MEDSURGE (prelims)

heart

pumps blood to lungs for oxygenated blood → back to the heart to be pumped to the body 

RBC

contains hemoglobin (where O2 binds to blood) to be delivered throughout the body

blood vessels

where blood flows 

• arteries = O2+ blood from heart to organs

• veins = O2- blood from organs to heart

• capillaries = where arterioles & venules meet

ANATOMY & PHYSIOLOGY OF HEART

• cone shaped hollow muscular organ in mediastinum between lungs; pumping 60ml/beat or 5L/min 

pericardium

protective covering of heart

3 layers of cardiac muscle

• epicardium - outermost layer 

• myocardium - middle layer

• endocardium - innermost layer

left anterior descending route

• LV, ventricular septum, chordae tendinae, papillary muscle, and RV (lesser extent)

circumflex coronary artery route

• LA, lateral & posterior surfaces of LV, part of interventricular septum, SA node, & AV node 

coronary arteries

supplies O2+ blood to heart muscles

blocked coronary arteries

causes MI (myocardial infarction) or heart attack

automaticity

initiates impulse spontaneously & repetitively

excitability (depolarization)

• responds to stimulus

conductivity

• transmits electrical impulses

contractility

• systole (contractions)

refractoriness

inability to respond until repolarization

SA node

conducts 80-100x/min.

AV node

• conducts 40-80x/min.

Bundle of His

Right & Left bundle branches

Purkinje fibers

conducts 20-40x/min.

preload (SV)

• blood volume distending ventricles at end of diastole before contraction

afterload (SV)

• resistance ventricles overcome to eject blood

VASCULAR SYSTEM FUNCTIONS

• provides conduits for blood to travel from heart to nourish body tissues

HISTORY TAKING

• to obtain information about client’s risk factors & symptoms of CVD

PHYSICAL ASSESSMENT (MAJOR SYMPTOMS OF CVD)

• pain / discomfort

• dyspnea on exertion / sitting (orthopnea) / when sleeping (paroxysmal nocturnal dyspnea)

• fatigue 

• palpitations

• weight gain - best indicator of edema (fluid retains)

• syncope - transient loss of consciousness due to low cerebral perfusion

• extremity pain due to ischemia & decreased venous return

PRECORDIUM (AREA OVER HEART)

• inspecting precordium → apical impulse

• palpation

• percussion

• auscultation = ab/normal heart sounds

S1 (closure of AV valves)

low pitch & long; best heard at apex of heart by palpating carotid pulse while listening

murmurs

• reflection of turbulence of blood flow through normal / abnormal valves

pericardial friction rub

sign of inflammation, infection, or infiltration

serum markers of myocardial damage (cardiac markers) 

• troponin T - less than 0.2ng/ml

• troponin I - less than 0.03ng/ml 

• creatinine kinase 

• myoglobin - less than 90mcg/L

C-reactive protein

should be less than 1.0mg/dl

blood coagulation tests

evaluates ability of blood to clot

chest radiography

determines size, silhouette, & position of heart

angiography (arteriography)

• invasive procedure involving fluoroscopy & contrast media

coronary arteriography (same technique for left heart catheterization) - complications

• MI, stroke, arterial bleeding, thromboembolism, lethal dysrhythmias, & death 

Intravascular ultrasonography (IVUS)

• catheter with miniature transducer (soundwaves) at distal tip to visualize coronary arteries

RADIOGRAPHIC TESTS : ELECTROCARDIOGRAPHY (ECG/EKG)

• graphically measures & records electrical current traveling through conduction system by heart 

• measured by electrodes placed on skin & connected to amplifier & strip chart recorder 

• standard 12-lead ECG (measures electrical current from 12 different views or leads)

ECG strip

• small block measuring 1 mm in height & width; standard speed = 25mm/sec

P wave (representation)

atrial depolarization

PR segment (representation)

• time required for impulse to travel through AV node (delayed) → Bundle of His → R&L bundle branches → Purkinje fiber network before ventricular depolarization

