Alterations of cardiac function Flashcards
(58 cards)
1
Q
Varicose veins
A
- Vein in which blood has pooled
- Distended, tortuous and palpable
- Cause: Trauma or gradual vein distention
- Typically the saphenous vein
2
Q
Chronic venous insufficiency
A
- Inadequate venous return over a long period due to varicose veins, valvular incompetence
- Venous stasis ulcers
3
Q
Venous stasis
A
Venous hypertension, circulatory stasis, and tissue hypoxia leads to an inflammatory reaction that causes fibrosclerotic remodeling of the skin. Ulceration and hyperpigmentation can occur
4
Q
Deep Venous Thrombosis
A
-Obstruction of venous flow leading to venous pressure.
-Factors (Virchow triad);
Venous stasis, venous endothelial damage, hypercoagulable states
-Post thrombotic syndrome
-Usually asymptomatic: prophylaxis for at risk individuals is crucial
5
Q
Post thrombotic syndrome
A
-Frequent complication of DVT characterized by chronic, persistent pain, swelling, and ulceration of the affected limb
6
Q
Thrombus formation
A
- Blood clot that remains attached to the vessel wall
- Thromboembolus (detached-has traveled)
- Arterial thrombi (more serious due to ischemia-Most common from mitral and aorta)
- Venous thrombi (more common low pressure, low flow system)
7
Q
Aneursym
A
- Local dilation or outpouching of a vessel wall or cardiac chamber
- True aneursym-all 3 layers of the arterial wall (fusiform, circumferential)
- False aneursyms (saccular) -Usually near a vascular graft and natural artery
- Most common site is aorta (htn, and arteriosclerosis are risk factors)
8
Q
Aortic dissection
A
dysphagia, dyspena, tearing of cp
-Infection, collagen disorders like marfans and chest trauma can also cause this
9
Q
Embolism
A
- Bolus of matter that circulates in bloodstream, then lodges obstructing blood flow.
- Dislodged DVT, air bubble, amniotic fluid, aggregate of fat, bacteria, cancer cells, or a foreign substance
- Many arterial emboli are from the heart (post MI, valve disease, endocarditis, dysrhythmias, HF)
10
Q
Peripheral artery disease (PAD)
A
- atherosclerotic disease of arteries that perfuse the limbs (esp lower)
- Risk factors: esp those with diabetes
- Intermittent claudication
- Often asymptomatic
11
Q
Intermittent claudication
A
- Obstruction of arterial blood flow in the iliofemoral vessels resulting in pain with ambulation
- Claudication-gets better with rest
12
Q
Peripheral artery diseases-Thromboangiitis obliterans (Buerger disease)
A
- Occurs mainly in young men who smoke
- Inflammatory disease of peripheral arteries resulting in nonathersclerotic lesions (Digital, tibial, plantar, ulnar, palmar arteries)
- Obliterates the small and medium sized arteries
- Produces dry gangrene
- Causes pain, tenderness, and hair loss in the affected area
- Symptoms are caused by slow sluggish blood flow
13
Q
Peripheral artery disease-Raynaud phenomenon or raynaud disease
A
- Episodic vasospasm (ischemia) in arteries and arterioles of the fingers, less commonly the toes
- Raynaud’s is secondary to other systemic diseases or conditions
- Primary vasospastic disorder of unknown origin
14
Q
Raynaud’s disease
A
- Collagen vascular disease (scleroderma), smoking, pulmonary hypertension, myxedema, and environmental factors (cold or prolonged to vibrating machinary)
- Endothelial dysfunction that causes decreased nitric oxide production (this is a potent vasodilator)
15
Q
Risk factors for hypertension
A
- Family hx
- age, gender (male greater than female)
- Black race, high sodium
- glucose intolerance
- heavy alcohol use, obesity, cigarrettes
- Low K, Mg, Ca
16
Q
Primary hypertension
A
- Genetics plus environment
- Other contributing factors: insulin resistance, dysfunction of SNS, RAAS, adducin, and natriuretic hormone, and inflamamtion
- This in turn causes vasoconstriction, renal salt and water retention, increased peripheral resistance, and increased blood volume
17
Q
Treatment of HTN
A
-diuretics, adrenergic blockers, Ca channel blockers, ACE inhibitors, ang 2 receptor blockers.
