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MARK BILLY L.

PERPETUA, MAN RN

CARDIOVASCULAR
SYSTEM DISORDERS
ANATOMY AND PHYSIOLOGY
HEART  Semilunar valves
 Pumps blood for Pulmonic valve
systemic circulation Aortic valve
 2 atria  AV valves
 2 ventricles Tricuspid valve
Bicuspid valve
ANATOMY AND PHYSIOLOGY
 Layers of the heart  Coronary arteries
 Endocardium  Supplies blood to the heart
 Myocardium  Right coronary artery

 Pericardium  Left anterior descending coronary


artery
 Visceral pericardium
 Left circumflex coronary artery
 Parietal pericardium
 *pericardial space: Fluid (approx. 50 mL)
CARDIAC ACTION POTENTIAL
 Dysrhythmia (arrhythmia)
 Any deviation from the normal rate or pattern of the heartbeat

 Cardiac Action Potential


 Depolarization: entry of calcium and sodium
 Phase 0: sodium influx
 Phase 1: initial repolarization (K exits the intracellular space)
 Phase 2: plateau (influx of calcium ions)
 Phase 3: rapid repolarization (efflux of potassium)
 Phase 4: resting membrane potential
ASSESSMENT AND
DIAGNOSTICS

MARK BILLY L. PERPETUA, MAN RN


PULSE PRESSURE
 Difference between the systolic and diastolic pressure
 Normal: 30-40 mmHg
 Determines the maintenance of GOOD cardiac output
 Increased or Widened pulse pressure:
 Conditions that elevate the stroke volume (anxiety, exercise,
bradycardia, raised ICP)
 Decreased or Narrowed pulse pressure
 Conditions of reduced stroke volume and ejection velocity (shock,
HF, hypovolemia)
JUGULAR VEIN PULSATIONS
 Can be a mean to estimate right-sided heart function
 Site: just above the clavicles, adjacent to the sternocleidomastoid
 Normally distended when patient is lying flat/supine
 Not apparent if head is elevated more than 30 degrees
 DISTENTION with head elevated at 45-90 degrees:
 Right ventricular failure
 Pulmonary hypertension
 Pulmonary stenosis
INSPECTION AND PALPATION (HEART)

 Aortic area  Tricuspid area


 Second intercoastal space, right of  Lower half of the sternum along the
the sternum left parasternal area
 Pulmonic area  Mitral (apical) area
 Second intercoastal space to the left  Left fifth intercoastal space at the
of the sternum midclavicular line
 Erb’s point  Epigastric area
 Third intercoastal space to the left of  Below the xyphoid process
the sternum
AUSCULTATION (HEART)
 NORMAL HEART SOUNDS  S2 (second heart sound)
 S1 and S2, produced by the closure of the  Created by the closure of the
AV valves and the semilumar valves pulmonic and aortic valve
respectively  Reffered to as the “dub”
 S1 (first heart sound)
 Aortic component is heard loudest
 Created by the closure of the over aortic and pulmonic area
tricuspid and mitral valve
 “lub” used to replicate the sound
 Heart loudest at the apical area
 Intensity increases during tachycardias
or mitral stenosis
AUSCULTATION (HEART)

 ABNORMAL HEART SOUNDS


 Produced due to structural or functional heart problems are
present
 S3, S4 gallops, opening snaps, systolic clicks, and murmurs
 These sounds are created by VIBRATION of the ventricle
and surrounding structure as blood meets RESISTENCE
during ventricular filling
 ABNORMAL HEART SOUNDS  S4 (fourth heat sound)
 S3 (third heart sound)  “Lub (s4) lub dub”
 “Lub-dub DUB”  Occurs late in diastole
 Occurs early in diastole during the  Generated during atrial contraction as
period of rapid ventricular filling blood forcefully enters a
 Physiologic S3 : normal in children and
NONCOMPLIANT ventricles
adults (35-40yo)  Summation gallop
 Elderly: sign of significant  When S3 and S4 are BOTH present,
pathophysiology creating a quadruple rhythm
 “LUB lub dub DUB”
ABNORMAL HEART SOUNDS
 MURMURS
Created by TURBULENT blood flow
Cause:
Narrowed valve
Ventricular wall defect (congenital)
Defect between aorta and pulmonary artery
Grading of Intensity (Murmurs)

