Finals Studying Flashcards
(116 cards)
1
Q
What are the 12 causes of PEA?
A
6 h's: hyperkalemia hypoxia hypothermia hydrogen ion excess (acidosis) hypovolemia hypoglycemia 6 t's: tamponnade tension pneumo thrombosis (pe) thrombosis (MI) toxins trauma
2
Q
What is the action potential cycle?
A
Phase 4 - polarized - resting membrane potential
Phase 0 - depolarization - Sodium inside
Phase 1 - early repolarization - Potassium out
Phase 2 - plateau phase - Calcium moves in
Phase 3 - rapid repolarization
3
Q
What are the qualities of cardiac cells?
A
Automaticity - ability to generate their own impulses
Rhythmicity - regular impulse generation
Conductivity - ability to transmit impulses to adjacent cells
Contractility - ability to respond to an impulse by contracting
Refractory Period - period of relaxation with no response to stimulation.
4
Q
Cardiac Output
A
The volume of blood pumped in one minute.
SV*HR=CO
5
Q
Stroke Volume
A
The amount pumped by one ventricle in one contraction.
6
Q
Starlings Law
A
The more the muscle fibres are stretched the greater their force of contraction. (Increased preload=pumping harder)
7
Q
How much can the heart stretch to accomodate?
A
Fully stretched, the heart can pump up to 5x its normal volume.
8
Q
What is polarization?
A
Relaxation
9
Q
What is depolarization?
A
Contraction
10
Q
What does the QRS complex represent?
A
Depolarization/contraction of the ventricles
11
Q
How many little boxes fit into one big box on ecg paper?
A
5
12
Q
How much time does each little box represent?
A
0.04 seconds
13
Q
How much time does each big box represent?
A
0.2 second (5*0.04=0.2)
14
Q
How long should the PRI be?
A
Less than 0.2, greater than 0.12.
15
Q
How wide should the QRS be?
A
Less than 0.12
16
Q
What are the 5 steps to reading an ecg?
A
Is the QRS wide or narrow? ID P waves and measure PRI. Determine relationship of P waves with the QRS. Determine rhythm regularity. Measure HR.
17
Q
When is the sequence method of HR determination used?
A
When the rhythm is regular and less than 6 seconds long.
18
Q
What are the numbers in the sequence method of determining HR?
A
300, 150, 100, 75, 60, 50, 43, 38, 33
19
Q
If the HR is between 2 numbers in the sequence method, how do you determine what it is?
A
Add the number before and after, then divide by 2.
20
Q
What is PSVT?
A
Paroxysmal Supraventricular Tachycardia
Runs of SVT that stop and start suddenly.
21
Q
What is MAT?
A
Multifocal Atrial Tachycardia - p waves that are arising from different locations in the atria.
22
Q
SA node pacemaker setting?
A
60-100
23
Q
Atrial cells pacemaker setting?
A
55-60
24
Q
AV node pacemaker setting?
A
45-50
25
Bundle of His and Bundle Branch pacemaker settings?
40-45
26
Purkinje fibres pacemaker settings?
35-40
27
Myocardial cells pacemaker settings?
30-35
28
If you're unsure whether a strip is showing fine v-fib or asystole, should you shock the pt?
Yes, better to err on the side of caution and shock if it could be fine v-fib instead of asystole.
29
What order are the 12 lead views in (which ones are contiguous)?
```
From right to left, ISAL:
Inferior
Septal
Anterior
Lateral
```
30
What are thebesian veins?
Small vessels arising directly from the ventricles - assist oxygenation of the heart.
31
What is the first thing you should give for ischemic chest pain?
ASA (have to do a 12 lead in order to give nitro)
32
Once a STEMI is ID'd, what is the first thing you should do?
Put on defib pads to prepare in case they code.
33
If QRS is greater than 0.12, what is going on?
A bundle branch block of some kind, either right or left.
34
If 12 lead is non-diagnostic, but pt is still experiencing chest pain, what do you do?
Still assess for ASA and nitro, go to ER CTAS 2, just no defib pads. Do 3 12-leads if non-diagnostic.
35
What tx can we do for hyperkalemia?
High dose ventolin (double our dose of salbutamol), which pushes calcium out of cells. Must patch to BHP to be able to do this.
