Synthesis Midterm 2

Systole

contraction

diastole

relaxation

atrial systole

blood moves into the atria and contracts 

atrial diastole 

blood enters right atrium, fills and distends 

left atrium recieves blood from pulmonary veins 

ventricular contraction

ventricles fill with blood and begin their own contraction, valves prevent blood flow

ventricular relaxation

coronary arteries nourish themselves and atria begin to fill + passive ventricular filling

SA node

initiates own electrical impulse

AV node

collects impulse and moves down the bundle of his, branches, and purkinje fibres

positive chronotropic effect 

increase HR

negative chronotropic effect

decrease HR

positive inotropic effect

increase myocardial contractility

negative inotropic effect

decrease myocardial contractility

positive domotropic effect 

increase in AV conduction velocity 

negative dromotropic effect

decrease in AV conduction velocity

pericardium

• tough outer layer

• serous pericardium contains serous fluid

myocardium

thick, muscular middle layer, responsible for pumping action

epicardium

• visceral layer of serous pericardium

• external layer of heart containing capillaries, nerve fibers, fat

tricuspid valve

• between right atrium and right ventricle

• 3 leaflets

mitral (bicuspid) valve

lies between LEFT atrium and ventricle

2 leaflets 

what are the 2 semilunar valves

• pulmonic valve

• aortic valve

signs and symptoms of decreased cardiac output

• acute changes in BP, mental status

• Cold, clammy skin

• colour changes

• crackles

• dyspnea

• dysrhythmias

• fatigue

• orthopnea

• restlessness

what is the primary pacemaker of the heart 

SA node 

atrial kick provides ____ of CO from atrial contraction

10-30%

intrinsic rate of SA node

60-100 bpm

how are impulses spread to AV node from SA node

internodal pathways 

intrinsic rate in bundle of his

40-60 bpm

intrinsic rate in purkinje fibres

20-40 bpm

small box on ECG = ?

0.04 seconds

large box on ECG = ?

0.20 seconds

what does the P wave represent

• activation of SA node

• atrial depolarization

P wave length

less than 0.11 seconds (3 boxes)

QRS interval meaning

ventricular depolarization

QRS interval length and characteristics

0.11 seconds or less 

Q characteristics 

• less than 0.04 seconds 

• less than 1/3 height of R wave

ST segment

end of S to beginning of T

PR interval

start of P to Start of Q wave

PR interval length 

0.12-0.20 seconds

QT interval duration 

0.40 - 0.45 seconds 

what is used to determine ventricular rate and regularity

R-R interval

what is used to determine atrial rate and regularity

P-P interval

steps in assessing EKGs

• assess rhythmicity

• assess rate 

• identify and examine waveforms 

• assess intervals (PR, QRS, QT) and examine ST segments

• interpret rhythm 

severe sinus bradycardia

rate less than 40 bpm

normal reasons for sinus brady

• sleep

• athletes

• rest

medications causing bradycardia 

• beta blockers 

• calcium channel blockers 

• digoxin

• amiodarone 

abnormal reasons for brady

• dysrhythmias (MI)

• high or low potassium

• hypoxia

• increased ICP (cushings triad)

• hypothyroid

• vagal stimulation

symptoms for sinus brady

• hypotension

• SOB

• fatigue

• chest pain

• clammy

treatment for symptomatic brady 

• pulse oximeter+ supplamental oxygen

• IV access 

• 12 lead ECG

• hold meds

• ATROPINE BUT MUST BE MONITORED AS CAN OVERTREAT

causes for sinus tachy

• MI

• stimulants (caffeine, nicotine)

• dehydration

• Exercise

• Emotions (fear, anxiety)

• hyperthyroid

• heart failure

• pain

• sympathetic stimulation

medications causing sinus tachy

• epinephrine

• atropine

• dopamine

• ventolin

treating sinus tachy

• depends on underlying cause 

• fluid replacement 

• pain relief 

• removal of meds or substances 

• reduce fever or anxiety 

Atrial fibrillation

• occurs due to altered automacity

• irritable sites in atria fire rapidly and therefore quiver

what does atrial fibrillation result in

• ineffectual atrial contraction

• decreased SV and CO

• loss of atrial kick

recognizing a-fib on ECG

• PR not measurable (P waves not present)

• QRS <0.10 seconds 

conditions associated with A fib

• ischemic heart disease

• age

• cardiomyopathy

• CHF

• pericarditis

• PE

• Diabetes

• Hypoxia

• Hypokalemia

• Hyperthyroidism

major associated risks with A fib

• increased stroke risk

• Pt loses atrial kick

A fib treatment

“O MI”

• oxygen 

• monitor digoxin levels 

• IV - amnioderone, metoprolol, bolus, ditiazem

• 12 lead ECG, tele, labs 

treatment of A fib if rapid rate and serious clinical manifestations

synchronized cardioversion BUT not if in a fib for longer than 48 hours

premature ventricular complexes (PVC)

