Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PCIV > Vol.3-Ch.2 "Cardiology" (Part 2) > Flashcards

Vol.3-Ch.2 "Cardiology" (Part 2) Flashcards

1
Q

When palpating edema what is the difference between “pitting” and “mild” edema?

A

When you palpate the edema, after you press in if the depression remains then it is “Pitting”, if it quickly goes back to normal than it is “Mild”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does cool, pale, diaphoretic skin actually specifically indicate?

What about mottled skin?

A

Pale, cool, and diaphoretic skin specifically indicates peripheral vasoconstriction and sympathetic stimulation

Mottled skin often indicates chronic cardiac failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are 3 subtle signs of previous cardiac medical history that may be seen on the pt?

A
  • Midsternal scars
  • Pacemakers
  • Nitro Skin Patches
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 4 possible heart sounds and what makes them?

Where are the 4 locations for heart sound auscultation but which one is the BEST place?

A

S1 = (First heart sound) is when the AV valves close during ventricular systole (tricuspid and mitral)

S2 = (Second heart sound) is when the Aortic and Pulmonary valves close during diastole.

S3 = (Third heart sound) is associated with CHF and is NOT a normal finding

S4 = (Fourth heart sound) occurs immediately before S1 and is associated with increased atrial contraction

The 4 classic sites of auscultation are:

  • Aortic
  • Pulmonic
  • Mitral
  • Tricuspid

But the Best point on the chest wall is known as the Point of Maximum Impulse (PMI) which is at the Apex of the heart so it is also called the Apical Impulse at the 5th intercostal space, midclavicular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is a Bruit?

A

A bruit is a murmur auscultated in an artery (could be carotid, abdominal or other major arteries) that indicates turbulent flow most likely caused by atherosclerosis,

If this is present in the carotids DO NOT attempt a carotid sinus massage as this may dislodge some plaque

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When and how is a Precordial Thump used?

A

It is most effective when used immediately following the onset of VFib or PVT

It may only be attempted once as the need for more energy to convert drastically increases over time, the only window of effectiveness is really right at the beginning.

Use by striking the mid sternum with the heel of your fist from about 10-12 inches high and with your forearm kept parallel to the chest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Atropine Sulfate

A

Type = Antiarrhythmic

Dose = 0.5mg every 3-5 min up to 3mg
(ACCORDING TO BOOK; AHA SAYS 1mg every 3-5)

It is a Parasympatholytic agent use for symptomatic (unstable) bradycardias, especially when arising from the atria. It is an anticholinergic. Will not be effective in 2nd and 3rd degree heart blocks!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Adenosine

Consistent with AHA

A

Type = Antiarrhythmic

Dose = 6mg initial, then 2nd & 3rd doses are 12mg ; max is 30mg total. MUST BE FOLLOWED BY NS FLUSH

It is used for:

  • stable, narrow tachy
  • unstable, narrow tachy (while prepping for SCV)
  • Stable, regular, monomorphic, wide tachy both as therapeutic and diagnostic

It is a naturally occurring nucleoside that acts on the sinus node to slow the rate and on the AV node to slow conduction and inhibit reentry pathways (like in WPW syndrome)

CONTRAINDICATIONS include 2nd and 3rd degree heart blocks b/c it only acts on above the ventricles (the SA and AV nodes/junction) so it would be pointless. As well as asthma, WPW,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Amiodarone

Consistent with AHA

A

AKA Cordarone

Type = Antiarrhythmic
It is also a Potassium channel blocker!

Dose = initial is 300mg, and 2nd dose is 150mg (that it)
(Antiarrhythmic infusion for stable wide tachy give first dose of 150mg over 10min, repeated as needed. Then for maintenance give 1mg/min for first 6 hours ; after that 6hrs give 0.5mg/min)

Works on:

  • Shockable cardiac arrest (if refractory to epi or epi not available, CPR, defib, and vasopressor therapy)
  • Stable, narrow tachy (atrial tachys)
  • Rapid vent rate b/c of accessory pathways in preexcited atrial arrhythmias (WPW syndrome)
CONTRAINDICATED IN:
- cardiogenic shock
- sinus brady
- and 2nd or 3rd heart blocks
(This is because is can CAUSE brady and heart blocks)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Lidocaine

consistent with AHA

A

Type = Antiarrhythmic

Recommended only as an alternative to Amiodarone in the presence of VFib or PVT (shockable rhythms)

