This document provides an overview of topics to be covered in NURS 216 Spring 2013 related to cardiovascular anatomy, physiology, and disorders. Key points include: - Review of cardiovascular anatomy, physiology, and mechanical functions of the heart. - Discussion of disorders such as atherosclerosis, hypertension, coronary heart disease, myocardial infarction, and venous disorders. - Objectives are to review cardiovascular concepts and discuss various cardiovascular disorders, including their causes, signs and symptoms, diagnosis, and treatment.

1. NURS 216 Spring 2013
Dr. Smith

2. 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.

3. 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

4.  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

6. 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

7. Pulmonary circulation:
smaller volume,
low pressure
Systemic circulation:
larger volume,
high pressure

8. 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

9. 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

10. 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
Vessel
radius
Intraluminal Wall
pressure tension

11. Layers of the Heart

12. Coronary Arteries

13. Conduction System

14. Electrocardiogram (EKG or ECG)

15. 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%

16. 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

18. 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

19. Arterial Disorders
 Hyperlipidemia and atherosclerosis (central)
 Peripheral arterial problems
 Aneurysms and dissections (usually central)

20. 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)

21. 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

22. Hyperlipidemia
 Types of lipoproteins are
categorized by the
amount of fat (density)
 “bad” and “good”
 Levels affected by diet,
activity level, and liver
function

23. 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

24. Xanthomas

25. 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)

28. 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

29. 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

30. 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

31. 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

33. 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

34. 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

35. 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)

36. 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

37. 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

38. Manifestations of Hypertension
 “the silent killer” Target Organ Damage
 Major risk factor for  Heart: LVH (LV
atherosclerosis hypertrophy), angina,
 Increases workload of MI, prior stents/CABG,
the LV heart failure
 TIA or strokes in brain
 Chronic kidney disease
 Peripheral vascular
disease
 retinopathy

39. 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

40. 3D reconstruction of CT angiography of an
infant with coarctation of the aorta
http://www.biij.org/2006/2/e11/

41. 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

42. Orthostatic Hypotension Causes
 Reduced blood volume
 Medications
 Aging
 Immobility, extended bed rest
 Autonomic nervous system dysfunction
 Treatment depends on identifying a cause

43. Coronary Arteries

44. 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

45. Varicose Veins

46. 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

47. 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?

49. Pericardial Disorders
 Pericardial effusion
-accumulation of fluid in the pericardial cavity
-can compress heart, lower SV
-diagnose with ultrasound/echo
-pericardiocentesis
-cardiac tamponade

50. Cardiac Tamponade

51. 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

52. 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)

53. Coronary Arteries

54. 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

55. 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

56. 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

57. 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

58. Signs and Symptoms of an MI
 Angina pectoris, chest pressure, possibly
radiating down left arm
 Diaphoresis
 Nausea
 Women often experience non-traditional
symptoms!

59. Diagnosis of an MI
 Blood markers: cardiac enzymes (troponin)
 EKG changes (ST elevation – “STEMI”)
 Cardiac catheterization
 Treatment:
-medications
-reperfusion (usually angioplasty and/or stent)

60. Myocardial Infarction
Left main
coronary
artery
Left anterior
descending
coronary
artery (LAD)

61. Zones of necrosis and ischemia

62. 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

63. 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

64. 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

65. 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

66. 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

67. 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

69. 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

70. 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

71. 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 unimpeded
blood 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

72. 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

73. 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

74. 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

75. 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