 Grade1  Grade 4
 Very faint and difficult for inexperienced  Loud and may be associated with a thrill
clinician to hear  Grade 5
 Grade 2
 Very loud, heard when stethoscope is
 Quiet, but readily perceived by the partially off the chest, associated with a
experienced clinician thrill
 Grade 3  Grade 6
 Moderately loud  Extremely loud, detected with the
stethoscope off the chest, associated
with a thrill
LIPID PROFILE
 Cholesterol
 Normal: <200 mg/dl
 High Density Lipoprotein (HDL)
 M: 35-75 F: 35-80
 Low Density Lipoprotein (LDL)
 Normal: <160 mg/dl
 Triglyceride
 (100-200mg/dl)
2D ECHOCARDIOGRAPHY

 Assesses the size, shape, and structure of the heart from


different views
 Uses ultrasound
 *with Doppler studies (assesses blood flow inside the
heart)
CARDIAC CATHETERIZATION
 Invasive diagnostic procedure in which radiopaque
arterial and venous catheters are introduced into
selected blood vessels of the right or left side of the
heart
 Post-procedure:
 Do not bend at waist or strain or lift
 Avoid tub baths
 WOF: bleeding and swelling
ANGIOGRAPHY

 A technique in which a contrast agent is injected into the


vascular system to outline the heart and blood vessel
 PRE-OP:
 Inquire for allergy to seafood and iodine
CAROTID ARTERY DUPLEX SCAN

 Ultrasound study done to assess the blood flow of the


arteries that supply blood from the heart thru the neck
to the brain
CARDIAC STRESS TEST
 Exercise stress test (threadmill)
 Pharmacologic stress test (given vasodilating agents) – reversed by aminophylline
 Dypirimadole
 Adenosine
 Dobutamine
 Detects:
 Presence of CAD
 Cause of chest pain
 Functional capacity of the heart after MI
 Effectiveness of antianginal or antidysrhythmic medications
 Occurrence of dysrhythmias
 Physical fitness program
Series of waves and
deflections recording the
heart’s electrical activity
from a certain view
CARDIAC ELECTROPHYSIOLOGY

 Automaticity: ability to initiate an electrical impulse


 Excitability: ability to respond to an electrical stimuli
 Conductivity: ability to transmit an electrical impulse
Sinoatrial Node (SA)
❑ Primary pacemaker
❑ Located at the junction of the superior vena cava and right
atrium
❑ Firing rate: 60-100/min
Atrioventricular Nove (AV)
❑ Located in the right atrial wall near tricuspid valve
❑ Coordinates electrical impulses from SA Node and after a
slight DELAY relays impulse to the ventricles
❑ Firing rate: 40-60/min
❑ Takes over if SA node fails
Ventricular Pacemaker sites
❑ Consists of Bundle of His branches and Purkinje fibers
❑ Takes over if SA and AV node fail
❑ Firing rate: 30-40/min
12-lead ECG
❑ Placement of ECG ❑ Views six leads:
LEADS ❑ Standard leads
❑ LIMB LEADS (bipolar): I,II,III
❑ Right arm (RED) ❑ Augmented leads
❑ Left arm (YELLOW) (unipolar): aVR, aVL,
❑ Right leg (BLACK) aVF
❑ Left leg (GREEN)
❑ CHEST LEADS ❑ Views six leads:
❑ V1 (4th ICS right of sternum) ❑ Unipolar
❑ V2 (4th ICS left of sternum) Precordial leads:
❑ V3 (directly between V2 and
V1-V6
V4)
❑ V4 (5th ICS left midclavicular
line)
❑ V5 (5th ICS anterior axillary
line)
❑ V6 (5th ICS midaxillary line)
P wave Atrial depolarization

