patho

Veins review

-Leaflet valves to prevent blood from flowing backwards
-leg muscles pump veins to return blood to the heart, against the effects of gravity
-when veins become varicose, the leaflets of the valves no longer meet, & the valves don't work
-allows blood to flow backwards & they enlarge even more

Varicose veins

_vein in which blood has pooled
-Distended, tortuous, & palpable veins
-Caused by trauma or gradual venous distention
-more common in superficial veins in the legs

Risk factors for Varicose veins

Age, female gender, family hx, obesity, pregnancy, DVT, prior leg injury

Chronic Venous insufficiency

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

Chronic Venous insufficiency S/S

Pruitis, hyperpigmentation of leg, chronic swelling of legs/ ankles....inc. risk of ulcers, cellulitis

Continues Chronic Venous insufficiency

Circulation to extremities so sluggish...metabolic demands of cells for O2/ nutrients & remove wastes barely met
Any trauma/ pressure...lower O2 supply further & causes cell death/nercrosis\= venous stasis ulcers

Tx of chronic venous insufficiency

SCDs, comp stocking, BP meds, elevate legs above heart level

Thrombus formation

Abnormal blood clot formed in vessel; remains attached to the vessel wall

Thrombus & emboli lumped together @ times

Ex: thromboembolus
Thrombophlebitis

Arterial Thromosis

Thrombus in artery
Potential of infarct of organs in body

Venous thrombi

blood clot form w/in vein

Thrombus formation in veins

Obstruction of venous flow from thrombus leading to increased venous pressure

DVT (deep vein thrombosis)

Thrombi most commonly occur in deep veins

3 factors promote venous thrombosis

Triad of Virchow
1. Venous stasis
2. Venous endothelial damage
3. Hypercoagulable state

Thrombus formation in vein, often near venous valve

accumulation of clotting factors & platelets lead to this

Inflammation occurs

around thrombus, further platelet aggregation, thrombus grows
-may or may not cause pain
-affected extremity painful, swollen, red, war, superficial veins may be engorged
-significant obstruction to venous blood flow, increase pressure in veins behind clot, edema of extremity

Tx of thrombi

most eventually dissolve w/o tx
some untreated DVT high risk for embolization
-heparin & warfarin

Embolism

Obstruction of a vessel by an embolus, a bolus of matter circulating in bloodstream
--key: floating, implies movment; usually breaks off from thrombi

Traveling embolus

in bloodstream until reaches vessel it cant fit through
May dislodged thrombus, air bubble, aggregate of fat, bacteria, CA cells, foreign substance

Arterial Embolism

Lodge in distal part of systemic circulation

Venous Embolism

PE often classified as such, because embolism forms in veins (DVT)

Hypertension (HTN)

Consistent elevation of systemic arterial blood pressure

Patho of HTN

Results from sustained increase in peripheral resistance (arteriolar vasoconstriction) increase in circulating blood volume or both
--sustained systolic blood pressur of 130 mm HG or greater or a diastolic pressure of 80 mm HG or greater
--persistent HTN one risk factor for stroke, MIT, HF, arterial aneurysm, leading cause of CKF

Primary HTN (essential)

Essential or idiopathic (increased ICP) HTN
Genetic & Environmental factors
Affects 92% to 95% of individuals w/ HTN
No obvious medical cause.

Risk factors for Primary HTN

High sodium intake
Natriuretic peptide abnormalities
Inflammation
obesity
insulin resistance

Primary HTN pathogenesis

Decreased renal salt excretion (Shift in pressure- natriuesis relationship)
-Increase SNS
-Genetics
-Decreased dietary potassium, magnesium & calcium
- increase dietary sodium intake
-insulin resistance
-obesity
-renal glomerular & tubular inflammation
-dysfunction of the natriuretic hormones
-endothelial dysfunction
Increase RAAS (respecially aldosterone)

Secondary HTN

Caused by a systemic disease process that raises peripheral vascular resistance or cardiac output
--Renal vascular or parenchymal disease, adrenocortical tumor, adrenomedullary tumors & drugs
\=5-10% cases

