Nur 333 Quiz 4

Cardiovascular 1 & 2

Blood Flow Regulation

Depends on CO & PVR

…..

Cardiac Output = CO

-amount of blood pumped by heart each minute

..

Peripheral Vascular Resistance = PVR

-resistance created by blood vessels

—vasoconstriction = increased resistance, vasodilation = decreased

—increased blood viscosity = increased resistance

…….

BP = CO X PVR

-raise BP by increasing CO = heart pumps more blood

-raise BP by increasing PVR = vasoconstriction

Cardiac Terms

Cardiac Cycle

-Systole = ventricular contraction

-Diastole = ventricular relaxation & filling

….

Blood Pressure

-Systolic BP = SBP = pressure during contraction

-Diastolic BP = DBP = pressure during relaxation

-Normally BP 120/80 mmHg

….

Stroke Volume SV

-Blood ejected per beat

-Normally 70mL

….

Cardiac Output CO

-CO = HR X SV

-Amount of blood pumped per minute

-Normally 5L/min

Laminar VS Turbulent Blood Flow

Laminar

-Smooth, parallel layers

-Low friction

-Normal in healthy vessels

….

Turbulent

-Irregular, swirling flow

-Occurs when vessels are narrowed, damaged, or obstructed

-Can produce a bruit

…………………………………..

Turbulent or stagnant blood flow increases risk of endothelial injury & clot formation

Blood Pressure Regulation

Body detects low perfusion

Kidneys activate RAAS

Vasoconstriction & fluid retention occurs, increasing BP

…..

Renin, Angiotensinogen, Angiotensin I, ACE, Angiotensin II, Vasoconstriction & Adrenal stimulation, Aldosterone,

-Increased Sodium & water retention

—Increased BV & BP

..

ADH increases water retention

—Increased BV & BP

Hypertension

Persistent elevation of BP

-SBP greater than 130mmHg or DBP greater than 80mmHg

-Silent killer = cause damage before symptoms appear

……

Types

-Primary = Essential

—90-95% of cases

—No single identifiable cause

—Influenced by genetics & lifestyle

-Secondary

—Caused by underlying conditions: kidney disease, endocrine, meds

…………

Major Effects

-Vascular damage = higher pressure injures endothelium

-Left ventricular hypertrophy = heart works harder to pump against

-Reduced oxygen supply to myocardium

…………

Major Complications

-Cardiac = MI, heart failure

-Vascular = atherosclerosis, aneurysm

-Cerebral = stroke

-Renal = chronic kidney disease

Arterial Wall Layers

Tunica Intima = Inner endothelium

-Site of atherosclerotic plaque formation

…

Tunic Media = Smooth Muscle

-Controls vasoconstriction & vasodilation

…

Tunica Adventitia = Outer connective tissue

-Provides structural support

Basic Arterial Disorder Concepts

Endothelial Injury arises from

-Hypertension, diabetes, high cholesterol, smoking

—Trigger inflammation & lipid accumulation in vessel wall

….

Arteriosclerosis = general term for hardening & loss of elasticity of arteries

..

Atherosclerosis = plaque buildup within the arterial wall

-plaque narrows lumen, reduced blood flow

—plaque rupture = thrombus formation = ischemia/infarction

…………………………

Lipids

-LDL = bad cholesterol = promotes plaques

—Elevated LDL = atherosclerosis

-HDL = good cholesterol = removes cholesterol from circulation

…

Glucose = Diabetes

-Chronic hyperglycemia damages endothelium

-Promotes inflammation & plaque formation

-Major risk factor for coronary artery disease

…

Nicotine = Smoking

-potent vasoconstrictor

-Increases BP & vascular injury

-Accelerates atherosclerosis development

Aortic Dissection

Tear in tunica intima allows blood to enter vessel wall

-Separates layers = false lumen forms

—Can lead to rupture or loss of organ perfusion

…

Symptoms

-Sudden, severe ripping or tearing in chest/back pain

—pain radiates between shoulder blades

…

Diagnosis

-CT angiography = gold standard

-Can use transesophageal echocardiogram TEE or MRI

…

Treatment = Medical Emergency

-IV beta blockers = reduce BP & aortic wall stress

-Emergency surgery for ascending dissections

…

Severity

-33% mortality in 24hr, 50% within 48hr

Heart Wall & Coronary Circulation

Heart Wall Layers

-Epicardium = outer layer

-Myocardium = thick layer responsible for contraction

-Endocardium = smooth inner layer of chambers & valves

….