36
Inotropic
Affects contraction
37
Dromotropic
Affects conduction
38
Chronotroic
Affects rate
39
Atherosclerosis
Thickening of blood vessel wall from accumulation of fatty material.
Can cause CVAs, angina, kidney problems, etc.
40
Angina Pectoris
AKA chest pain
Occurs when there's a defficiency of o2 for the heart muscle. Can occur when the heart is working harder than usual and needs more o2 or when blood supply to the myocardium is impaired.
41
Stable Angina
Predictable pain, location, severity, etc
Insufficient o2 supply - anaerobic metabolism and accumulation of lactic acid and co2
Typically lasts 1-5 mins and is relieved by rest.
42
Unstable Angina
Caused by insufficient o2 supply causing anaerobic metabolism and accumulation of lactic acid still, but with more severe pain than stable angina, not easily relieved by rest or meds.
Typically lasts more than 15 minutes.
Often indicative of pre-MI angina.
Doesn't follow same pattern as their usual angina.
43
Angina Symptoms
Substernal chest pain, usually triggered by physical or emotional stress.
Tightness or pressure in the chest that often radiates into the neck or left arm.
Pallor, diaphoresis, and nausea.
Lasts anywhere from a few seconds to much longer.
44
Angina Tx?
```
Full assessment with detailed questioning.
Assess need for o2
ASA
12 lead
Nitro
IV therapy.
Vitals every 5 minutes minimum.
```
45
Acute Coronary Syndrome
Results from prolonged cardiac disorder causing myocardial ischemia or infarction. (STEMI Non-STEMI, and unstable angina)
Typically caused by a rupture of the plaque in the arteries and subsequent thrombosis of the coronary artery.
Plaque builds up with a fibrous cap over it, and when that cap ruptures a blood clot forms attached to the plaque, which blocks the artery.
46
How do you manage Acute Coronary Syndrome pre-hospital?
Be calming, place pt at rest.
determine presence of possible acs
opqrst
care must begin immediately to limit the size of the infarct
Perform a 12 lead, assess for ASA and o2. After 12-lead is acquired, consider nitro and do your secondary. If STEMI positive, rapid transport and defib pads.
Only administer o2 if necessary.
47
ASA pharmacology
Platelet aggregating inhibitor (anticlotting)
Administered orally (chewed)
Significantly decreases mortality with MI.
48
Nitro pharmacology
Vasodilator - can relieve vasospasm and improve blood flow, relaxes peripheral vasculature and may reduce afterload to reduce the cardiac workload.
Typically won't relieve MI pain as it has little to no effect on the blockage.
Doesn't reduce mortality - not life saving.
Administered sublingually.
Side effects: hypotension, headache (if pt has used nitro properly before calling EMS, they should have a headache)
NEVER use in pts with RVI.
49
Dissecting Aortic Aneurysm
Result of degenerative changes in the middle layer of the aorta, leads to "ungluing" of inner layer of aorta, which tears, then begins dissecting as blood is pumped into the unnatural space between the inner and middle layer, which stretches and weakens the vessel. If it dissects into the valves it may prevent the valve from closing and results in blood entering back into the left ventricle during systole.
Main concern - could rupture.
50
S+S of Dissecting Aortic Aneurysm
Middle aged+, with chronic htn.
Main complaint is chest pain, often described as the worst pain they've ever felt, ripping or tearing, like a knife.
Pain usually comes on suddenly, located in the anterior chest or back, between the shoulder blades, can radiate into the back or abdomen.
Difference in BP between the 2 arms due to disruption of blood flow through the artery.
51
Management of Aortic Dissection
```
Calm and reassure pt.
O2
IV
Cardiac Monitor
Transport with no delay, can do nothing prehospital to stabilize them, they need the ER NOW.
```
52
Conditions to take ASA
Age greater than or equal to 18 years old
Unaltered LOA
Able to chew and swallow
53
Contraindications for ASA
Allergy or sensitivity to NSAIDS
If asthmatic, no prior use of ASA
Current active bleeding
CVA or TBI in the previous 24 hours
54
ASA dosing?
160-162mg PO, 1 dose max.
55
Nitro Conditions?
Age greater than or equal to 18 years old.
Unaltered LOA
HR 60-159
Normotensive
Prior use of nitro or IV access obtained.
