Patho Exam 3

Inferior/Superior Vena Cava → right atrium → tricuspid valve → right ventricle → pulmonic valve → pulmonary artery → pulmonary veins → left atrium → mitral/bicuspid valve → left ventricle → aortic valve → aorta → body

What is the normal blood flow through the heart?

systemic

What system is high pressure?

pulmonary

What system is low pressure?

the main purposes of the CV system

• transport

  • O2, nutrients, hormones

• remove CO2/wastes

pericardium, epicardium, myocardium, endocardium

What are the 4 layers of the heart?

pericardium

• outer fibrous layer

• inner serous layer

  • parietal

myocardium

• “muscle,” involuntary

• intercalated disks/gap junctions

  • allow action potential to rapidly move cell to cell

  • contract as one unit

• less intracellular storage of calcium

• contain actin and myosin filaments

endocardium

• thin membrane connective and endothelial tissue

• lines heart/valves

s1 sound

atrioventricular valves closing during systole (ventricles contract)

s2 sound

semilunar valves closing during diastole (atrium contracts)

systole

blood flows to body and lungs during…

diastole

blood is returned back to the heart to fill ventricles during…

on the surface of the myocardium

Where are the coronary arteries located?

right coronary artery

Which artery supplies the right atrium, right ventricle, and septum

left coronary artery

Which artery supplies the left anterior descending (LAD), left ventricle, septum

75%

How much of O2 is used at rest by myocardium?

collateral circulation

When new blood vessels form around clot in artery to provide more blood flow

SA node, AV node, Bundle of His (AV bundle), Right and left branches, and Purkinje fibers

What is the path of the conduction system through the heart?

SA node

normal pacemaker of heart (rate 60-100)

CO = SV x HR

What is the calculation for cardiac output?

preload, after load, and contractility

What are the determinants of cardiac output?

preload

volume of blood at diastole, determined by venous return/stretch of cardiac muscle

afterload

the pressure the heart works against

contractility

how strong the heart contracts

• increased afterload

• decreased preload

• bradycardia (low HR)

• reduced contractility

What situations decrease CO?

arteries

thick walled, elastic

veins

thin walled, distensible

• valves

• muscle and respiratory pump

capillaries

single endothelial cell, thick

the veins

Most of the bodys blood is held where?

the capillaries

Where does oxygen and nutrient delivery occur?

• increases heart rate and contractility

• vasoconstriction

How does the SNS control BP?

decreases HR

How does the PNS control BP?

local factors

• O2, metabolic wastes (H+, K+. Co2)

How does auto regulation control BP?

Norepi/epi, angiotensin II, and histamine

How does the humoral control BP?

• nitric oxide

  • vasodilation

  • inhibit platelet aggregation

• Endothelin

  • vasoconstriction

How does endothelial control, control BP?

increases BF

increased diameter of a blood vessel foes what to BF? (Poiseuille’s Law)

• pressure

• resistance

  • viscosity

  • vessel diameter/length

• Blood Flow = change in pressure over resistance

What factors affect BF?

• more pressure to maintain blood flow through vessels

• increases risk of clots/thrombi

• ex. plaques, clots

What is turbulent blood flow and give an example of something that could cause turbulent BF.

• drains excess interstitial fluid which keeps fluid in vessels balanced

• immune system

How does the lymphatic system interact with the CV system?

dyslipidemia

abnormal lipid levels

hyperlipidemia

elevated lipids in the blood

• hypercholesterolemia

• hypertriglyceridemia

• combined hyperlipidemia

Lipids

cholesterol and triglycerides

• essential for cell membrane and hormone synthesis

Hydrophilic outer layer, hydrophobic inner layer, and apolipoproteins

What makes up a lipoprotein structure?

hydrophilic outer layer

proteins and phospholipids

hydrophobic inner layer

triglycerides and cholesterol

Apolipoproteins

• attach to receptors on cells/tissue

• activate enzymes for normal lipoprotein metabolism

the exogenous and endogenous pathways

What are the two pathways to create cholesterol?

exogenous pathway for cholesterol

• lipids absorbed from GI tract (food)