Coronary Circulation

-Right Coronary Artery RCA
—Supplies RA & RV, and part of conduction system

-Left Coronary Artery LCA

—Divides into Left Anterior Descending LAD & Circumflex artery

—LAD o widow maker = most involved in MI, anterior wall & septum

—Circumflex artery = lateral wall of heart

Angina Pectoris AKA Chest Pain

Temporary myocardial ischemia = decreased oxygen to heart muscle

-Common causes = atherosclerotic plaque narrowing, thrombus formation, coronary vasospasm

…

Stable Angina

-predictable, occurs with exertion

-relieved with rest or nitroglycerin

..

Unstable Angina = Medical Emergency

-Occurs at rest or worsening pattern

-Indicates high risk for MI

Cardiac Ischemia Diagnosis

Initial Assessment

-Vital Signs, BP

-Physical Exam Findings

…

Lab Tests

-Lipid Profile

-Cardiac Biomarkers

—Troponin, CK-MB

…

Diagnostics

-ECG

-Chest X-Ray

-CT Coronary Angiography

…

Invasive Testing

-Cardiac Catheterization

Electrocardiogram ECG/EKG

Shows electrical activity of heart

…

12 Lead

-Provides multiple views of cardiac electrical activity

-Helps detect ischemia, infarction, & rhythm abnormalities

………………

P Wave = atrial depolarization & contraction

QRS Complex = ventricular depolarization & contraction

T Wave = ventricular repolarization & recovery phase

…..

NSTEMI = Non-ST Elevation MI

STEMI = ST Elevation MI

Myocardial Infarction AKA Heart Attack

Pathophysiology

-Plaque rupture = thrombus formation

-Coronary artery obstruction

-Ischemia = myocardial necrosis

……………………..

Symptoms

-Typical

—Crushing chest pain, radiation to jaw/left arm, diaphoresis, nausea

-Atypical

—Dyspnea, fatigue, epigastric pain

……………………

Diagnostic Findings

-ECG changes

-Elevated troponin

-Cardiac catheterization confirms occlusion

Cardiac Dysrhythmias

Supraventricular

-Originates above the ventricles

-Atrial fibrillation

……

Ventricular

-Originates in the ventricles

-More serious

…………………………………………

Rate-Based Classification

-Tachyarrhythmia = fast HR

-bradyarrhythmia = slow HR

……

Heart Block

-Delay or interruption in electrical conduction

…

Ectopic Pacemaker

-Electrical impulse originates outside normal pathway

Conduction Disturbances Post-MI

Atrioventricular AV Block

-Delayed conduction through AV node

-May cause bradycardia

……..

Atrial Fibrillation

-Irregularly irregular rhythm

-No distinct P waves

……..

Premature Ventricular Contractions PVCs

-Early ventricular beats

……..

Ventricular Tachycardia

-Rapid ventricular

……..

Ventricular Fibrillation

-Chaotic rhythm = cardiac arrest

Heart Failure

Inability of the heart to pump enough blood to meet metabolic demands

-Caused by impaired contractility, filling, or both

-HF doesn’t = cardiac arrest

—Heart is weak but still beating

…….

LVEF

-Normal = 60-70%

-Heart Failure < 40%

……………………………………………………….

Pathophysiologic Changes that lead to HF

-Fluid overload = increase preload, myocardium stretching

-Impaired ventricular filling = stiff/thickened ventricles = diastolic dysfunction

-Degeneration of ventricular muscle = loss of contractile strength = systolic dysfunction

-Decreased ventricular contraction = reduce cardiac output & perfusion

…….

Major Causes

-Ischemic Heart Disease, MI

-Chronic Hypertension

-Valve Disease

-Dysrhythmias, especially AFib

-Pulmonary disease = right heart strain

Cardiac Output

Cardiac Output CO

-Stroke Volume X HR

…..

Preload = amount of blood filling the ventricle before contraction

-end diastolic pressure

-Increased in hypervolemia, regurgitation of cardiac valves, heart failure

…

Afterload = resistance the ventricle must pump against

-Increased in hypertension & vasoconstriction

-Increased = increased cardiac workload

Left-Sided Heart Failure

Left Ventricle cannot pump blood effectively to the body

……………

Backward Effects = Blood backs up into pulmonary circulation

-Pulmonary congestion, crackles

-Pink frothy sputum

-Dyspnea, orthopnea

…….

Forward Effects = Decreased perfusion to body

-Fatigue, confusion

-Decreased urine output

Right-Sided Heart Failure

Right Ventricle cannot pump blood effectively to the lungs

…………

Backward Effects = Blood backs up into systemic venous circulation

-JVD

-Peripheral edema, ascites, hepatomegaly

…………

Forward Effects = Reduced blood flow to pulmonary circulation

-Often develops secondary to left-sided HF

…….