• arise from irritable focus within ventricle

• occurs earlier than next expected sinus beat

PVC on ECG

• QRS >0.12 seconds - “wide and bizarre”

• T wave in opposite direction of QRS complex

3 sequential PVCs

runs or bursts

bigeminal PVCs

every other beat is a PVC

trigeminal PVCs

every 3rd beat is a PVC

quadrigeminal PVC

every 4th beat is a PVC

medications causing PVCs

• sympathomimetics — ventolin

• cyclic antidepressants

• phenothiazines

causes of PVCs

• age

• hypoxia

• stress

• exercise

• digitalis toxicity

• acid-base or electrolyte imbalance

• MI

• ACS

• stimulants

patients with PVCs may complain of… 

• palpitations 

• racing heart 

• skipped beats 

• chest or neck discomfort 

ventricular tachycardia

3 or more PVCs occur in a row at a rate of more than 100 BPM (typically 160)

v tach on ECG

regular, wide, bizarre

causes of v tach 

• ACS

• cardiomyopathy

• tricyclic antidepressant OD

• digitalis toxicity 

• valvular heart disease 

• cocaine abuse 

• mitral valve prolapse 

• acid-base or electrolyte imbalance 

• trauma

clinical manifestations of V tach

• occurs with or without a pulse

• monomorphic VT can degernate to polymorphic VT or V fib

• syncope or near-syncope from abtupt onset

• chest pain, hypoxia, SOB, alternate LOC

V tach with pulse treatment

• airway and oxygen

• BP

• IV access and meds depending on narrow (adenosine) or wide (adenosine or amioderone) complexes

V tach poor perfusion with pulse treatment 

low bp, altered mental status, shock, heart failure

synchronize cardioaversion immediately/amioderone

pulseless v tach treatment

defibrillation followed by medicatiosn

synchronized cardioversion

• patient with pulse who show signs of lower hemodynamic instability

• 100 jouls

defibrillation

• for pulseless VF, VT, higher energy delivered asynchronously

• 320-350 jouls

ventricular fibrillation 

• chaotic rhythm beginning in the ventricles 

• no organized depolarization of the ventricles 

V fib causes

• increase SNS activity

• vagal stimulation

• electrolyte imbalance

• antiarrythmics

• hypertrophy

• ACS

• heart failure

• environmental factors

V fib treatment

• CPR and defibrillator

• tracheal intubation

• IV access

indications for defibrillation 

• pulseless VT

• V fib 

Heart failure

the heart is too weak to pump efficiently and therefore cannot provide proper cardiac output to maintain the body’s metabolic needs

“FAILURE” - F

fatty heart valves — stenosis, regurgitation, infected heart

“FAILURE” - A

arrhythmias - A fib or tachycardia 

“FAILURE” - I

infarction 

“FAILURE” - L

lineage - congential, fam hx

“FAILURE” - U

uncontrolled HTN

“FAILURE” — R

recreational drug use 

“FAILURE” — E

evaders — viruses or infections

risk factors for heart failure

• smoking

• obesity

• alcohol

• substance use

left ventricular systolic dysfunction 

• issues with squeezing phase 

• low EF <40%

• less circulation to tissues and backs up into the lungs 

• echo, catheterizarion, nuclear stress test 

left ventricular diastolic dysfunction

• ventricle too stiff to allow for normal filling BUT contracts normally

• pulmonary symptoms — crackles, SOB, orthopnea

• can lead to right sided heart failure

right sided heart failure

blood backs up into vena cavas and out through peripheral area

• caused by left sided HF, cor pulmonale, HTN, COPD

Clinical manifestations of right HF

“swelling:

• swellings of hands, legs, liver

• weight gain

• edema (pitting)

• large neck vein (JVD)

• lethargic 

• irregular HR (a fib)

• nocturia

• girth (abdomen increased in size, ascites)

Clinical manifestations of left HF

“Drowning”

• dyspnea

• rales (crackles)

• orthopnea 

• weakness 

• nocrtunal paroxysmal dyspnea 

• increased HR 

• nagging cough

• gaining weight (2-3 lb/day)

Dx heart failure

• BNP (300-900+)

• cxr

• echo

• HRT cath

• nuclear stress test

Nursing interventions heart failure

• assess meds (HR, BP, volume)

• labs (k+, BUN, creatinine, digoxin, BNP, troponin)

• fluid restriction diet

• elevate legs and HOB

about how much sodium can a person with HF have

no more than 2-3 G per day

how much fluid can a person in HF have

no more than around 2L a day

what weight is important for patients in HF

• 2-3 lbs/day

• 5 lbs per week

Meds for HF

• ACEs and ARBs

• loop or potassium sparing diuretics 

• beta blockers 

• anticoagulants 

• vasodilations 

• digoxin

Ace inhibitors

• “-pril”

• first line

• vasodilation, decresed BP, kidney excretes Na

• side effecrs: increased potassium, nagging cough