It is a WEAK Calcium Chanel Blocker

Dose = initial 1-1.5mg/kg, but id needed repeated every 5-10min at 0.5-0.75mg/kg to a max of 3.0 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Diltiazem

A

Type = Antiarrhythmic

It is a Calcium Channel Blocker that ALSO slows down heart rate

Used for SVT (stable, narrow tachy) that is uncontrolled or unconverted by adenosine or vagal maneuvers

It is ALSO something that can be prescribed to patients to help control recurring AFib or A-Flutter

Dose = initial 15-20mg over 2 minutes, 2nd dose of 20-25mg after 15 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Epinephrine

consistent with AHA

A

Type = Vasopressor

Used as first line drug for cardiac arrest ; acts on both Alpha and Beta adrenergic receptors

Given 1mg of 1:10k every 3-5
(For IV infusion in Brady therapy when refractory to Atropine give 2-10mcg/min titrated to pt response)

If given endotracheally increase to 2-2.5mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Norepinephrine

A

Type = Vasopressor

It is a sympathomimetic and actually has MORE effect on Alpha adrenergic receptors but LESS on the Beta

Similar to Dopamine it is used for symptomatic (unstable) bradycardias refractory to Atropine ; ALSO used for cardiogenic and septic shock patients but DO NOT give it to pts who are in shock specifically caused by hypovolemia as it can also cause bradycardia

Dose = initial is 8-10mcg/minute to attain a BP of 80-100mmHg. For maintenance use 2-4mcg/minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Dopamine

A

AKA Intropin

Type = Vasopressor

Stimulates Alpha and Beta receptors to increase cardiac output

Similar to Norepinephrine it is used for symptomatic (unstable) bradycardias refractory to Atropine

Dose = 2-10mcg/kg/min
(AHA states 5-20mcg/kg/min titrated to pt response)

DO NOT give to hypovolemic shock pts until fluid resuscitation has been completed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Dobutamine

A

Type = vasopressor

Increases cardiac output by increasing stroke volume. Has little effect on heart rate and is occasionally used for isolated left heart failure until other meds like digitalis can take effect. DO NOT use solely for hypovolemic shock pts.

Dose = 2-10mcg/kg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Vasopressin

A

Type = Vasopressor

It is a naturally occurring hormone called Antidiuretic Hormone that is secreted by the posterior pituitary gland. High doses have sympathomimetic effects, B/c when given during CPR is increases coronary perfusion pressure, vital organ blood flow, VFib median frequency, and cerebral O2 delivery. It has once been suggested as an alternative to Epi but no longer so.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Nitroglycerin

A

It is an organic nitrate that dilates peripheral arteries and veins, thus reducing preload, afterload, and myocardial oxygen demand. It can also cause some coronary artery dilation by increasing blood flow through collaterals.

Nitro admin DOES NOT relieve MI symptoms but it will angina. So it can be diagnostic for MI vs Angina.

It should also be given before morphine when appropriate (not hypotensive, recent ED pill, or signs of inferior MI) b/c it works in conjunction with Morphine Sulfate in an MI

Dose = 1 sublingual tablet repeated every 5 minutes up to 3 tablets ; monitor blood pressure before each dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Morphine

A

Aids in MI because it reduces pain but also reduces myocardial oxygen demand by reducing preload and afterload b/c it reduces sympathetic nervous system discharge.

Dose = 3-5mg increments slow IV push
(According to book)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Fentanyl

A

It is a synthetic opiate analgesic chemically unrelated to morphine. It is considerably shorter than morphine and has an immediate onset making it have a safer side-effect profile.