Complicated HTN

Chronic hypertensive damage to blood vessels & tissues leading to target organ damages in heart, kidney, brain & eyes

CV complications

Myocardial hypertrophy
HF
CAD
MI
Sudden Death

Orthostatic (postural) Hypotension

Decrease in both systolic & diastolic blood pressure while standing
--decrease in SBP of as least 20 mmHg or DBP of as least 10 mmHG w/in 3 minutes of moving to standing position

Orthostatic lacks

normal blood pressure compensation in response to gravitational changes on the circulation

Normal Orthostatic

stands: gravity changes or circulation compensated by reflex arteriolar/ venous constriction, increase HR; closure of valves in venous system, contraction leg muscles, stretch receptor that response to shift in volume, increase HR, constricts systemic artierioles

Abnormal Orthostatic Hypotention

standing, blood pool, normal arterial pressure not maintined

Aneurysm

Local dilation or outpouching of vessel wall or cardiac chamber
-Aorta most susceptible, esp. abdominal d/t amount of pressure & blood flow

Causes of Aneurysm

Atherosclerosis: plaque formation erodes vessel wall, contributes to inflammation & relase of enzyems further weaken wall
Hypertension: increase wall stress

Aneurysm can lead to

aortic dissection or rupture (AAA: abdominal aortic aneurism)

Aneurysm are most common after

MI when intraventricular tension stretches noncontracting infarcted muscled, infarct expansion, weak/thin layer of necrotic muscles, fibrous tissues that bulges w/ systole

S & Sx of aneurysm

Aortic no signs until rupture, sever pain, hypotention
If impaired flow to extremity, ischemia
Heart: dysrythmia, HF, embolism of clots to brain

Arteriosclerosis

Chronic disease of the arterial system

When does arteriosclerosis occur?

When blood vessels that carry O2 & nutrients from your heat to the rest of body (arteries) become thick & stiff..sometimes restricting blood flow to organs & tissues

Healthy arteries

Are flexible & elastic but over time walls can harden

Atherosclerosis & artheriosclerosis

Often used interchangeably, but are two different things

Atherosclerosis Caused

by accumulation of lipidpladen macrophages w/in arterial wall, leads to plaque development

Not single disease, pathologic process that can affect vascular systems throughout the body, result in ischemic syndroms

Leading causes of Atherosclerosis?

CAD, CVD (coronary artery & vascular disease)

Atherosclerosis Progression/ patho

-Begins w/ injury to endothelial cells that line artery walls, inflammation of endothelium
-Cellular proliferation
- macrophage migration & adherence
LDL oxidation (foam cell formation)
_Fatty streak
- Fibrous plaque
_complicated plaque

Risk factors for Atherosclerosis

diabetes, smoking, hyperlipidemia/dyslipidemia, hypertension

Atherosclerosis results in

inadequate perfusion, ischemia, necrosis

S & Sx of atherosclerosis

result from inadequate profusion r/t obstruction of vessels

Peripheral Arterial Disease (PAD)

Atherosclerotic disease of arteries that perfuse limbs, especially lower extremities

PAD increase risk

Risk w/DM
Gradual increased obstruction to arterial blood flow to legs

S & Sx PAD

Common: intermittent claudication: atherosclerosis in iliofemoral vessels leads to pain w/ ambulation
May be asymptomatic in early stages

Tx form PAD

Decrease risk factors, antiplatelet therapy

Coronary Artery Disease (CAD)

Any vascular disorder that narrows or occludes the coronary arteries leading to myocardial ischemia
--end resuls of accumulation of plaques w.in walls of coronary arteries that suppply myocardium w/O2 & nutrients, obsrtuction of lumen of coronary artery

Pts with CAD may

suffer 1 or more MI, and may have addl symtoms such as angina at rest

CAD most common cause

Atherosclerosis

Lab marker for CAD

Troponin I

Risk Factors for CAD Nonmodifiable (can't do anything about)

Increase age
Family hx
Male gender or female gender postmenopause

Risk factors for CAD Modifiable (can control)

