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CCP 2 Review > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What are some causes of Long QT

A

Congenital

  • genetic disease of K and Na channels
  • Autosomal DOminant
Acquired
-Meds (Sotolol, Amiodarone, Zofran
- Electroylytes Hypo Mag/Hypokalemia, Hypocalcemia
- Hear ICM/HCM
- SAH
Malnutrition (Lytes).
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2
Q

Treatment for Long QT

A

Congenital

  • continue bb therapy
  • correct electrolytes

Acquired
- stop offending medications
Magnesium 2 G alive 4 grams dead

  • treat Hypo K, Hypo Ca, Hypomg
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3
Q

Review of cardiac actionable potential

A

Phase 4= -90 mv closed sodium channels, NAK pump working 3-2

Phase 0- Depolarization fast sodium channels +20ish

Phase 1 Fast NA close, K Efflux opens

Phase 2 Clacium influx occurs causing plateau phase

Phase 3 Calcium influx stops and K efflux continues (depolarization)

Phase 4 K efflux happens and NAK pump continues ( sodium calcium exchanger

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4
Q

Mechanism of Ashton of antyarrythmics

A

Lidocaine - decrease conduction velocity, decrease refractory period, decrease automaticity

Beta blocker
- decrease conduction velocity, no change to refractory period, decrease automaticity

Class 3 ( Pottassium blocke)- increases refractor period

Class 4- decrease velocity, increased refractory period. Decrease automaticity

Digoxin, CCB, BB, Adensoine all work on the AV node which decreases automaticity Also

Lidocaine works on conduction pathway in the LBB RBB and my coyotes

Amiodarone works on both

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5
Q

Torsades vs polymorphic VT

A

Only called TORSADES if the underlying QTc was long
- give Mg

Amiodarone, lidocaine, correct electolytes, defibrillate

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6
Q

Indications for ICD

A

1) cardiac arrest due to VT or VG not due to transient or reversible cause (class 1 evidence)

2) spontaneous or sustained VT ( Class 1)
- in association with structural heart disease
-

3) syncope NYD with EPS induced hemodynamically significant sustained VT/VF (CLass 1)
4) sever symptoms (syncope) attributed to sustained VT while awaiting transplant

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7
Q

What is Brugada Syndrome

A

Autosomal dominant genetic mutation of sodium channels

Can be intermittent and most common middle aged males

THEY NEED AN ICD

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8
Q

Brugada Syndrome types

A

Type 1 2mm ST elevation in V1-V3 followed by a negative T wave

  • diagnosis with clinical criteria, VT;VF, Family hx SCD <45, coved type ECGS in family members, Inducibility of VT, Syncope, Nocturnal atonal respiration’s

Type 2 Saddleback shape ST Elevation

Type 3 Morphoology of 1 and 2 with 2mm st elevation

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9
Q

Layers of the heart outside n

A 
Fibrous Pericardium
Parietal Pericardium
Pericardial Cavity
Visceral Pericardium
Myocardium
Endocardium
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10
Q

Oxygen Delivery equation

A

D02= Co x Ca02

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11
Q

Oxygen consumption equation

A

V02= COx (Ca02-Cv02)

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12
Q

Cardiac output equation

A

C0=HR x SV

Volume of blood ejected by heart in 1 minute

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13
Q

Stroke volume is affected

A

Preload
Afterload
Contractility

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14
Q

How to get ejection Fraction

A

EF= SV/EDVx100%

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15
Q

Define Preload

A

Wall stress at the end of diastole

- related to degree to which myocardial fibres are stretched therefore the MAXIMAL resting length of the sarcomere

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16
Q

Frank staling curve

A

As you increase contractility you will increase SV

As you decrease Contractility you will decrease Contractility

As you increase preload you will increase contractility until you have maximal stretch and the you will plate you

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17
Q

Frank starling Curve GRAFT

A

What is the Concept of mean systemic filling pressure

If the pressure in the right atrium is greater than or equal to Mean systemic filling pressure there will be no flow

There has to have a pressure gradient that drives venous return

Mean systemic fill pressure average 7-8

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18
Q

Define Contractility

A

Inherent capacity of the myocardium to contract independently of changes in preload or afterload

This is secondary to interactions between Ca ions and contractile proteins

Ex able to increase contractile with exercise, adrenergic stimulation and inotropic medications

