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A&P Panel Questions > Cardiac > Flashcards

Cardiac Flashcards

1
Q

CPR Rates:
Adult
Child
Newborn

A

Adult:

30: 2 pausing for ventilations
15: 1 no pause for ventilation once advanced airway inserted.

Children:

30: 2 single responder
15: 2 dual response
15: 2 dual response no pause with advanced airway

Newborn:

3: 1 single responder
3: 1 dual response

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2
Q

Reasons for adrenaline in arrest (4)

A

Alpha effects – vasoconstrictive qualities. An increase in peripheral vascular resistance
increases venous return and eventually cardiac output and coronary perfusion pressures.

Beta 1 – increases the irritability of the ventricles and hopefully enable the generation of
a rhythm.

Beta 1 – increases myocardial contractility and hopefully cardiac output.

Has a short ½ life

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3
Q

ICP role in cardiac arrest

A
  • Insertion of a definitive airway – ETT
  • Further drug therapy for prevention, or control of lethal arrhythmias.
  • Education
  • Treat complications arising from clinical presentations and prevent them from occurring.
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4
Q

LMA Indications and Contra indications

A

Indications:

  • Unconscious patient without gag reflex
  • Ineffective ventilation with BVM/oxysaver and airway Mx (OPA / NPA)
  • > 10/60 assisted ventilation required
  • Unable to intubate - difficult/failed intubation

Contraindications:

  • Intact gag reflex or resistance to insertion
  • Strong jaw tone + trismus
  • Suspected epiglottitis or upper airway obstruction
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5
Q

LMA Precautions

A
  • Inability to prepare the patient in the “sniffing position”
  • Pts who require high airway pressures eg advanced pregnancy, morbid obesity,
    decreased pulmonary compliance (stiff lungs due to pulmonary fibrosis) or increased
    airway resistance (severe asthma)
  • Pts less than 14 years of age due to enlarged tonsils
  • Significant volume of vomit in airway
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6
Q

Function of the Heart

A

The heart is a muscle located in the central chest to the left. Its primary function is the pumping
of blood around the body, providing nutrients and removing waste.

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7
Q

Flow of blood

A

Blood enters from the body into the right atrium via the superior vena cava
↓
From right atrium through the tricuspid valve into the right ventricle
↓
From the right ventricle into the pulmonary vein to the lungs
↓
Blood returns from the lungs to the left atrium via the pulmonary vein
↓
From the left atrium through the mitral valve into the left ventricle
↓
From the left ventricle to the body via the aorta

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8
Q

Define ACS

A

The spectrum of conditions ranging from unstable angina through to NSTEMI to STEMI, which
all share the common pathophysiology of a disrupted atherosclerotic lesion.

Unstable angina (UA) and NSTEMI are characterized by a non-totally occlusive white thrombus;
the difference being that UAP resolves prior to death of any myocardium and NSTEMI involves
some myocardial death. STEMI is characterized by a totally occlusive red thrombus.
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9
Q

Define AMI

A

Necrosis or death of myocardial tissue, usually due to prolonged ischemia resulting from an
atherosclerotic plaque with superimposed thrombus.

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10
Q

Define Angina pectoris

A

Angina is an episodic, clinical syndrome that results from transient myocardial ischemia, causing
pain in any of the cardiac sites.

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11
Q

Define Unstable Angina

A

Advanced angina with presence of transient thrombi formation over atherosclerotic lesions.
There is impending infarction.

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12
Q

Define Atherosclerosis

A

Initiated and compounded by inflammatory response, it is a progressive disease characterized by
thickening and hardening of an artery over time, caused by soft deposits of lipids, cellular debris,
fibrin, and calcium in the lining of large arteries (in the intima).

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13
Q

Define Atheroma

A

A sub-intimal collection of lipids and cellular debris leading to raised plaques and complicated
lesions subject to fissuring, haemorrhage or rupture.

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14
Q

Pathophysiology of Coronary Artery Disease and Acute Coronary Syndrome

A

Build up of fatty plaque, lipids and blood products
↓
Injury to tunica intima wall
↓
Infiltration of lipoproteins, RBC‟s, WBC‟s, macrophages, collagen, with smooth muscle proliferation – all
within the wall of the tunica intima
↓
Formation of non-obstructive fatty streak
↓
Atherosclerotic plaque formation will begin to project into the lumen of coronary arteries.
↓
The plaque cap is disrupted causing the contents of the plaque to mix with passing blood.
↓
Contact between tissue products and blood, this can cause platelet aggregation on the surface of the intima.
↓
Activation of a clotting factor creates a continues in a cascade until fibrinogen is converted into fibrin.
↓
Clot grows and forms an occlusion of the blood vessel

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15
Q

ACS Risk Factors

A 
P - Post menstural
H - HTN
A - age over 40 (men)
D - Diabetes
H - HyperChol
H - History (family)
O - Obesity
R - Race (black)
S - Smoking
S - Sedintary
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16
Q

Chest Pain Assessment

A 
Sweating
Palpitations
Nausea/Vomiting
Dizziness/Lightheaded
SoB
Calf Pain
Peripheral Oedema
BP L vs  R
Diarrhea
Constipation
17
Q

AMI Path Flow Chart

A

Occlusion

No O2 supply. Irritation, ECG changes

Anerobic Metabolism

Increased intraacellular sodium

Cell swells, and ruptures

Released enzymes and ions - further ECG changes

Cell death

18
Q

Cardiogenic Shock with Right Ventricular Involvement

A

Approx 1/3 of patients with inferior AMI have right ventricular involvement.
The most serious complication of right ventricular infarction is SHOCK – decrease in preload, less in right
ventricular ejection therefore less returning to left side of heart – causing decrease in stroke
volume

19
Q

Cardiac Failure – LVF

A

Up to 20% of AMI patients present with some congestive failure. Generally speaking the more
severe the LLVF the higher the mortality.

