Pathophysiology - Exam 3 - UTA (Urban)

Arteriosclerosis

Thick and Hardened artery

HTN | Smoking | Diabetes

Intima is damaged and walls stiffen. Elasticity and compliance decreases.

Atherosclerosis

Fatty Deposits

Plaques form | tissue inflamed | High amount of LDL's (low-density lipoproteins=more fat than protein)

Hypertension

the force of the blood against the artery walls is too high.

Pre - Stage I - Stage II

Preload

Volume of blood returning from the heart.

Normal volume = 4-6ml

Afterload

Amount of blood ejected from the heart

Contractility

How effectively the heart works to eject blood "toned"

Arterial Insufficiency

Muscle tone and the state of the lumen are compromised.

Aneurysms

A ballooning and weakened area in an artery.

Venous Disorders

Chronic Venous Insufficiency (CVI)

Deep Vein Thrombosis (DVT)

Valvular Disorders

Gravity Winning - not necessarily pathogenic

Valve Incompetence - pathology invlolved

Cardiogenic Shock

Heart suddenly can't pump enough blood to meet your body's needs

What side of the heart is the Arterial side?

The LEFT. OXYGENATED blood is going "out" via aorta to all arteries and tissues

What side of the heart is the Venous side?

The RIGHT. DEOXYGENATED blood if flowing "in" from all the veins and tissues.

Inotropic

POSITIVELY or NEGATIVELY modifying the force or speed of contraction of muscles.

pos- pumps faster

neg- pumps less

Systemic Vasodilation

from anaphalaxis or Sepsis

Analyphalyaxis

severe, potentially life-threatening allergic reaction. It can occur within seconds or minutes of exposure to something you're allergic to.

Low blood pressure (hypotension)

A weak and rapid pulse

In a case of HIGH preload

Volume too LARGE- heart is working too hard.

CAUSES: Fluid Excess States

1. heart failure

2. iatrogenic fluid overload

3. hormonal imbalances (SIADH)

In a case of LOW preload

Volume too SMALL - not enough to sustain good perfusion

CAUSES:

Fluid volume deficit (bleeding, dehydration, hormonal imbalances like DI)

Systemic vasodilation (blood pools in periphery- sepsis, anaphylaxis)

Afterload problems

Resistance - ANY resistance to forward flow

RV Afterload Pathologies

Pulmonary Vascular Resistance

Too High due to: athero/arteriosclerosis of pulmonary vasculature (narrowed stiff pulmonary artery) Stiff noncompliant lung tissue (lung disease)

If RV afterload too high, can result in RIGHT heart failure. COR PULMONALE

LV Afterload Pathologies

Systemic Vascular Resistance

Too high due to :

athero/arteriosclerosis (narrowed stiff vasoconstricted aorta & systemic arteries) high resistance

If LV afterload too high, can result in LEFT heart failure. (LHF)

Too Low:

Arterial vasodilation (sepsis, anaphylaxis)

if LV too low, can result in Shock

Normal HR

60-100

Describe potassium changes to HR and Rhythm

Hyperkalemia = Increased rate

Hypokalemia = Decreases rate

Stroke Volume

Amount ejected by the LEFT VENTRICAL with every contraction

Normal = 70ml/beat

Conditions that facilitate good venous return and prevent backflow

Good drainage of tissues, proper functioning valves in legs, well toned working muscle.

Venous Congestion Issues

Gravity winning, being on feet too long, Valve Incompetence (venous insufficiency)

Chronic Venous Insufficiency

Leg vein valves wearing out "floppy"

valves not closing properly during diastole causing back flow. Pool of nonmoving blood is called VENOUS STASIS. results in increased hydrostatic pressure. pressure pushes fluid into the tissues causing EDEMA (dry, tight, brownish skin) Further engorgement leads to tissue breakdown and VENOUS STASIS ULCERS- back flow can go further into the surface veins, twisting and distorting them causing VARICOSE VEINS (local back flow)

Name a few causes of Edema

HTN

right-sided heart failure

venous problems

kidney disease

injury

lymphatic problems

hypoosmolar problems

Deep Vein Thrombisis

A clot the develops ON THE WALL of the vein (deep veins of calves and thighs)

THROMBOPHLEBITIS

vein becomes inflamed or swollen

Virchows Triad

the three broad categories of factors that are thought to contribute to thrombosis.