Dyslipidemia
HTN
Cigarette smoking
DM (Diabetes mellitus)
Obesity/ Sedentary lifestyle
Atherogenic diet

Coronary arteries normally supply blood flow....

sufficient to meet demands of myocardium

CAD can decrease

myocardial blood supply leading to myocardial ischemia (MI)

Myocardial Ischemia (MI)

Local, tempoary deprivation of the coronary blood supply
Ischemia: amt of blood supplies to tissue inadequate
--myocardium doesn't fxn optimally
--larger areas..impairment in relaxation & contraction of myocardium

MI infarction: tissue irreversible death

1 Stable angina
2 Prinzmetal angina
3 Silent ischemia

Stable angina

chest pain caused by MI; substernal chest discomfort. Usually relieved w/ rest, nitrates

Prinzmetal angina

CP that occur unpredictably & often at rest, often at night; caused by vasospasm of coronary arteries; vasospasm of CA

Silent ischemia

ischemia may be asymptomatic: fatigue, SOB, unease, more common in women

MI mainfestations

Sudden sever CP; may radiate
Nausea, vomiting
Diaphoresis
Dyspnea

Complications of MI

Sudden cardiac arrest due to ischemia, left ventricular dysfunction, & electrical instability. Apply oxygen!

acute coronary syndrome (ACS)

Sudden coronary obstruction r/t thrombus formation over ruptured or ulcerated atherosclerotic plaque

Unable angin with ACS

Angina pectoris that worsens/ changes
At least 1 of 3 features: occurs at rest lasting \>10 min., severe & new onset, crescendo pattern ( increase and decrease of intensity)
May be indicator of impending HA. Sense of "impending doom"

MI interruption

Interruption of blood supply to part of the heart r/t blockage of coronary artery, O2 shortage, if untreated heat cells damaged or die

Disorders of the pericardium

(heart wall) (fibrous sac surrounding the heart)

Acute Pericarditits

Acute inflammation of the pericardial membrane
Pericardial membranes become inflamed & rough, pericardial effusion may develop (serous, purulent, fibrinous)

Causes of Acute pericarditis

viral or bacterial infection of pericardium, idiopathic, sepsis, MI, Surgery

May have CP, Lead to pericardial effusion, tamponade
Exam: low grade fever, tacyhy, friction rub

Pericardial Effusion

Fluid around the heart

Cardiac tamponade: happens when fluid leads to increase pressure, adversely affects heart fxn
Tx: pericardiocentesis (aspiration of fluid) underlying tx

Disorders of endocardium (inner most lining of heart wall)

Damage heart valves, composed of endocardial tissue
--Inflammatory, ischemic, traumatic, infectious, remodeling chagnes

Disorders of endocardium develop

Valvular stenosis: aortic valve consists of 3 leaflets (trileaflets) flow of blood from left ventricle to aorta & rest of body during ventricular systole

Aortic stenosis

aortic valve become progressively stenotic, pressure gradient created between LV and aorta since blood not adequately pumped through narrow orifices. Slow HR, heart murmur

Mitral Stenosis

inflammation and scarring of valvular leaflets impaired flow of blood from left atrium to left ventricle; pulmonary congestion, right HF, diastolic murmur. aka Myocardial hypertrophy.

Valvular regurgitation

1. Aortic regurgitation (AR)
2. Mitral regurgitation (MR)
3. Tricuspid regurgitation (TR)

aortic regurgitation (AR)

leaking of aortic valve that causes blood to flow in revers direction during ventricular diastole, from aorta into left ventricle

Mitral regurgitation (MR)

mitral valve doesn't close properly when heart pumps, backflow of blood from left ventricle into left atrium during ventricular systole

Tricuspid regurgitation(TR)

failure of heart's tricuspid valve to close properly during systole w/ each heartbeat some blood passes form right ventricle to right atrium, opposite the normal direction

Dysrthythmias

1 Normal (QRS)
2. Irregular (heart quivers)
3 Asystole (no movement)

Heart Failure

General term used to describe several types of cardiac dysfunction that result in inadequate perfusion of tissue w/ blood-borne nutrients