PR interval (representation)

• time required for atrial depolarization and impulse to travel; measured from beginning of P wave to end of PR segment (0.12-0.20 seconds)

QRS complex

• ventricular depolarization; measured from QR wave to S wave (0.04-0.10 seconds)

ST segment

• early ventricular depolarization

T wave

• ventricular repolarization

U wave

• late ventricular repolarization

QT interval

• total time required for ventricular depolarization & repolarization; measured by beginning of QRS complex to end of T wave

NORMAL HEART RHYTHM CHARACTERISTICS

• HR 60-100 BPM

• P waves before QRS complex

• PR interval (0.12-0.20 seconds)

• QRS complex (0.04-0.10 seconds)

• conduction forward & cyclical

• rhythm regular with no delay

echocardiography

• ultrasound waves to assess cardiac structure & mobility at valves

hemodynamic monitoring

• assessed volume & blood pressure in heart and vascular system by surgically inserted catheter

direct BP monitoring

• uses radial, brachial, or femoral artery; catheter tip contains sensor measuring & transmitting fluid pressure to transducer

CVP / central venous pressure monitoring

• pressure by venous blood in right atrium (normally, 2-7 mmHg)

HEART FAILURE

• acute / chronic clinical syndrome from any structural / functional cardiac disorder impairing heart’s ability to fill / eject blood throughout body

RA&RV

failure leads to venous congestion of organs (O2- is received, not O2+) 

symptoms : 

peripheral venous congestion = RA doesn’t receive all the blood from organs → increased jugular vein pressure (JVP) = hepatomegaly (large liver, but size doesn’t affect its function), caused by cardiac cirrhosis (O2- backflows to the lungs)

RA&RV

failure due to increased pulmonary vascular pressure

symptoms : 

pulmonary circulation = LV doesn’t function so RV doesn’t function as well increasing the pressure in pulmonary circulation = chronic lung disease (cor pulmonale)

LA/LV

pulmonary vein returns blood from lungs → failure leads to pulmonary congestion and pressure (lungs = most affected organ)

symptoms : 

increased pulmonary venous pressure leading to pulmonary congestion (O2+ doesn’t come back to LA causing systemic resistance)

LA/LV +

supplies blood to body organs → failure leads to low organ perfusion and hypoxia 

RSHF

dyspnea not as prominent = due to pulmonary congestion is on the left side

hepatosplenomegaly = due to backflow of blood

distended abdomen = due to ascites

weight gain = due to edema

history & physical exam

• fluid status (I/O and HCT = measures plasma)

• perfusion status (PO2)

• BP (high/low)

• weight (if +edema)

• temperature of extremities (cool clammy = increased venous return)

NON-INVASIVE CARDIAC TESTING : ECHOCARDIOGRAM / 2D ECHO

• gold standard for diagnosing & ongoing evaluation of patient with heart failure 

• determines LV/RV size & function, wall motion (wall thickness), valvular function (+/- backflow), diastolic function, presence / absence of pericardial or intracardiac masses abnormalities, and evaluate intracardiac filling pressures

• estimate of LVEF (left ventricular ejection fraction) - to determine if patient has reduced ejection fraction (less than 40%)

NON-INVASIVE CARDIAC TESTING : CHEST X-RAY

• to assess for cardiomegaly, pulmonary congestion = may show cardiac chamber enlargement (to make way for cardiomegaly), increased pulmonary venous pressure, interstitial or alveolar edema, valvular or pericardial calcification (rigid valves due to murmur/backflow from ventricles to aorta), or co-existing thoracic diseases

B-type natriuretic peptide (BNP)

• BNP & N-terminal pro BNP levels to evaluate patients with dyspnea for heart failure

liver function tests

• elevated transaminases (ALT&AST)  & LDH (lactate dehydrogenase) and total bilirubin levels may be present due to liver congestion

arterial blood gas

• altered oxygenation & acid-base balance may occur due to decreased perfusion / fluid overload