Increased pulmonary oedema.

20
Q

Coronary Blood Supply

SA, AV, Atrium and Ventricles

A

SA supplied by
55% RCA 45% LCx

AV and Bundle of HIS supplied by
90% RCA 10% LCx

Right Atrium: sinus node artery (which is a branch of the RCA in 55% of cases & LCx in 45%)

Left Atrium: is supplied by the LCx

Right Ventricle (posterior portion): RCA and posterior descending branch (PDA) & LAD

Right Ventricle (anterior portion): RCA and LAD

Left Ventricle (posterior) is supplied by LCx, PDA & LAD, Anterior Left main, LAD & LCx

Apex is supplied by LAD

Septum is supplied by septal branches of LAD, PDA and AV nodal branch of RCA.

21
Q

Define Collateral Circulation

A

An arteriolar to arteriolar anastomosis between branches of the same of different coronary
arteries. Collateral circulation develops when circulation to an area declines. They develop more
efficiently when obstruction to the area is gradual as opposed to sudden.

22
Q

Goals of Treatment - ACS

A

Increase O2 delivery to the heart
Decrease myocardial O2 demand
Reduce BP to minimize further plaque rupture
Prevent cardiac failure
Minimize progression of injury/infarction
Minimize clot formation and platelet aggregation

23
Q

ACS Treatment

A 
ICP
Aspirin
Monitor
Oxygen if required
GTN
Pain Relief
Anti emetics if required
24
Q

Define Cardiac Failure

A

The inability of the heart to independently provide adequate cardiac output to perfuse the tissues
with vital blood-borne nutrients

25
Q

LVF Signs (12)

A 
dyspnoea, DOE, use of accessory muscles, 
crackles (usually fine end expiratory), 
pink/white frothy sputum, 
fatigue, 
lethargy, 
weakness, 
anorexia,
insomnia, 
tachycardia, 
diaphoresis, 
pallor, 
low SpO2
26
Q

RVF Signs (9)

A 
weight gain, 
oedematous lower limbs, 
abdominal distention,
ascites, 
hepatomegaly, 
splenomegaly, 
neck vein distension, 
anorexia, 
nauseam feeling of gastric fullness
27
Q

Define Cardiogenic Shock

A

Shock of cardiac cause, give that shock is a progressive syndrome of inadequate cardiac output.

Normal metabolic demand for O2 and nutrients is not met and metabolic waste products
accumulate in the cell. Progressive cell and organ ischemia leads to death of the cell, organ and organism.

28
Q

Sympptoms Cardiogenic Shock

A

Hypotension
Tachycardia
Altered conscious state

29
Q

Define Pulmonary Oedema

A

Leakage of fluid from the pulmonary circuit and interstitium into the alveolar spaces.

Whether Cardiogenic or non-Cardiogenic in origin, regulation and balance between capillary hydrostatic
and oncotic pressure, lymphatic drainage and alveolar permeability is compromised.
This results in the shift and thus accumulation of fluid in the alveoli, causing respiratory
compromise

30
Q

Causes APO (5)

A 
Volume overload
Pressure overload
Filling disorders
Myocardium dysfunction
High output states
31
Q

Patho APO secondary to LVF

A

LEFT VENTRICULAR DYSFUNCTION (↓SV & CO)
↓
PULMONARY PRESSURE ↑ - LEADING TO HYDROSTATIC RESSURE OVERCOMING ONCOTIC PRESSURE
↓
FLUID SHIFTS INTO THE INTERSITIUM (CAN CONTAIN UP TO 500ML)
↓
WITH FURTHER ACCUMULATIONS THE FLUID CROSSES THE ALVEOLAR EPITHELIUM INTO THE ALVEOLI – LEADING TO ALVEOLAR FLOODING AND SURFACTANT WASH AWAY.
↓
ABNORMALITIES IN GAS EXCHANGE, VITAL CAPACITY AND OTHER RESPIRATORY VOLUMES ARE SUBSTANTIALLY REDUCED - HYPOXEMIA

32
Q

Treatment APO

A 
ICP
Positioning
Monitoring
Oxygen
Assisted ventilation with PEEP
GTN
33
Q

Infective vs APO

A 
Infective:
Febrile
Sepsis
Cough
Hx of infection
Unilateral
APO:
CCF
Cardiac Meds
Bilateral
Usually between 0300 and 0600
34
Q

Action Potential

A

In a ventricular myocardial cell there is a higher concentration of potassium inside the cell in
relation to outside the cell and a higher concentration of sodium outside the cell that inside the
cell. The net electrical effect of these concentration differentials is a potential of -90mV inside
the cell, this is maintained by the Na/K pumps, which use energy in the form of ATP to pump
3Na out of the cell and 2K into the cell

35
Q

Myocardial Cell Electrocardiology

A

Phase 0: Depolarisation
rapid Na entry

Phase 1: Early Repolarisation
K moves out

Phase 2: Plateau Phase
K out and Ca in

Phase 3: Rapid Repolarisation
Slow leak of Na into cell

Phase 4: Resting membrane potential
No movement

36
Q

Action Potential Cell

A

Phase 0- voltage gated Ca channels open, slow Na channels open
Phase 3- K leaves cell to try a decrease membrane potential toward resting membrane potential
Phase 4- Slow leakage of Na into cell, membrane potential becomes slowly negative until membrane potential reached

Resting membrane potential = -50mV (fast Na channels don’t activate b/c start at -50mV (fast Na channels open at -60mV)

A&P Panel Questions (8 decks)

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