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19
Q

Define Afterload

A

Wall stress generated by muscle fibres during systole

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20
Q

La places law

A

Wall Stress= pressures radius / 2x wall thickness

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21
Q

How to we measure Cardiac output

A

CO= MAP-CVP/SVR

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22
Q

Arterial oxygen content equation

A

Ca02= (Hgbx1.34xSa02+ .003xPa02)

Cv02= ( Hgbx1.34xSv02+0.003+Pv02)

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23
Q

What is the solubility coefficient of 02

A

0.003

24
Q

What are the major determinants of myocardial oxygen demand uptake

A

1) HR
2) Wall Stress
3) Contractility

25
Q

What will high wall tenson result in for metabolic demand

A

Increase metabolic demand and increase oxygen consumption of the heart

26
Q

What will decrease myocardial oxygen supply

A

1) decrease coronary blood flow
2) increased HR ( less diastolic filling time)
3) increased diastolic volume
4) deceased 02 content
Decrease hematocrit
Decreased 02 saturation

27
Q

At rest does the heart already have maximal 02 extraction

How do you increase 02 extraction

A

At rest the heart already has maximal 02 extraction so the only way to increase it is to increase deliver and increase coronary flow.

Exercise will increase coronary blood flow by 4-5 x

28
Q

What are the main 4 Coronary arteries

A

Left main
Right
LAD
Circumflex

29
Q

Explain the left and right dominance for blood supply

A

The posterior descending artery feads the AV node

In 2/3 of population the PDA comes offf the RCA

1/3 of people it comes off the Left Circumflex artery

Co dominant it comes of RCA and LCx

30
Q

What arteries come of RCA

A

RCA
Nodal Branch
Acute marginal
Posterior descending 2/3 of people

31
Q

What branches of LAD

A

S1 S2 septal branches towards middle or septum

D1 D2 D3 diagonal arteries towards left

There is also the S1S2 which branches off posterior descending arteries

32
Q

Coronary Perfusion Territories

A

RCA- inferior segments, posterior 1/3 IVS+ as node and AV node

LCx All lateral segments and occasionally SA and AV node

LAD all anterior segments and 2/3 IVS + septum

33
Q

WHen does the Coronaries receive blood

A

LV 85 percent during diastole 1 percent systole

RV both systole and diastole

Blood flow is drained by Coronary sinus and empties into RA 85 percent and 15 percent into thesbian veins ( Empty into Left side heart) along with bronchial veins and pulmonary veins (causing a physiological shunt)

34
Q

In order what the the CVP wave forms and what do they represent

A

A, C, X, V, Y

A= Right atrial contract at end of Diastole

  • you will lose a wave in A-FIB
  • A wave will increase in Tricuspid and pulmonic stenosis
  • Cannon A waves are in heart blocks, V TAC secondary to contraction agains a close tricupsid Valve

C= Early systole

  • Tricuspid valve bulging into RA from RV congtraction
  • Tricuspid regurgitation causes fusion of C and V waves with x descending blunted

X- (mid systole) which is the RA relaxation

  • Incresed x descent in constrictive pericarditis
  • Decreased ascent with Tricuspid Regurg as increased RA pressures suggest RV dysfunction

V= (late Systole)
Rapid Filling of RA
- increaed V wave in Tricuspid recurg from increased RA pressure

Y=

35
Q

Systole steps

A

1) Isovolumetric contraction is when MV closes and AV is still closed as ventricule builds up pressure
2) Rapid Ejection 2/3 volume ejected
3) Slower Ejection: 1/3 volume Ejected

36
Q

Diastole Phases (4)

A

1) Isovolumetiric relaxation: AV closed and MV still closed as LA builds up pressure
2) Early ventricular filling: MV opens, passive LV fills LAP> LVP (70-80 final stroke volume)
3) Late Diastolic filling/diastasis: LVP approaches LAP, dependent on chamber compliance
4) Atrial systole/kick contracts 15-20 percent

37
Q

Pressure Volume Loop starting from bottom left corner

A

A= End systolic Volume

B= Early Ventricular Filling/Late Ventricular Filling

C= Mitral Valve closes

Isovolumetric Contraction

D= Aortic Valve Closes

E= stroke volume/ejection

F= Aortic Valve Closes

Isovolumetric Relaxation

A

38
Q

What is a normal Cardiac Output

A

4.o-8.0 l/min

39
Q

Pacemaker Action Potential

A

Phase 4= sodium leaks into cell - 60mv

Phase 0 depolarization occurs with Ca channels opening

Phase 3- depolarizations with potassium out.