INVASIVE CARDIAC TESTING

• left sided catheterization

• coronary angiography

• endomyocardial biopsy

• hemodynamic monitoring (elevated filling pressures, hypoperfusion, and altered vascular tone)

fluid volume excess

• diuretics = increases urine

• sodium restriction = to restrict water

decreased cardiac output

• (+) inotropes = digoxin & digitoxin

• vasodilators = pressins

• temporary/permanent pace makers for sinus rhythm

• control tachycardia by decreasing activity & stress

SA node (sinoatrial)

where electrical impulses begin

AV node (atrioventricular)

delayed to complete emptying

NORMAL SINUS RHYTHM (NSR)

• rhythm regular 

• rate 60-100 bpm

• P waves uniform & upright

• P & QRS ratio 1:1

• PR interval 0.12-0.20 seconds

• QRS complex narrow & less than 0.12

if there’s P wave = QRS complex

• to get the BPM = 5 x 0.2 (duration per p wave) = 1 second x 6 (number of p waves) = 6 x 10 (to get a full minute) = 60 bpm

SINUS ARRHYTHMIA

• irregular rhythm & HR increases gradually with inspiration and decreases with expiration (HR = 60-100 bpm)

• P waves uniform & upright

• P & QRS ratio 1:1

• PR interval 0.12-0.20 seconds

• QRS complex narrow & less than 0.12

sinus arrhythmia etiology

• may be a result of reflex enhancement of sympathetic tone during inspiration and parasympathetic tone with expiration 

SINUS BRADYCARDIA

• rhythm originates at SA node but decreased rate (less 60 bpm) for atria and ventricles

• rhythm regular 

• rate less than 60 bpm

• P waves uniform & upright

• P & QRS ratio 1:1

• PR interval 0.12-0.20 seconds

• QRS complex narrow & less than 0.12

atropine sulfate (sinus bradycardia)

• increases BP as sinus bradycardia can cause vagal stimulation which lowers BP

SINUS TACHYCARDIA

• rhythm originates at SA node but increased rate (100+ bpm) for atria and ventricles

• rhythm regular 

• rate 100+ bpm

• P waves uniform & upright

• P & QRS ratio 1:1

• PR interval 0.12-0.20 seconds

• QRS complex narrow & less than 0.12

SUPRAVENTRICULAR TACHYCARDIA (SVT)

• rapid dysrhythmia originating above ventricles in atria or AV junction; atrial & ventricular rate of 120+ bpm (150-250 bpm)

• rhythm usually very regular but beats are abnormal

ATRIAL FLUTTER

• rhythm regular / irregular

• rate 250-350 bpm (atrial); ventricular rate slower

• P waves not observable but saw-toothed flutter waves

• PR interval not measurable

• QRS complex normal (0.06-0.10 seconds)

ATRIAL FIBRILLATION

• rhythm irregular 

• rate 350+ bpm (atrial); ventricular rate slow / normal / fast

• P waves absent (erratic waves)

• PR interval absent

• QRS complex normal but may widen if conduction delays

1ST DEGREE ATRIOVENTRICULAR BLOCK (DELAY)

• conduction delay to ventricles; usually asymptomatic & not indicated for tx.

• rhythm regular 

• rate 60-100 bpm but depends on rhythm

• P waves uniform & upright

• P & QRS ratio 1:1

• PR interval 0.20+ seconds 

• QRS complex narrow & less than 0.12 unless conduction delay

• close observation of hemodynamic status 

2ND DEGREE ATRIOVENTRICULAR BLOCK (DELAY)

• not all impulses from atria conducts to ventricles; SA node electrifies at regular intervals but some impulses are blocked at AV junction

• usually asymptomatic

2nd degree AVB types

• Mobitz 1 / Wenckebach and Mobitz 2 (more serious)

• Mobitz 1 / Wenckebach 

• rhythm regularly irregular (repeating patterns, dropped QRS complex)

