NURS 216 Spring 2013

Dr. Smith

Reading You must read Chapter 17 for review of the structure

and normal function of the cv system. Slides 5-20 in this lecture should be review from A&P and we will only briefly discuss them.

We will discuss most parts of Chapter 18 except for HTN in special populations.

We will discuss most parts of Chapter 19 except for heart disease in infants and children.

Objectives Review important concepts of cardiovascular anatomy:

layers of the heart, valves, electrical conducting system

Review important concepts of cardiovascular physiology: mechanical function, hemodynamics, regulation of cardiac output and blood flow

Review components of the systemic circulation and blood vessels

Discuss disorders of arterial function: artherosclerosis, peripheral arterial disorders, aneurysms and dissections

Discuss control of blood pressure and hypertension

Discuss disorders of venous function: varicose veins and venous thrombosis

Discuss coronary heart disease: chronic and acute

Discuss pericardial, myocardial, endocardial, and valvular disorders

Mechanical Functions The heart’s job is to pump blood throughout the

circulatory system

Cardiac muscle is similar to skeletal, with addition of intercalated disks

Atria and ventricles must be coordinated and healthy to achieve ideal blood flow and circulation

Pulmonary circulation:

smaller volume,

low pressure

Systemic circulation:

larger volume,

high pressure

Arterial vs. Venous System Difference in type and thickness of layers

Vascular smooth muscle

Arterial system: high-pressure “resistance” vessels, blood moves through b/c of pressure pulsations from LV

Venous system: low-pressure “capacitance” vessels, blood moves through by muscle pumps

-valves

-effects of gravity

Volume and Pressure One influences the other

In the systemic circulation:

-pressure is highest in the arteries, lowest in the veins

-volume is lowest in the arteries, highest in the veins

Veins are extremely compliant and distensible, so they are able to expand and store large volumes of blood

The whole circulatory system is closed, but blood can shift between systemic and pulmonary systems and between central and peripheral circulation

Pressure, Resistance, and Flow Blood flow (cardiac output) = Δ pressure/resistance

-higher pressure gradient means more blood flow

-higher resistance means less blood flow

Resistance is affected by radius of the vessel and blood viscosity

Ideally, blood flow is laminar, not turbulent

Laplace law: P = T/r may restate: T = P*r

Intraluminal

pressureWall

tension

Vessel

radius

Layers of the Heart

Coronary Arteries

Conduction System

Electrocardiogram (EKG or ECG)

Cardiac Cycle During systole, AV valves are closed, semilunar valves open,

and ventricles eject their blood into the pulmonary arteries and aorta

During diastole, semilunar valves are closed, AV valves open, and atria drop blood down into ventricles

At end of diastole, there is an “atrial kick”

End Diastolic Volume (EDV) = volume in ventricles at end of diastole

End Systolic Volume (ESV) = volume at end of systole

Stroke Volume (SV) = EDV-ESV usually ~ 70 mL

Ejection fraction (EF) = SV/EDV usually ~ 60-70%

Cardiac Output Determinants Cardiac output (CO) = SV x HR, measured in L/min

-varies greatly with metabolic demands, activity

-anywhere from 4 to 8 L/min

Preload = EDV, “volume work” or “prestretch”

-to a limit, higher preloads cause a stronger contraction (due to arrangement of muscle fibers)

Afterload = pressure that LV must overcome to pump blood into aorta “pressure work” (blood pressure)

Contractility = increased strength of contraction independent of preload

Control of Cardiovascular Function CV system is innervated by the autonomic nervous

system (ANS)

Effects of sympathetic and parasympathetic systems

Vagus nerve

SNS is the main controller of blood vessels

Autoregulation in the tissue beds

-histamine, serotonin, kinins, prostaglandins

Endothelial control

-nitrous oxide (NO), angiotensin II

Arterial Disorders Hyperlipidemia and atherosclerosis (central)

Peripheral arterial problems

Aneurysms and dissections (usually central)

Atherosclerosis The development of fibrous, fatty lesions in the intima

of large and medium-sized arteries (aorta, coronary arteries, cerebral arteries)

MOST COMMON CAUSE OF CORONARY HEART DISEASE!!!

