Alterations of cardiac function Flashcards
Varicose veins
- Vein in which blood has pooled
- Distended, tortuous and palpable
- Cause: Trauma or gradual vein distention
- Typically the saphenous vein
Chronic venous insufficiency
- Inadequate venous return over a long period due to varicose veins, valvular incompetence
- Venous stasis ulcers
Venous stasis
Venous hypertension, circulatory stasis, and tissue hypoxia leads to an inflammatory reaction that causes fibrosclerotic remodeling of the skin. Ulceration and hyperpigmentation can occur
Deep Venous Thrombosis
-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
Post thrombotic syndrome
-Frequent complication of DVT characterized by chronic, persistent pain, swelling, and ulceration of the affected limb
Thrombus formation
- 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)
Aneursym
- 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)
Aortic dissection
dysphagia, dyspena, tearing of cp
-Infection, collagen disorders like marfans and chest trauma can also cause this
Embolism
- 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)
Peripheral artery disease (PAD)
- atherosclerotic disease of arteries that perfuse the limbs (esp lower)
- Risk factors: esp those with diabetes
- Intermittent claudication
- Often asymptomatic
Intermittent claudication
- Obstruction of arterial blood flow in the iliofemoral vessels resulting in pain with ambulation
- Claudication-gets better with rest
Peripheral artery diseases-Thromboangiitis obliterans (Buerger disease)
- 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
Peripheral artery disease-Raynaud phenomenon or raynaud disease
- 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
Raynaud’s disease
- 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)
Risk factors for hypertension
- Family hx
- age, gender (male greater than female)
- Black race, high sodium
- glucose intolerance
- heavy alcohol use, obesity, cigarrettes
- Low K, Mg, Ca
Primary hypertension
- 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
Treatment of HTN
-diuretics, adrenergic blockers, Ca channel blockers, ACE inhibitors, ang 2 receptor blockers.
Arteriosclerosis
-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
Atherosclerosis
- 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
Risk factors of atherosclerosis
- 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
Progression of atherosclerosis
- Inflammation of endothelium
- cellular proliferation
- macrophage migration
- LDL oxidation (foam cell formation)
- Fatty streak
- Fibrous plaque
- Complicated plaque
Endothelial injury
- 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
Complications of atherosclerosis
- Calcification of fibrous plaque
- Rupture or ulceration of plaque
- Hemorrhage of plaque
- Embolization of fragments
- Weakening of vessel wall
Coronary artery disease
- Any vascular disorder that narrows or occludes the coronary arteries
- Atherosclerosis is most common cause
Risk factors for CAD
-Dyslipidemia, hypertension, smoking, DM, Obesity, defect in the production of precursor endothelial cells
Non-traditional risk factors for CAD
- Markers of inflammation of thrombosis
- C reactive protein, fibrinogen, protein C, and plasminogen and activator inhibitor
- Infections
- Hyperhomocysteinemia
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
Triglycerides
-In chylomicrons
VLDL
-Mainly triglycerides + carrier protein
LDL
-Mainly cholesterol + carrier protein
HDL
Mainly phospholipids + carrier protein
Coronary arteries
-Two major left main and RCA
Left main coronary artery
- LAD supplies to LV, RV and septum
- Circumflex supplies LA and lateral wall
RCA
-Supplies posterior RV, and some to the LV
Prinzmetal angina
-abnormal vasospasm of coronary vessels results in unpredictable chest pain
Silent ischema
-MI that doesn’t cause detectable symptoms
Myocardial ischemia
- When coronary blood flow is interrupted for an extended period, myocyte necrosis occurs-MI
- Two major types of MI
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
Acute coronary symptom assessment
-measuring serum enzymes such as creatinine kinase and troponins and ECG changes (ST elevation)
Acute coronary syndromes
- Transient ischemia
- Unstable angina
- Sustained ischemia
- MI
- Myocardial inflammation and necrosis
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)
MI
- cellular injury, cellular death,
- structural and functional changes (2-hibernating myocardium, 3-myocardial remodeling, 1-myocardial stunning)
- Repair
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
Disorders of heart wall: Pericardium
- acute pericarditis (drug therapy, infections, tumors)
- Pericardial effusions (tamponade)
- constrictive pericarditis
Disorders of myocardium: Cardiomyopathies
- Dilated cardiomyopathy (congestive cardiomyopathy)
- Hypertrophic cardiomyopathy
- Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
- asymmetric septal hypertrophy cardiomyopathy
- Hypertensive (valvular hypertrophic) cardiomyopathy
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
Hypertrophy
-increase in absolute wall thickness
Restrictive cardiomyopathy
- infiltration of myocardium and reduced compliance
- Ventricular filling is reduced
- Systolic functions and myocardium wall thickness are normal or near normal
Disorders of the endocardium
- Valvular dysfunction
- Valvular regurg
- Mitral valve prolapse syndrome
Valvular Stenosis
Mitral stenosis
Aortic stenosis
Valvular regurg
Aortic regurg
Mitral regurg
Tricuspid regurg
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
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)
Congestive HF
- Systolic HF
- Diastolic HF
Systolic HF
Inability of the heart to generate adequate CO to perfuse tissues
Diastolic HF
Pulmonary congestion despite SV and CO
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)