40
Q

Normal axis

A

30 to -90 degrees

Positive I. Positive AVF

41
Q

Left Axis Deviation

A

Positive lead I

Negative AVF

0 to -90

42
Q

RAD

A

Negative Lead I

Positive AVF

+ 90 to +180

43
Q

Extreme axis deviation

A

Negative Lead 1

Negative AVF

-90 to -180

44
Q

Either a hypertrophy axis shifts towards or a damaged part of the heart axis moves away.

A

What causes axis deviation

45
Q

What is atherosclerosis and its patho genesis

A

Is a type of arteriosclerosis (thickening and hardening of artery walls) affects primarily medium and large size muscular arteries affecting the intima

This is caused by a chronic inflammatory response in the walls of the arteries which is a slow progression of fat(cholesterol) build up within the artery causing intimacy lesions called Atheromas, atheromatous or fibrofatty plaques.

46
Q

Angina Pectoris Definition

A

Imbalance of myocardial oxygen supplyly and demand

Stable, predictable with increased activity and resolves with rest or NTG

Typically requires >70 percent occlusion

47
Q

What are our Hemodynamic goals with CAD

A

1) Small chamber size + low LVEDP
2) SLow HR, Increased diastolic filling time
3) reduced contractility
4) Adequate perfusion pressure

LV only gets perfusion during diastole where as RV gets perfusion from systole and diastole

1) Decrease preload
2) maintain afterload (hypertension is better than hypotension
3) Decrease contractility
4) Decrease Rate and keep in SINUS Rhtym

48
Q

Therapy to treat Coronary ischemia

A

NTG 0.5-3mcg/kg/min

Nitride 0.5-3 mcg/kg/min

Phenylephrine/norepinephrine/ vasopressin for hypoperfusion

BB, CCB do decrease HR, improve diastolic filling time

MgS04 for hypomagneisa which has coronary vasodilation properties which decreases size of infarct in acute ischemia and reduces mortality during infarction

49
Q

How do Nitrates Work

A

Nitrates increase 02 supply by dilation of large epicardial coronary arteries

Low doses decrease preload which decreases wall stress and decreases to cardiac 02 demand

Higher doeses decreases afterload and decreases myocardial 02 demand.

50
Q

What can exacerbate myocardial ischemia

A

HTN, Fever, Tachycardia, anemia, hypoxemia, valvular disease

Standard of Care

BB,CCB, Nitrates, Statin, antiplatelet, ACEi, ARBS

51
Q

Type 1 Vs Type 2 MI

A

Type 1 mi is causes by a sympathetic hyperactivity from catecholamines causing a plague rupture or erosion causing increased Coagulability and decreaed fibrinolysis which causes a Acute Coronary Thrombosis

Type 2 is from sever Stable CAD whic an increased myocardial 02 demand causing increase HR increased sympathetic hyperactivity, increased BP, increaed LVEDP, causing a supply and demand issue
Usually prolonged ST depression

52
Q

Type 1) Occlusive MI

Type 2) Infarction secondary to supply and demand

Type 3) Sudden cardiac death

Type 4) PCI causing infarction

Type 5) CABG causing infarction

A

Types of MIs

53
Q

Difference between a OMI and. NOMI

A

OMI is a complete vessel occlusion

NOMI is a narrowed vessel no totally occluded.

54
Q

Non MI Troponin elevation cause

A

Sepsis, CHF, Renal Failure, Stroke

55
Q

What happens to ST segments during NSTEMI AND STEMI AND WHY

A

During NSTEMI subendocardial cells are more susceptible to ischemia.
- Pottaium leak arrives from ischemic tissue causing a partial depolarization towards the electrode which causes the baseline to shift upward.

This looks like ST depression

During Stemi
- potassium leak happens prior to electric stimulation and produces a force away from the electrode cause it an upward shift of baseline

Looking like ST elevation

Q waves
- necrotic muscles does not generate electrical forces

CCP 2 Review (2 decks)

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