Cardiovascular Disease (Patho)

Most common in lower limbs

Chronic Disease of arterial system (abnormal THICKENING or HARDENING of vessel walls)

Risk Factors: High sodium intake, natriuretic peptide abnormalities, inflammation, obesity, insulin resistance

Decrease in systolic and diastolic BP upon standing, lack of normal BP compensation in response 2 gravity in circulation

Clinical Manifestations: significant hypotension (>20 mmHg), lighthead/dizzy, blurry vision, weak, syncope, confusion

ECG changes during episodes of pain, increased likelihood of progressing to MI, may NOT have Troponin in blood

Extravascular hematoma that continues w/intravascular space

Caused by labile coronary artery thrombus, reversible myocardial ischemia, NOT relieved by typical nitroglycerin

Artery walls are under pressure & local dilation or outpouching of a vessel or cardiac chamber

Unpredictable, Not related to exercise or stress, Caused by Coronary artery spasm, happens mainly AT NIGHT,

Myocardial Ischemia (coronary art getting clogged up makes oxygen less available to the heart)

Aorta is most susceptible, esp abdominal & causes include atherosclerosis & hypertension

Modifiable Risk Factors: Dyslipidemia(high blood cholesterol), hypertension, smoking, diabetes mellitus,

Clinical Manifestations: aching pain, swelling, brawny skin discoloration, venous stasis ulcers

inadequate venous return over a long period due to varicose veins or valvular incompetence

Nonmodifiable Risk Factors: Increased age, family history, gender

Sudden and extended obstruction of myocardial blood supply & sustained ischemia

Foreign substance: illicit drugs

Caused by genetic and environmental factors

Risk Factors: varicose veins, heart disease, previous DVT, history of extremity trauma and phlebitis

Risk Factors: Smoking, Diabetes, Obesity- BMI over 30, HTN, High Cholesterol, Increasing age

Blood clot that remains attached to the vessel wall

Complications: CVI (Chronic Venous Insufficiency) and Pulmonary Embolus

Types: Transmural Infarction (STEMI) Most dangerous & goes through all levels of heart & ECG Changes

Types: Nontransmural/ Subendocardial Infarction (NSTEMI) ECG Changes. Not extended to all layers of heart

Dislodged thrombus, air bubble, cancer cells, bacteria loves to travel to the heart, aggregate from fat to bone marrow

Clinical Manifestations: Headache, SOB, nosebleed (epistaxis), fatigue, s4 gallop

Thickening and Hardening caused by accumulation of lipen-laden macrophages (fats) in arterial wall leading to plaque

More common in Women

Risk Factors: Diabetes, Smoking, Hyperlipidemia, Dyslipidemia(high blood cholesterol lvl), Hypertension

Progression: Macrophage migration & adherence, LDL Oxidation (foam cell formation), fibrous plaque, complicated plaque

Atherosclerotic disease of the arteries that perfuse limbs, Ischemia is bc blood flow gets interrupted,

Pt had stable angina then became unpredictable, angina that is OCCURING AT REST, or increasing in severity or frequency

obstruction of venous flow leading to increased venous pressure

Increased in hypertension and vasoconstriction

Clinical Manifestations: swelling, pain, redness, warmth

Normal Adult: 5L/ min.

Modifiable Risk Factors: Obesity/Sedentary lifestyle and Atherogenic diet: high fat intake

HR X Stroke Volume

Comes on with exertion (tell pt. to sit and rest)

Chronic hypertensive damage to blood vessels and tissue lead to target tissue damage to organ (ie heart, kidney, brain)

Volume inside ventricle at end of diastole; left ventricular end-diastolic volume

Complications: Sudden cardiac arrest due to ischemia, Left Ventricular dysfunction, & electrical instability

Fusiform (Circumferential & Saccular)

Ischemia, angina, acute coronary symptoms (unstable angina & MI) & any vascular disorder that narrows or coronary art

Formation of arteriosclerosis

Myocardial metabolism is the function of the heart as the consumer and provider of energy (oxygen consumption)

Risk Factors: older age, dehydration, heart arrhythmias, endocrine disorders, neurological disorders

Normal Healthy <3: 55-70%

factors that make the heart work harder to pump blood to the body, increased = increased cardiac output

CAD produces myocardial ischemia when atherosclerotic coronary arteries supply INSUFFICIENT OXYGENATED BLOOD to tissues

amount, or percentage of blood that is pumped (or ejected) out of ventricles

Clinical Manifestations: Sudden Severe cheat pain that may radiate, N/V, Diaphoresis, Dyspnea

Risk Factors: Virchow's triad (venous stasis, hypercoagulable state, venous endothelial damage)

stroke volume and preload

Local temporary deprivation of the coronary blood supply, nitroglycerin used to treat vasodilation to arteries

Results in Structural/Function Changes bc trying to use scar tissue to contract. (not as good as healthy tissue)

Secondary to something else and appears suddenly and usually higher than pulmonary primary hypertension

Caused by underlying condition renal vascular or parenchymal disease, adrenocotical tumors, adrenomedullay tumor, drugs

Aorta is most susceptible, esp abdominal & can lead to aortic dissection or rupture

Progression: inflammation of the endothelium (due to chronic inflammation), cellular proliferation, fatty streak

Bolus of matter that is circulating the blood stream

increased hypervolemia, regurgitation of cardiac valves, heart failure

Clinical Manifestation: Intermittent Claudication (pain w/walking) & diminished pulses in affected extremity

Virchow's Triad (Venous Stasis, Hypercoagulable states, venous endothelial damage)

Risk Factors: Hypercoagulable state (birth control, smoking, dehydration, high RBC, high platelet, pregnancy)

Complications: Cardiogenic Shock, Pericarditis, Pericardial tamponade

(PRESSURE) Resistance to ejection of blood from left ventricle & determined by system vascular resistance (SVR) in aorta

Treat By: elevating legs, walking eases the pain, wear support stockings