18
Q
Arteriosclerosis
A
-Chronic disease of arterial system
-Abnormal thickening, and hardening of vessel walls
-Smooth muscle cells and collagen fibers migrate to the tunica
intima
-This can be an inevitable result of aging w/ cross linking of collagen and deposits of Ca
19
Q
Atherosclerosis
A
- Form arteriosclerosis
- Thickening and hardening by accumulation of lipid-laden macrophages in the arterial wall
- Plaque development
- This is leading cause of CAD and CVD
20
Q
Risk factors of atherosclerosis
A
- inflammatory disease that begins with endothelial and progresses through several stages of fibrotic plaque
- elevated CRP, increased serum fibrinogen, oxidative stress, infection, and periodontal disease
21
Q
Progression of atherosclerosis
A
- Inflammation of endothelium
- cellular proliferation
- macrophage migration
- LDL oxidation (foam cell formation)
- Fatty streak
- Fibrous plaque
- Complicated plaque
22
Q
Endothelial injury
A
- Endothelium stops making normal antithrombotic and vasodilatory subtances, like nitric oxide and prostaglandins
- Leukocytes and macrophages adhere to the endothelium and release cytokines
- Oxidation and phagocytosis of LDL
23
Q
Complications of atherosclerosis
A
- Calcification of fibrous plaque
- Rupture or ulceration of plaque
- Hemorrhage of plaque
- Embolization of fragments
- Weakening of vessel wall
24
Q
Coronary artery disease
A
- Any vascular disorder that narrows or occludes the coronary arteries
- Atherosclerosis is most common cause
25
Risk factors for CAD
-Dyslipidemia, hypertension, smoking, DM, Obesity, defect in the production of precursor endothelial cells
26
Non-traditional risk factors for CAD
- Markers of inflammation of thrombosis
- C reactive protein, fibrinogen, protein C, and plasminogen and activator inhibitor
- Infections
- Hyperhomocysteinemia
27
Lipids
- Strong link between lipoproteins and CAD
- Fat metabolism
- Dietary fat package in chylomicrons for absorption in small instenstine
- Good cholesterol in transported lipids to the liver for disposal
28
Triglycerides
-In chylomicrons
29
VLDL
-Mainly triglycerides + carrier protein
30
LDL
-Mainly cholesterol + carrier protein
31
HDL
Mainly phospholipids + carrier protein
32
Coronary arteries
-Two major left main and RCA
33
Left main coronary artery
- LAD supplies to LV, RV and septum
| - Circumflex supplies LA and lateral wall
34
RCA
-Supplies posterior RV, and some to the LV
35
Prinzmetal angina
-abnormal vasospasm of coronary vessels results in unpredictable chest pain
36
Silent ischema
-MI that doesn't cause detectable symptoms
37
Myocardial ischemia
- When coronary blood flow is interrupted for an extended period, myocyte necrosis occurs-MI
- Two major types of MI
38
Two types of MI: Subendocardial infarction and transmural infarction
-in addition to myocyte necrosis other changes in the heart with MI include hibernating, stunning and remodeling
39
Acute coronary symptom assessment
-measuring serum enzymes such as creatinine kinase and troponins and ECG changes (ST elevation)
40
Acute coronary syndromes
- Transient ischemia
- Unstable angina
- Sustained ischemia
- MI
- Myocardial inflammation and necrosis
41
Unstable angina
- Partially occlusive thrombus. EKG shows no ST elevation, no elevation in troponin
- Presents with chest pain, can occur at rest, usually a new onset and severe pain (NSTEMI)
42
MI
- cellular injury, cellular death,
- structural and functional changes (2-hibernating myocardium, 3-myocardial remodeling, 1-myocardial stunning)
- Repair
43
Clinical eval of MI
- ECG changes
- Cardiac enzymes (Troponins-see in 2-4 hours and can be elevated for 7-10 days)
- CK-MB (see in 2-4 hours, peaks in 24 hours)
- LDH (hyperglycemia 72 hours post MI)
- Creatinine kinase
- Complications: dysrhythmias, congestive HF, and death
44
Disorders of heart wall: Pericardium
- acute pericarditis (drug therapy, infections, tumors)
- Pericardial effusions (tamponade)
- constrictive pericarditis
45
Disorders of myocardium: Cardiomyopathies
- Dilated cardiomyopathy (congestive cardiomyopathy)
- Hypertrophic cardiomyopathy
- Restrictive cardiomyopathy
46
Hypertrophic cardiomyopathy
- asymmetric septal hypertrophy cardiomyopathy
| - Hypertensive (valvular hypertrophic) cardiomyopathy
47
Dilated cardiomyopathy
- increase in radius with no change in wall thickness
- greater the wall tension generated greater myocardial O2 demand. If blood supply doesn't meet o2 demand pump will eventually fail
- More prone to fail
48
Hypertrophy
-increase in absolute wall thickness
49
Restrictive cardiomyopathy
- infiltration of myocardium and reduced compliance
- Ventricular filling is reduced
- Systolic functions and myocardium wall thickness are normal or near normal
50
Disorders of the endocardium
- Valvular dysfunction
- Valvular regurg
- Mitral valve prolapse syndrome
51
Valvular Stenosis
Mitral stenosis
| Aortic stenosis
52
Valvular regurg
Aortic regurg
Mitral regurg
Tricuspid regurg
53
Rheumatic fever
- Diffuse inflammatory disease caused by a delayed response to infection by group A beta-hemolytic streptococci
- Febrile illness (Inflammation of joints, skin, nervous system, and heart)
- If left untreated can result in rheumatic heart disease
54
Infective endocarditis
- Inflammation of endocardium
- Agents (bacteria, virus, fungi, rickettsiae, and parasites)
- Sources (prothestic valves, indwelling catheters, open heart surgery)
- Pathogensis (Prepared endocardium, blood-borne microorganism adherence, proliferation of microorganisms)
55
Congestive HF
- Systolic HF
| - Diastolic HF
56
Systolic HF
Inability of the heart to generate adequate CO to perfuse tissues
57
Diastolic HF
Pulmonary congestion despite SV and CO
58
Right HF
- Commonly caused by a diffuse hypoxic pulmonary disease
- Can result from increase in LV filling pressure that's reflected back in pulmonary circulation
- Can occur from LHF, diffuse hypoxic disease (pulmonary, COPD, cystic fibrosis, ARDS)