Vessels become narrowed, blood flow decreases, leads to ischemia (chronic)

A portion of the lesion or plaque can break off and completely block blood flow (acute)

Atherosclerosis Why? Response-to-injury hypothesis

The intima is damaged (HTN + high LDL = danger)

Injury to the endothelium changes the permeability and causes an inflammatory response

Monocytes and platelets are attracted to the injury

Monocytes and oxidized LDL molecules burrow under intima

Lesion under intima grows, core may become necrotic, may harden due to calcium deposits

Thrombosis, hemorrhage, or rupture of fibrous cap may occur

Hyperlipidemia Types of lipoproteins are

categorized by the amount of fat (density)

“bad” and “good”

Levels affected by diet, activity level, and liver function

Hypercholesterolemia Specifically, too-high levels of LDL or Total Cholesterol

Primary (familial) or secondary

Measure with a fasting lipid profile/panel

Treat with diet, exercise, then medications

More aggressive depending on other CHD risk factors

Goal levels:

-LDL <100 mg/dL

-TC < 200

-HDL > 60

Xanthomas

Atherosclerosis Always monitor risk factors, work with patient to

improve/reduce them

If patient develops s/sx:

-exercise/stress test

-cardiac catheterization

May need angioplasty, stents, or coronary artery bypass grafting (CABG)

CHD Risk Factors Biologic: male gender, increasing age, family history

Modifiable: hyperlipidemia, hypertension, smoking, diabetes mellitus, obesity, sedentary lifestyle

Negative risk factor: high HDL-C

Peripheral Arterial Disease Can also have atherosclerosis in peripheral arteries,

often superficial femoral and popliteal

Same risk factors as CHD

Blood flow to the extremity is reduced

Intermittent claudication

Diagnose by signs of hypoxia in limb, palpation of pulses, ultrasound

Address risk factors, avoid injury, medications

May need a stent

Aneursyms and Dissections Atrophy or weakness of the medial layer causes a

dilation of the artery

Can occur in any artery of the body, commonly abdominal aorta

Degeneration caused by atherosclerosis, connective tissue disorders, increased blood pressure around a stenotic area

Example types: berry, fusiform, saccular, dissection

Aneursyms and Dissections Increasing radius at the weakened spot increases

tension inside artery (LaPlace Law)

Danger of eventual rupture

Abdominal aortic aneurysm:

-usually over age 50, increase with age

-often asymptomatic, possible pulsating mass

Aortic dissection:

-most common site is the ascending aorta

-rupture, hemorrhage into vessel wall

-abrupt, intense pain, BP quickly falls – usu FATAL

Blood Pressure definitions BP is measured in an

artery, usually the brachial

Measured in mmHg

BP is the pressure inside an artery caused by the movement of blood through it

BP = CO * PVR

Short-Term Regulation of BP Neural

-baroreceptors: pressure sensors, in carotids and aortic arch

-chemoreceptors: chemical sensors, in carotids and aortic arch

Humoral

-RAA System (renin is released by the kidneys)

-vasopressin/ADH: released in response to decreased BP or increased osmolality of blood

RAA System Renin release stimulated by:

-increased SNS activity

-decreased BP, ECF volume, or ECF Na concentration

Renin changes to angiotensin I in the blood, then into angiotensin II in the lungs

Angiotensin II effects:

-vasoconstriction of arterioles (short-term control)

-stimulates aldosterone release, causing Na and water retention (longer-term control)

Long-Term Regulation of BP Mainly by the kidneys via their control of ECF volume

ECF excess causes higher rates of Na and H2O excretion

ECF deficit causes lower rates of Na and H2O excretion

Many blood pressure medications work through changing kidney function

Essential Hypertension Aka “primary” HTN, accounts for 90-95% of HTN

Normal BP = <120 and <80

HTN = >140 or >90

Biological risk factors:

Lifestyle risk factors:

Criteria for HTN diagnosis: at least 2 separate readings

Treatments: lifestyle modifications, medications

Manifestations of Hypertension “the silent killer”

Major risk factor for atherosclerosis

Increases workload of the LV

Target Organ Damage

Heart: LVH (LV hypertrophy), angina, MI, prior stents/CABG, heart failure

TIA or strokes in brain

Chronic kidney disease

Peripheral vascular disease

retinopathy

Secondary Hypertension d/t another condition, correcting that condition often

improves BP

Kidney disease

Excess aldosterone or glucocorticoids

Pheochromocytoma – tumor usually in the adrenal medulla

Coarctation of the aorta

Malignant HTN

http://www.biij.org/2006/2/e11/

3D reconstruction of CT angiography of an

infant with coarctation of the aorta

Orthostatic Hypotension AKA postural

hypotension

SNS reflexes don’t work properly

BP quickly drops, decreasing CBF -> dizziness & syncope

With position change, see BP drop and HR increase

Orthostatic Hypotension Causes Reduced blood volume

Medications

Aging

Immobility, extended bed rest

Autonomic nervous system dysfunction

Treatment depends on identifying a cause

Coronary Arteries

Venous Disorders – Varicose Veins Legs contain superficial and deep veins

Varicose veins – dilated, enlarged superficial veins

Occur due to impaired or blocked flow in deep veins, increased pressure is superficial veins

More common after age 50, in obese persons & women

Long-term increased venous pressures eventually weaken valves, worsening the vein distension

Support stockings, surgical repair

Varicose Veins

Chronic Venous Insufficiency Commonly caused by reflux/backflow through

damaged veins

Worsened by prolonged standing

s/sx: varicose veins, tissue congestion, edema, eventual impaired nutrient delivery to tissues (necrosis, dermatitis, stasis ulcers, thin/shiny skin)

Most common in lower legs

Venous Disorders - DVTs Deep Vein Thrombosis (DVT)

Risk factors: blood stasis, vessel wall injury, increased coagulability (Virchow’s triad)

-what clinical conditions could lead to these risk factors?

May be asymptomatic when small, but gradually tend to increase in size

S/sx: pain, swelling, tenderness (usually unilateral, often in calf)

Complications?

Pericardial Disorders Pericardial effusion

-accumulation of fluid in the pericardial cavity

-can compress heart, lower SV

-diagnose with ultrasound/echo

-pericardiocentesis

-cardiac tamponade

Cardiac Tamponade

Pericarditis Acute – can be after infections or trauma

-increased capillary permeability allows exudate into pericardial cavity

-S/sx: chest pain, pericardial friction rub, EKG changes

Chronic – exudate may remain for months, years

-often due to systemic diseases

-symptoms usually minimal

-still needs to be monitored

Coronary Heart Disease Heart disease due to impaired coronary blood flow,

usually d/t atherosclerosis

-stable plaque (usually leads to ischemia/angina)

-unstable plaque (often leads to MI)

CHD (MIs, heart failure, etc) is the leading cause of death in the United States for men and women

Projected costs of CHD in 2010: 316.4 billion (direct and indirect) (CDC data)

Coronary Arteries

An Oxygen Problem The balance between myocardial oxygen supply and

demand must be maintained!

Demand influenced by: HR, contractility, muscle mass, ventricular wall tension (afterload)

Supply influenced by: coronary blood flow, O2 carrying capacity, vascular resistance

Remember that blood flow (perfusion) is necessary for oxygen delivery

Effect of reduced oxygen: ischemia

Effect of absent/acute lack of oxygen: infarction

Myocardial Ischemia Ischemia occurs when O2 demand is greater

than supply

O2 shortage forces myocardium to use anaerobic metabolism -> pain (angina pectoris)

Mild increases in HR and BP usually occur before chest pain – the SNS is compensating

Possible EKG changes

All changes are reversible if O2 supply is restored

Angina Pectoris Stable – predictable onset, pain is constricting,

pressure-like, subsides with rest or medication

Silent – ischemia without angina

Variant or vasospastic – due to spasmodic narrowing of the coronary arteries, unpredictable, often at night, often associated with cocaine use

Acute Coronary Syndromes AKA myocardial infarction, “heart attack”

Sudden blockage of one or more coronary arteries stops blood flow to a part of the myocardium

The myocardium quickly begins to die: infarction/necrosis

MIs are most common in the LV

Locations: Anterior, inferior, lateral, septal

LOCATION AND SIZE OF INFARCT DEPEND ON LOCATION OF CORONARY ARTERY BLOCKAGE

Signs and Symptoms of an MI Angina pectoris, chest pressure, possibly

radiating down left arm

Diaphoresis

Nausea

Women often experience non-traditional symptoms!

Diagnosis of an MI Blood markers: cardiac enzymes (troponin)

EKG changes (ST elevation – “STEMI”)

Cardiac catheterization

Treatment:

-medications

-reperfusion (usually angioplasty and/or stent)

Myocardial InfarctionLeft main

coronary

artery

Left anterior

descending

coronary

artery (LAD)

Zones of necrosis and ischemia

Effects of an MI Reduced contractility & compliance

Abnormal wall motion

Reduced SV & EF

dysrhythmias

These changes combine to depress overall ventricular function

Severity depends on:

-function of the uninvolved myocardium

-collateral circulation

-general compensation of the cardiovascular system

Compensatory Mechanisms SNS will react to < CO and cause vasoconstriction of

systemic arteries and veins

SNS also causes > HR and > contractility (HR and BP usually maintained)

Kidneys retain Na and water

The increased preload increases ventricular contractility to a point (Frank Starling)

The body’s compensations for decreased ventricular function are limited

The ventricles (LV) gradually dilate and hypertrophy due to increased volume and workload

Worst-Case Scenario Outcomes Cardiogenic shock – when MI affects > 40% of LV, the

severe drop in systemic and cardiac circulation causes death

Papillary muscle rupture – usually affects mitral valve

Cardiac rupture – the necrotic area of the ventricle wall ruptures, leads to massive bleeding into pericardium

MIs often result in heart failure

Myocardial Disorders All the other causes of myocardial dysfunction besides

CHD

Myocarditis: inflammation of myocardium, usually d/t infection

-wide variation of s/sx

-diagnose by EKG changes, cardiac enzymes, biopsy

Cardiomyopathies

-primary and secondary

-dilated, hypertrophic, restrictive

Hypertrophic Cardiomyopathies(HCM) Ventricular wall enlargement “enlarged heart”, walls

become stiff and less compliant -> heart failure

Common in young adults, cause of sudden cardiac death

A primary type of cardiomyopathy, genetic

Variation in S/sx and prognosis

-dyspnea, chest pain, fatigue – worse with exertion

-arrhythmias

Medication and surgical treatments

Dilated Cardiomyopathies(DCM) Pathogenesis: a gradual enlargement (dilation) of the

ventricle chambers (left ventricle) -> heart failure EF drops to 40% or lower A primary type of cardiomyopathy, caused by:

-infectious myocarditis-alcohol/drug abuse-NMS diseases-genetic, idiopathic

S/sx: dyspnea on exertion (DOE), othopnea, weakness, edema, dysrhythmias

Treatment focuses on preventing further damage, maintaining heart function, possible transplant

Infective Endocarditis Rare but life-threatening

Often d/t bacteria that invade the endocardium and valves -> common cause of valve disorders

Staphylococci, streptococci, enterococci

Requires an already-damaged endocardium and an organism gaining entry into the circulatory system

Vegetations often develop on heart valves

Pt may have systemic infection s/sx, heart murmur

Risk factors: heart disease, IV drug use

Diagnose with blood cultures, echo

Acute Rheumatic Fever Multisystem inflammatory disease that may occur

after group A β-hemolytic streptococcal pharyngitis

Theory is that the infection causes a systemic autoimmune response

Rheumatic Heart Disease (RHD) is the cardiac manifestation of RF, may involve all three layers of the heart

Autoantibodies react with host tissue – cause damage to the valves, both stenosis and regurgitation

Progression is gradual

Valvular Heart Disease A problem with any of the four heart valves creates

abnormal blood flow and increases cardiac work

Normal valves allow unidirectional and unimpededblood flow

Regurgitation: valve doesn’t close properly and allows backflow – creates volume work

Stenosis: valve opening is restricted, preventing forward flow – creates pressure work

Both problems can occur together in the same valve

Regurg or stensosis cause murmurs

Pathogenesis of Valve Disease Destruction by infective endocarditis (ex: rheumatic

fever)

Connective tissue defects

Rupture of papillary muscles

Damage from an MI

Congenital malformations (mitral valve prolapse)

Mitral and aortic valves most commonly affected

Manifestation variables: valve involved, severity of damage, rapidity of onset, any compensatory mechanisms

Mitral Valve Stenosis Resistance to blood flow from LA->LV, LA must

work harder

Pressure from LA backs up into pulmonary circulation, pulmonary pressures rise

Increased pressure may travel through pulmonary system to the RV -> RV hypertrophy -> R heart failure

Sx appear at ~50% stenosis

Increasing exertional dyspnea, tachycardia, atrial dysrhythmias

Mitral Regurgitation During systole, some blood flows backward into LA

instead of all moving forward through aortic valve

Causes: RHD, mitral valve prolapse

LA dilates to accommodate backflow, eventually fails and pressures in pulmonary circuit rise -> L heart failure

LV will become dilated and hypertrophied

Acute mitral regurg usually fatal

Aortic Stenosis Narrowed aortic valve obstructs blood flow into aorta

from LV during systole

Pressure work -> LV hypertrophy

Compensation works for a while

Sx begin at ~50% narrowing

Angina, syncope, LV failure

Loud systolic murmur

Onset of sx: 5 year survival

Usually fatal before causing right heart failure