension & Right heart failure may develop
- S4 gallop
29
Q
What is and what causes right heart failure?
A
- It is the inability of the right ventricle to provide adequate blood flow into the pulmonary circulation at a normal CVP.
- Often results from LHF when the ↑ if LV filling pressure goes back into the pulmonary circulation → ↑ CVP → ↑ emptying resistance from the right ventricle → Right hear dilating and failing → JVD, venous distention, peripheral edema, hepatosplenomegaly
- RHF can also occur from pulmonary hypertension from COPD or ARDS
30
Q
What is ventricular remodeling?
A
- Is a process that is mediated by angiotensin II, aldosterone, catecholamines, adenosine, oxidative tress, and inflammatory cytokines
- This results in myocyte hypertrophy, scarring, and loss of contractile function
- These changes can be limited and even revered through ace inhibitors, beta-blockers, statins, pacemakers, and ventricular assist devices.
31
Q
What is Kawasaki disease?
A
- An acute self-limiting systemic vasculitis that may result in cardiac sequelae.
- Is a disease of young children
- Disease progresses in 4 stages
33
Q
What are some characteristics of acyanotic congenital heart defects?
A
- They are defects that increase pulmonary blood flow
- There is a left to right shunt
- Types: Patent ductus arteriosus, atrial septal defect, ventricular septal defect, tetralogy of Fallot, tricuspid atresia
34
Q
What are some characteristics of cyanotic congenital heart defects?
A
- They are defects that decrease pulmonary blood flow
- There is a right to left shunt
- Types: tetralogy of Fallot, tricuspid atresia
35
Q
Describe the pathophysiology of coarctation of the aorta
A
- It is a narrowing of the lumen of the aorta that impedes blood flow → ↑’d pressure proximal to the stenosis and ↓’d distal to it → this leads to ↑’d work for L. ventricle → LV hypertrophy → HF
- May develop because of abnormal contractile ductal tissue that constricts at the time of ductal closure
- https://www.youtube.com/watch?v=HbUrfLgE2FE.
