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CARDIOVASCULAR > CARDIOVASCULAR- Physiology > Flashcards

CARDIOVASCULAR- Physiology Flashcards

1
Q

Which ia the formula to calculate Cardiac output?

A

Stroke volume X heart rate

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2
Q

Using Fick principle how do you calculate Cardiac output?

A

CO= Rate of O2 consumption
———————————————————
arterial O2 content- venous O2 content

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3
Q

What is the mean arterial Pressure?

A

Cardiac output X Total peripheral resistance

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4
Q

Formula to calculate Mean arterial pressure

A

MAP= 2/3 diastolic pressure+ 1/3 systolic pressure

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5
Q

How do you calculate Pulse pressure?

A

Pulse pressure= Systolic pressure- diastolic pressure

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6
Q

What is the pulse pressure?

A

Is proportional to Stroke volume, inversely proportional to arterial compliance

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7
Q

In order to calculate Stroke volume we need this formula

A

SV= End Dyastolic Volume- End systolic Volume

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8
Q

During early stege of excercise how is Cardiac output maintan?

A

↑ Heart rate and ↑ Stroke volume

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9
Q

During late stages of excercise how is the Cardiac output affected?

A

↑ Heart rate only (Stroke volume plateu)

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10
Q

How is Diastole affected with ↑ Heart rate?

A

Diastole is prefetentially shortened with ↑ Heart rate

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11
Q

How is Cardiac Output affectedif Diastole is shortened with ↑ Heart Rate?

A

Less filling time → ↓ CO (eg Ventricular tachycardia)

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12
Q

When is Pulse pressure increased?

A

In hyperthyrodism, aortic regurgitation, arteriosclerosis, obstructive apnea (sympathetic tone), exercise (transient)

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13
Q

In these situation pulse pressure is decreased

A

Aortic stenosis, cardiogenic shock, cardiac tamponade, and advanced hear failure

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14
Q

Who affects Stroke volume?

A

By Contractility, Afterload, Preload

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15
Q

When does Stroke volume increases?

A

↑ contractility, ↑ preload or ↓ afterload

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16
Q

When do Contractility and Stroke volume (SV) increase?

A

Cathecholamines
↑ increased intracellular Ca2+
↓ extracellular Na+ (↓ activity of Na+/Ca2+ exchanger)
Digitalis

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17
Q

How digitalis increase contractility?

A

Blocks Na+/ K+ pump → ↑ intracellular Na+ → ↓ Na+/Ca2+ exchanger → ↑ intracellular Ca2+

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18
Q

Explain the mechanism of how cathecolamins increase contractility

A

↑ activity of Ca2+ pump in sarcoplasmic reticulum

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19
Q

In these situations Contractility and Stroke volume is decreased

A 
β 1 blockade (↓cAMP)
Heart failure with systolic dysfunction
Acidosis
Hypoxia/ Hypercapnea (↓ PO2/ ↑ PCO2)
Non dihydropyridine Ca2+ blockers
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20
Q

These are normal situations that increase Stroke volume

A

Anxiety, excercise, pregnancy

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21
Q

How does a failling heart affects Stroke Volume?

A

↓ Stroke Volume (both systolic and diastolic dysfunction)

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22
Q

Which situation increase Myocardial O2 demand?

A

↑ afterload
↑ contractility
↑ Heart rate
↑ ventricular diameter (↑ wall tension)

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23
Q

Which measured is approximated to Preload?

A

Ventricular End dyastolic Volume (EDV)

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24
Q

Preload depends on this factors

A

Venous tone and circulating blood volume

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25
Q

What decreases preload?

A

Venodilators (nitroglicerin)

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26
Q

Which measured is approximated to Afterload?

A

By MAP (Mean Arterial pressure)

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27
Q

What does Laplace’s law states related to Afterload?

A

Relation of Left Ventricle size and afterload

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28
Q

Laplace’s law formula

A

Wall tension = pressute X radius
—————————-
2 X wall thickness

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29
Q

Law related to After load

A

Laplace’s Law

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30
Q

What is the result of ↑ After load?

A

LV compensates for ↑ Afterload by thickening (hypertrophy) to ↓ wall tension

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31
Q

This drug Decreases just Afterload?

A

Vasodilators (hydralazine) ↓ Afterload (arterial)

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32
Q

These drugs decrease both Atferload and Preload

A

ACE inhibitors and ARBs

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33
Q

Which chronic situation can lead to Left ventricle hypertrophy?

A

Chronic hypetension (↑ MAP)

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34
Q

Formula to calculate Ejection Fraction

A

SV EDV- ESV
EF= ——- = —————-
EDV EDV

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35
Q

What does Left ejection means?

A

Index of ventricular contractility

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36
Q

Which is the normal value of Ejection Fraction?

A

> 55 %

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37
Q

When is Ejection Fraction decreased?

A

In systolic heart failure

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38
Q

How is Ejection fraction in dyastolic heart failure?

A

Normal

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39
Q

Force of contraction is proportional to…

A

End diastolic length of cardiac muscle fiber

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40
Q

What is End diastolic length of cardiac muscle fiber?

A

Preload

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41
Q

When is Contractility decreased?