…….

Heart Valves

Tricuspid = RA & RV

Pulmonary = RV & pulmonary artery

Mitral/Bicuspid = LA & LV

Aortic = LV & aorta

………

Atrioventricular AV = Tricuspid & Mitral

-Supported by chordae tendineae & papillary muscles to prevent backflow during contraction

Semilunar = Pulmonic & Aortic

Valvular Heart Disease

Structure & Function

-Maintain one-way blood flow

-Thin fibrous flaps lined with endothelium

…………..

Causes

-Congenital malformation

-Degenerative & calcific changes

-Infection or inflammation

……..

Diagnosis

-ECHO = visualizes valve structure & blood flow

—Determines severity of stenosis or regurgitation

……..

Management

-Monitor disease progression

-Meds for symptom control

—Diuretics = reduce fluid overload

—Beta blockers = reduce cardiac workload

—Anticoagulants = prevent thrombus formation, especially with Afib

-Surgical repair or valve replacement if severe

—Valvotomy/valvuloplasty = open narrowed valves

—Replacement: bioprosthetic or mechanical

Heart Sounds

First = Lub = S1

-Closure of AV valves

-Marks start of systole

—Valves open during diastole

…..

Second = Dub = S2

-Closure of semilunar

-Marks start of diastole

—Valves open during systole

Heart Murmurs

Extra heart sounds heard because of turbulent flow

….

Occur with increased flow

-fever, pregnancy, anxiety

Usually don’t cause symptoms

……

Caused by valve deformity/dysfunction

-Stenosis regurgitation

May require medical management

Valvular Dysfunctions

Stenosis

—Leads to increased cardiac workload & hypertrophy

-Narrowed valve opening = blood flow obstructed

-Increased resistance = pressure build up behind valve

-Blood moves inefficiently forward, leaves volume behind

………..

Regurgitation/Insufficiency

—Overtime leads to decreased cardiac output & potential heart failure

-Valve fails to close tightly = backward leakage of blood

-Causes volume overload in the chamber behind the valve

-Results in less forward ejection & chamber dilation

……………………………………………………………..

Consequences

-Dysrhythmias

—Chamber stretching disrupts electrical pathways

—May cause atrial fibrillation or other rhythm disturbances

-Thrombus formation

—Turbulent or stagnant flow increases risk of clot formation

-Stroke

—Clots can embolize to brain = ischemic stroke

-MI & Heart Failure

—Increased workload & hypertrophy raise oxygen demand

—Can progress to ischemia or heart failure if untreated

Mitral Valve Stenosis

Narrowed mitral valve impedes blood flow from LA to LV

-Decreased CO = less blood enters the LV

-Increased LA pressure & volume = atrial enlargement & pulmonary congestion

……….

Causes

-calcification from aging or atherosclerosis

-Rheumatic heart disease RHA = most common

………

Symptoms

-dyspnea on exertion, orthopnea due to pulmonary congestion

-fatigue & reduced exercise tolerance due to cardiac output

-nocturnal dyspnea & palpitations from atrial enlargement/dysrhythmia

Mitral Valve Insufficiency/Regurgitation

Mitral valve fails to close completely during ventricular contraction = systole

-Blood leaks backward from LV to LA with each heartbeat

-Volume overload in both LA & LV leads to dilation & hypertrophy

-Forward cardiac output decreases

…..

Causes

-papillary muscle damage after MI

-mitral valve prolapse

-infective endocarditis

……

Symptoms

-fatigue, dyspnea, orthopnea due to pulmonary congestion

-palpitations from atrial dilation/dysrhythmias

Mitral Valve Prolapse MVP

Valve leaflets bulge into LA during systole

Common cause of mitral regurgitation

Often asymptomatic & discovered incidentally

-Don’t require treatment usually

Aortic Valve Stenosis

Narrowed aortic valves restricts blood flow from LV to aorta

-Increased afterload forced LV to work harder = left ventricular hypertrophy LVH

-Over time reduces cardiac output & impairs coronary perfusion

…….

Causes

-Aortic sclerosis & calcification

-Rheumatic heart disease RHD

-Congenital bicuspid aortic valve

……..

Classic Symptom Triad

-Angina = via poor coronary perfusion of hypertrophied LV

-Syncope = via reduced cerebral perfusion during exertion

-Dyspnea = via pulmonary congestion from elevated LV pressures

Aortic Valve Insufficiency/Regurgitation

Aortic valve fails to close completely during diastole

-Blood leaks backward from aorta to LV

-Creates LV volume overload = ventricular dilation & reduced contracility

-Progression = pulmonary congestion & reduced cardiac output

……..

