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CARDIOVASCULAR

SYSTEM
• EMERITA C. MENDOZA,
• R.N., M.D.
Scope
• Anatomy and Physiology
• Assessment
• Diagnostic and Lab
• Disorders
“Closer look”
Anatomy Key Points!
• Layers
• Chambers
• Valves
• Conduction
• Blood Supply
• Circulatory System
• Accessory Structures
Layers
• Epicardium outer
• Myocardium middle
• Endocardium inner
(enclosed by the pericardium)
• Pericardial sac space between the
pericardium and
epicardium
Chambers

• Left and right atrium


• Left and right ventricles (thick muscles)

inter-atrial septum – divides the


left and right
atrium
inter-ventricular septum – divides the
left
and right
Valves
• AV atrioventricular valves
– Tricuspid
– Mitral or bicuspid
• Semilunar valves
– Aortic
– Pulmonic
PAMT
Conduction System and
Innervation

• SA and AV node are innervated by . . .


ANS
Conduction System and
Innervation
• SA
• pacemaker of the heart
• located at the posterior wall of RA
• 70-80 beats per minute (atrial
contraction)
Conduction System and
Innervation
• Bachmann’s bundle
• Internodal pathways
– Anterior
– Middle (wenckebach’s),
– Posterior (thorel’s)
Conduction System and
Innervation
• AV Node
• Reserved generator
• Located at the interventricular septum
• 40-60 beats/min
Conduction System and
Innervation