HF FAILURE

F-faulty heart valves- (stenosis/regurgitation/infection)
A- arrhythmia -(A-Fib/tachycardia)
I- infarction -CAD, muscle ischemia, MI)
L- lineage (congenital/ family)
U- Uncontrolled HTN- (stiffening of heart wall)
R- Recreational drug use- (Illicit drugs & alcohol abuse)
E- evaders- (Virus/Infection)

Left heart failure (congestive heart failure)

1 Systolic heart failure
2 diastolic heart failure
More common than RHF

systolic heart failure

-inability of the heart to generate adequate cardiac output to perfuse tissue
-Ventricular remodeling
-causes include mycardial infarction, myocarditis, cardiomyopathy

diastolic heart failure

-pulmonary congestion despite normal stroke volume and cardiac output
-Causes include myocardial hypertrophy & ischemia, diabetes, valvular & pericardial disease

Manifestation of left heart failure

-Result of pulmonary vascular congestion & inadequate perfusion of the systemic circulation
-Include dyspnea, orthopnea, cough of frothy sputum, fatigue, decreased urine output & edema
-Physical examination often reveals pulmonary edema (cyanosis, inspiratory crackles, pleural effusions,) hypotentsion or hypertension, an S3 gallop, and evidence of underlying CAD or HTN

Right heat failure

-most commonly caused by a diffuse hypoxic pulmonary disease
-can result form in increase in left ventricular filling pressure that is reflected back into the pulmonary circulation

DROWNING

-LEFT heart failure-
D- Dyspnea
R- rales -crackles
O-Orthopnea (sit-up to breath)
W-weakness
N-nocturnal paroxysmal dyspnea ( SOB @ night)
I-increased heart rate
N- Nagging cough (frothy)
G-Gain weight 2-3lbs daily

SWELLING

-RIGHT heart failure-
S- swelling (peripheral)
W-weight gain
E- edema (pitting)
L-large neck vein (JVD)
L-Lethargy (tired)
I-irregular heat rate
N-nocturia (urine @ night)
G- Girth (abd increase size, nausea & anorexia)

Shock

-Cardiovascular system fails to perfuse the tissues adequately
-Leads to impaired cellular metabolism
--impaired O2 use
--Impaired glucose use
-Manifestation vary based on stage but often include hypotenstion, tachycardia, increase respiratory rate

Types of Shock

1. Cardiogenic
2. Hypovolemic
3. Neurogenic
4. Anaphylactic
5. Septic

Cardiogenic

Inadequate circulation of blood r/t primary failure of ventricles of heart to fxn effectively
--decrease cardiac output & evidence of tissue hypoxia

Hypovolemia

state of decrease blood volume caused by loss of whole blood, plasma, or interstitial fluid
--begins to develop when intravascular volume has decreased by 15%

Neurogenic (also called vasogenic shock)

shock resulting in hypotension, bradycardia, attributed to disruption of autonomic pathways within spinal cord
--hypotension occurs r/t decrease systemic vascular resistance, pooling of blood w/in extremities lacking sympathetic tone
--can result from severe CNS damage; trauma causes sudden loss of sympathetic stimulation of blood vessels, causes them to relax, sudden decrease in BP

anaphylactic shock

anaphylaxis associated with systemic vasodilation that results in low blood pressure, leading to decrease tissue perfusion & impaired cellular metabolism
--also associated with severe bronchoconstrction to the point where the individual is unable to breathe.

Septic shock

caused by decreased tissue perfusion and oxygen delivey as a result of severe infection and sepsis, though the microbe may be systemic or localized to a particular site. Decreased B/P, diaphoretic, and lethargic. Lactic Acid level is measured when released with strenuous exercise & other conditions heart failure, and decreased flow of O2 in body.

Multiple Organ Dysfunction Syndrome (MODS)

Progressive dysfunction of two or more organ systems resulting from an uncontrolled inflammatory response to sever illness or injury