Dose = 50-100mcg
onset = immediate
peak effects = 3-5minutes
lasts = 30-60 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Alteplase

A

AKA tPA

A fibrinolytic agent manufactured by recombinant DNA tech that allows for very limited allergic reactions, b/c it is so close to the real thing. It can be given within 6 hour onset of occlusion (ACCORDING TO BOOK) (AHA says 3hrs but with exceptions can be 4.5)

Dose = 100mg over 1.5-2 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Tenecteplase

A

AKA TNKase

A newer form of fibrinolytic that is more fibrin specific than tPA. The Half-life is longer than tPA but the pt outcomes are consistent with tPA.

Dose = 30-50mg bolus over 5 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Furosemide

A

AKA Lasix

Potent loop diuretic that relaxes the venous system. IT CAN CAUSE FETAL ABNORMALITIES.

Dose = 40mg slow IV push(40mg/min)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are some things that can influence the success of defibrillation? (x8)

A
  • Time from VFib onset
  • Condition of myocardium
  • Heart Size and body weight
  • Pad size
  • Pad placement
  • Pad-skin interface
  • Pad contact
  • Properly functioning defibrillator
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Indications for synchronized cardioversion (4x)

A
  • perfusing VTach
  • Paroxysmal SVT
  • Rapid AFib
  • A-Flutter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is a carotid sinus massage and when should it be used?

A

It can convert paroxysmal SVT into sinus rhythm by stimulating the baroreceptors in the carotid bodies. This increases vagal tone and decreases heart rate (similar to vagal or Valsalva maneuvers).

Have Atropine on stand by, have O2 flowing, DO NOT ATTEMPT if bruits are present, place fingers on carotid as close to jaw/neck as possible, STOP as soon as you see a reduction in heart rate OR if it has been 15-20seconds, may repeat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the most common presentation of cardiovascular emergencies?

A

Chest pain

It is also the 2nd most frequent reason people call for EMS in general

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is Acute Coronary Syndrome?

A

AKA Acute Ischemic Coronary Syndrome

It is the spectrum of coronary artery disease processes of myocardial ischemia to injury to infarction.

28
Q

What is the definition of Stable vs Unstable Angina and Acute Myocardial Infarction??

A
  • Stable Angina is transient chest pain that comes as “episodes” stemming from myocardial ischemia, specifically during increased times of myocardial oxygen demand like during exertion
  • Unstable Angina (aka Pre-infarction Angina) is angina that meets one of the three following criteria:
  • Lasts longer than 20 min
  • New onset
  • Crescendo angina (increasing pain, frequency, and duration)
  • *Unstable angina is a sign that the underlying disease causing angina is worsening and may indicate an imminent MI. It is usually resistant to treatments
  • Acute Myocardial Infarction is irreversible injury (necrosis) to the myocardium
29
Q

What are the 3 typical things needed for diagnosis of an Acute MI?

A
  • clinical history suggestive of coronary artery disease
  • Evidence of ischemic changes on an ECG
  • Elevated myocardial enzymes in the blood
30
Q

What are atheromas?

A

They are the specific spots of development of thick, hard plaques in atherosclerosis

31
Q

What is Prinzmetal’s Angina, aka Atypical Angina, aka Vasospastic Angina?

A

It is abnormal spasms of the coronary arteries that can cause angina. It often occurs at rest and can cause ST elevation mimicking a STEMI but it does still indicate ischemia all the same.

32
Q

How long do angina episodes usually last and what do they usually cause on an ECG?

A

Angina usually lasts around 3-5 minutes, but can go up to 15 minutes. However, it is usually relieved by rest and/or nitro.

The most common ECG finding is ST segment depression

33
Q

What is the main process of an MI starting?

Where do most MI’s occur?

A

It is most often associated with Atherosclerotic Heart Disease, precipitated by a thrombus stemming from plaque that broke off, and then became lodged at another atherosclerotic location further down the coronary artery

Most MI’s occur in the LEFT VENTRICLES

34
Q

Transmural Infarctions VS Subendocardial Infarctions

A

Transmural Infarction: (STEMI)

  • Affects the FULL DEPTH of the myocardium
  • This is how Pathological Q waves develop!!
  • However, since it can take some time for patho Q’s to develop, it is more easily recognized by the immediate ST Elevation which is why these are called STEMI’s!!