56
Nitro Contraindications?
Allergy or sensitivity to nitro
Phosphodiesterase inhibitor use in the last 48 hours
SBP drops by more than 1/3 or more of its initial value after nitro is administered.
12 lead ecg compatible with Right Ventricular MI.
57
Non-STEMI Nitro dosing?
SBP of at least 100mmhg, 0.3 or 0.4 mg every 5 minutes, max 6 doses. Sublingual.
Note - start vitals at the 3 minute mark after dosing, so that at 5 minutes you are able to administer more nitro if indicated.
58
Aorta
Exits the left ventricle, largest artery in the body.
| Right and left coronary artery emerge from the aorta close to where it exits the ventricle.
59
Name the coronary arteries.
Right coronary artery,
Left coronary artery, which divides into the
Circumflex artery (which wraps around the back of the heart) and
Left anterior descending artery
60
What are the deadly dozen chest injuries?
```
9 primary:
- Flail chest
- Open pneumo
- Massive hemothorax
- Tension pneumo
- Cardiac Tamponnade
- Airway obstruction
- Tracheal or Bronchial injury
- Diaphragmatic tears
3 Secondary:
- Myocardial contusion
- Aortic rupture
- Pulmonary contusion.
```
61
What is flail chest?
Two or more adjacent ribs fractured in two or more places.
| Underlying pulmonary contusion is common with flail segments.
62
Do we stop RTS to apply an Asherman seal?
No, just get someone to put a hand on the injury, keep going and address it after RTS is done.
63
How to tx rib #'s?
Give supplementary o2, don't coach to breath more deeply, that would hurt. They're already self-splinting by not breathing too deeply, just get them to hospital.
Remember that there could be underlying injuries, keep high suspicion for threats to breathing caused by the #.
64
Sternal #s
1/4 of these pts will die. Pt will complain of anterior chest pain, look for deformity, flail sternum, and ecg changes. There's a risk of myocardial contusion. Supportive tx only, get moving to ER.
65
Simple Pneumothorax
Accumulation of gas in pleural cavity, caused by direct thoracic injuries or barotrauma. Presentation depends on size of pneumothorax.
A small pneumo may cause only mild dyspnea and pleuritic chest pain. Breath sounds may be diminished.
Large pneumo will produce increased respiratory compromise - absent breath sounds, hypoxia, tachycardia, cyanosis.
Simple pneumos can also be spontaneous in tall skinny males - if no trauma, but presenting with s+s. May also have happened to them before, ask hx.
66
Simple pneumo tx?
ABCs, deliver high concentration o2. Keep reassessing to find out if it's progressing to a tension pneumo.
67
Tension pneumothorax
Life-threatening condition that results from continued air accumulation w/in the intrapleural space. Less than 50% inflation.
May occur from open thoracic injury, blunt trauma, barotrauma, or shearing forces.
S+S:
Increasing dyspnea,
absent breath sounds on affected side,
tachycardia,
JVD (a late sign),
tracheal deviation (a late sign),
hypotension due to blood not being able to return to the heart from the venous system.
68
Tx of tension pneumo?
High flow o2, rapid transport, ALS backup.
69
Massive Hemothorax
```
Blood fills the potential space between the parietal and visceral pleura. Each lung can hold up to 3000 ml of blood. Occurs in approx 25% of chest trauma pts.
S+S:
lack of jvd,
may have trach deviation if massive,
hemoptysis,
dull to percussion.
```
70
Massive hemothorax tx?
Supportive care for abcs, high flow o2, tx for shock.
71
Pulmonary contusion
Damage to alveoli and capillaries from compression of lung tissue against the chest wall, results in reduced delivery of oxygen across the alveolar-capillary membrane.
May have hemoptysis. Look for signs of overlying injury like crepitus, tenderness, or contusions.
72
Pulmonary contusion tx?
Airway management, supportive care.
73
What is Beck's Triad?
Muffled heart tones
Hypotension
JVD
74
What does Becks Triad mean?
The pt likely has pericardial tamponade.
75
Pericardial tamponade tx?
O2, rapid transport to trauma centre for surgery.
76
Myocardial Contusion
Blunt cardiac injury caused by the heart colliding with the sternum, leading to local tissue contusion, hemorrhage, edema, and cellular damage. May lead to dysrhythmias.
