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Step 1 - Cardiovascular > Physiology > Flashcards

Physiology Flashcards

1
Q

Cardiac output

A

Stroke volume x Heart rate

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2
Q

Cardiac output according to Fick’s principle

A

Rate of oxigen consumption / (arterial O2 content - venous O2 content)

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3
Q

Mean arterial pressure

A

CO x total peripheral resistance (TPR)

2/3 Dyastolic pressure x 1/3 systolic pressure

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4
Q

Pulse pressure

A

Systolic pressure - diastolic pressure

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5
Q

Pulse pressure is proportional to _______ and inversely proportional to ________

A

Stroke volume

Arterial compliance

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6
Q

End diastolic volume - end systolic volume

A

Stroke volume

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7
Q

CO is mantained by ____ and _____ during EARLY stages of exercise

A

Heart rate

Stroke volume

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8
Q

During LATE stages of exercise CO is mantained by

A

Heart rate only

Stroke volume plateaus

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9
Q

Preferentially shortened by high heart rate

A

Diastole

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10
Q

Isolated systolic hypertension in elderly

A

Aortic stiffening

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11
Q

Stroke volume depends on

A
  1. Contractility: directly
  2. Preload: directly
  3. Afterload: inversly
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12
Q

Contractility increases with

A
  1. Cathecolamine stimulation via B1 Rc
  2. Higher intracellular Ca
  3. Lower extracellular Na
  4. Digitalis (Blocks Na/K pump: more ic Na: less Na/Ca exchanger: more intracellular Ca)
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13
Q

Cathecolamine stimulation via B1 receptor effects

A
  1. Ca channels phosphorilated: more Ca entry: more Ca induced ca release and Ca storage in sarcoplasmic reticulum
  2. Phospholamban phosphorylation: active Ca ATPase: Ca storage in sarcoplasmic reticulum
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14
Q

Contractility decreases with

A
  1. Beta 1 blockade: less cAMP
  2. Heart failure with systolic dysfunction
  3. Acidosis
  4. Hypoxia/hypercapnia
  5. Non dihydropyridine Ca channel blockers
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15
Q

Myocardial oxygen demand increases with

A
  1. Contractility
  2. Afterload
  3. Heart rate
  4. Diameter of ventricle: more wall tension
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16
Q

Wall tension

A

Follows Laplace’s law:

Pressure x radius

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17
Q

Wall stress

A

Pressure x radius (tension) / 2 x wall thickness

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18
Q

Decreases preload

A

Venous vasodilators: nitroglycerin

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19
Q

Decreases afterload

A

Arterial vasodilators: hydralazine

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20
Q

Decrese preload and afterload

A 
ACE inhibitors (IECA)
ARB (ARA-II)
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21
Q

Chronic hypertension (increased MAP) produces

A

Left ventricle hypertrophy to overcompensate for high afterload in order to decrease wall tension