• packaged as chylomicrons

• transported to → adipose tissue, skeletal muscle, liver

endogenous pathway for cholesterol

• Liver

• synthesis of VLDL, LDL, HDL

• storage

LDL

bad cholesterol

• if excess → injury to blood vessel

HDL

transport excess cholesterol from peripheral tissue to liver

• excreted in bile

risk factors for high cholesterol

• diet

• obesity/sedentary lifestyle

• Genetics

  • ex. familial hypercholesterolemia

  • autosomal dominant: lack of LDL receptors

• Diabetes Mellitus

• Medications: beta blockers, HIV

metabolic syndrome

• associated w/ increased cardiovascular disease

• elevated fasting glucose (or having diabetes)

• elevated blood pressure (or tx for hypertension)

• elevated waist circumference

• dyslipidemia → high triglycerides or low HDL

To be diagnosed with metabolic syndrome, you have to 3 or more of the following..

• smoking

  • contributes to HTN

  • reduces HDL, elevates LDL

  • causes inflammation → damage endothelium

• hypertension

  • endothelial/vessel damage

• diabetes/insulin resistance

  • endothelial damage

  • increased lipoproteins

• obesity → abdominal obesity strong risk factor

• physical inactivity

• hyperlipidemia/dyslipidemia

What are the modifiable risk factors for atherosclerosis?

• age

• gender: occurs earlier in males

  • rate equalizes post menopause

• family history

• genetics

  • alterations in cholesterol/lipid metabolism

What are the non-modifiable risk factors for atherosclerosis?

Complications of atherosclerosis

• ischemia and infarction

  • limb ischemia

  • cerebral ischemia and stroke

  • myocardial ischemia and myocardial infarction

1. endothelial injury

2. migration of inflammatory cells

3. lipid accumulates/smooth muscle proliferation

4. Fibrous cap and plaque

What are the stages of the development of an atherosclerotic plaque?

endothelial injury (development of atherosclerotic plaque)

• causes: smoking, high LDL levels, HTN

• endothelial damage → inflammation

• adhesion macrophages and platelets

migration of inflammatory cells (development of an atherosclerotic plaque)

• macrophages migrate into intimal layer of blood vessel

  • engulf lipoproteins

  • fatty streak

lipid accumulates / smooth muscle proliferation (development of atherosclerotic plaques)

• macrophages

  • oxidize and engulf LDL → foam cells

  • release growth factor → smooth muscle and extracellular matrix proliferation

Fibrous cap and plaque formation (development of an atherosclerotic plaque)

• Fibrous cap of smooth muscle and extracellular matrix (collagen and elastic fiber)

• core of lipids, foam cells, fatty debris

• step 4

myocardial infarction

Stable plaques in coronary arteries become inflamed → unstable plaque → platelet aggregation → clot formation → infarction of cardiac tissue

stable plaque

older lesions may be stable; calcified

unstable plaque

inflammation contributes to rupture, high inflamed plaque poses risk → “vulnerable” or “unstable”

• rupture, ulceration, erosion → thrombus in blood vessel

infarction

Disease produced in coronary arteries due to an acute/unstable plaque.

coronary artery disease

Disease produced due to a chronic stable plaque in the coronary arteries.

acute arterial occlusion

disease produced in peripheries due to acute, unstable plaques.

Peripheral arterial disease

disease produced in peripheries due to chronic, stable plaques.

acute arterial occlusion

• sudden interruption of BF

• thrombus → erosion or rupture of a plaque

• thromboembolus (often from heart)

seven p’s: pistol shot, pallor, pain, polar, pulseless, paresthesia, and paralysis

What are the signs and symptoms of an acute arterial occlusion?

peripheral arterial disease

• atherosclerosis in the extremities

• common arteries of the leg (femoral, popliteal)

• age

• race

• *smoking*

• *diabetes*

• hyperlipidemia

• HTN

What are the risk factors for peripheral arterial disease?

walking to increase collateral circulation

What is the treatment for peripheral arterial disease?

• decreased flow and tissue oxygenation

• complications: ulcers, necrosis, poor sound healing, amputation

What are the consequences of peripheral arterial disease?

• s/s are gradual

• Claudication, thin skin, brittle nails, muscle atrophy, cool feet, dependent rubor, delayed wound healing

What are the signs and symptoms of peripheral arterial disease?