Causes

-Infective endocarditis

-Rheumatic Heart Disease RHD

-Marfans syndrome

-Long-term hypertension via aortic root dilation

-Congenital defects or trauma

……..

Symptoms

-Dyspnea & fatigue due to decreased CO

-Orthopnea & pulmonary congestion

-Bounding pulse & widened pulse pressure

-Palpitations or awareness of heartbeat

-Signs of progressive left-sided HF

Venous Disorders

Varicose Veins

Chronic Venous Insufficiency

Venous Ulcers

Deep vein Thrombosis DVT

Vein Structure & Function

Layers:

-Tunica intima, media, & adventitia

…

Types:

-superficial, deep, perforating

….

Function: return blood to the heart

-thin-walled, flexible vessels

-low-pressure system aided by valves & skeletal muscle contraction

Venous Dysfunction Core Issues

Valve Failure

-blood reflux & pooling

..

Venous Stasis

-slowed blood flow

..

Elevated Venous Pressure

-fluid leakage into tissues

Varicose Veins

Abnormally dilated superficial veins caused by valve incompetence

-Increased venous pressure = valve failure = blood pooling & vein dilation

-Most common in legs due to gravity & upright posture

………..

Risk Factors

-Prolonged standing/sitting

-Obesity, pregnancy = increased venous pressure

-Aging = loss of vessel elasticity

-Female gender = hormonal influence aka progesterone

-Family history, prior venous disease

………..

Symptoms

-visible, tortuous, bluish veins

-leg heaviness, aching, cramping

—worse with standing

-mild ankle edema

-may progress to chronic venous insufficiency if untreated

………..

Treatment

-Conservative: leg elevation, compression stockings, regular exercise

-Procedural: sclerotherapy, laser/radiofrequency ablation, vein stripping

Chronic Venous Insufficiency

Valve damage = venous reflux & pooling = increased venous pressure = edema & skin changes

-Chronic venous congestion = impaired oxygen exchange & tissue breakdown

……….

Risk Factors

-Prolonged standing or immobility

-Obesity, pregnancy = increased venous pressure

-Leg trauma, prior DVT

……..

Symptoms

-Leg swelling, heaviness, aching

—worsen with standing

-Shiny, thickened skin with brown discoloration

-Stasis dermatitis & itching

-Poor wound healing

—venous ulcers near ankles

……..

Diagnosis

-Doppler = assesses venous reflux & valve function

……..

Treatment

-Compression therapy

-Leg elevation & ambulation

-Venous ablation, surgical repair in advanced disease

Venous Ulcers

Caused by chronic venous insufficiency & venous hypertension

-Poor venous return = increased hydrostatic pressure = fluid & RBC leakage into tissues

-Leads to skin breakdown, inflammation, necrosis

….

Common Sites

-Near medial malleolus = inner ankle

-May also occur on lower leg or shin

….

Symptoms

-shallow, irregularly shaped ulcer with red wound base

-Surrounding skin = brownish discoloration, thickened, itchy

-Pain relieved by leg elevation

—Distinguishing feature from arterial ulcers

-Associated edema & weeping

….

Treatment

-compression therapy to improve venous return

-Leg elevation, ambulation

-Wound care: moist dressings, debridement if needed

-Address underlying venous insufficiency

—Surgery, ablation, vein repair

Virchow’s Triad: Venous Thrombosis

Venous Stasis

-Immobility

-Surgery

-Prolonged Travel

-Heart Failure

……………………..

Endothelial Injury

-Trauma

-Surgery, IV catheters

-Inflammation

……………………

Hypercoagulability

-Cancer

-Pregnancy, Estrogen therapy

-Inherited clotting disorders

DVT & PE

Blood stasis promotes thrombus formation in deep vein

—Often leg or pelvis

-Piece may dislodge = embolus, travels via vena cava to right heart to lungs

—Lodging in pulmonary artery = PE

—PE can block pulmonary circulation = impaired gas exchange = hypoxia or sudden death

…………………..

Diagnosis

-DVT

—Duplex ultrasound = gold standard

—D-dimer for screening

-PE

—CT angiography = gold standard

—V/Q scan if contrast contraindicated

……………………

Treatment & Prevention

-Prevention

—SCDs, early ambulation, leg elevation, compression stockings

-Medication

—Anticoagulants = heparin, warfarin

—Thrombolytics if severe

-Procedures

—IVC filter if anticoagulation contraindicated

—thrombectomy