PR-Segment 0.04 sec (delay by AV Node for completion of


ventricular filling)

QRS Complex Ventricular depolarization

ST segment Early ventricular repolarization

T wave Actual ventricular repolarization

U wave Repolarization of the mid-myocardial cell

PR-Interval Represents transition of impulse from SA node


to Purkinje fibers

QT-interval Duration time from ventricular depolarization


to ventricular repolarization
TIME (Secs) AMPLITUDE
(mV)
SMALL box 0.04 secs 0.1 mV
LARGE box 0.20 secs 0.5 mV
1-sec strip: 5 large boxes or 25 small boxes
P wave 0.06-0.12 sec
QRS 0.05-0.10 sec
T wave Not measured
PR interval 0.12-0.20 sec
ST-segment Not measured
T wave inversion: Ischemia
Tischemia
ST-segment elevation: Injury
STinjury
Pathologic Q-wave: Old MI
InfarQion
T wave inversion: Ischemia
Tischemia
ST-segment elevation: Injury
STinjury
Pathologic Q-wave: Old MI
InfarQion
BLOOD VESSEL
DISTURBANCES

MARK BILLY L. PERPETUA, MAN RN


HYPERTENSION

MARK BILLY L. PERPETUA, MAN RN


HYPERTENSION
 Defined as a systolic blood pressure of 140 mm Hg or higher
or a diastolic blood pressure of 90 mm Hg or higher, based
on the average of two or more accurate blood pressure
measurements taken 1 to 4 weeks apart by a health care
provider.
 TYPES:
 Primary/Essential (unidentified etiology 90-95%)
 Secondary (identified cause 5%)
HYPERTENSION
 Risk factors: personality)
 E – xcessive alcohol intake  I – increased weight (Obesity)
 S – tress  A – ge (increased age)
 S – moking  L – ifestyle
 E – xcessive intake of caffeine
 N – a increase in diet
 T – ime urgent (type A
HYPERTENSION
 Normal:  Stage II
 Less than 120/80 mm Hg  Systolic at least 140 or diastolic at
least 90 mm Hg
 Elevated:
 Systolic between 120-129 and
 Hypertensive Crisis
diastolic less than 80  Systolic over 180 and or diastolic
over 120 mm Hg
 Stage I
 Systolic between 130-139 or
diastolic between 80-89
HYPERTENSION
 HYPERTENSION CRISES
 Hypertension emergency
 Needs to be lowered within 6 hrs (if not, will lead to irreversible compli)
 IV anti-hypertensives (Nicardipine or Nitroprussides)
 Hypertension urgency
 Needs to be lowered within 24 hrs, no symptoms of serious problem
 Oral anti-hypertensive drugs
HYPERTENSION
 Manifestations:  Dx:
 BRAIN: Headache, Dizziness, CVA,  Blood Chemistry
TIA  ECG
 EPISTAXIS  Echocardiography
 EYES: Hemorrhages, Papilledema
 CVS: Chest pain, MI, Hypertrophy
 KIDNEYS: Renal failure
HYPERTENSION
 Mngt:
 P –rovide DASH diet (Dietary Approaches to Stop Hypertension)
 R –elaxation techniques
 E –xercise
 S –top alcohol
 S –top smoking
 U –nnecessary medications assoc. with HPN should be eliminated
 R –educe weight and Restrict Na to 2g daily
 E –mphasize importance of medication compliance
HYPERTENSION
 Medications  Action:
(ANTIHYPERTENSIVES)  Decreases BP
 Calcium Channel Blockers  Decreases cardiac workload
 “dipine”  SE:
 Nifedipine  Headache
 Amlodipine  Orthostatic hypotension (WOF: fall, light
 Felodipine headedness, dizziness)
 Verapamil*
 Diltiazem*
HYPERTENSION
 Medications  Contraindication:
(ANTIHYPERTENSIVES)  Pregnancy (teratogenic)
 ACE inhibitors  Asthma (trigger)
 “pril”  SE:
 Enalapril
 Agranulocytosis
 Captopril
 Angioedema (edema of lips, tongue and
 Consideration: neck)
 Given an hour before meals (food prevents  Hyperkalemia (muscle weakness)
absorption)
 Avoid salt substitutes and orange juice
(may contain high potassium)
HYPERTENSION