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22
Q

Ejection fraction

A

Stroke volume / End diastolic volume

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23
Q

Index of ventricular contractility

A

Ejection fraction

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24
Q

loss of contractility

A
  1. Loss of myocardium: myocardial infarct
  2. Beta blockers
  3. Non dihydropypiridine Ca
  4. Channel Blockers
  5. Dilated cardiomyopathy
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25
Digoxine is a
Positive inotrope
26
_____ account for most of TPR
Arterioles
27
Highest cross-sectional area | Lowest flow velocity
Capillaries
28
Volumetric flow rate (Q)
Flow velocity x cross sectional area
29
Viscosity depends mostly on
Hematocrit
30
Viscosity increases in (examples)
Hyperproteinic states: multiple myeloma | Polycitemia
31
Viscosity decreases in
Anemia
32
Inotropic + effect
Cathecolamines | Digoxin
33
Inotropic - effect
Uncompensated HF Narcotic overdose Sympathetic inhibition
34
Increases venous return
Fluid infusion | Sympathetic activity
35
Decreases venous return
Accute hemorrage | Spinal anesthesia
36
Decreases total peripheral resistance
Exercise | AV shunt
37
Increase total peripheral resistance
Vasopressors
38
Period of the highest ventricular O2 consumption
Isovolumetric contraction
39
Isovolumetric contraction
Between mitral valve closing and aortic valve opening
40
Isovolumetric relaxation
Between aortic valve closing and mitral valve opening
41
Rapid filling
Period just after mitral valve opening
42
Reduced filling
Period just before mitral valve closing
43
Phases of left ventricle
1. Isovolumetric contraction 2. Systolic ejection 3. Isovolumetric relaxatio 4. Rapid filling 5. Reduced filling
44
S1
Mitral and tricuspid valve closure
45
S2
Aortic and pulmonary valve closure
46
S3: when, meaning, pathological/normal
- Early diastole, during rapid ventricular filling - High filling pressures: mitral regurgitation, HF - Dilated ventricles, normal in children and young adults
47
S4: when, meaning, pathological/normal
- Late diastole, atrial kick - High atrial pressure - Ventricular noncompliance: hypertrophy: left atrium must push against stiff LV wall - ABNORMAL, regardless of patient age
48
S4 is normal when
IT's never normal, regardless of patient's age
49
a wave (JVP)
atrial contraction
50
a wave is absent in
atrial fibrillation: a=atrial
51
c wave
RV contraction: c=contraction | Closed tricuspid valve bulging into atrium
52
x descent
Downard displacement of closed tricuspid valve during rapid ventricular ejection phase
53
v wave
high atrial pressure due to filling against closed tricuspid valve
54
y descent
RAtrium emptYing into RV
55
Prominent y descent
Constrictive pericarditis
56
Absent y descent
Cardiac tamponade
57
Normal splitting of S2 occours
During inspiration due to the higher venous return and higher RV filling because of the drop in intrathoracic pressure
58
Wide spitting of S2 occours in
Conditions that delay RV emptying: - Pulmonic stenosis - Right bundle branch block
59
Fixed splitting
Atrial septal defect: left to right shunt: higher Righ atrial and right ventricle volume
60
Paradoxical splitting
Delayed aortic valve closure: -Aortic stenosis -Left bundle branch block On inspiration P2 moves closer to A2, thereby paradoxically eliminating the split
61
Increases intensity of right heart sounds
Inspiration
62
Increases intensity of hypertrophic cardiomyopathy murmur
``` Valsalva (phase II) Standing up (decreases preload) ```
63
Decreases intensity of hypertrophic cardiomyopathy
Handgrip | Squating
64
Hand grip...
Increases afterload: - Less intensity of HCM - More intensity of MR, AR, VSD murmurs
65
Decreases intensity of most murmurs
Valsalva phase II | Standing up
66
Earlier onset of MVP click/murmur
Valsalva | Standing up
67
Aortic stenosis murmur
Crescendo-decrescendo systolic ejection murmur | Click may be present
68
Aortic stenosis symptoms
SAD: Syncope Angina Dyspnea
69
Most common cause of aortic stenosis
Age related calcification in older patients: >60 years old | Early onset calcification of bicuspid aortic valve
70
Mitral/tricuspid regurgitation: murmur characteristics
Holosystolic | High pitched: blowing murmur
71
MR is often due to
Ischemic heart disease: post-MI Mitral valve prolapse Left Ventricle dilatation
72
TR is often due to
Right ventricle dilatation
73
Most frequent valvular lesion
Mitral valve prolapse
74
Mitral valve prolapse: murmur characteristics
Late systolic crescendo murmur with midsystolic click
75
Midsistolic click in mitral valve prolapse is due to
Chordae tendinae sudden tensing
76
Mitral valve prolpase can be caused by
Myxomatous degeneration: Marfan, Ehler-Danlos Rheumatic fever Chordae tendinae rupture
77
Ventricular septal defect murmur
Holosystolic Harsh-sounding Loudest at tricuspid
78
Can predispose to infective endocarditis
Mitral valve prolapse
79
Pulsus parvus et tardus
Aortic stenosis: pulses are weak with a delayed peak
80
Aortic regurgitation murmur
High pitch Early diastolic Decrescendo
81
Watson's water hammer pulse or corrigan pulse or magnus and celer pulse
Aortic regurgitation
82
Severe aortic regurgitation can produce _____ when severe and chronic
head bobbing
83
Aortic regurgitation is due to
Aortic root dilation Bicuspid aortic valve Endocarditis Rheumatic fever
84
Interval between S2-OS and severity of mitral stenosis
Shorter interval=higher severity
85
Mitral stenosis murmur
Opening snap: abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips Mid to late diastolic murmur
86
Late and highly specific sequela of rheumatic fever
Mitral stenosis
87
Chronic Mitral Stenosis can result in
LA dilatation
88
Continuous murmur
Patent ductus arteriosus: continuous machine like murmur loudest at S2 Due to congenital rubella or prematurity
89
Phases of myocardial action potential
0: rapid upstroke and depolarisation 1: initial repolarisation 2: plateau 3: rapid repolarization 4: resting potential
90
Phase 0 of myocardial action potential
Rapid upstroke and depolarisation | Voltage gated Na channels open
91
Phase 1 of myocardial action potential
Initial repolarisation: inactivation of voltage gated Na channels Voltage gated K channels begin to open
92
Phase 2 of myocardial action potential
Ca influx through voltage gated Ca channels balances K efflux Ca influx from ECF triggers Ca release from sarcoplasmic reticulum and myocyte contraction
93
Phase 3 of myocardial action potential
Massive K efflux due to opening of voltage gated slow K channels and closure of voltage gated Ca channels
94
Phase 4 of myocardial action potential
Resting potential | High K permeability through K channels
95
3 differences cardiac muscle vs skeletal muscle
1. Cardiac muscle action potential has a plateau, due to Ca influx and K efflux 2. Cardiac muscle contraction requires Ca influx from ECF to induce Ca release from sarcoplasmic reticulum 3. Cardiac myocytes are electrically coupled to each other by gap junctions
96
Refractory periods in cardiac cycle
1. Absolute refractory period: no stimulus can cause depolarisation 2. Effective refractory period: may allow for non propagated depolarization 3. Relative refractory period: allows a normal than stronger stimuli to cause a full depolarization 4. Supranormal period: hyperexcitable period, even a weak stimulus can trigger an action potential
97
Pacemaker action potentials occour in
SA and AV nodes
98
Phase 0 of pacemaker action potential
Upstroke: opening of voltage gated Ca channels
99
Phase 1 of pacemaker action potential
Doesn't exist
100
Phase 2 of pacemaker action potential
Doesn't exist
101
Phase 3 of pacemaker action potential
Inactivation of Ca channels and activation of K channels: K efflux
102
Determines HR
Slope of phase 4 in the Sa node
103
Adenosine effect on phase 4 of pacemaker action potential
Like ACh decreases the rate of diastolic depolarization and decreases HR
104
Phase 4 of pacemaker action potential
Slow spontaneous diastolic depolarisation due to If: funny current If channels are responsible for a slow mixed Na/K inward current
105
AV node blood supply
Right coronary artery
106
pacemaker rates vs speed of conduction
SA>AV>Bundle of His>Purkinje/ventricles | Speed of conduction: Purkinje>atria>ventricles>AV node
107
Bachmann bundle
Conducts from AV node to left atrium
108
AV node location
Posterioinferior part of interatrial septum
109
PR interval
Time from start of atrial depolarization to start of ventricular depolarization Usually less than 200 msec= 0.2 seg= 5 squares
110
QT interval
Ventricular depolarization Mechanical contraction of the ventricles Ventricular repolarisation
111
T wave
Ventricular repolarization | T wave inversion may indicate ischemia or recent MI
112
J point
Junction between end of QRS complex and start of ST segment
113
ST segment
Isoelectric, ventricles depolarised
114
U wave
Prominent in: - Hypokalemia - Bradycardia
115
Torsades de pointes
Ventricular tachycardia | Can progress to ventricular fibrillation
116
_________ predisposes to torsades de pointes
Long QT interval
117
Drug induced long QT
``` ABCDE AntiArrhythmics: class IA, III AntiBiotics: macrolides Anticychotics: haloperidol AntiDepressants: TCA AntiEmetics: ondansetron ```
118
Treatment of torsades de pointes includes
magnesium sulfate
119
Congenital long QT syndrome
Inherited disorder of myocardical repolarisation typically due to ion channel defects Increase risk of sudden cardiac death (SCD) due to Torsades de Pointes
120
Congenital QT syndrome includes
- Romano-Ward syndrome | - Jervell and Lange-Nielsen syndrome
121
Romano Ward syndrom
Congenital QT syndrome | Pure cardiac phenotype (no deafness)
122
Jervell and Lange Nielsen syndrome
Congenital QT syndrome Autosomal recessive Sensorineural deafness
123
Brugada syndrome
Autosomal dominant Asian males ECG pattern of pseudo-right bundle branch block + ST elevations in V1-V3 Risk of ventricular tachyarrhytmias and SCD Prevent with implantable Cardioverter defibrillator (ICD)
124
Most common type of ventricular pre excitation syndome
Wolff-parkinson White
125
Wolff parkinson white syndrome
- Abnormal fast accessory conduction pathway from atria to ventricle (Bundle of Kent) - Bypasses the rate slowing AV node - Ventricles depolarize earlier: delta wave with widened QRS complex and shortened PR interval on ECG - May result in reentry circuit: SV tachycardia
126
Atrial fibrillation
Chaotic and erratic baseline with no descrete P waves in between IRREGULARLY spaced QRS complexes
127
Atrial fibrillation tratment
- Anticoagulation - Rate control - Rhythm control - Cardioversion
128
Atrial flutter
A rapid succession of IDENTICAL, back to back atrial depolarization wave: sawtooth pattern
129
Definitive treatment of flutter
Catheter ablation
130
No discernible rhythm
Ventricular fibrillation
131
AV block: First degree
PR >200 mseg | Benign and asymptomatic, no treatment required
132
Progressive lengthing of PR interval until a beat is dropped: P wave not followed by QRS
AV block: Second degree: Mobitz type I: Wenckebach
133
Mobitz type II
Dropped beats are not preceded by a change in the length of the PR interval May progress to 3rd degree block Treat with pacemaker
134
Third degree (complete block)
Atria and ventricles beat independently of each other. P waves and QRS complexes not rhytmically associated Atrial rate >Ventricular rate
135
Can be caused by Lyme disease
Third degree (complete) block
136
Third degree block treatment
pacemaker
137
Mobitz type II treament
pacemaker
138
Atrial natriuretic peptide is released from, when, effects
- atrial myocites - increase in blood volume and atrial pressure - increase cGMP, vasodilation and less Na absorption at renal collecting tubule. Dilates afferent renal arterioles and constricts efferent arterioles, promoting diuresis - Contributes to aldosterone escape
139
Brain natriuretic peptide is released from, when, effects
- ventricular monocytes - response to high tension - Similar action to ANP, longer half life - Dx of HF: High NPV - Nesiritide for treating HF
140
Cushing reflex
Triad: - hypertension - bradycardia - respiratory depression
141
Central chemoreceptors respond to
pH and Pco2 of brain | Doesn't respond to PO2
142
Peripheral chemoreceptors respond to
Low PO2 (<60 mmHg) High PCO2 Low pH blood
143
Aortic arch chemo and baroreceptors transmit via
Vagus nerve to solitary nucleus of medulla
144
Carotid sinus baroreceptor transmits via
Glossopharyngeal nerve to solitary nucleus
145
Good aproximation of left atrial pressure
Pulmonary capillary wedge pressure
146
PCWP in mitral stenosis
PCWP> LVED pressure
147
PCWP is measured with
Pulmonary artery catheter: Swan Ganz catheter
148
Causes vasodilation in brain
CO2: lower pH
149
Determine fluid movement through capillary membranes
Starling forces: - capillary pressure - intersticial fluid presure - plasma oncotic presure - intersticial oncotic pressure

Step 1 - Cardiovascular (5 decks)

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