Cardiac Flashcards
What are the intrinsic rates of the heart
SA node 60-100
Atrial cells 55-60
AV node 40-60
Bundle of His 40-45
Bundle branch 40-45
Purkinje fibers 20-40
What are the cardiac cells
Automaticity- generates own electrical impulses
Excitability- irritability and ability to respond to a charge
Conductivity- pass a charge onto next cell
Contractility- ability to shorten and contract
Refractory period
Approx. 0.5ms
Absolute refractory- won’t respond to any stimulus no matter how strong
Relative refractory- the membrane only responds to very strong stimulus and a few secs after absolute where the membrane repolarizes
Polarization of an ECG
P wave- atrial polarization
QRS- ventricular depolarization
T wave- ventricular polarization
U wave (if present)- repolarization of Purkinje fibers
Limb leads
bipolar
White electrode- RA
Red electrode- LL
Black electrode- LA
Green electrode- RL
Chest leads
unipolar
V1- right side of sternum 4th intercostal
V2- left side of sternum 4th intercostal
V3- between V2, V4
V4- 5th intercostal direct below the nipple
V5- between V4, V6
V6- 6th intercostal mid auxiliary line
Baroreceptors
Sense pressure changes
Aortic and carotid receptors and aortic and carotid bodies
Chemoreceptors
Impulses sent via receptors to medulla when excess CO2 or low O2 levels are in the blood
Atherosclerosis
Thickening of the artery wall due to accumulation of fatty tissues
Chronic can be asymptomatic until the blockage impacts blood flow then becomes symptomatic
Acute rupture/ thrombus formation causes acute infarction- no blood flow distal to block
Affects predominantly coronary, renal, aortic, femoral, carotid artery
Types of anginas
Stable, unstable, variant angina
Stable angina
Follows the same pattern for the patient
Lasts 1-5 min and is relieved by rest
When the person is at rest there is enough blood flow to meet sedentary needs but when demands increased and is not met angina occurs
Unstable angina
Same etiology as stable but the pain is more severe and isn’t as easily relieved by meds/ rest
Lasts >15 min and indicative of pre-MI angina
Greater degree of obstruction in coronary arteries leading to an increased risk of imminent MI that could benefit from early treatment and prevention
P wave
precedes QRS, less than 110ms, amplitude <2.5mm
PR interval
normally between 0.12 seconds and 0.20 seconds, shorter= wolff, longer= 1st degree block
QRS complex-
less than 0.12 sec
J point-
QRS ends, and ST segment begins
ST segment
line between QRS and t wave
T wave
asymmetric, less than half the height of QRS and in the same direction, faster downstroke than upstroke
TP segment-
isoelectric line (baseline) that is flat, straight, horizontal that begins at T and ends at P
QT interval-
0.36s- 0.44s
Starlings law
the greater amount of blood volume (preload) into the ventricle of the heart during diastole (the relaxed phase) the greater the amount of blood volume ejected out of the heart during the systolic(contraction phase)
Aplastic anemia
Failure of bone marrow to function causing a loss of stem cells and a decreased number of RBCs, leukocytes, and platelets
Sickel cell anemia
Altered hemoglobin changes to a sickle cell shape and crystalizes, changing the life span to 20 days from 120. The altered shape causes less oxygen to be carried and a risk of thrombi and necrosis
Hemolytic anemia
Premature destruction of RBCs that is inherited of acquired. May not appear as anemia if bone marrow can produce enough RBCs
Polycythemia
Primary: increased production of RBCs in bone marrow for no reason
Secondary: increased RBC secondary to hypoxia (needs more RBCs for o2 carrying capacity)
Hemophilia
Deficiency of clotting factors that can be mild where only bleeding occurs after an accident or severe where bleeding is frequent and spontaneous
Disseminated intravascular coagulation (DIC)
Excessive bleeding and clotting factors that causes unneeded clots and the factors are unavailable during excessive bleeding
Multiple myeloma
Cancer of plasma cells that causes affected plasma cells to rapidly multiply and infiltrate marrow leading to organ death/ failure
Leukemia
Leukocytes multiply uncontrollably in marrow and are released into circulation suppressing production of other cells leading to anemia
Hodgkins’s lymphoma
Involves a single lymph node that spreads to two or more regions on the same side of the diaphragm, then affects lymph nodes on both sides of the diaphragm then involves bones, liver, or lungs
Non-Hodgkins lymphoma
Multiple lymph node involvement through the body that is non organized pattern of widespread metastases that involves intestinal nodes and organs
HIV
Immune deficiency from a virus that affects lymphocytes and suppresses the immune system and attacks t cells leading to low numbers and increases the risk of infections and cancer
Pathway of blood through the heart
Deoxygenated blood -> superior vena cava/ inferior vena cava -> right atrium -> tricuspid valve -> right ventricle -> pulmonary valve -> pulmonary artery -> lungs to collect O2/ dump CO2 -> pulmonary veins -> left atrium -> bicuspid valve -> left ventricle -> aortic valve -> aorta -> body
Sodium potassium pump
It starts in polarization where potassium is inside, and sodium and calcium are outside. Moves to depolarization during a contraction causing the opening of sodium channels to allow sodium inside, calcium also moves inside, and potassium moves outside. Repolarization occurs during a termination of action potential where potassium channels open allowing potassium to leave the cell.