STASIS

HYPERCOAGULABILITY

INJURY

Dangerous Sequela of DVT

DVT > IVC > RA > RV > PA

part of thrombus breaks free and gets stuck in pulmonary arteries.

PULMINARY EMBOLUS

S&S- SOB > Shock > Hemoptysis (blood in sputum) > Death

Treatment for Venous Problems

Encourage mobility

Encourage hydration

Elevate feet

Blood thinners (Heparin, Coumadin)

Asprin- prevents clotting

Blood Pressure (Systolic and Diastolic)

Blood Pressure- simply the fluid pressure in the arterial system

Desired range: 110/60 - 115/70

Systolic- pressure in the arteries exerted when the heart is contracting and ejecting blood OUT

Diastolic- pressure of fluids existing in the arteries when the heart is between contractions

Prehypertension

SYSTOLIC - 120-139

DIASTOLIC - 80-89

Stage I Hypertension

SYSTOLIC - 140-159

DIASTOLIC - 90-99

Stage II Hypertension

SYSTOLIC - 160-above

DIASTOLIC - 100-above

S&S of decreased perfusion and ischemia

Ischemic pain- increases with exertion and diminishes with rest. (Exertion=more O2 demand)

this pain is in the tissue distal to the plaque or narrowing. (femoral arteries affected, pain in the calves)

Diminished pulses, delayed CRT, skin pale/cool, sometimes blue , delayed healing, delayed Cardiac Output, altered consciousness, Stroke, diminished urine output.

Risk Factors of arterial narrowing

NON-MODIFIABLE = family history, advancing age

MODIFIABLE = Diet, obesity, alcohol, sedentary lifestyle, cigarette smoking

Lipodystrophy

a disorder in which the body is unable to produce fat. characterized with DM2- increased circulating LDL's

5 Specific Arterial Diseases related to Atherosclerosis

Peripheral arterial disease (PAD)

Arterial thrombi and emboli

Aneurysms

Hypertension

Coronary artery disease

Peripheral arterial disease (PAD)

Peripheral arterial insufficiency:

disease of any arterial vessels outside if the heart especially the legs. Intermittent claudication "limping"

the P's of PAD

Pain

Parathesia

Pallor

Pulselessness

Poikilothermia

Arterial disease ischemia

no hair on legs, skin shiny, cool and pale feet, skin ulcers, diminished pulses.

Arterial thromboembolitic problems

a clot in a vessel flowing from the heart. distal tissue ischemia.

Hypertension - HTN

consistent elevation of systemic arterial blood pressure.

Normal BP

110/70

anything over 140/90 = hypertensive

anything under 90/60= hypotensive

Secondary Hypertension

uncommon - caused by altered hemodynamics associated with disease such as adrenal tumor or renal problems.

Primary Hypertension

Caused by complex set of factors.

Athersclerosis

overactivity of the sympathetic nervous system

overactivity of the RAAS

Risk factors: high sodium intake, water retention, high pressure in circulatory system

Overactivity of the SNS

due to sustained stressors, genes, Epinephrine overstimulates Beta receptors and over-increases HR and contractility. this in turn leads to a greater cardiac output and sustained increased BP

Overactivity of RAAS

normally RAAS is compensatory in a drop in BP causing vasoconstriction and increased blood volume. in this case it is chronically overactive thus blood volume and pressure is high.

HTN affects the vasculature in what 3 systems?