S+S:
Pt complains of sharp, retrosternal chest pain.
Lung sounds may reveal crackles, due to left ventricular dysfunction.
ECG changes may occur - sinus tach, atrial fib, atrial flutter, pac's/pvc's
77
Myocardial contusion management?
Fluid therapy
abcs, freq reassessment of vital signs
monitor cardiac rhythm.
78
Myocardial rupture
acute perforation of the ventricles, atria, septum, chordae, muscles, or valves, caused by severe blunt force compression.
S+S:
may present with acute pulmonary edema or signs of cardiac tamponade.
79
Myocardial rupture management
Supportive care, rapid transport to a trauma centre.
80
Commotio Cordis
Immediate cardiac arrest caused by blunt trauma during the heart's repolarization period (the beginning of the t wave).
Pt appears in ventricular fibrillation and respond well to defibrillation if performed quickly.
81
What are cheyene-stokes respirations?
Periodic breathing, periods of apnea.
82
What are signs and symptoms of left sided heart failure?
- restlessness
- agitation
- confusion
- severe SOB
- tachypnea
- abnormally high or low bp
- crackles, possibly wheezes
- frothy pink sputum
83
Management of left sided heart failure?
Position pt upright unless impossible due to bp or loa (have legs dangling from stretcher if possible). Laying these pts down could kill them.
vitals, cardiac monitor, spo2, etco2
o2
iv
12 lead
nitro - 0.4-0.8mg SL, depending on bp.
bronchodilators should be avoided, will worsen CHF.
84
If both crackles and wheezes are present, which should you tx?
the crackles (nitro, CPAP)
85
What is the most common cause of right sided heart failure?
Left sided heart failure.
As blood backs up from the left side of the heart into the lungs, the right side of the heart has to work harder to pump blood into the engorged pulmonary arteries.
May also result from PE or pulmonary htn (increased resistance of blood through the lungs).
86
Cardiogenic shock
occurs when the heart is too damaged to pump sufficient blood to maintain tissue perfusion.
When 40% or more of the left ventricle has been infarcted.
Can occur after ROSC
87
S+S of cardiogenic shock
confusion/comatose due to decreased cerebral perfusion, restless/anxious if awake.
pale, cool skin - from massive peripheral vasoconstriction.
poor spo2 readings - fingers and hands barely perfused.
rapid, shallow respirations - often crackles
rapid, thready pulse.
88
Management of cardiogenic shock
Focused on improving oxygenation and perfusion w/o increasing the workload on the heart.
100% supplemental o2.
Pt supine unless pulmonary edema present.
IV TKVO
Cardiac monitor and 12 lead.
Transport quickly.
89
Hypocalcemia
Increases permeability and excitability of the nerve membranes - spontaneous stimulation of the skeletal muscles
Severe - laryngospasms and airway obstruction
Heart - contractions are weak, conduction delayed, arrhythmias develop, cardiac output drops. Heart muscle has no nerves, so contraction is directly affected by calcium levels only available through calcium channels.
90
Hypercalcemia
Depressed neuromuscular activity - muscle weakness and loss of tone.
Interfere with ADH - less water absorption - polyuria
Severe - blood volume drops, renal function impaired, wastes accumulate, cardiac arrest.
Heart - contractions increase in strength and duration with dysrhythmias developing
Bones - excess Parathyroid Hormone (PTH), calcium intake - bone density and strength are affected.
91
Hypocalcemia s+s
tetany, muscle spasms
tingling fingers, mental confusion, irritability
arrhythmias, weak contractions of the cardiac muscles
92
hypercalcemia s+s
lethargic, anorexia, nausea, constipation, polyuria, thirst
Kidney stones
arrhythmias - prolonged cardiac contractions
Increased BP
93
Functions of sodium?
- affects osmotic pressure (extracellular fluid volume)
- nerve impulse conduction
- muscle contraction
94
Hyponatremia
Low sodium
Impaired nerve conduction
Fluid imbalances - fatigue, muscle cramps, abdo discomfort or cramps with nausea and vomiting.
Decreased osmotic pressure outside cells - fluid shift into the cells - hypovolemia and drop in bp
Brain swelling - CNS effects (headache, confusion, seizures)
95
Hypernatremia
Too much salt.