Left ventricular failure
Most commonly damaged during an MI
Happens when the left side of the heart can’t pump blood from the pulmonary vessels so blood backs up behind the left side causing increased pressure in the left atrium and pulmonary veins and serum to be forced from pulmonary capillaries and into alveoli.
Right side heart failure
A result of left sided heart failure where when blood is pumped back into the lungs the right side must work harder to pump blood back into the pulmonary arteries and eventually the right side cannot keep up and fails
Respiratory distress standard
Consider life/limb/function threats like ACS, AMI, dissecting aorta, tension pneumo/ pneumothorax, respiratory disorders, pulmonary edema, pericarditis
Acquire a 12-lead and perform a secondary assessment of the chest for subcutaneous emphysema, accessory muscle use, urticaria, indrawing, shape, symmetry, and tenderness, assess the lungs for decreased air entry and adventitious sounds through auscultation, abdomen per standard, neck for tracheal position and JVD, and extremities for ankle/leg edema
STEMI hospital bypass standard
> 18, have chest pain or equivalent consistent with cardiac ischemia or MI, current episode <12 hours from onset, 12 lead showing a STEMI: 1mm elevation in 2 anatomical leads or 2mm elevation in leads V1-V3 and the paramedic agrees
Contraindications: CTAS 1 w/ unstable airway/ ventilate, 12 lead is consistent with LBBB, ventricular paced or any other STEMI imitator, transport to hospital that performs percutaneous coronary intervention >60 min from pt contact, pt has a complication requiring primary care diversion like mod/sev resp distress or CPAP, hemodynamically unstable, symptomatic SBP is <90mmHg, VSA w/o ROSC
ACP diversion ventilation inadequate despite assistance, hemodynamic instability unresponsive to ACP treatment/ management, VSA w/o ROSC
Oxygen therapy standard
Administer oxygen using a device and flow rate to attempt to maintain oxygen saturation between 92-96 as measured by SPO2 unless specified otherwise. Continuously administer oxygen for pts with CO, cyanide, noxious gas exposure, upper airway burns, scuba-diving related disorders, ongoing cardiopulmonary arrest, complete airway obstruction, sickle cell anemia w/ suspected Vaso-occlusive crisis. Also give oxygen to pts with critical findings like age-specific hypotension, respiratory distress, cyanosis/ ashen colour/ pallor, altered LOC, abnormal pregnancy/labour.
Acute cardiogenic pulmonary edema medical directive
Nitro: >18, HR- 60-159bpm, SBP- normotension
Contraindications: allergy/ sensitivity to nitrates, phosphodiesterase inhibitor use within previous 48 hours, SBP drops by 1/3 or more of initial value after administration
SBP >100-<140, 0.4 mg, 5 min dose interval, max 6 doses
Cardiac ischemia medical directive
ASA: >18, LOA- unaltered, other: able to chew and swallow
Contraindications: allergy/ sensitivity to NSAIDS, no prior use if asthmatic, current active bleed, CVA/TBI in previous 24 hours
ASA: dose- 160-162mg, max dose- 162mg, max # of doses-1
Nitro: >18, LOA- unaltered, HR- 60-159, SBP- normotension, other- prior med hx or iv access obtained
Contraindications: allergy/ sensitivity to nitrates, phosphodiesterase inhibitor use within previous 48 hours, SBP drops by 1/3 or more of initial value after administration, 12 lead compatible with RVI
STEMI- SBP- >100, 0.4mg, dose interval- 5 min, max # of doses- 3
No STEMI- SBP- >100mmhg, dose- 0.4 mg, dose interval- 5 min, max # of doses- 6
Normal sinus rhythm
60-100 bpm
Regular
Present p wave that proceeds qrs
<0.12 qrs width
Sinus bradycardia
<60 bpm
Regular
Present p wave that proceeds qrs
<0.12 qrs width
Sinus tachycardia
> 100bpm
Regular
Present p wave that proceeds qrs
<0.12 qrs width
Sinus arrest
The same as NSR but SA node fails to generate an impulse
Sinus arrhythmia
Slight variation of a sinus rhythm- longer TP segment
SA block
Rate varies
Irregular
Present p waves unless dropped
P:qrs- 1:1
Normal QRS
Wandering atrial pacemaker
Regular
60-100 bpm
Normal qrs
P:qrs- 1:1
P waves present but inconsistent
PAC
Underlying rhythm resets SA node firing and causes a “skipped beat”
QRS looks like it has a friend and they are social distancing from other QRS friends
Supraventricular tachycardia (SVT)
P wave is there but inside T wave
140-280bpm
Regular
Qrs- <0.12
Atrial flutter
250-350 bpm
Regular
Qrs normal
P waves present but saw toothy
P:qrs- 2:1 or more
Atrial fibrillation
No discernable p waves
QRS- innervated but <0.12
Irregularly irregular
Bpm variable
Multifocal atrial tachycardia (MAT)
100-150 bpm
Irregularly irregular
P waves: present but 3 distinct morphologies
QRS: <0.12
Junctional rhythm
40-60 bpm
QRS: 0.12- but no relationship with atrial activity
Regular
P waves: inverted, retrograde/antegrade
Accelerated junctional rhythm
60-100 bpm
Regular
P wave: absent, antegrade/ retrograde
QRS: normal
P:QRS: 1:1 if absent then none
Junctional tachycardia
> 100bpm0- if exceeds 150 SVT may occur
P waves: retrograde
QRS: narrow
PR interval is short
Regular
Premature junctional complex (PJC)
Narrow QRS w preceding p wave or retrograde P wave
Occurs sooner than next beat is expected
First degree heart block
Rate is dependent on underlying rhythm
Regular
Normal p waves
PR interval increases with each beat (>0.20)
2nd degree heart block type 1
Regularly irregular
PRI lengthens until the beat is dropped and it restarts
P:qrs- variable
2nd degree heart block type 2
Irregular or regular
Grouped beats with one dropped beat between the groups
Third degree heart block
<60bpm
Everything sends out its own impulses, so ventricles develop their own
Non conducted p waves
Absence of AV conduction
Idioventricular
20-40 bpm
Regular
Absent p waves
P:QRS- n/a
QRS: >0.12
Accelerated idioventricular
40-100 bpm
Regular
P waves: absent
QRS: >0.12
Monomorphic v tach
Regular
Uniform QRS
Ventricular tachycardia
> 100bpm
QRS: >0.12 and monomorphic
Regular with no variation
P waves: not visualized
Sustained: >30 sec or requires intervention from hemodynamic instability
Unsustained: non sustained: 3 or more consecutive ventricular complexes ending spontaneously in <30 sec
Polymorphic v tach
QRS varies in size and shape
Torsades de pointes
Prolonged QT interval
Type of polymorphic v tach
Can convert to NSR or v fib- notifier of death
Premature ventricular complex (PVC)
Unifocal but occurs earlier than the next expected beat caused by a premature firing of the ventricle
The ventricle is in a refractory state when normal impulse tries to get through so ventricles don’t fire at normal time
V fib
Cardiac death (straighter arctic monkeys’ wave)
Asystole
Flatline
No more heart contracting so generally a confirmation of death