Subendocardial Infarctions: (NSTEMI)
- Affects only the subendocardial layer
- Aka a Non-Q Wave Infarct
- These show the classic signs preceding a STEMI, or early STEMI signs of ST depression and inverted T waves
(Because they have not gone full depth yet)

35
Q

What is a basic flow chart of things to see on an ECG in order from ischemia to infarct?

A

Ischemia : ST depression and inverted T waves

Injury: ST elevation

Infarction: Usually a patho Q wave

36
Q

What is the most common complication of MIs and what is the most common cause of death?

What are some other things that may develop post MI? (5x)

A

The most common complication AND cause of death in an MI is Arrhythmias

These can also occur:

  • Destruction of large mass of myocardial muscle mass may lead to CHF that ultimately leads to Left or Right sided heart failure or both
  • Heart Failure is when the heart is inefficient but adequate (it’s ability to pump is impaired but it can meet the body’s demands)
  • Cardiogenic Shock is when inadequate tissue perfusion occurs because the heart is now inefficient AND inadequate
  • Ventricular Aneurysms of the myocardial wall can result b/c the dead tissues weaken the walls
  • Pump Failure
37
Q

What is the definition of a pathological Q wave?

A

It is a Q wave deeper than 5mm or wider than 0.04seconds

38
Q

What is the time window for administration of fibrinolytics?

A

within 6 hours of onset of symptoms

AHA says 3-4.5 but that may just be for strokes

39
Q

What is the process of a Percutaneous Transluminal Coronary Angioplasty (PTCA) (what happens in a CATH Lab)

A

A pt is taken into the Cath lab where they place a catheter (normally in the femoral) and advance it into the heart where they release radiographic dye to visualize the arteries and locate if and where there is a block. (TO this point it is called a CORONARY ANGIOGRAM) Next when it becomes a PTCA is if there is a block they will advance in a balloon right where the block is and inflate it to bust up the clotted area, next they will wait to see if the area stays expanded and if not then they will place a Stint to keep it open in a process called Primary Coronary Stenting

40
Q

What is a CABG?

A

It is a Coronary Artery Bypass Grafting (usually only done after the pt is stable) where they take a saphenous vein from the leg and use it to circumvent or replace part of a coronary artery

41
Q

What are the 4 Cardiac Enzymes to took at for diagnosis of a MI?

A

Creatine Kinase:

  • Has 3 forms: CK-BB in the brain, CK-MM in the skeletal muscle, and CK-MB in the heart
  • Obviously we are watching for elevated CK-MB will begin to rise in 3-4 hours post infarct and peak at 24hours
Lactic Dehydrogenase (LDH):
- LDH is found in a lot of different places but LD1 is found in the heart and will rise within 24hrs after infarct

Myoglobin:

  • Myoglobin is where O2 is stored in Striated muscle (skeletal and heart) but when that muscle is damaged it is released into the blood stream.
  • It will begin to rise within 2 hours of infarct and peak at 6-8 hours

Troponin: ***
- Proteins within the contractile regions of cardiac fibers. There are 3 types but Troponin I (TnI) is the form most frequently assessed because it is very specific for cardiac injury and not found in the serum of a healthy person. Begins to rise in 4-6 hours and peaks in 12-16 hours.

42
Q

What is Heart Failure?

A

it is a clinical syndrome in which the heart’s mechanical performance is compromised so that cardiac output cannot meet the body’s needs.

It usually involves either Right or Left sided heart failure, but as a side note, Left sided heart failure ALWAYS eventually leads to Right sided heart failure.
(The most common cause of right sided HF is left sided HF)

43
Q

Besides Left Sided heart failure what is another common cause of JUST Right sided heart failure (with left side still intact)

A

Pulmonary Hypertension secondary to COPD

Cor Pulmonale = heart failure due to pulmonary disease

Right under that is a PE which also places a lot of pressure that the Right Vent is pushing against

44
Q

What is Congestive Heart Failure?

A

Congestive Heart Failure is when the heart’s reduced stroke volume causes an overload of fluid in the body’s other tissues causing edema (can be in the lungs, peripheral extremities {usually lower leg from ankle to knee}, sacral, or peritoneal)

The reduction in stroke volume can arise from anything that comprises the hearts ability to fill properly or contract properly, that is to say when there is Mechanical Failure of any cause

It is the MOST COMMON cause of hospitalization in patients over 65!!