 Medications  Alpha 2 agonist


(ANTIHYPERTENSIVES)  Clonidine

 Angiotensin Receptor Blockers  Methyldopa

 “sartan”  CI: Liver disease

 Increases potassium (but no SE like ACE  SE: increased Na and water retention,
inhibitors) depression, impotence and constipation
 Alpha 1 blockers  Beta Adrenergic Blockers
 “sozin”  “olol”
 Not for COPD and Asthma patients
ANEURYSM

MARK BILLY L. PERPETUA, MAN RN


ANEURYSM
 Localized sac or dilation of an
artery formed at a weak
point in the vessel wall
 ETIOLOGY:
 Inflammatory
 Congenital
 Infections
 Mechanical
 Pregnancy-related
 Traumatic
 Anastomotic
ANEURYSM
 TYPES:
 Accdg to STRUCTURE:
Saccular (one-sided outpouching)
Fusiform (entire wall outpouching)
Dissecting (Splitting of tunicas)
ANEURYSM
 TYPES:
 Accdg to LOCATION:
 Thoracic Aortic Aneurysm (TAA)
 Boring pain when supine

 Abdominal Aortic Aneurysm (AAA)


 Throbbing pain on the abdomen when supine
 Pulsatile mass in the abdomen
 Blue-toes syndrome (r/t impaired circulation in the lower ex when the aneurysm
progresses)
ANEURYSM
 Dx:
 Chest radiograph
 Angiogram
 Transesophageal echocardiography
 MRI
ANEURYSM
 Mngt: (<2 inches – control pressure, >2 inches – surgery)
 A –nti-hypertensives (DOC: Beta blockers)
 N–otify MD
 E –mphasize follow-up check up
 U –ltrasound
 R –esection/excision
 Y –ou should modify the risk factors
 S –trict control of BP
 M –edication that reduces cardiac contractility (negative inotropes)
PERIPHERAL VASCULAR
DISEASE

MARK BILLY L. PERPETUA, MAN RN


BUERGER’S DISEASE
(THROMBOANGITIS OBLITERANS)

MARK BILLY L. PERPETUA, MAN RN


BUERGER’S DISEASE

 Diffuse inflammation of the SMALL and MEDIUM


ARTERIES followed by the veins
 Also involves FIBROSIS of the NERVES
 Affects the FEET or lower extremities (BILATERAL)
 Cause: UNKOWN/AUTOIMMUNE
BUERGER’S DISEASE
 PREDISPOSING FACTORS:  MANIFESTATIONS:
 Men (20-35)  Pain d/t Intermittent claudication
 Heavy Smoking  COLD sensitivity
 Chewing of Tobacco  Skin color changes (Reddish to
bluish then becomes darkened)
 Diminished peripheral pulses
 Ulceration and gangrene
BUERGER’S DISEASE
 Dx:  Debridement
 Segmental limb BP  STOP smoking
 Contrast angiography  BKA/AKA
 Duplex UTZ (patency of vessel)  Stump:

 Mngt:  elevated (prevent edema)


 Figure of 8 bandage
 Vasodilators:
 Nitroprusside/NTG (Improve
circulation)
RAYNAUD’S DISEASE

MARK BILLY L. PERPETUA, MAN RN


RAYNAUD’S DISEASE
 Characterized by INTERMITTENT arteriolar
vasoconstriction that affects the FINGERS and
TOES
 Usually affects the HANDS and FINGERS
(UNILATERAL)
 Cause: Unknown/Autoimmune
RAYNAUD’S DISEASE
 PREDISPOSING FACTORS:  Dx:
 Women (16-40)  Same with Buerger’s dse
 COLD climates  Mngt:
 Heavy SMOKING  Avoid stimuli that causes
VASOCONSTRICTION

 MANIFESTATIONS:  Layers of clothing (winter)