• rate atrial rate greater than ventricular due to dropped QRS

• P waves uniform & upright

• P & QRS ratio some P waves doesn’t have QRS complex

• PR interval lengthens with cycles until P wave isn’t followed by QRS complex

• QRS complex narrow & less than 0.12

Mobitz 2 (less common)

• more serious as it may progress to 3rd degree AVB & bradycardic in nature; block occurs below bundle of His in bundle branches

• rhythm regular but may be irregular for ventricular rhythm

• rate atrial rate greater than ventricular due to dropped QRS

• P waves uniform & upright

• P & QRS ratio some P waves doesn’t have QRS complex

• PR interval normal / prolonged & constant for conducted P waves

• QRS complex may be narrow & normal / widened due to coexisting bundle branch block

3RD DEGREE ATRIOVENTRICULAR BLOCK (COMPLETE HEART BLOCK) / AV DISSOCIATION

no impulses from atria are conducted through AV junction to ventricles; they beat independently

temporary block

• acute myocardial infarction: (inferior MI) 

• temporary block medications - beta blockers, calcium channel blockers (diltiazem) or digoxin

• inflammation = myocarditis, rheumatic fever or Lupus

• infections = toxoplasmosis (acquired by cat feces)

• permanent block 

• acute myocardial infarction (anterior MI)

• degeneration of conduction system due to : advanced age or cardiac calcification of mitral or aortic valve 

• iatrogenic damage: due to arrhythmia ablation at the site of AV Junction or valve surgery (Tricuspid valve replacement)

• caused by medical managements

AV NURSING PRIORITIES

• decreased cardiac output R/T failure of heart to pump blood to meet metabolic needs manifested by hypotension

• acute chest pain R/T decreased blood flow to myocardium through coronary arteries

• ineffective tissue perfusion R/T decreased cardiac output manifested by syncope 

• fatigue R/T increased hypoxic tissue and slowed removal of metabolic wastes 

BUNDLE BRANCH BLOCK

type of IV conduction block; conduction delay in 1 of 2 main bundle branches, unblocked bundle branch conducts normally then depolarization spreads from first ventricle (cell-cell) to second ventricle instead of both ventricles being depolarized simultaneously

BBB (bundle branch block) etiology

• may be permanent conduction disorder from congenital heart disease, rheumatic heart disease, cardiomyopathy, severe aortic stenosis, or others / temporary which may occur after acute conditions like MI / heart failure

PREMATURE VENTRICULAR CONTRACTIONS (PVC)

• occurs earlier than expected normal QRS & wider; bizarre QRS morphology and preceding P wave is absent

VENTRICULAR TACHYCARDIA

• 120-320 bpm and can lead to ventricular fibrillation

monomorphic

ventricular node fires the impulse

polymorphic

• different nodes fires the signal 

VENTRICULAR FIBRILLATION

• rhythm irregular & patient unconscious since there’s no cardiac output

rate 300+ disorganized

• causes ventricles to quiver than contract in rhythm

VENTRICULAR ASYSTOLE / CARDIAC STANDSTILL

• absent electrical activity & no ventricular activity = no QRS complex, ventricular contraction, and cardiac output

PULSELESS ELECTRICAL ACTIVITY

• clinical situation where organized electrical activity is present but patient is pulseless due to absent / inadequate mechanical activity of heart to fill or contract 

IV KCL

to replenish potassium; do not push as it burns the veins & can cause death (this is given by side drip or infusion pump)

DISTURBANCES IN OXYGENATION

• Infectious Disorders = Pericarditis, Myocarditis, Endocarditis, RHD 

• Coronary Artery Disease = Atherosclerosis, Angina pectoris, & Myocardial infarction 

• Congestive Heart Failure 

• Pulmonary edema 

• Arrhythmias

CHRONIC CONSTRICTIVE PERICARDITIS (HEART BEING CHOKED)

• chronic pericardial inflammation causes fibrous thickening of the pericardium → pressure builds up in heart = rigid pericardium where heart can’t expand nor contract → inadequate ventricular filling = low cardiac output which activates RAAS = heart failure

MYOCARDITIS

due to inflammation = abnormal function