Weakness
Agitation
Increased thirst with dry, rough mucous membranes
Decreased urinary output (ADH secretions)
Increased urinary output if the cause is ADH insufficiency.
96
Hyponatremia s+s
anorexia, nausea, cramps
fatigue, lethargy, muscle weakness
headache, confusion, seizures
decreased bp
97
Hypernatremia s+s
thirst with dry tongue and mucosa
weakness, lethargy, agitation
edema
elevated bp
98
What does insulin do with potassium?
Insulin promotes the movement of potassium into the cells.
99
With acidosis, what happens with potassium?
Shifts potassium out of the cells.
Hydrogen ions move into cells and displace K ions to maintain electrical neutrality. K in the fluids diffuse into the blood, leading to hyperkalemia.
100
With alkalosis what happens with potassium?
shifts potassium into the cells.
101
Role of potassium
- regulates intracellular fluid volume
- metabolic processes in the body
- nerve conduction
- contraction of all muscle types
- membrane potential
102
Hypokalemia
cardiac dysrhythmias - prolonged repolarization - arrest
Neuromuscular function interference - muscles are less responsive to stimulus - fatigue, muscle weakness.
Parasthesias
Decreased GI motility - anorexia and nausea
Weak respiratory muscles - shallow resps
Renal malfunction - polyuria
103
Hyperkalemia - causes
```
renal failure
deficit of aldosterone
k sparing diuretics
k leakage out of cells with tissue damage (crush injuries, smiling death)
acidosis - displaces k
```
104
Hyperkalemia - results
ECG:
- p waves wide and flat
- longer pri
- wide, flat qrs
- t wave is high and wide
```
Muscle weakness - paralysis
Fatigue, nausea, diarrhea
paresthesias
Arrhythmias - arrest
oliguria
```
105
Hyperkalemia tx
depends on level of suspected hyperkalemia, currently only ACPs can follow the directive, call for ALS backup.
High dose ventolin - 1600 mcg MDI or 10 mg neb. (Could patch BHP about this?)
106
How thick are capillary walls?
1 cell thick.
107
Peripheral resistance
resistance to blood flow imposed by the force of friction between the blood and the vessel walls. Partly bc of viscosity (higher proportion of RBC and protein molecules in blood), partly from diameter of arterioles and capillaries.
108
Does SNS activation increase or decrease peripheral resistance?
SNS activation causes vasoconstriction and an increase in peripheral resistance.
109
Where is the vasomotor mechanism controlled?
The medulla - the vasomotor/vasoconstriction centre.
When stimulated - initiates an impulse outflow by sympathetic fibres that end in the smooth muscles of the vessel walls - causes constriction.
110
What happens when there's an increase in arterial bp?
-stimulation of aortic and carotid baroreceptors, stimulates cardiac control center to lower the HR.
-inhibits vasoconstriction center
-more impulses per second go out over parasympathetic fibers to slow the HR and dilate the blood reservoirs.
-strives to bring bp back to normal
(homeostasis)
111
What happens when there's a decrease in arterial bp?
baroreceptors are stimulated when they sense the pressure drop, stimulates the cardiac control center to elevate HR.
Sends more impulses to the medulla to stimulate vasoconstriction, stimulates SNS, increasing HR and vasoconstriction, raising bp to normal levels (homeostasis)
112
What are the four factors that affect BP?
```
Cardiac output
Blood volume
Peripheral resistance
Blood viscosity
An increase in any one of these relates to an increase in BP.
```
113
Peripheral Resistance
Friction of blood against the vessel walls
114
RAAS
Kidneys release renin when low BP is detected.
Renin activates angiotensin 1 (vasoconstrictor)
Angiotensin 1 is affected by angiotensin converting enzyme (ACE) and you get angiotensin 2 (powerful vasoconstrictor)
Then angiotensin 2 stimulates the release of aldosterone (also a strong vasoconstrictor).
RAAS raises bp long term.
115
What do kinins do?
Produce relaxation in the smooth muscles of the arteries, increase the capillary permeability, vasoconstrict the venules.
Lower bp.
ACE inhibitors fall into this category.
116
Cor Pulmonale
Hypertrophy of the right ventricle due to increased vascular resistance in the pulmonary artery. (Causes heart failure)