Raynauds disease

• intense vasospasm of arteries/arterioles in fingers and less often toes

• primary cause → cause unknown

  • common in young women

  • exposure to cold and emotional stress, possibly hyperactive SNS response

• Secondary → associated w/ diseases/situations that cause vasospasm

  • collagen diseases, frostbite, trauma

skin pale to cyanotic, cold sensation, numbness/tingling

What are the s/s of Raynaud’s disease?

aneurysm

ballooning out of vessel wall (or chamber of heart)

true aneurysm

ballooning out of complete vessel wall

• fusiform or saccular

false aneurysm (pseudoaneurysm)

tear in arterial wall w/ extravascular hematoma

dissecting aneurysm

• intimal tear

• blood b/t layers of vessel wall

aortic dissection

• acute, life threatening hemorrhage into the vessel wall

• most common in ascending aorta

• associated w/ trauma, HTN, atherosclerosis

atherosclerosis, HTN, congenital weakness, Marfan syndrome, infection, trauma

What are the risk factors for aneurysms?

• thoracic: pain back, neck, substernal

• abdominal (AAA): most common type

  • often asymptomatic

  • abdominal/back pain

  • palpable if > 4cm (in thin person)

What are the s/s of a true aneurysm?

law of Laplace

increase in size = increase risk of rupture

abrupt onset severe pain in chest or back, altered pulses upper extremities , syncope, hemiplegia paralysis

What are the s/s of a dissecting aneurysm?

ventricular contraction

When does systolic BP occur?

ventricular relaxation

When does diastolic BP occur?

• SNS and baroreceptors

• RAA system

• ADH

What mechanisms control BP in the short term?

SNS & baroreceptors (short term regulator of BP)

• increase sympathetic activity

  • vasoconstriction, increase HR, increase contractility (increase C.O.)

  • Parasympathetic: decrease HR

  • trigger release of ADH

RAAS (short term regulator of BP)

• aldosterone: increase Na+ and O2 reabsorption

• angiotensin II: vasoconstriction

ADH (short term regulator of BP)

• osmoreceptors

  • increased osmolality

• baroreceptors

  • decreased BP

• increase H2O reabsorption (kidney)

• kidneys

  • regulate BP by regulation of fluid volume

  • BP increases → diuresis/natriuresis increase (increase H2) and Na+ excretion)

  • a shift in the pressure-natriuresis/diuresis relationship is part of the pathophysiology of primary HTN

What controls BP longterm?

Primary (95%, unknown cause) and secondary (caused by disease)

What are the two types of HTN?

• renal disease (acute or chronic)

  • Na+/H2O retention, HTN

• Renal Artery Stenosis

  • excessive activation of RAAS

• Endocrine disorders → cushings, hyperaldosteronism

• Pheochromocytoma

  • adrenal medulla tumor produces catecholamines

• Coarctation of the aorta: narrowing of aorta

• oral contraceptive drugs

• obstructive sleep apnea

What are the causes of secondary HTN?

patho of primary HTN

• vasoconstriction/ increased pressure

  • remodeling of arterioles/arteries

  • hypertrophy of arterial smooth muscle

  • permanently narrowed lumen

• Key initiating factors

  • dysfunction of SNS, RAA system

  • inflammation and endothelial dysfunction

    • loss of normal local vasodilators (nitric oxide)

    • increase sensitivity to vasoconstrictors (endothelin)

  • lead to vasoconstriction, increased vascular resistance, renal sodium and water retention, increased blood volume, and sustained HTN

• combination of genetics/environment

• family history

• increasing age (general 50)

• gender (earlier in men)

• african american

• diet: high Na+ intake

• obesity (central obesity = increased risk)

• diabetes

• smoking

• excessive ETOH (alcohol)

What are the risk factors for HTN?

• primary

  • obesity

  • family hx, dyslipidemia, type 2 diabetes

• secondary

  • most common d/t renal problems

  • correction of the aorta

Risk factors of HTN in children

• Cardiovascular damage

  • affects large and small vessels

  • accelerated atherosclerosis

  • changes in the myocardium: high SVR, increase workload (after load), LV hypertrophy (can lead to heart failure)

• Kidney damage

  • glomerular damage from vasoconstriction and tissue ischemia

  • nephrosclerosis and chronic kidney disease

  • acceleration of diabetic kidney disease

• Cerebrovascular damage

  • risk of stroke, aneurysm, intracranial hemorrhage

  • hypertensive encephalopathy

• Retinopathy

  • vessels weakened, retinal hemorrhage

  • papilledema (optic disc edema)

• aorta → aneurysms, dissections

• PAD

What are the consequences of HTN?