IT IS MECHANICAL FAILURE CAUSING EDEMA ELSEWHERE; ALMOST BETTER THOUGHT OF AS HEART FAILURE CAUSED CONGESTION

This most often leads to death b/c of pulmonary edema, then respiratory failure, and death.

When pulmonary edema is getting worse pts will present with pink frothy sputum, difficulty breathing, acute edema or weight gain in other places, and often Paroxysmal Nocturnal Dyspnea (dyspnea that comes and goes at night when laying down)

45
Q

What are some common medications that a CHF pt may be on that you want to look for?

A
  • Loop diuretics like Furosemide (Lasix)
  • Hypertension Meds (might also be lasix)
  • Digoxin to increase heart’s contractility
  • ACE inhibitors to decrease afterload (this cuts off the RAAS System)
46
Q

What is Pulsus Alternans?

A

When a pulse alternates between weak and strong

47
Q

Why are CPAP and Nitro in unison the best thing you can do for a CHF pt?

What are some secondary line defenses against CHF pts; what was the old and new theories?

A

CPAP helps push the fluids in the lungs back across the respiratory membrane back into the capillaries, then the Nitro helps vasodilates peripheral and coronary collateral vessels (not as much on the coronary) to allow for there to be more space in the tank for the fluids pushed back into the container

CPAP should be started out at a PEEP of 5 cm H2O but if needed to increase go to 7.5-10 cm H2O

The OLD theory for CHF was to give a loop diuretic with morphine, but this is no longer the recommendation b/c studies show that the pts are usually already on and most likely taken their diuretic so it takes a very high amount to work and morphine typically did not have as much vasodilation effects as needed and had too much suppression of the CNS and respiratory drive leading to more intubations

The NEW theory is that giving an ACE inhibitor is best secondary line of action because it decreases afterload. This is b/c is stops the RAAS system before Angiotensin 1 can become Angiotensin 2 which has vasoconstrictive properties.

48
Q

CPAP VS PEEP

A

CPAP is continuous positive pressure during inspiration and expiration (i.e. continuous)

PEEP is positive end expiratory pressure and it only gives positive pressure during expiration.

Normally a pressure of 2.5-5 mmH2O is all that is needed but it can go up to 10.
Above 10 starts to increase pressure within the chest cavity to a point where it reduces the left side ventricles from filling properly and can reduce cardiac output

because of this it is important to use the LOWEST AMOUNT NEEDED

49
Q

What is the normal amount of fluid within the pericardial sac (between the visceral and parietal pericardium)

A

25mL

50
Q

What are the normal medications used for Cardiac Tamponade?

A

since management is usually just supportive care is limited. Medication to help may include:

  • Dobutamine
  • Dopamine
  • Furosemide (lasix)
  • morphine

The main care needed is a Pericardiocentesis where a cardiac needle is inserted into the pericardium to drain the blood, pus, air, or serum.

51
Q

What constitutes a hypertensive emergency?

A

Hypertension itself is considered a BP of 160mmHg over 90mmHg or greater

A Hypertensive Emergency is an increase in blood pressure that is accompanied by end or target organ changes. Often caused by noncompliance with hypertension medication.

It often occurs with Hypertensive Encephalopathy, a condition of acute or subacute consequences of severe hypertension characterized by AMS, vomiting, visual disturbances (such as transient blindness), paralysis, seizures, stupor, and coma.

On occasion it can cause Left Vent Failure, pulmonary edema, or stroke

Another big hypertensive crisis is Eclampsia, which can occur anywhere between the 20th week of pregnancy to birth, and is marked by a blood pressure of at least 140/90mmHg

52
Q

Heart Attack VS Cardiac Arrest

A

Heart Attack = Circulation Problem

Cardiac Arrest = Electrical Problem

53
Q

What is Cardiac Arrest?

What is Sudden Death?