A

Loss of myocardium (eg. MI), β blocker, calcium channel blockers, dilated cardiomyopathy

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42
Q

Which are the parameters measured in Starling curve?

A

Stroke Volume (or Cardiac Output) compared to Ventricular End diatolic Volume (Preload)

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43
Q

In which situation is Starling curve above normal range

A

Excercise

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44
Q

When is Starling curve below normal range?

A

CHF+ digoxin

CHF

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45
Q

What is ΔP?

A

Changes in pressure (pressure gradient)

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46
Q

What is Q?

A

Flow

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47
Q

Meaning of R

A

Resistance

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48
Q

Formula to calculate Pressure gradient

A 
Pressure gradient (ΔP) = Flow (Q) X Resistance (R)     
ΔP = Q X R
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49
Q

Which other formula is similar to ΔP = Q X R?

A

Ohm’s law: ΔV = IR

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50
Q

In order to calculate Resistance what is needed?

A

driving pressure (ΔP) 8 n (viscosity) X length
R= ——————————– = ———————————–
flow (Q) πr4

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51
Q

How is Total resistance of vessels in series calculated?

A

TR= R1+ R2+ R3…..

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52
Q

For Total resistance of vessels in parallel this is the Formula

A

1 1 1 1
—- = — + — + — ….
TR R1 R2 R3

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53
Q

On what mostly depends the viscosity?

A

On Hematocrit

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54
Q

When is Viscosity increased?

A

Polycythemia
Hyperproteinemic states (multiple myeloma)
Hereditary spherocytosis

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55
Q

When is viscosity decreased?

A

Anemia

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56
Q

How does pressure gradient drives flow?

A

From high pressure to low pressure

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57
Q

What is directly proportional to resistance?

A

Directly proportional to viscosity and vessel

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58
Q

Resistance is inversely proportional to….

A

the radius to the 4th power

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59
Q

They regulate capillary flow

A

Arterioles account for most of Total Peripheral Resistance

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60
Q

What happens in inotropy?

A

Changes in contractility → altered Cardiac Output for a given Right Atrium pressure (preolad)

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61
Q

They are inotropy positive

A

Catecholamines, digoxin

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62
Q

Examples of inotropy negative

A

Uncompensated heart failure, narcotic overdose

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63
Q

What causes Venous return changes?

A

Altered Rigth Atrium pressure for a given Cardiac output. Mean systemic pressure changes with volume/ venous tone.

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64
Q

In venous return, when does the mean systemic pressure changes?

A

With volume/ venous tone

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65
Q

Example of Positive venous return

A

Fluid infusion, sympathetic activity

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66
Q

Name situation that negatively stimulates venous return

A

Acute hemorrhage, spinal anesthesia

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67
Q

What causes Total peripheral resistance changes?

A

Altered Cardiac Output at a given Rigth Atrial pressure; however, mean systemic pressure is unchanged

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68
Q

What causes positive total peripheral resistance?

A

Vasopresors

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69
Q

In this situation exist negative total peripheral resistance

A

Exercise, AV shunt

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70
Q

How are cardiac and vascular functions affected by excersice?

A

Reinforcing:
↑ inotropy
↓ Total peripheral resistance
To maximize Cardiac Output

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71
Q

How are cardiac and vascular functions affected by heart?

A

↓ inotropy

Fluid retention to ↑preload to maintain Cardiac Output

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72
Q

Which are the phases of Pressure volume loops and cardiac cycle?

A

1) Isovolumetric contraction
2) Systolic ejection
3) Isovolumetric relaxation
4) Rapid filling
5) Reduced filling

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73
Q

When does the isovolumetric contraction occurs?

A

Period between mitral valve closing and aortic valve opening

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74
Q

When is the period of highest O2 consumption?

A

During isovolumetric contraction

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75
Q

Period of Systolic ejection

A

Period between aortic valve opening and closing

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76
Q

Period between aortic valve closing and mitral valve opening

A

Isovolumetric relaxation

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77
Q

Period just after mitral valve opening

A

Rapid Filling

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78
Q

Reduced Filling

A

Period just before mitral valve closing

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79
Q

What does S1 means?

A

Mitral and tricuspide valve closure

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80
Q

Where is the loudest area to hear S1?

A

Mitral area

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81
Q

What is the meaning of S2?

A

Aortic and pulmonary valve closure

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82
Q

Where is better heard S2?

A

Left Sternal border

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83
Q

What does S3 means?

A

In early diastole during rapid ventricular filling phase

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84
Q

Which situations are associated to S3?

A

↑ Filling pressures (eg. mitral regurgitation, CHF) and common in dilated ventricles

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85
Q

When is S3 consider normally?

A

Normal in children and pregnant women

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86
Q

Alternative name for S4?

A

Atrial kick

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87
Q

When is S4 heard?

A

In late diastole

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88
Q

What does S4 means?

A

High atrial pressure

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89
Q

If we heard a S4 what should we think?

A

Associated with ventricular hypertrophy. Left atrium must push against stiff LV wall

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90
Q

Which are the four waves in Jugular venous pulse?

A

a, c, x, v, y

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91
Q

What does a wave in Jugular venous pulse means?

A

Atrial contraction

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92
Q

Which is the meaning of c wave in Jugular venous pulse?

A

RV contraction (closed tricuspid valve bulging into atrium)

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93
Q

What does x descent in Jugular venous pulse means?

A

Atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction

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94
Q

When is x descent absent?

A

In tricuspid valve

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95
Q

v wave in Jugular venous pulse means

A

↑ right atrial pressure due to filling against closed tricuspid valve

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96
Q

Meaning of y descent wave

A

Blood flow from Right Atrium to Right Ventricle

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97
Q

What happens in normal heart splitting sound?

A

Inspiration → drop in intrathoracic pressure→ ↑ venous return to the RV→ ↑ RV stroke volume → ↑ RV ejection time→ delayed closure of pulmonary valve

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98
Q

What else happens during insipiration?

A

↓ pulmonary impedance (↑ capacity of the pulmonary circulation)

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99
Q

What contributes to delayed closure of pulmonic valve?

A

↓ pulmonary impedance (↑ capacity of the pulmonary circulation)

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100
Q

How is represented Normal splitting?

A

Expiration I I I
S1 A2 P2
Inspiration I I I

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101
Q

When is heard the wide splitting of Heart sounds?

A

Seen in conditions that delayed RV emptying:
Pulmonic stenosis
Right bundle branch block

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102
Q

What does delay in RV causes?

A

Delayed pulmonic sound (regardless of breath)

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103
Q

How is wide splitting heard?

A

An exaggeration of normal splitting

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104
Q

Represent the wide splitting

A

Expiration I I I
S1 A2 P2
Inspiration I I I

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105
Q

When is Fixed splitting seen?

A

Atrial Septal Defect

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106
Q

Which are the repercussions of Atrial Septal Defect?

A

Atrial Septal Defect → left to right shunt → ↑ Ra and RV volumes → ↑ flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed

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107
Q

How is the fixed splitting pattern?

A

Expiration I I I
S1 A2 P2
Inspiration I I I

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108
Q

When is paradoxical splitting heard?

A

In conditions that delay LV emptying

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109
Q

Which situations delay LV empting?

A

Aortic stenosis, left bundle branch block

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110
Q

What is the difference of a normal splitting and paradoxical spliting?

A

Normal order of valve closure is reversed so that P2 sounds occurs before delayed A2 sound

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111
Q

This is the reason why is a paradoxical splitting

A

On insporation, P2 close later and moves closer to A2, thereby “paradoxycally” eliminating the split

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112
Q

Schematically how is Paradoxical splitting?

A

Expiration I I I
S1 P2 A2
Inspiration I II

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113
Q

What can be heard in Aortic area?

A

Systolic murmur

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114
Q

Systolic murmurs in Aortic area?

A

Aortic stenosis
Flow murmur
Aortic valve sclerosis

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115
Q

What can be heard in left sternal border?

A

Diastolic and Systolic murmurs

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116
Q

You might identify these diastolic murmur pathologies in the left sternal border

A

Airtic regurgitation

Pulmonic valve regurgitation

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117
Q

You might identify these systolic murmur pathology in the left sternal border

A

Hypertrophic cardiomyopathy

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118
Q

what can be heard in Pulmonic area?

A

Systolic ejection murmur

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119
Q

What can a systolic ejection murmur in pulmonic area mean?

A 
Pulmonic stenosis
Flow murmur (physiologic murmur)
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120
Q

This is what can be heard in Tricuspid area

A

Pansystolic murmur

Diastolic murmur

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121
Q

Pansystolic murmur in Tricuspid area can mean…

A

Tricuspid regurgitation

Ventricular Septal defect

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122
Q

Diastolic murmur in Tricuspid area can mean…

A

Tricuspid stenosis

Atrial septal defect

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123
Q

Mitral area sounds can be classified as

A

Systolic and Dyastolic murmurs

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124
Q

Systolic murmur in mitral area means…

A

Mitral regurgitation

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125
Q

Diastolic murmur in Mitral area means…

A

Mitral stenosis

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126
Q

How can a Atrial Septal Defect be presented?

A

Pulmonary flow murmur (↑ flow across tricuspid); blood flow across the actual ASD does not cause a murmur because there is no pressure gradient

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127
Q

How the murmur of Atrial septal defect can evolve?

A

The murmur later progresses to a louder diastolic murmur of pulmonic regurgitation from dilation of the pulmonary artery

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128
Q

During inspiration how are heart sounds modified?

A

↑ intensity of right heart sounds

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129
Q

What is the effect of Hand grip maneuver?

A

↑ systemic vascular resistance

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130
Q

What can be heard with Hand grip maneuver?

A

↑ intensity of MR, AR, VSD murmurs

↓ intensity of AS, hypertrophic cadiomyopathy murmurs

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131
Q

How can Had grip maneuver affect Mitral valve prolapse sounds?

A

↑ murmur intensity, later onset of click/murmur

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132
Q

When is better apreciated Valsalva maneuver?

A

phase II

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133
Q

What is the effect of Standing in systemic circulation?

A

↓ venous return

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134
Q

If Valsalva maneuver or Standing is realizaed Which murmurs are affected?

A

↓ intensity of most murmurs (including AS)

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135
Q

Which murmurs are ↑ with Valsalva maneuver or Standing?

A

Hypertrophic cardiomyopathy murmur

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136
Q

How can Valsalva maneuver or Standing affect Mitral valve prolapse sounds?

A

↓ murmur intensity, earlier onset of click/murmur

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137
Q

Which are the effects of Rapid squating?

A

↑ venous return, ↑ preload, afterload with prolongued squating

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138
Q

What murmur is ↓ in intensity with Rapid squating?

A

Hypertrophic cardiomyopathy murmur

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139
Q

Which murmur is ↑ in intensity with Rapid squating?

A

AS (aortic stenosis)murmur

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140
Q

How can Rapid squating affect Mitral valve prolapse sounds?

A

↑ murmur intensity, later onset of click/murmur

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141
Q

What pathologies does Systolic heart sounds include?

A

Aortic/ pulmonic stenosis, Mitral/ tricuspid regurgitation, ventricular septal defect

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142
Q

These pathologies are included in Diastolic heart sounds

A

Aortic/ pulmonic regurgitation, mitral/tricuspid stenosis

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143
Q

How is Mitral/Tricuspid regurgitation heard?

A

Holosystolic, high pitched blowing murmur

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144
Q

Where is better heard mitral?

A

Loudest at apex and radiates toward axilla

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145
Q

What enchance Mitral sounds?

A

By maneuvers that ↑ Total peripheral resistance

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146
Q

Which are common reasons of Mitral regurgitation?

A

Ischemic heart disease, Mitral Valve prolapse, Left ventricle dilation

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147
Q

Where is Tricuspid sound better heard?

A

Loudest at tricuspid areaand radiates to right sternal border

148
Q

When is Tricupid enhance?

A

By maneuvers that ↑ Rigth Atrial return (eg inspiration)

149
Q

Which is the common cause of Tricuspid Regurgitation?

A

Right ventricle dilation

150
Q

Which pathology can cause either Mitral Regurgitation of Tricuspid Regurgitation?

A

Infective Endocarditis

151
Q

This is the murmur caused by Aortic stenosis

A

Crescendo-decrescendo systolic ejection murmur

152
Q

What happens in Aortic stenosis?

A

LV» aortic pressure during systole

153
Q

Where is Aortic Stenosis better heard?

A

Heart base; radiates to carotids

154
Q

Which pulse is seen in Aortic Stenosis? What does it means?

A

“Pulsus parvus et tardus”- pulsesare weak with delayed peak

155
Q

Which could be the results if Aortic Stneosis?

A

Syncope, Angina, Dysnea on exertion

156
Q

These are reasons of Aortic Stenosis

A

Age related calcific aortic Stenosis or Bicuspid aortic valve

157
Q

What can be heard in Ventricular Septal Defect?

A

Holosystolic, harsh sounding murmur

158
Q

Where is better heard Ventricular Septal Defect?

A

Loudest at tricuspid area

159
Q

What accentuates Ventricular Septal Defect murmur?

A

Hand grip maneuver due to ↑ afterload

160
Q

What is heard in Mitral Valve prolapse?

A

Late systolic crescendo murmur with midsystolic click

161
Q

Why is Midsystolic click heard in Mitral valve prolapse?

A

Due to tensing of chordae tendineae

162
Q

Which is the most frequent valvular lession?

A

Mitral valve prolapse

163
Q

Where is better heard mitral valve prolapse?

A

Over Apex

164
Q

When is better heard mitral valve prolapse?

A

Loudest just before S2

165
Q

How is the prognosis of Mitral valve prolapse?

A

Usually Benign

166
Q

What can Mitral valve prolapse predispose?

A

Infective endocarditis

167
Q

Which could be the causes of Mitral valve prolapse?

A

Myxomatous degeneration, rheumatic fever, or chordae rupture

168
Q

What predisposes an earlier apperance of Mitral valve prolapse?

A

Maneuvers that ↓ venous return (standing or Valsalva)

169
Q

How are Heart murmurs classified?

A

Systolic
Diastolic
Continuous

170
Q

Name systolic murmur causes

A

Mitral/ Tricuspid regurgitation
Aortic Stenosis
Ventricular Septal Defect
Mitral Valve prolapse

171
Q

These are Diastolic murmur causes

A

Aortic regurgitation

Mitral stenosis

172
Q

In this pathology we can heard a Continuous murmur

A

Patent Ductus Arteriosus

173
Q

What is heard in Aortic regurgitation?

A

High pitched “blowing” early diastolic decrescendo murmur

174
Q

When Aortic regurgitation is chronic what can be seen?

A

Wide pulse pressure; can present with bounding pulses and head bobbing

175
Q

These are possible causes of Aortic Regurgitation

A

Aortic Root dilation
Bicuspid aortic valve
Endocarditis
Rheumatic fever

176
Q

When is aortic regurgitation better heard?

A

↑ murmur during hand grip

177
Q

What decreases intensity of murmur in Aortic regurgitation?

A

With Vasodilators

178
Q

In mitral Stenosis what is heard?

A

Follows opening snap

179
Q

Which is the reason of Opening snap in Mitral Stenosis?

A

Due to abript half in leaflet mition in diastole, after rapid opening due to fusion at leaflet tips

180
Q

When is Mitral Stenosis heard?

A

Delayed rumbling late diastolic murmur

181
Q

In mitral Stneosis what correlates with increased severity?

A

↓ Interval of between S2 and Opening Snap

182
Q

This is what happens in Mitral Stenosis

A

LA&raquo_space; LV pressure during diastole

183
Q

Which is the most common reason of Mitral Stenosis?

A

Secondary to Rheumatic Fever

184
Q

What could be the result of Chronic Mitral Stenosis?

A

Left Atrial Dilation

185
Q

What enhances Mitral stenosis?

A

Maneuvers that ↑ Left Atrial return (expiration)

186
Q

What is heard in Patent ductus arteriosus?

A

Continuous machine-like murmur

187
Q

When is Patent ductus arteriosus murmur better heard?

A

Loudest at S2

188
Q

Common causes of Patent ductus arteriosus

A

Congenital Rubella

Prematurity

189
Q

Where is Patent ductus arteriosus murmur better heard?

A

At left infraclavicular area

190
Q

Where else does Ventricular action potential takes place?

A

Bundle of His and Purkinje fibers

191
Q

How many phases does Ventricular action potential has?

A

0, 1, 2, 3, 4

192
Q

What happens in Phase 0 of Ventricular action potential?

A

Rapid upstroke and depolarization

193
Q

Which channles are open in Ventricular action potential phase 0?

A

Voltage gated Na+ channels

194
Q

This phase is known as initial repolarization in Ventricular action potential

A

Phase 1

195
Q

Which channels interact in Phase 1 of Ventricular action potential?

A

Inactivation of Voltage gated Na+ channels

Voltage gated K+ channels begin to open

196
Q

How is phase 2 of Ventricular action potential known?

A

Plateau

197
Q

Which channels are affected in Plateau phase of Ventricular action potential?

A

Ca+ influx through voltage gated Ca2+ channels balances K+ efflux

198
Q

During phase 2 of Ventricular action potential what does Ca2+ influx triggers?

A

Triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction

199
Q

Also known as Rapid repolarization phase in Ventricular action potential

A

Phase 3

200
Q

What happens in Rapid repolarization phase during Ventricular action potential?

A

Massive K+ efflux due to opening of voltage gated slow K+ channels and closure of gated Ca2+ channels

201
Q

What is phase 4 of Ventricular action potential?

A

Resting potential

202
Q

Which channels are permeable in Resting potential?

A

High K+ permeability through K channels

203
Q

Which is the difference in channels between skeletal muscle and Cardiac muscle?

A

Cardiac Miscle action potential has a plateau, which is due to Ca2+ influx and K+ efflux
Myocite contraction occurs due to Ca2+ induced Ca2+ release from the sarcoplasmic reticulum

204
Q

When are Cardiac nodal cells depolarize?

A

During Diastole

205
Q

What is the result of cardiac nodal cells depolarization?

A

Automaticity due to If channels

206
Q

What are If channels?

A

“Funny current” channels responsible for a slow, mixed Na+/ K+ inward current

207
Q

What other difference do Cardiac cells have from Skeletal muscle cells?

A

Cardiac Myocytes are electrically coupled to each other by gap junctions

208
Q

From how many mV does Ventricular action potential goes?

A

More than 0 mV to -85 mV

209
Q

How much time does Efective refractory period last?

A

200 msec

210
Q

From which phases does Efective refractory period takes place?

A

From phase 1 to phase 4

211
Q

What is the Efective refractory period?

A

Is the time when the cardiac cell can’t be depolarize

212
Q

Where does Pacemaker action potential occurs?

A

In the SA and AV nodes

213
Q

What happens in Phase 0 of Pacemaker action potential?

A

Upstoke- Opening of voltage gated Ca2+ channels

214
Q

What happens to the fast voltage gated Na+ channels in Pacemaker action potential?

A

Are permanently inactivated

215
Q

Why are fast voltage gated Na+ channels in Pacemaker action potential inactivated?

A

Because of less negative resting voltage of these cells

216
Q

Which is the result inactivated fast voltage gated Na+ channels in Pacemaker action potential?

A

Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles

217
Q

What happens in phase 2 of pacemaker action potential?

A

Phase 2 is absent

218
Q

Which channels are affected in phase 3 of pacemaker action potential? and How?

A

Inactivation of Ca2+ channels and ↑ activation of K+ channels → ↑ K+ efflux

219
Q

How is phase 4 of pacemaker action potential known?

A

Slow diastolic depolarization

220
Q

What happens during phase 4 of pacemaker action potential?

A

Membrane potential spontaneously depolarizes as Na+ conductance ↑

221
Q

Which channels are different in pacemaker action potential and Ventricular action potential?

A

If different from INa in phase 0

222
Q

Which phase acounts as the automaticity of SA and AV nodes?

A

Phase 4

223
Q

In the pacemaker action potential what determines the Heart rate?

A

The slope of phase 4 in the SA node determines Heart Rate

224
Q

What is the effect of ACh/ adenosine in heart?

A

↓ the rate of diastolic depolarization and ↓ Heart rate

225
Q

What ↓ the rate of diastolic depolarization and ↓ Heart rate?

A

ACh/ adenosine

226
Q

These is the effect of catecholamines in heart?

A

↑ depolarization and ↑ Heart Rate

227
Q

Who ↑ depolarization and ↑ Heart Rate?

A

Catecholamines

228
Q

What is the effect of Sympathetic stimulation in heart?

A

↑ the chance that If channels are open and thus ↑ Heart Rate

229
Q

From how many mV does pacemaker action potential goes?

A

Little less -60 to little more than 0

230
Q

In electrocardiogram what does P wave means?

A

Atrial depolarization

231
Q

Who masks Atrial repolarization in Electrocardiogram?

A

By QRS comlex

232
Q

What does PR interval means?

A

Conduction delay through AV node

233
Q

How much time does PR interval normally last?

A

< 200 msec

234
Q

What is QRS complex?

A

Ventricular depolarization

235
Q

Time that QRS normally lasts?

A

< 120 msec

236
Q

What happens in QT interval?

A

Mechanical contraction of the ventricles

237
Q

What is the T wave?

A

Ventricular Repolarization

238
Q

What electrocardiogram change indicates recent MI?

A

T wave inversion

239
Q

What happens in ST segment?

A

Isoelectric, ventricles depolarized

240
Q

When is U wave present in electrocardiogram?

A

Caused by hypokalemia, bradycardia

241
Q

How is the speed of conduction?

A

Purkinje> atria> ventricles> AV node

242
Q

How are classify the Pacemakers?

A

SA> AV> bundle of His/ Purkinje/ ventricles

243
Q

How is the conduction Pathway?

A

SA node→ Atria → AV node → common bundle→ bundle branches → Purkinje fibers → ventricles

244
Q

Which are the characteristics of SA node?

A

Pacemaker inherent dominance with slow phase of upstroke

245
Q

Which is the delay of AV node?

A

100 msec

246
Q

What does the Atrioventricular delay allows?

A

Allows time for ventricular filling

247
Q

How is the potential measured in Electrocardigram?

A

In mV

248
Q

From how many mV RS goes?

A

1.0 to -0.5

249
Q

What are Torsades de Pointes?

A

Polymorphic ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG

250
Q

Which is the possible progression of Torsades de Pointes?

A

To Ventricular fibrillation

251
Q

What predisposes to Torsades de Pointes?

A

Long QT interval

252
Q

Who causes Torsades de Pointes?

A

Drugs, ↓ K+, ↓ Mg2+, other abnormalities

253
Q

What is included in the treatment of Torsades de Pontes?

A

Magnesium sulfate

254
Q

Which medicines can cause Torsades de Pointes?

A 
Some Risky Meds Can Prolong QT
Sotalol
Risperidone 
Macrolides
Chloroquine
Protease inhibitors (navir)
Quinidine (class Ia, also class III)
Thiazides
255
Q

Inherited disorder of myocardial repolarization

A

Congenital long QT syndrome

256
Q

Which is the reason of Congenital long QT syndrome?

A

Typically due to ion channel defects

257
Q

Which are the risks of Congenital long QT syndrome?

A

Increased risk of sudden cardiac death due to torsades de pointes

258
Q

Which are Congenital long QT syndrome?

A

Romano Ward syndrome

Jervell and Lange Nielsen syndrome

259
Q

Genetically which is the inheritance mode of Romano Ward syndrome?

A

Autosomal dominant

260
Q

What is the phenotype affection in Romano Ward syndrome?

A

Pure cardiac phenotype (no deafness)

Congenital long QT syndrome

261
Q

Inheritance mode for Jervell and Lange Nielsen syndrome

A

Autosomal recessive

262
Q

Phenotype Characteristics of Jervell and Lange Nielsen syndrome

A

Sensorioneural deafness

Congenital long QT syndrome

263
Q

Most common type of ventricular pre excitation syndrome

A

Wolff Parkinson White syndrome

264
Q

What is Wolff Parkinson White syndrome?

A

Most common type of ventricular pre excitation syndrome

265
Q

Which is the defect in Wolff Parkinson White syndrome?

A

Abnormal fast accessory conduction pathway from atria to ventricle bypasses tje rate slowing AV node

266
Q

Which is the Abnormal fast accessory conduction pathway from atria to ventricle in Wolff Parkinson White syndrome?

A

Bundle of Kent

267
Q

What are the results of Bundle of Kent in Wolff Parkinson White syndrome?

A

Ventricles begin to partially depolarize earlier, giving rise to characteristic delta wave with shortened PR interval on ECG

268
Q

What is the Delta wave?

A

Partial Ventricles depolarization earlier

269
Q

Which could be the complication of Wolff Parkinson White syndrome?

A

May result in reentry circuit → Supraventricular tachycardia

270
Q

Which is the ECG pattern of Atrial Fibrilation?

A

Chaotic and erratic baseline(irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes

271
Q

Which are the possible outcomes of Atrial fibrilation?

A

Can result in atrial stasis and lead to Thromboembolic stroke

272
Q

Which are the treatments for Atrial Fibrilation?

A

Includes rate control, Anticoagulant, and possible pharmacological or electrical cardioversion

273
Q

How is Atrial flutter seen in EKG?

A

A rapid succession of identical, back to back atrial depolarization waves

274
Q

Which appearance do flutter waves have?

A

Sawtooth appearance

275
Q

Which is the Pharmacological treatment for Atrial Flutter and what is its purpose?

A

Pharmacological conversion to sinus rhythm, Class IA, IC or III antiarrhythmics
Rate control

276
Q

Which is the pharcmacological treatment for Atrial Flutter for Rate control?

A

β blocker or Calcium channel blockers

277
Q

Definitive treatment for Atrial Flutter

A

Catheter ablation

278
Q

On ECG what is seen in Ventricular Fibrilation?

A

A completely erratic rhythm with no identifiable waves

279
Q

Which could be the prognosis of Ventricular Fibrilation?

A

Fatal arrythmia without immediate CPR and defibrillation

280
Q

What happens in 1st degree AV block?

A

The PR interval is prolonged (> 200 msec)

281
Q

How is the prognosis of 1st degree AV block?

A

Benign and asymptomatic

282
Q

Which is the treatment for 1st degree AV block?

A

No treatment required

283
Q

How are AV blocks Classified?

A 
1st Degree
2nd Degree
       Mobitz Type I 
       Mobitz Type II
3rd Degree
284
Q

How else is Mobitz Type I known?

A

Wenckebach

285
Q

What happens in Mobitz I?

A

Progressive lenghtening of the PR interval until a beat is dropped (a P wave not followed by QRS complex)

286
Q

Explanation of Mobitz II

A

Dropped beats that are not preceded by a change un the length of the PR interval (as in type I).
It is often found as 2:1 block, where there are 2 or more P waves to 1 QRS response

287
Q

Which is the prognosis of Mobitz II?

A

Might progress to 3rd degree block

288
Q

How is Mobitz often treated?

A

With Pacemaker

289
Q

AV block known as complete block

A

3rd degree

290
Q

What happens in 3rd degree block?

A

The atria and the ventricles beat independiently of each other

291
Q

Which is the ECG pattern of 3rd degree block?

A

Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes

292
Q

Which rate is faster in 3rd degree block?

A

Atrial rate is faster than the ventricular rate

293
Q

How is 3rd degree block ussually treated?

A

With pacemaker

294
Q

Which infectious disease can result in 3rd Degree block?

A

Lyme disease

295
Q

Who produces Atrial natriuretic peptide?

A

Released from atrial myocytes

296
Q

When do atrial mycytes produce Atrial natriuretic peptide?

A

in response to ↑ blood volume and atrial pressure

297
Q

Which is the effect of Atrial natriuretic peptide?

A

Vasodilation and ↓ Na+ reabsorption at the renal collecting tubule

298
Q

Which is the renal effect of Atrial natriuretic peptide?

A

Constricts efferent renal arterioles and dilates afferent arterioles via cGMP, promoting diuresis and contributing to “aldosterone escape” mechanism

299
Q

Another name for B type natriuretic peptide

A

Brain natriuretic peptide

300
Q

Who releases B type natriuretic peptide?

A

Ventricular myocytes

301
Q

When is B type natriuretic peptide release from ventricular myocytes?

A

In response to ↑ tension

302
Q

How is B type natriuretic peptide compared to Atrial natriuretic peptide?

A

Similar physiologic action to ANP, with longer half life

303
Q

What is the purpose to measured B type natriuretic peptide in blood test?

A

Diagnosing Heart failure (very good negative predictive value)

304
Q

This is the recombinant form of B type natriuretic peptide

A

Nesiritide

305
Q

When is Neseritide recommended?

A

For treatment of Heart failure

306
Q

How does aortic arch transmits to solitary nucleus?

A

Via Vagus nerve

307
Q

Where is Solitary nucleus located?

A

Medulla

308
Q

Which stimulates are needed for Receptors in Aortic arch to respond?

A

Respond only to ↑ Blood pressure

309
Q

Where is carotid sinus located?

A

Dilated region at carotid bifurcation

310
Q

How does carotid sinus transmits to solitary nucleus?

A

Via Glossopharingeal nerve

311
Q

Which stimulates are needed for Receptors in carotid sinus to respond?

A

Respond to ↓ and ↑ Blood pressure

312
Q

Which is the importance of Barorreceptors?

A

Important in the response to severe hemorrhage

313
Q

From Hypotension to Increased Blood Pressure how do Barorreceptors interact?

A

Hypotension- ↓ arterial pressure→ ↓ strecth → ↓ Afferent baroreceptor function → ↑ efferent sympathetic firing and ↓ efferent parasympathetic stimulation → Vasocontriction, → ↑ HR, ↑ contractility, ↑ BP

314
Q

Which is the chain of events caused with Carotid massage?

A

↑ pressure on carotid sinus → ↑strethc → ↑afferent baroreceptor firing → ↑ AV node refractory period → ↓ HR

315
Q

For what do Barorreceptors contribute?

A

To Cushing Reaction

316
Q

What is the Cushing reaction?

A

Triad of hypertension, bradycardia and respiratory depression

317
Q

How Baroreceptors contribute in Cushing reaction?

A

↑ Intracraneal pressure constricts arterioles → cerebral ischemia and reflexes sympathetic ↑ in perfussion pressure (hypertension) → ↑ stretch → Reflex baroreceptor induced-bradycardia

318
Q

When is consider PO2 is decreased?

A

< 60 mmHg

319
Q

Name the types of Chemoreceptors

A

Peripheral

Central

320
Q

In peripheral chemoreceptors who are stimulated?

A

Carotid and aortic bodies

321
Q

In peripheral chemoreceptors what stimulates Carotic and aortic bodies?

A

↓ PO2
↑ PCO2
↓ pH of blood

322
Q

How do Central chemoreceptors work?

A

Are stimulated by changes in pH and PCO2 of brain interstitial fluid, which in turn are influenced by arterial CO2

323
Q

Which Chemoreceptors do not directly respond to PO2?

A

Central

324
Q

Organ with largest blood flow

A

Lung

325
Q

Percentage of Cardiac output that flows through Lungs?

A

100%

326
Q

Largest share of systemic cardiac output

A

Liver

327
Q

Highest blood flow per gram of tissue

A

Kidney

328
Q

Largest arteriovenous O2 difference

A

Heart

329
Q

Why is heart conisder to have Largest arteriovenous O2 difference?

A

Because O2 extraction is 80%

330
Q

In heart what increases O2 demand?

A

↑ Coronary blood flow, not by ↑ extraction of O2

331
Q

What is PCWP?

A

Pulmonary Capillary wedge pressure

332
Q

Which is the purpose to measuse Pulmonary Capillary wedge pressure?

A

Is a goof approximation of left atrial pressure

333
Q

Which is the normal range for PCWP?

A

< 12 mmHg

334
Q

In this pahology PCWP> LV diastolic pressure

A

Mitral stenosis

335
Q

How is Pulmonary Capillary wedge pressure meassured?

A

Pulmonary artery catheter (Swan Ganz catheter)

336
Q

Expected pressure of Right Atrial

A

<5 mmHg

337
Q

Pressure of Right ventricle

A

25/5

338
Q

In Right ventricle this is the normal pressure

A

130/10

339
Q

Expected pressure in Aorta

A

130/90

340
Q

What is the autoregulation?

A

How blood flow to an organ remains constant over a eide range of perfusion pressures

341
Q

Main Organs that have autoregulation

A 
Heart
Brain
Kidneys
Lungs
Skeletal muscle
Skin
342
Q

Factors determining autoregulation in Heart

A 
Local metabolites (vasodilatory):
CO2, adenosine, NO
343
Q

Which factor determines autoregulation in Brain?

A 
Local metabolities (vasodilatory)
CO2 (pH)
344
Q

Factors determining autoregulation in Kidneys

A

Myogenic and tubuloglomerular feedback

345
Q

Which factor determines autoregulation in Lungs?

A

Hypoxia causes Vasoconstriction

346
Q

Which vasculature is unique in that hypoxia causes Vasoconstriction?

A

Pulmonary vasculature

347
Q

Which pulmonary areas are perfused?

A

Only well ventilated areas are perfused

348
Q

What is the effect of Hipoxia in the organs, other than the lungs?

A

Hypoxia causes dilation

349
Q

Factors determining autoregulation in Skeletal muscle

A

Local metabolites:

Lactate, adenosine, K+, H+, CO2

350
Q

Which is the factor determinining autoregulation in Skin?

A

Sympathetic stimulation most important mechanism- Temperature control

351
Q

What do Starling forces determine?

A

Fluid movement through capillary membranes

352
Q

Which are the factors in Starling forces?

A 
Pc= Capillary pressure
Pi= Intersticial fluid pressure
πc= Plasma colloid osmotic pressure
πi= Interstisial fluid colloid osmotic pressure
353
Q

What does Capillary pressure does?

A

Pushes fluid out of capillary

354
Q

Effect og Interstitial pressure

A

Pushes fluid into capillary

355
Q

What effect does plasma colloid osmotic pressure has on capillary?

A

Pulls fluids into capillary

356
Q

Which effect does interstitial fluid colloid osmotic pressure has?

A

Pulls fluid out of capillary

357
Q

How is Net filtration pressure calculated?

A

Pnet= (Pc-Pi)- (πc-πi)

358
Q

In Starling forces what is Kf?

A

Filtration constant

359
Q

Who determines the Filtration constant?

A

Capillary permeability

360
Q

For capillary fluid exchange What is Jv?

A

Net fluid flow

361
Q

How do you calculate Net fluid Flow?

A

Jv= (Kf)(Pnet)

362
Q

What is edema?

A

Excess fluid outflow

363
Q

Which are the common causes of Edema?

A

↑ capillary pressure
↓ plasma proteins
↑ capillary permeability
↑ interstitial fluid colloid osmotic pressure`

364
Q

Example of ↑ capillary pressure

A

↑ Pc; heart failure

365
Q

Which cases have ↑ capillary permeability?

A

↑ Kf; toxins. infections, burns

366
Q

Name an example of ↑ interstitial fluid colloid osmotic pressure

A

↑ πi; Lymphatic blockage

CARDIOVASCULAR (6 decks)

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