• Purkinje system
• Bundle of His
• Right and left bundle
• Purkinje fibers
• Purkinje network
BLOOD SUPPLY TO
MYOCARDIUM
• COMMON CORONARY ARTERY
• RIGHT AND LEFT C.A.
Circumflex branch – left ventricle
Arch of the AORTA
Accessory Structures
• Pericardium
• Mediastinum
• Thoracic Cavity
The Pericardium
• A membrane that surrounds the
heart and great vessels
The Mediastinum
• The space between the lungs, which
includes the
heart
pericardium
aorta and
vena cava.
The Thoracic Cavity
• The chest wall composed of the
sternum and the rib cage
• The cavity is separated by the
diaphragm, the most important
respiratory muscle
Vascular System
• Composed of the arteries, veins and
capillaries
• Transport blood to all parts of the body
and back to the heart
• Inner layer – tunica intima
• Middle layer – tunica medialis
• Outer layer – tunica adventitia
Blood Circulation
• Pulmonary circuit
from the heart to lungs then back to
heart
• RA → Tricuspid Valve → RV
• → Pulmonic Valve
• PA → Lungs → 4 PV
• LA → Mitral Valve → LV
• → Aortic Valve
• Systemic Circuit
Blood Supply to:
• Bone – Haversian canal and
Volkmann’s canal
• Blood Vessel – vasa vasorum
• Heart – coronary arteries
• Brain – common carotid artery –
external and internal carotid artery,
anterior, middle and posterior cerebral
artery (Circle of Willis)
• Upper Extremities – basillic – cephalic
– brachial – radial and ulnar
Blood Supply to:
• Eyes – choroids (between sclera and
retina) cornea gets 02 from the
atmosphere
• Kidneys – renal artery – interlobar
artery – arcuate artery – interlobular
artery – afferent arteriole – glomerulus
– efferent arteriole - vasa recta – back
to the heart
• Liver – celiac artery – hepatic artery
and hepatic portal vein (food laden) -
Regulation of Arterial BP and
Distribution of Blood :
• Vasomotor and Cardiac Center in the
Medulla Oblongata ↑ or ↓ BP
• Pressor area – causes
vasoconstriction to increase BP
• Depressor area - causes
vasodilation to decrease BP
• Cardioinhibitor –
parasympathetic stimulation to
decrease BP
• Cardioaccelerator – sympathetic
REGULATIONS
• The Baroreceptor Reflex to increase
BP
Decreased BP initiates ADH secretion
and increases HR to increase BP.
• The Chemoreceptor Reflex to increase
BP
Lack of oxygen – vasoconstriction to
increase BP
It is only activated when BP is below 60
mm Hg
REGULATIONS
• The CNS Ischemic Response
• When CO2 is elevated in the blood and
there is insufficient blood supply to the
brain the vasomotor becomes very
hyperactive causing peripheral
vasoconstriction to increase BP.
REGULATIONS
• The Renin-Angiotensin-Aldosterone
Responses RAAP
• A decreased blood flow to the kidneys
activates JGA to release RENIN enzyme
to increase BP.
• Renin → liver → angiotensinogen
→ angiotensin I → adrenal cortex
• → aldosterone →
• Angiotensin I → lungs →
angiotensin II
REGULATIONS
• The Atrial Natriuretic Peptide
• Stored in the atrial cells, opposes the
RAAP, decreasing intravascular blood
volume by excreting water into the
kidneys
TERMS
• CARDIAC OUTPUT
• STROKE VOLUME
• BLOOD PRESSURE
• PULSE
• PULSE DEFICIT
• PULSE PRESSURE
ASSESSMENT
• Chest pain Dyspnea
• Cyanosis Pallor
• Fatigue Palpitations
• Syncope Edema
• Arrhythmia Murmur
• Gallop Pericardial friction
rub
ASSESSMENT
• Chest Pain
• Most common
• Due to Ischemia or Myocardial
Infarction
• Precipitated by stress or can be
relieved by Nitroglycerin (NTG)
• In MI it is more intense unrelated to
activities and can’t be relieved by NTG
ASSESSMENT
• 2. Dyspnea
• Labored breathing
• Dyspnea on exertion is due to
increased O2 demand of myocardium.
• Orthopnea is related to blood pooling
in the pulmonary bed, suspect
Pulmonary Edema
• Any sudden or acute dyspnea may be a
sign of Pulmonary Embolism
ASSESSMENT
• 3. Cyanosis
• Bluish discoloration of the skin and
mucous membrane
• Sat O2 is below 94%
• 4. Fatigue
• Maybe due to Anemias or related to
decreased Cardiac Output
ASSESSMENT
• 5. Palpitations
• Awareness of rapid or irregular heart
beat
• Autonomic Nervous System and
Adrenal Glands response (stress)
• 6. Syncope
• Transient loss of consciousness
• Due to decreased cerebral tissue
perfusion
ASSESSMENT
• 7. Edema
• Increased Hydrostatic Pressure (HP)
• Decreased Colloidal Oncotic Pressure
(COP)
• Obstructed Lymphatic or Vascular
System
• Anasarca
ASSESSMENT
• Bilateral edema
= CHF or Renal Failure
• Unilateral edema
= Vascular or Lymphatic obstruction
• Non-pitting edema
= Inflammatory related
• Pitting edema
= HP and COP derangement
ASSESSMENT
• 8. Skin
• Color, temperature, hair growth, nails,
capillary refill,
• clubbing or spooning of fingers
evaluation.
ASSESSMENT
• 9. Cardiac rate and rhythm
• Tachycardia
• Bradycardia
• Heart block
• Arrhythmias
• Sinus arrest
ASSESSMENT
• S1 closure of AV valves (lub)
• S2 closure of SL valves (dup)
• S3 & S4 diastolic filling sound
• S3 is heard after S2, if present
suspect CHF
• S4 is heard prior to S1,
if present suspect non-
compliant ventricles although
this is common among
elderly
ASSESSMENT
• Murmurs turbulence of blood flow, if
positive watchout FEV, this is normal
until 1 year old
• Pericardial Friction Rub “squeking
sound” suspect pericardial effusion
and pericarditis if this is heard
• Muffled Heart Sound Deadening sound,
if this is positive rule out Cardiac
Tamponade and other similar problem
like Effusion
ASSESSMENT
ASSESSMENT
Dx and Lab Tests
• Cardiac enzymes
• Serum analysis
• CARDIAC CATH
– Angiography (technetium 99, thallium)
– CVC
– SWAN-GANZ
• EKG
• Pacemaker
• PTCA
Disorders
• Hyperlipidemia
• Coronary Artery Disease
• Angina
• Myocardial Infarction
• Congestive Heart Failure
Coronary Artery Disease
CAD
• fatty deposits in the inner layer of
coronary arteries.
• mainly from hypercholesterolemia
Coronary Artery Disease
• Risk Factors:
• Hypertension
• Cigarette Smoking
• Diabetes Mellitus
• Obesity
• Sedentary Lifestyle
• Stress
• Atherosclerosis
• Hyperlipidemia
Coronary Artery Disease
• Incomplete occlusion of the coronary
arteries lead to Angina (ischemia)

• Complete occlusion of the coronary


arteries lead to Myocardial Infarction
Angina
• Diminished O2 supply to the
myocardium
• Types:
• Stable – ↑activity = pain, relieved
by rest
• Unstable – ↑activity = pain,
relieved by NTG
• Pre infarction – pain at rest,
relieved by NTG
Angina
• Diagnostic Evaluation:
• Characteristic of chest pain:
• Substernal or retrosternal pain that
radiates to arms neck and jaws
• Squeezing, heavy, tightness of the
chest
• Precipitated by cold, eating, emotions
and exertion
• Lasts a few minutes and then subsides
Angina
• NTG test (relief from pain)
• ECG (ST and T wave changes)
• Thallium 201 Imaging
• Technetium-99 Imaging
Angina
• Nursing Diagnosis:
• Pain related to imbalance in myocardial
oxygen demand
• Decreased cardiac output related to
reduced preload and after load
• Anxiety related to pain, uncertain
prognosis and threatening environment
Angina
• Management:
• Give antianginal drugs
• Administer O2
• Maintaining cardiac output
• Decreasing Anxiety
Myocardial Infarction
• Absent of O2 supply to the
myocardium
• Necrosis or death to the myocardial
tissue
• Attack may be sudden or gradual
Myocardial Infarction
Myocardial Infarction
• Chest pain:
• Severe, steady crushing and squeezing
• Not relieved by rest or NTG
• May continue for 15 minutes
• Levine’s sign
• May produce anxiety and fear resulting
to increased HR, BP and RR
• Diaphoresis, cold clammy skin, facial
pallor
Angina
• Diagnostic Evaluation:
• Characteristic of chest pain:
• Substernal or retrosternal pain that
radiates to arms neck and jaws
• Squeezing, heavy, tightness of the
chest
• Precipitated by cold, eating, emotions
and exertion
• Lasts a few minutes and then subsides
Myocardial Infarction
• Diagnostic Evaluation:
• Chest pain can’t be relieved by NTG
• ST segment depression and T wave
inversion
• Cardiac enzymes: increased
• Troponin-T (CT and T)
• CK MB (CREATINE PHOSPHOKINASE)
• LDH (lactate dehydrogenase)
• AST (aspartate aminotransferase)
CK -MB
• it rises in serum within 2 to 8
hours of onset of acute
myocardial infarction.
• Serial measurements every 2 to
4 hours for a period of 9 to 12
hours after the patient is first
seen will provide a pattern to
determine whether the CK-MB is
rising, indicative of myocardial
injury.
Myocardial Infarction
• Nursing Diagnosis:
• Pain related to an imbalance in oxygen
supply and demand
• Anxiety related to chest pain, fear of
death and threatening environment
• Decreased cardiac output related to
impaired contraction of the heart
Myocardial Infarction
• Altered tissue perfusion (myocardial)
related to coronary stenosis
• Activity intolerance related to
insufficient oxygenation
• Risk for injury (bleeding) related to
dissolution of clots
• Ineffective individual coping related to
threats to self esteem
Myocardial Infarction
• Management:
• CBR without BP
• Oxygen therapy
• Pain control
• Morphine or Meperidine
• Vasodilator (NTG)
• Anxiolytic (Benzodiazepine)
Myocardial Infarction
• Pharmacologic Therapy
• Thrombolytic Agents
• TPA tissue plasminogen activator
• Streptokinase (streptase)
• Urokinase
• Anticoagulant
• Heparin
• Warfarin
• Beta adrenergic blocking agents
Myocardial Infarction
• Surgical revascularization:
• PTCA Percutaneous Transluminal
Coronary Angioplasty

• CABG coronary artery bypass graft


Congestive Heart Failure
• inability of the heart to pump blood into
the circulatory system.
• usually due to inability of the ventricles
to pump blood
• leading to
• ↓
• Pulmonary congestion
• ↓
• Pulmonary hypertension
CHF
• left sided heart failure will manifest
• ↓
• Pulmonary in Nature
• dyspnea, labored breathing,
orthopnea,
• moist hacking cough, bi-basilar
crackles,
• increased PAWP
• ↓
CHF
• right ventricle will pump harder just to
• pass blood into the congested
pulmonary capillaries
• ↓
• resulting to right ventricular
hypertrophy
• Right Ventricular Failure (Cor
Pulmonale)
• ↓
CHF
• blood will be congested into the right
side
• ↓
• right sided heart failure will
follow
• ↓
• Venous congestion
• distended neck veins,
hepatomegaly,
CHF
• venous pooling in the lower extremities
• bi-pedal edema, varicosities, DVT
• ↓
• until all venous system becomes
congested with fluid
• ↓
• periorbital edema or
• generalized edema
• ANASARCA
CHF
• Predisposing Factors:
• Myocardial Infarction
• Arrhythmias
• Pregnancy
• Pulmonary Embolism
• Anemia
• Renal Failure
CHF
• Diagnosing CHF:
• Daily weighing reveals unexplained
weight gain
• Abdominal girth measurement shows
ascites
• EKG detects heart strain
• Chest X-ray may highlights
cardiomegaly and pleural effusion
• CVC Central Venous Catheter and
SWAN-GANZ
CHF
• Nursing Considerations:
• The goal of treatment is to improve
pump function and reverse the
compensatory mechanism of the heart.
• Observe complete bed rest and reduce
myocardial oxygen demand.
• Employ FEV (forced expired volume)
management and prevent the
complications to occur.
• Give Diuretics and Digoxin (0.5 – 2.0
CHF
• Complications:
• Acute Pulmonary Edema
• Treatment:
• Bed rest and maintain high fowler’s
position
• O2 therapy
• Morphine administration to dilate
blood vessels
• Dopamine to increase myocardial
CHF
• Complications:
• Cardiac Arrhythmias
• Disturbances in regular rate and
rhythm due to changes in electrical
automaticity or conduction
• Irregular HR, rhythm and regularity
Cardiac Arrhythmias
• ATRIAL A.
• Premature atrial contraction (PAC) –
more than 100 bpm
• Atrial flutter – 250-300 bpm
• Atrial fibrillation – higher than 500 bpm

• VENTRICULAR A.
• Premature ventricular contraction
Premature ventricular
contraction
• AV Block
• Impulse is delayed from SA node
to AV node
• 1st degree –
• 2nd degree –
– Mobitz type I – asymptomatic (ventricular
contraction is adequate)
– Mobitz type II – critical (atrial contraction is
not synchronized with the ventricle)
• Treatment:
• Cardiac Arrest
• Heart stops beating or
contraction is ineffective
• Watch-out for ↓ tissue perfusion
manifestations:
Restlessness (early sign)
Tachycardia and
tachypnea
Shallow respirations
Palpable BP
• Cardiac Arrest
• Treatment:
• Increase CO
• Cardiovascular drugs and
mechanical equipment
utilization
• Cardiovascular Drugs:
• IV Dopamine (vasopressor)
• IV Dobutamine (diuretic effects)
Disorders
• Venous Thrombus
• Chronic Venous Insufficiency
• Arteriosclerosis
• Raynaud’s Phenomenon
• Hypertension
Venous Thrombus

• Due to:
• Stasis of blood
• Injury to the vessel wall
• Altered blood coagulation
Venous Thrombus
• High Risk:
• Fractures, cast and joint replacement
• Obesity and smoking
• Immobilized patient
• Heart problems
Venous Thrombus
• May progress to:
• Phlebitis-inflammation of the vessel
wall
• Superficial thrombophlebitis-greater
and lesser saphenous veins are
affected.
• Deep vein thrombosis-deep veins are
affected, pulmonary embolism is a
known complication of this.
Venous Thrombus
• Manifestations:
• (+) Homan’s sign
• fever chills
• swelling and cyanosis
Venous Thrombus
• Diagnostic:
• Venous duplex ultrasound
• Impedance plethysmography
• RF testing (radioactive fibrinogen)
fibrinogen I 125
• Venography
• Coagulation Profiles:
– APTT
– PT/INR
Venous Thrombus
• Management:
• Prevent complications
• Bed rest for 5 days
• Prevent muscle contraction if possible
to prevent dislodging the clot
• Elevation of affected part 10-20 degree
above the heart
• Anticoagulant
• Thrombolytic
Chronic Venous Insufficiency
• Destruction of the valves because of
chronic blood pooling or trauma.
• Venous return is decreased
• ↓
• chronic venous stasis
• ↓
• resulting to edema and swelling
formation
• ↓
Arteriosclerosis
• It is hardening of the arterial blood
vessel walls related to aging.
• Atherosclerosis-common type of
arteriosclerosis due to atheromas.
Arteriosclerosis
• Aging and atheromas
• ↓
• impeding the lumen of the
arterial walls
• ↓
• it may be incomplete or
incomplete occlusions
• ↓
• producing systemic effects
Arteriosclerosis
• maybe asymptomatic or it may
manifest only if the damaged is severe

• systemic effects

• 1. ↑ PVR = heart strain to
hypertension
• 2. weakening the muscles of the
wall that leads to aneurysm
Arteriosclerosis
• 3. TIA to CVA
• 4. Angina to MI
• 5. ATN to Renal Failure
• 6. Retinopathy to Blindness
• 7. Peripheral Occlusive Disease (TAO)
to Gangrene Formation
• 8. Hepatic Infarction
• 9. Pulmonary Infarction
Arteriosclerosis
• Diagnostic Evaluation:
• Arteriography
• CT Scan
• MRI
• Duplex UTZ
• EKG
Arteriosclerosis
• Management:
Modification of risk factors
(CAD and hyperlipidemia)
• Anticoagulants
• Antiplatelets
• Lipid Lowering Agent
• Antihypertensive
• Vascular Rehabilitation/Exercise
Arteriosclerosis
• Surgical Intervention:
• PTA-Percutaneous Transluminal
Angioplasty
• Laser Angioplasty
• Embolectomy-removal of clot from the
artery
• Thrombectomy-removal of thrombus
from the artery
• Endarterectomy-removal of plaque
TAO
• THROMBOANGITIS OBLITERANS
(TAO) OR Buerger’s Disease
• Occlusion of the peripheral blood
vessels (lower extremities)

• Cause: heavy smokers


(common), ARTERIOSCLEROSIS,
HYPERLIPIDEMIA, DM
TAO
• Dx: Arteriography

• Management: promote collateral


circulation (exercise), stop from
smoking or control other risk
factors, no elevation above the
heart, warm compress

• DRUGS: anticoagulants,
fibrinolytics, vasodilators,
Raynaud’s Phenomenon
• This is a vasospastic disease with
unusual sensitivity to cold or emotional
stress.
• The cause is unknown but it may be
secondary to Autoimmune Disease.
Raynaud’s Phenomenon
• Due to arteriolar constrictions
Manifestations:
• Coldness
• Pain
• Pallor of finger tips, toes and tip of the
nose
• Color changes:
– White - blanching (vasospasm)
– Blue - cyanotic (blood pooling)
Raynaud’s Phenomenon
• Diagnostic:
• Rule out secondary problem (chronic
arterial disease and connective tissue
disorder)
Raynaud’s Phenomenon
• Management:
• Avoid extreme temperatures Control
pain with analgesic, reassure that it is
only temporary
• Calcium channel blockers is used to
reduce vasospasm
• NTG or sympatholytics may help
• Antiplatelet, Dipyridamole (Persantin)
to prevent occlusion
Hypertension
• “Silent killer”
• Is a disease of vascular regulation that
leads to high blood pressure
BP = CO x PR
• Mainly due to alteration of:
– Central Nervous System
– Renin-Angiotensin-Aldosterone System
– Extracellular Fluid Volume
Hypertension
• Primary or Essential Hypertension
• Other cause are absent
• Average BP exceeds the upper limits
(taken at rest 3x with several days
interval)
• Diastolic is 90 mm Hg or higher
• Represents 95% of patients with
hypertension
Hypertension
• Secondary Hypertension
• Due to:
• Renal Pathology
• Coarctation of the Aorta
• Endocrine Disturbance
• Drugs (estrogens, sympathomimetics,
NSAIDs, steroids)

Malignant Hypertension
Hypertension
• Risk Factors:
• Old age
• Race
• Overweight
• Family History
• Smoking
• Sedentary Lifestyle
• Diabetes Mellitus
Classification
• Stage I = 140-159/90-99
• Stage II = 160-179/100-109
• Stage III = >or=180/>or=110
Hypertension
• Manifestations:
• Usually asymptomatic
• Headache, flashes, nausea and
vomiting
• Monitor the complications
– Heart strain
– Aneurysm
– Kidney Failure
– CVA
Hypertension
• Diagnostic Evaluation:
• Monitor BP
• Evaluate all of the risk factors:
• Eg. EKG, Blood Sugar, Blood Chem
etc.
Hypertension
• Management:
• Control of all risk factors
• Eg. Lose weight, limit alcohol, cut
sodium to 2.4 g/day, stop smoking,
reduce dietary saturated fat and
cholesterol, reduce coffee intake.
• Diet, Exercise and Weight reduction
• Despite lifestyle changes and BP
remains high
• drug therapy should be started:
• Diuretics Furosemide (Lasix)
• Adrenergic Inhibitor
• Peripheral Agent: Reserpine
(Serpasil)
• Central Alpha-Agonist
Methyldopa (Aldomet)
• Alpha-Blockers Prazosin HCl
(Minipress)
Cardiovascular Drugs
• Anti Anginal
• Opiate Analgesic – Morphine Sulfate
• ↓ cardiac workload and BP,
improve LOC and sedative effect

• Vasodilators
• Nitroglycerin NTG
• Relax smooth muscle, dec. BP
and alleviate headache
Cardiovascular Drugs
• Calcium Channel Blockers
• Nifidepine (Procardia) Diazepam
(Cardizem)
• Decrease muscle tone, interferes
contraction, decrease BP
• S.E. – bradycardia, diarrhea and rashes

• Beta Blocking Agent


• Propranolol
Cardiovascular Drugs
• Digitalis, Digoxin
• Positive Inotropic (Increases
contraction of the heart)
– Increase emptying capacity of the heart
• Negative chronotropic (Decreases HR)
AV node control
– Increase CO (improves stroke volume)
• S.E. – GIT disturbance, CNS depression
and flashes of light
Cardiovascular Drugs
• Dopamine – diuresis effect
• Increase Na excretion (kidney)
• Vasodilators
• Norepinephrine effect
• Dobutamine
• Increase CO
• More potent on contraction
Cardiovascular Drugs
• Diuretics
• Spironolactone (Aldactone) – K sparer
• Furosemide (Lasix) – K waster

• Anti hypertensive
• ACE inhibitors – Captopril
(Capoten)
Cardiovascular Drugs
• Anti dysrhythmic drug
• Lidocaine (Xylocaine) for PVC
• Atropine for Mobitz type I
• Isoproterenol (Isuprel) for sinus
bradycardia
• Norepinephrine (Levophed) powerful
vasoconstrictor
• Epinephrine – increase conduction,
contractility and automaticity
Cardiovascular Drugs
• Thrombolytic/Fibrinolytic Agent
• Streptokinase – lyses the clot (20T IU IV
bolus or 4T IU/min drip)
• Urokinase – avtivates plasminogen to
plasmin (intracoronary)
• TPA – tissue plasminogen activator
• Antidote – Amino Caproic Acid
Cardiovascular Drugs
• Blood thinner
• Heparin – prevent formation of new clot

(4-8T IU/30 min)


• Check APTT
• Antidote – Protamine Sulfate

• Warfarin (Coumadine) – decrease


viscosity of blood (PO) home meds
EKG
PACEMAKER