A

Cardiac Arrest is the absence of ventricular contraction that immediately results in systemic circulatory failure

Sudden Death is any death that occurs within 1 hour of onset of symptoms

Cardiac Arrest and Sudden Death account for 60% of all deaths from Coronary Artery Disease

54
Q

Quick Overview of the 3 phases of Cardiac Arrest and their details

A 
Phase 1 of Cardiac Arrest (VFib): ELECTRICAL
- 0-4 min of arrest
- Adequate O2
  Adequate Energy Stores
  Near normal pH
  No myocardial Ischemia
  No myocardial infarction
- Treatment: DEFIBRILLATION
- Good-Excellent survival Chances
Phase 2 of Cardiac Arrest (VFib): CIRCULATORY
- 4-10 min of arrest
- Inadequate O2
  Inadequate Energy Stores
  Falling pH
  Possible Myocardial Ischemia
  No myocardial infarction
- Treatment:
  CPR(at least 90 sec)/Defibrillation/Epi
- Good-Fair survival chances
Phase 3 of Cardiac Arrest (VFib): METABOLIC
- 10+ min of arrest
- Profound Acidosis
  Electrolyte disturbances
  Cellular Death
  Bowel Flora translocation
  Myocardial toxins
- Treatment:
  Induces hypothermia
  metabolically-focused therapies
  prevent injurious factors during reperfusion
  anti-endotoxin antibodies
- None-Very Low survival chances
55
Q

In depth overview of the Phase 1 of cardiac arrest: Electrical Phase

A

Phase 1: Electrical
- Occurs in first 4 minutes of arrest.

The heart still has energy and O2 because of the stores in Myoglobin (even though it only has 2 subunits instead of 4), there is still O2 in the current blood supply so if compressions are started immediately there will be a small window where perfusion can be prolonged; sometimes the pt may even still be breathing for a brief period at the beginning of arrest, hopefully providing a brief period of respiration. So at this point there is not any major damage to the myocardial muscle. With there still being available O2 and energy (ATP), there is still aerobic metabolisms occurring so Acidosis has not begun yet.

Because the main problem in this phase is the disorder of electrical function the MAIN course of action is to get defibrillation as soon as possible

56
Q

In depth overview of the Phase 2 of cardiac arrest: Circulatory Phase

A

Phase 2: Circulatory
- Occurs in 4-10 minutes of arrest.

By this phase there is no longer adequate O2 or Energy stores so the myocardium is in distress; ie ischemia is possible. In this phase we switch from aerobic to anaerobic metabolisms which produces lactic acid and we begin to see a fall in pH levels (more acidic).

As opposed to phase 1 where defib is the first thing we want to do, since the myocardium is not prepared to depolarize, we now need to prep it by giving at LEAST 90 seconds of CPR BEFORE trying to defibrillate. This may also include the need for epinephrine administration to best prepare for defib success

57
Q

In depth overview of the Phase 3 of cardiac arrest: Metabolic Phase

A

Phase 3: Metabolic
- Occurs at 10+ minutes of arrest

At this phase the chances of survival severely drop.
Now we have severe hypoxia, severe acidosis, inadequate O2 and energy, and possible myocardial injury and infarction.

One of the first major impairments of the cardiac system in this phase is the failure of the sodium-potassium pump. As the pump fails, the cell wall fails and the extracellular sodium begins to fill the cell and causes water to follow; once water floods the cell behind the sodium, it will eventually cause the cell to swell, rupture, and die.

This same process occurs in the GI tract, and as the walls of the GI tract begin to fail accordingly, the special bacteria that resides there (normally Gram Negative) is allowed to enter the body. When these bacteria die inside the body they release various toxic chemicals including endotoxins and cytokines; both of which suppress myocardial function.

Therefore, even is resuscitation is successful and there is ROSC, these endotoxins, cytokines, and metabolic acids (lactic acid) are going to be be sent off to other organs where they can cause damage or failure. Even the administration of Epo can be very harmful for a pt in this phase b/c epi shunts blood away from the nonessential organs (like the GI tract) to the brain, heart, lungs, and kidneys.

Treatment for pts in this stage (which we can’t even really do most) include induced hypothermia, electrolyte corrections, acidotic buffers, antiendotoxin antibodies, and inflammatory agents.