Neurological- brain and eyes

Renal - hematuria or proteinuria

cardiovascular - workload of heart

Aneurysms

localized dilation or out-pouching or arterial vessel wall. weakened walls from HTN or atherosclerosis create bulging. can happen in the brain, aorta, abdominal aortic, thoracic aortic.

HDL value

should be at least 40mg/dl

Medical approaches to combat arterial problems.

Overactivity of the SNS - beta blockers

Overactivity of RAAS - ACE inhibitors

Coumadin or Heparin to combat clots.

Stroke Volume

amount of blood ejected per contraction

~ 70ml/beat

P wave

Atrial depolarization

QRS complex

ventricular depolarization

T wave

ventricular repolarization

ST wave

time interval between end of ventricular depolarization (S) and repolarization (T)

Hear rate

the rate of impulses generated by the SA node. Normal is 60-100

Three factors of healthy arteries

Good Perfusion

Good vasomotor tone

Patent Lumen

Inotroipc

describes the effect in different factors of contractility.

Positive = enhances contractility

Negative = decreases contractility

Pulmonary Vacsular Resistance

Normal RV afterload

Normal Systemic Restiance

Normal LV afterload

Some possible causes of Tachycardia

Neurohormonal - sympathetic = epinephrine - binds to BETA receptors

electrolyte changes - hypokalemia - causes hyperpolerization - ischemia from RCA

glitches in the SA or AV node

Some possible causes of Bradycardia

Neurohormonal = parasympathetic

vages nerve secretes acetylcholine

hypokalemia - causes hyperpolerization - ischemia from RCA

glitches in the SA or AV node

Dysrhythmia

aka- Arrhythmia

ischemic or infarct tissue interferes with normal conduction. electrolyte imbalances. age related wear and tear.

Atrial Fibrillation

chaotic impulses in the atria. diminished CO due to no "atrial kick" blood can coagulate.

Thrombi in the left atrium can cause

emboli out to the body- it can go to the brain and cause a stroke

Thrombi in the right atrium can cause

emboli out to the lungs

Ventricular Fibrillation

chaotic impulses in the ventricles. this is the most deadly because it can result in NO CARDIAC OUTPUT

Increased preload problems

TOO MUCH VOLUME

increased blood volume in the heart. Fluid volume overload. increases the workload on a sick heart

Decreased preload problems

TOO LITTLE VOLUME

decreased blood volume in the heart. Decreased CO and low BP

Increased afterload from the RV

atherosclerosis of pulmonary branches and artery. lung disorder - chronic bronchitis

Increased afterload from the LV

atherosclerosis of the aorta and systemic arteries.

HTN - high blood volume - peripheral arterial vasoconstriction.

Coronary Artery Disease - CAD

disorder where the coronary arteries are narrowed or occluded

Homocysteine

an amino acid that can contribute to atherosclerosis via oxidative damage, similar to free radicals.

some people have higher amounts than others.

Risk of getting CAD

increased Homocysteine

Elevated C-reactive protein

C-reactive protein - CRP

CRP is linked to the inflammatory process of plaque formation in the coronary arteries (if you have coronary atherosclerosis, your CRP will likely be elevated.)

Patho of CAD

1.) Ischemia- coronary vessels are narrowed and occluded by plaques, due to the atherosclerotic / inflammatory processes.

2.) ischemia to cardiac cells is a negative inotropic (squeeze) influence on the heart = decreased cardiac output.

3.) Ischemia leads to cellular death (necrosis)

4.) necrosis in the heart is known as myocardial infarction (MI)

infarction = irreversable

Angina

a painful constriction or tightness- chest pain - painful ischemia to the heart.

Characteristics of classic angina

patient often will describe it as tightness, heaviness ("elephant sitting on me"); sometimes burning, indigestion-like; will sometimes place clenched fist over sternum

Pathophysiology of Angina Perception

a) buildup of lactic acid and abnormal stretching of ischemic myocardium irritate myocardial nerve fibers

b) the afferent sensory nerve fibers in the area transmit the pain impulses to areas of the spinal tract that include C3 to T4

c) the variety of nerve root areas causes the variation in pain each individual has

explains why some patients may have radiation of pain into

classic areas such as left arm, jaw, & back

Stable Angina

pain pattern is very predictable and well-controlled by lifestyle changes. nitroglycerin or aspirin (reduces inflammation- leakiness and swelling, and, inflammation debris) can relieve/treat it

A slow development of plaque forms - small and subtle ischemia to tissues stimulates

Arteriogenesis

a type of angiogenesis (general word for "new blood vessel creation") End result of this is the establishment of COLLATERAL CIRCULATION composed of new branches of the coronaries that develop and can "feed" tissue beyond an occluded or nearly-occluded vessel.

The better the collateral circulation, the more stable the CAD.

Acute Coronary Syndrome (ACS)

one of several possible coronary-artery-flow-blocking situations occurs

1) sudden clot development.

2) an arterial embolus flows into a narrowed coronary artery

3) an existing plaque ruptures & its contents fill up the lumen.

Unstable Angina

When someone with stable angina develops a change for the worse (usually sudden)

Usually indicates worsening or change in existing coronary plaques -worsening of ischemia

1) Substantial change in pain now needs 3 NTG tabs

2) EKG shows acute ischemic changes

c) patient admitted to the hospital, treatment is still geared towards maximizing coronary patency & perfusion with acute interventions such as IV NTG, IV morphine, possibly angioplasty, heart surgery, etc.

Myocardial Infarction

Myocardial cells are starting to undergo necrosis

S&S usually include

1)severe, unrelenting pain

2)EKG changes = ischemia & certain degree of necrosis

3) lab test findings that show increases in:

non-specific enzymes released by injured and dying cells = creatine kinase (CK) - troponin.

Troponin

specific substance only released by injured and dying myocardial cells

the higher the serum titer, the more extensive the damage

Miscellaneous S&S that often occur in ACS

tachycardia - epinephrine "fight or flight"

bradycardia, dysrhythmias, large amount of sweating, fatigue, weakness, mental status change, deterioration of responsiveness, hypotension, dyspnea, prolonged CRT, low urine output

Cardiomegaly

Enlarged heart -- increase in size of cells over time due to cells "working harder" to compensate for less oxygen

Heart Valvular Disorders

disease processes such as rheumatic fever (post-strep autoantibodies invade & inflame heart valves, joints, and/or kidneys)

Problems depend on severity & which valves involved, generally negatively affect CO in one way or another.

also caused by bacterial endocarditis, or birth defects

Stenosis

Valvular narrowing or stiffening

affects "full opening"

2) valve orifice is constricted & narrowed, blood cannot easily flow through it.

3) smaller opening generates more turbulence-there is a rumbling sound know as a MURMUR

Valvular Incompetence aka valvular prolapse, insufficiency or regurgitation

Floppiness affects "full closing"

- regurgitation of blood back into the chamber it came from

- back flow of regurgitation also can cause turbulence - MURMUR

Heart Failure (HF)

the failure of the heart to eject / propel blood forward effectively - preload, afterload, and or contractility problem

either LEFT or RIGHT

Fluid overload of the heart

Congestive heart failure

3 Things that contribute to Heart Failure

PUMP PROBLEM: contractility weakened

INCREASED RESISTANCE: increased afterload to forward flow.

INCREASED PRELOAD: fluid volume overload (increased preload)

What would the body do to compensate for diminished Cardiac Output?

the RAAS kicks in, bit in this case it is harmful. increased preload & afterload MAKE THE ALREADY STRUGGLING HEART HAVE TO WORK EVEN HARDER

S&S of fluid backup into lungs

Pulmonary Edema

Crackles upon auscultation of lungs

Lung congestion

-Cough, often with frothy blood-tinged sputum (hemoptysis)

-Orthopnea--SOB upon lying down

-increased respiratory rate (RR)

-decreased SO2 (oxygen saturation)

With LHF, where does the backup occur?

In the lungs