 COLDNESS, pain, pallor, cyanosis  Gloves


followed by HYPEREMIA, numbness,  Ca channel blockers
tingling, and burning pain
INFLAMMATORY DISORDERS OF
THE HEART

MARK BILLY L. PERPETUA, MAN RN


ENDOCARDITIS

MARK BILLY L. PERPETUA, MAN RN


ENDOCARDITIS
 Inflammation of the INNER lining of the heart
including the valves
 Cause:
 Infection (Staph.Aureus/Strep.Viridans)
 Trauma
 Prosthesis
 Idiopathic
ENDOCARDITIS
 MANIFESTATIONS:  Dx:
 S/Sx of infection  Blood GS/CS
 Dysrhytmias  Elevated ESR and WBC
 Heart murmur  Echocardiography
 OSLER’s NODE (reddish lesions on  ECG
FINGER PADS)
 Mngt:
 JANEWAY’s NODE (non-tender
hemorrhagic lesions on PALMS and  Antibiotic agents
SOLES)
 Treat underling cause
PERICARDITIS

MARK BILLY L. PERPETUA, MAN RN


PERICARDITIS
 Inflammation of the OUTER lining of the heart
 Cause:
 Infection (Viral)
 Neoplasms
 Renal failure
 Radiation
 Inflammatory disorders/Autoimmune
PERICARDITIS
 MANIFESTATIONS:  Mngt:
 CHEST PAIN aggravated by  Analgesics
BREATHING and relieved by  Treat the underlying cause
SITING/LEANING FORWARD
 Antibiotics (infection)
 FRICTION RUB on auscultation
 Dx:
 Elevated WBC
 ECG
 Echocardiography
PERICARDITIS
 COMPLICATION:  Mngt:
 CARDIAC TAMPONADE  Pericardiocentesis
 EXCESS fluid in the pericardial  Pericardial windowing
sac that interferes with cardiac
filling
 BECK’s TRIAD:
 JVD
 Distant/Muffled heart sound
 Pulsus paradoxus
CARDIOMYOPATHY

MARK BILLY L. PERPETUA, MAN RN


CARDIOMYOPATHY
 Abnormality of heart’s MUSCLE
 Causes:
 Unknown
 Viral
 Chronic alcohol abuse
 Pregnancy
CARDIOMYOPATHY

 TYPES:
 Dilated cardiomyopathy (most common)
 Restricted cardiomyopathy
 Hypertrophic cardiomyopathy
CARDIOMYOPATHY

 Mngt:
 Monitor S/Sx of HEART FAILURE
 Rest (dec. cardiac workload)
 No medical theraphy
 Avoid ALCOHOL (cardiac depressant)
 Diet: Low Na
CORONARY ARTERY DISEASE

MARK BILLY L. PERPETUA, MAN RN


CORONARY ARTERY DISEASE

 Atherosclerosis
 Plaque build-up in the arteries
 Arteriosclerosis
 Hardening of the arteries
CORONARY ARTERY DISEASE
 Risk factors:  F –atty/Salty foods
 R –ace (African-  A –ge (>40)/Alcohol
American)/Regions that are  C –igarette Smoking
industrialized
 T –ype A behavior
 I –nfection/Inc. BP
 O –besity/Oral
 S –tress contraceptives
 K –nowing a sedentary  R –esult of DM
lifestyle
CAD

Chronic Ischemic Heart Disease Acute Coronary Syndrome

Stable Variant Silent Non ST-segment


Angina Angina Myocardial ST-segment
Elevation MI
Ischemia Elevation MI
(Unstable Angina)
ANGINA PECTORIS
 Chest pain due to inadequate supply  PAIN:
of OXYGEN in the myocardium
 Substernal, paroxysmal, transient
leading into myocardial ISCHEMIA
 Anterior chest
 Predisposing factor:
 Vague (Radiates to the neck,
 Extremes of Emotions
jaw, shoulders)
 Excessive Eating
 Relieved by rest and nitroglycerine
 Extremes of temperatures
 Short duration (<15minutes)
 Excessive Exercise
 Exertion
ANGINA PECTORIS
 Stable Angina  Variant/Prinzmetal
 Pain is predictable  Caused by vasospasm
 Relieved by rest and NTG  Pain even at rest
 Occurs during exertion
 Unstable  Dx:
 Aka pre-infarction angina  ECG: Inverted T-wave
 Sx increased in frequency
Tischemia
 Not relieved by NTG
ANGINA PECTORIS
 Mngt:  NTG:

 R –est  Action: VASODILATOR


 Max dose: 3 tablets
 O –xygen
 Interval: q 5 mins
 N –itroglycerine
 Storage: Amber-colored/ tightly sealed
 A -spirin/Antiplatelets/Anticoagulants bottle
 B –Beta-blockers  SE: Headache/Dizziness
 PATCH: ACW (use gloves)
 C –alcium channel blockers
 Avoid: hairy areas/wounds and abraisions
 Check BP first!
MYOCARDIAL INFARCTION
 Chest pain due to almost complete obstruction of coronary arteries leading
into cardiac cell necrosis/infarction
 Predisposing factor:
 5E’s
 Pain:
 Substernal HEAVINESS (elephant on the chest)
 Duration: >15 mins
 Hallmark: LEVINE’s sign (hand clutching on CHEST)
MYOCARDIAL INFARCTION
 Dx:
 ECG:
 ST-segment elevation (site of INJURY)
 STinjury
 Pathologic Q-wave (denotes OLD MI)
 infarQtion
 T-wave invertion (site of ISCHEMIA)
 Tischemia
MYOCARDIAL INFARCTION
 Dx:
 Cardiac Enzymes
 Tropinin I (early) and T (late)
 Most DEFINITIVE of cardiac damage
 CK-MB

 Cardiac specific, increased later than Troponin and first to decrease


 Myoglobin
 Lactic Dehydrogenase
MYOCARDIAL INFARCTION

 Mngt:
 Morphine (Check VS/antidote: Naloxone)
 Aspirin (antiplatelet)
 Nitrate (vasodilator)
 Anticoagulant (Heparin/Enoxaparin)
 Statins (anticholesterol)
MYOCARDIAL INFARCTION
 Mngt:  Encourage leg exercises
 Thrombolytics  CABG
 Streptokinase  Vessels used:
 t-PA (alteplase)  Internal mammary artery
 SE: Bleeding  Cephalic vein

 Surgical:  Saphenous vein (Longest life)

 Percutaneous Transluminal Coronary  Gastroepipoic artery


Angioplasty (PTCA)  Radial artery
 Avoid vigorous coughing
HEART FAILURE

MARK BILLY L. PERPETUA, MAN RN


HEART FAILURE
 Inability of the heart to PUMP
blood to meet body’s metabolic
demand
 LEFT SIDED
 RIGHT SIDED
 Coughing
 Hepatomegaly
 Hemoptysis
 Edema
 Orthopnea
 Ascites
 Pulmonary congestion
 Distended neck veins
 Paroxysmal Nocturnal Dyspnea
HEART FAILURE
 Dx:  Mngt:
 CXR: cardiomegaly  ACE inhibitors (-pril)
 Echocardiogram: Dec. Ejection fraction  Diuretics (dec. pulmonary congestion)
 CVP: elevated in RSHF  Dilators (dec. preload)
 Diet: Low Salt
 Digoxin
HEART FAILURE
 Digoxin:  Toxicity:
 (+) inotropic – increased the force of  Neuro S/Sx
contraction
 N/V, Anorexia
 (-) chronotropic – decreased HR
 YELLOW HALOS around lights
 (-) dromotropic – changes rhythm
 Normal level: 0.5 – 2 ng/ml  ANTIDOTE: Digitalis Immune Fab
(DIGIBIND)
 Check: Apical pulse (1 full minute)
 HR <60bpm: HOLD  *Check electrolyte: Potassium
level
 (+) vomiting: DO NOT double the dose
 Hypokalemia: potentiates the
effect of digoxin

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