58
Q

What are 4 unusual causes of cardiac arrest?

A
  • Brugada Syndrome:
    A hereditary condition associated with high risk of sudden cardiac death caused by a Right BBB and ST segment elevation in leads V1-V3 usually caused by fast polymorphic ventricular tachycardia.
  • Long QT Syndrome:
    Is a group of disorders that increase the risk for sudden death from an arrhythmia. It can be inherited or acquired. It most commonly results in Torsades De Points
  • Hypertrophic Cardiomyopathy:
    A disease in which the myocardium thickens and stiffens, especially in the ventricles and septum. It can be inherited or acquired. If acquired it is often b/c of hypertension and aging. IT IS THE LEADING CAUSE OF DEATH IN YOUNG ATHLETES
  • Commotio Cordis:
    It usually occurs in healthy young males in athletics and is when they are struck by a sudden, blunt, nonpenetrating blow to the anterior chest that results in immediate cardiac arrest/VFib. Can usually be corrected by CPR and early defib
59
Q

Atherosclerosis VS Arteriosclerosis

A

Atherosclerosis is the formation of plaque (fats- lipids & cholesterol) on mid to large arteries under the tunica intima (inner layer), calcium often deposits on these plaque sites that will later chip off and become thrombi.

Arteriosclerosis is when the intimal surface gets destroyed (often b/c of atherosclerosis) and the vessel looses it’s elasticity, often resulting in hypertension.

60
Q

What does Aneurysm mean and what are the 5 types?

A

Aneurysm = “dilation of a vessel”

Types include:

  • Atherosclerotic
  • Dissecting
  • Infectious (rare but usually caused by syphilis)
  • Congenital
  • Traumatic

Most involve Atherosclerotic aneurisms at the aorta ; They occur when blood surges into the aortic wall through a tear in the aortic tunica intima

61
Q

Location/cause, symptoms, and target population of Abdominal Aortic Aneurysms?

A

Location:
- Commonly results from atherosclerosis of the aorta below the renal arteries and above the bifurcation of the common iliac arteries.

Symptoms:

  • Abdominal pain
  • Back and flank pain
  • Hypotension
  • Urge to defecate caused by the retroperitoneal leakage of blood
  • The book didn’t say this but obviously a large pulsating mass in the abdomen

Target Pop:

  • 10x more likely in men
  • Ages 60-70
62
Q

Location, cause, and target population of Dissecting Aneurysms?

A

Location/Cause:
- Caused by degenerative changes in the smooth muscle and elastic tissue of the aortic media; this can result in a hematoma and subsequently an aneurysm. The original tear is often from Cystic Medial Necrosis, a degenerative disease of connective tissue often associated with hypertension and aging. Most involve the Ascending Aorta but then spreads.

Target Pop:

  • Hypertensive pts
  • 40-50+yo
  • Hereditary
  • Pregnancy
63
Q

What is Vasculitis?

A

It is inflammation of blood vessels

Inflammation within the media of a muscular artery tends to destroy the internal elastic lamina.. Necrosis and hypertrophy of the vessel occur and the vessel wall has a high likelihood of breaching, leaking fibrin and red blood cells into the surrounding tissue. Possible leading to partial or total vascular occlusion and subsequent necrosis.

64
Q

What is commonly associated with Peripheral Arterial Atherosclerotic disease and where does it normally affect?

A

It is commonly associated with diabetes mellitus and commonly strikes in the calf but can occur in any leg muscle. B/c it leads to diminished arterial supply to the areas there is typically no edema, but there is pain from ischemia and over time without blood gangrene or necrosis may set in.

It causes Intermittent Claudication which is diminished blood flow in exercising the muscle

65
Q

What is Homan’s sign and what does it indicate?

A

It is pain behind the knee while dorsiflexing the foot and may be indicative of a deep vein thrombosis (which usually occurs in the thigh or calf)

66
Q

What are the 5 Ps of Vascular Disorder Assessment?

How do you treat Vascular Disorders?

A
  • Pallor
  • Pain
  • Pulselessness
  • Paralysis
  • Paresthesias

Mostly treat supportively, with O2 or pain management as needed

PCIV (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions