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1 STEP Uworld cardio > Shock + HF > Flashcards

Shock + HF Flashcards

1
Q

Low CVP in shock?

A

Hypovolemic and distributive

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2
Q

High CVP in shock?

A

Cardiogenic and obstructive

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3
Q

Low PCWP in shock?

A

Hypovolemic, obstructive and distributive

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4
Q

High PCWP in shock?

A

Cardiogenic

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5
Q

Low cardiac index and SvO2 in……………………

A

Neurogenic shock due to impaired sympathetic reflexes

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6
Q

Low cardiac index (CO) in shock?

A

Hypovolemic, cardiogenic, obstructive

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7
Q

Why there is increase PCWP in cardiac tamponade?

A

due to external compression of the heart despite low left-sided preload

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8
Q

High CO in shock?

A

Distributive shock

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9
Q

Low SVR in shock?

A

Distributive

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10
Q

High SVR (afterload) in shock?

A

Hypovolemic, cardiogenic, obstructive

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11
Q

Low SvO2 in shock?

A

Hypovolemic, cardiogenic, obstructive

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12
Q

High SvO2 in shock?

A

Distributive (in neurogenic is low)

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13
Q

Right-sided preload is called ……….

A

Central venous pressure (CVP)

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14
Q

Left-sided preload/left ATRIAL pressure is called ………

A

Pulmonary capillary wedge pressure (PCWP).

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15
Q

Why PCWP is decreased in septic shock?

A

Due to decreased venous return

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16
Q

Venous dilation in sepsis is caused due to ……… (2)

A

Peripheral venous dilation –> pooling of blood in dilated veins
Increased vascular permeability (third-spacing)

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17
Q

SVR decreased in sepsis is due to ……….

A

Arteriolar vasodilation

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18
Q

How changes action of the heart in sepsis when sympathetic drive increases?

A

Increased HR and contractility –> increased CO

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19
Q

What causes compensatory increase in sympathetic drive in sepsis? (2)

A

Hypotension and inflammation from sepsis

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20
Q

Why CO is increased in sepsis despite low ventricular preload?

A

Due to compensatory activation of sympathetic NS

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21
Q

What 2 factors affect increase of CO in sepsis?

A

Decr. afterload and baroreceptor reflex-mediated increase in HR (tachycardia)

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22
Q

CO in early and late stage of sepsis?

A

Early - increased due to compensation of SNS and dec. afterload
Late - decreased due to tissue ischemia and accumulation of cytotoxic mediators

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23
Q

Low CO results in ………..

A

inadequate oxygen delivery to the organs –> end-organ damage

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24
Q

Why there is increased mixed venous oxygen saturation in sepsis?

A

Increased CO cause rapid blood transit through the peripheral capillaries and incomplete oxygen uptake by the tissue

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25
Q

In neurogenic shock primary disturbance is in ………………..

A

Peripheral vasodilation

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26
Q

Difference in response between septic and neurogenic shock?

A

In sepsis - there is increase in sympathetic response –> high HR and contractility
In neurogenic - nerve injury –> no sympathetic response –> no increase in HR and contractility –> low CO

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27
Q

Why increase of TPR is important in shock?

A

To maintain end-organ perfusion

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28
Q

How changes distribution of the blood in the body when there is shock?

A

Blood shunts from extremities and skin to vital organs

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29
Q

What causes increase of venous return?

A

Systemic venous constriction

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30
Q

What is kidney reaction to shock?

A

Increased RAAS –> increase of Na and water retention

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31
Q

Treatment of hypovolemic shock?

A

Blood transfusion and crystalloid infusion (saline)

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32
Q

What changes cause infusion of saline in shock? (2)

A

Increase intravascular and LV end-diastolic volume

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33
Q

Shock. Treatment = saline. How it changes heart work of fibers/SV/CO?

A

Incr. LV EDV –> stretch of myocardium and increased length of sarcomere at the end of diastole –> Frank Starling mechanism –> contraction –> increased SV and CO

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34
Q

With shock, poor organ and tissue perfusion leads to tissue …………… and increased …………….. metabolism

A

Tissue hypoxia –> increased anaerobic metabolism –> lactatic acidosis

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35
Q

Metabolic disturbance in shock?

A

Metabolic (lactatic) acidosis –> with compensatory respiratory alkalosis due to increased CO2 exhalation since there is reduction in pH

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36
Q

If hypovolemic shock is with diarrhea, how it worsens presented metabolic disturbance?

A

Loss of bicarbonate from GI tract worsens metabolic acidosis and increase a ventilation even more

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37
Q

Location of primary disturbance in cardiogenic shock?

A

Typically left ventricular failure

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38
Q

MI –> acute LV failure and cardiogenic shock. 3 symptoms?

A

Hypotension + pulmonary crackles + audible S3

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39
Q

Pulmonary embolism symptoms? (7)

A 
Acute-onset chest pain + shortness of breath.
Tachycardia
Tachypnea
JVD
Clear lung
May manifest syncope/near syncope
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40
Q

ABG in PE?

A

Hypoxemia + acute resp. alkalosis due to hyperventilation

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41
Q

PE. Changes in pulmonary artery and RV?

A

Increase in pressure.

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42
Q

Increase in pressure in RV in PE cause ……………. (change of RV?)

A

Dilation/RV cavity dilation - due to RV wall tension and cardiac muscle stretching.

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43
Q

How changes RV myocardial oxygen consumption and coronary artery perfusion in PE? It leads to ……….

A

O2 demand increases and coronary artery perfusion decreases.

Leads to supply/demand mismatch and RV ischemia

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44
Q

Why there is decreased coronary artery perfusion in PE?

A

decreased RV output due to obstruction –> decr. LV preload and CO –> decr. RV O2 supply (because myocardium gets oxygenated blood from left ventricle) –> RV ischemia

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45
Q

Incr. RV O2 demand and decr. coronary artery perfusion results in …………… –> …………………. (RV changes)

A

RV ischemia –> RV failure (cannot pump blood –> even more decreased left-side preload –> decr. CO)

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46
Q

In what pathologies manifest and doesn’t thickening of RV?

A

RV thickening manifest in chronic pulmonary hypertension.

There is no thickening of RV wall in acute PE, because it is not enough time.

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47
Q

LV CAVITY changes in acute PE?

A

LV is normal or somewhat reduced in size due to reduced blood flow from right heart.

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48
Q

LV WALL changes in acute PE?

A

Nothing. Thickening is expected not with PE, but with systemic hypertension or severe aortic stenosis

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49
Q

Pulmonary arterial hypertension in chronic respiratory diseases. 2 factors.

A
  1. Hypoxia induced pulmonary vasoconstriction

2. Associated vascular remodeling, therefore RV must work harder

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50
Q

Patient has pulmonary arterial hypertension thus is predisposed to RHF. What 2 conditions can lead to RHF?

A
  1. Subacutely from progressive pulmonary hypertension

2. Acutely due to PE (sudden obstruction of an already comprosmised pulmonary capillary bed)

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51
Q

Pulmonary arterial hypertension. CVP, RV size, PCWP and CO?

A

CVP increased;
RV size - increased due to volume overload;
PCWP - decreased
CO - decreased

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52
Q

Symptoms of decreased CO? (4)

A

Dyspnea
Fatigue
Exertional angina
Syncope

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53
Q

Right atrial pressure and LVEDP in RHF?

A

RAP - increased

LVEDP - normal/decreased due to impaired RV output - less blood in the left heart

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54
Q

Right atrial pressure and LVEDP in LHF?

A

RAP = normal/decreased

LVEDP - increased

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55
Q

When manifest RHF due to LHF?

A

In advanced stage

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56
Q

RV dysfunction results in the backup of blood within the venous circulation, leading to increased CVP, which is transmitted to …………

A

PORTAL CAPILLARIES (ie, hepatic sinusoids).

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57
Q

Hydrostatic pressure and oncotic pressure in ascitis?

A

Increased and normal.

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58
Q

When manifest hypoalbuminemia in RHF caused ascitis?

A

Albumin half time is ~21d, therefore hypoalbuminemia may manifest after several weeks, therefore in early disease oncotic pressure is normal

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59
Q

Hepatic sinusoid in ascitis. 2 characteristics.

A

Sinusoidal engorgement due to congestion, but permeability unaffected.

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60
Q

What pressures would resolve ascitis?

A

High oncotic and low hydrostatic pressure in portal capillaries

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61
Q

In what case can be increased portal capillary permeability?

A

In hepatic malignancies which disrupt portal capillary integrity

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62
Q

LVEDP and RAP in LHF?

A

LVEDP increased, RAP ir normal/decreased (in early disease)

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63
Q

RAP in late stage of LHF?

A

Invariably/always elevated

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64
Q

How chronic hypertension causes HF?

A

Concentric LV hypertrophy and resulting diastolic dysfunction

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65
Q

Acute pulmonary edema caused due to …………………………. pressure

A

increased alveolar capillary hydrostatic pressure

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66
Q

How looks alveoli in acute cardiogenic pulmonary edema?

A

Engorged alveolar capillaries (storos raudonos lyg susisukusios kraujagysles)

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67
Q

What material is in alveoli in acute cardiogenic pulmonary edema?

A

Pink, acellular material - results from transudation of fluid plasma

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68
Q

When RBCs leak to the alveoli?

A

RBCs leak to the alveoli in chronic pulmonary congestion, when too high pressure breaks vessels

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69
Q

histopathology of acute and chronic pulmonary congestion.

A

Acute: engorged alveolar capillaries with pink, acellular material within alveoli
Chronic - RBCs extravasate into alveoli –> hemosiderin-laden macrophages

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70
Q

How is formed hemosiderin in chronic HF?

A

RBCs phagocytosed by macrophages –> iron from heme is converted to hemosiderin

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71
Q

What iron stores can detect Prussian blue stain?

A

Ferritin and hemosiderin

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72
Q

Where can be founded siderophages and identified by Prussian blue stain?

A

In any tissue where macrophages encounter extravasated RBCs

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73
Q

In which vessel increased pressure cause pulmonary edema when HF?

A

ELEVATED PULMONARY VENOUS PRESSURE

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74
Q

What is reaction in Prussian blue stain + RBCs in alveoli in chronic HF?

A

Colorless potassium ferrocyanide is converted to blue-black ferric ferrocyanide by iron

75
Q

RBCs in chronic HF extravasate into …….. (2)

A

Alveoli and lung parenchyma

76
Q

What indicates alveolar hemorrhage?

A

hemosiderin-laden macrophages

77
Q

RBCs extravasation into lung parenchyma results in ………………………….. (2)

A

Stiffening of alveolar walls and decreased lung compliance

78
Q

Gross appearance of the heart in chronic hypertension?

A

Uniformly thickened left ventricle walls (–> decreased LV cavity size)

79
Q

Histology of the heart in chronic hypertension?

A

Enlarged cardiomyocytes with highly visible nuclei (prominent nuclei)

80
Q

What 2 mediators are released in the heart in chronic hypertension?

A

Angiotensin II and endothelin

81
Q

Which 1 drug prominently provide reduction in remodeling in chronic hypertension LVH? Why?

A

Angiotensim II receptor blockers. Because in chronic hypertension there is increased local expression of angiotensin II and endothelin in the heart, which participate in development of LHF.

82
Q

There is expression of angiotensin II and other factor in the heart in chronic hypertension. What factor? What medication is used to reduce expression and in what pathology treatment?

A

Endoothelin.
Endothelin receptor blockers (bosentan).
Bosentan is not typically used in hypertension, but it may be used to treat pulmonary arterial hypertension which would lead to reduction of right ventricular hypertrophy

83
Q

What factor plays a role in development of eccentric LHV when volume overload?

A

Same as in concentric - local angiotensin II

84
Q

In what states is increased adenosine expression?

A

Myocardial ischemia and reperfusion of the heart.

85
Q

What is the effect of adenosine?

A

Dilates blood vessels, especially coronary arteries, to improve circulation. Therefore compensatory increase is seen in myocardial ischemia and reperfusion

86
Q

Calcitonin gene related peptide. Function? effect on heart?

Blockers used in?

A

Potent vasodilator. May play a role in protecting the heart from HF and LVH.
CGRP blocker - in migraine to reduce dilated vessels in the brain

87
Q

IL-1 effect on the heart?

A

Implicate in atherosclerosis development. High levels expected in CAD, but not LVH.

88
Q

IL-1 blockers used for ……..

A

the treatment on autoimmune inflammatory conditions (eg rheumatoid arthritis)

89
Q

NO effect for LVH?

A

Protective against LVH

90
Q

NO synthase function?

A

catalyzes production of NO, which is potent vasodilator

91
Q

What levels of NO synthase is expected in LVH?

A

Low levels. NO is protective against LVH, but in development play a role angiothensin II and endothelin

92
Q

Reduced LV EF (<50proc) + no HF symptoms. Pathology?

A

Asymptomatic LV systolic dysfunction

93
Q

Preserved LV EF (>50proc) + no HF. Pathology?

A

HF with preserved EF - diastolic dysfunction eg in systemic hypertension

94
Q

What compensatory mechanisms are seen in early stage of HF to maintain asymptomatic stage? (2)

A
  1. Eccentric/concentric hypertrophy

2. Neurohormonal mechanisms: RAAS and SNS

95
Q

How is kept normal CO in early HF?

A

Activation of SNS (due to decreased stretch of aortic and carotid baroreceptors)

96
Q

What does SNS when decreased CO in HF?

A

Released catecholamines: vasoconstriction, incr. HF and contractility

97
Q

When is activated RAAS in HF?

A

When decreased renal perfusion

98
Q

What is the effect of RAAS activation in HF?

A

Increased Na and H2O reabsorbtion due to aldosterone and vasoconstriction due to angiotensin II

99
Q

RAAS activation effect on preload and afterload?

A

increased preload due to increased volume retention;

Increased afterload due to vasoconstriction

100
Q

2 aims in the early stage of HF

A

Maintain CO and organ perfusion

101
Q

Why long-term effects of the SNS and RAAS are detrimental?

A

Increased hemodynamic stress and neurohormonal-induced cardiac remodeling –> decompensated HF

102
Q

What cause opposite effect to SNS and RAAS?

A

Atrial and brain natiuretic peptide. Increase Na and H2O excretion. BUT EVENTUALLY THIS PATHWAY IS OVERWHELMED

103
Q

What 3 factors induce hemodynamic stress?

A

Incr. HR and contractility;
Vasoconstriction;
Incr. Extracellular volume

104
Q

What 3 neurohormonal factors cause it’s prolonged activation effect which leads to deterious cardiac remodleing??

A

SNS activation;
RAAS activation;
ADH secretion

105
Q

What induces neurohormonal activation in HF?

A

DECREASED CO

106
Q

How is inhibited neurohormonal effect in HR with medications?

A

Beta blockers; Ace inhibitors; ATII blockers–> primary toward inhibition of detrimental effect of neurohormonal pathways (SNS and RAAS)

107
Q

2 factors which indicate decompensated HF?

A

Elevated LVEDP and decr. CO

108
Q

What is mixed venous O2 content in HF?

A

Reduced, because due to decreased CO, tissue starve for O2, therefore there is increased O2 extraction from the available capillary blood.

109
Q

SV in early and late HF?

A

Early - generally maintained, as CO

Late - decreased as decompensation takes place

110
Q

Cardiomyocytes properties (3)

A

Contractile;
Electrical conduction;
Endocrine capability to regulate blood volume

111
Q

What is an endocrine capability to regulate blood volume of the cardiomyocytes?

A

Release of ANP and BNP

112
Q

Which part of the heart release ANP and BNP?

A

ANP - atrial myocardium

BNP - ventricular myocardium

113
Q

What factor induces release of ANP and BNP?

A

Volume overload which causes stretching and increased wall stress

114
Q

What is the effect of natiuretic peptides on vessels?

A

venous and arterial dilation –> decreased both preload and afterload

115
Q

What is the effect of natiuretic peptides on kidney?

A

Increased Na and H2O excretion = facilitate diuresis

116
Q

If patient has shortness of breath + incr BNP =?

A

Probably HF. If shortness of breath and normal BNP, the cause is not cardiac

117
Q

Natiuretic peptides. Opposite action element?

A

Renin from RAAS

118
Q

Acute or chronic pulmonary edema. What is activated in lung?

A

Alveolar juxtacapillary receptors.

Activated either by engorged by blood or when pulmonary edema occurs as in CHF.

119
Q

What is the function of the alveolar juxtacapillary receptors?

A

Increase respiratory rate in response to pathologic alveolar processes such pulmonary edema or pneumonia.

120
Q

Where are the alveolar juxtacapillary receptors?

A

In the alveoli near the pulmonary capillaries.

121
Q

BNP is increased in HF. In what other heart pathology it’s increased?

A

MI

122
Q

Elevated blood pressure effect on baroreceptors.

A

Increased BP causes stretching of aortic baroreceptors –> triggered reduction in SNS –> alleviated vasoconstriction (SNS slopinimas nesukelia vasodilatacijos, tai slopina vasokonstrikcija) and reduced myocardial contractility

123
Q

………… of preload cause ……….. of CO

A

decrease; decrease

124
Q

What enzyme breaks down and therefore inactivates natiuretic peptides?

A

Metalloprotease neprilysin

125
Q

What is the neprilysin inhibitor? Result effect?

A

Sacubitril.

Prevents neprilysin degradation –> enchanced effect of natiuretic peptides

126
Q

What secondary factor is used in natiuretic peptide function pathway?

A

Natiuretic peptide receptors activate guanylate cyclase –> cGMP

127
Q

Taget organs of natiuretic peptides?

A

Kidney, adrenal and blood vessels

128
Q

Natiuretic peptide effect on adrenal glands?

A

Inhibits secretion of aldosterone –> no Na and H2O reabsorbtion

129
Q

Natiuretic peptide effect on kidney?

A

Dilation of afferent and constriction of efferent –> increased GRF –> increased urinary excretion (diuresis) of Na and H2O.
Renin inhibition

130
Q

Natiuretic peptide effect on blood vessels?

A
  1. Arteriolar and venular smooth muscle relaxes –> vasodilation
  2. Increased vascular permeability –> extravasation into the interstitium –> decreased blood volume
131
Q

What and how regulates hepatic blood flow?

A

Hepatic stellate cells (perisinusoidal cells of Ito) release local mediators

132
Q

How vascular endothelial cells regulate blood flow?

A

NO and prostacyclin - vasodilation

Endothelin and TXA2 - vasoconstriction

133
Q

Increased levels of ANP and BNP are beneficial or detrimental effect on heart?

A

Beneficial. Protects against the deterious remodeling and fibrosis that occur in heart failure

134
Q

Neprilysin breaks down natiuretic peptides. What other molecule also is broken down?

A

ATII2

135
Q

Neprilysin inhibitors should be prescribed in concomitant with ………….. because…………..

A

Angiotensin II receptors blockers.

Neprilisyn breaks down both natiuretic and ATII - inhibitors like sacubitril would prevent breakdown of ATII –> therefore vasoconstriction and fluid retention

136
Q

ANP and BNP effect on afterload and preload?

A

VASODILATION
Incr. venous compliance –> decr preload
Decr. peripheral arterial resistance –> decr afterload
IN TOTAL: REDUCED CARDIAC WORK

137
Q

ANP and BNP versus ATII? Which effect conteracts other?

A

ATII > ANP and BNP

138
Q

Sacubitril-valsartan effect on cardiac contractility?

A

Not significantly affected

139
Q

Angiotensinogen is synthesized in ………..

A

Liver

140
Q

Activation of RAAS maintains…………………. and ………..

A

effective blood volume and organ perfusion

141
Q

ATI is converted to ATII by ………… from ………………

A

ACE; from lung

142
Q

Renin converts ……… to ……….. Where?

A

Angiotensinogen to ATI.

In systemic circulation

143
Q

Where is converted ATI to ATII?

A

Small pulmonary vessels. By ACE

144
Q

In which vessel is higher levels of ACE in lung?

A

In pulmonary vein than pulmonary artery (on the way out of lungs than on the way into the lungs)

145
Q

How ATII worsens CO?

A

Arterial vasoconstriction –> increased peripheral systemic pressure = increased afterload –> decreased CO

146
Q

What enzymes are responsible for ATII and other structurally similar enzymes? Where they are found?

A

Angiotensinases.

In multiple tissues

147
Q

Fissure sign is ………..

A

created by fluid trapped between the right upper and middle lobe.

148
Q

Created by fluid trapped between the right upper and middle lobe. What term is used to describe it on x-ray?

A

Fissure sign

149
Q

Pleural effusion on xray?

A

Blunting of the costophrenic angles

150
Q

Blunting of the costophrenic angles on xray. What it indicates?

A

Pleural effusion

151
Q

What indicate patchy, bilateral opacification on xray?

A

Pulmonary edema

152
Q

Pulmonary edema on xray seen as ………….

A

Patchy, bilateral opacification

153
Q

Pulmonary vessels on xray? (one word)

A

Prominent pulmonary vessels

154
Q

What 2 signs may be seen as well in ADHF?

A

Kerley B lines and cardiomegaly

155
Q

What are Kerley B lines?

A

Short, horizontal lines perpendicular to the pleural surface that represent edema of the interlobular septa.

156
Q

Edema of the interlobular septa is seen on x ray and called ………

A

Kerley B lines

157
Q

Cardiomegaly ration on xray

A

cardiac-to-thoracic width ratio >50proc

158
Q

Expression of contractile proteins in hypertrophic cardiomyopathy?

A

Increased

159
Q

LVEDP in hypertrophic cardiomyopathy?

A

Increased. Graduallly it transmits to pulmonary veins –> pulmonary edema

160
Q

LVEDV in hypertrophic cardiomyopathy?

A

Eventually declined

161
Q

EF and SV in hypertrophic cardiomyopathy?

A

EF preserved but SV decreases despite it

162
Q

S4 on cardiac auscultation as …………………………..

A

S4 on cardiac auscultation as blood strikes the stiff LV wall during atrial systole.

163
Q

Dilated cardiomyopathy results from …………………..

A

A direct insult to cardiomyocytes that impairs their contractile function

164
Q

What is heart compensation to volume overload (incr. left ventricular volume)?

A
  1. Early stage - Frank-Starling mechanism

2. Later - eccentric hypertrophy to maintain CO

165
Q

Overwhelming wall stress in dilated cardiomyopathy eventually leads to (3)

A
  1. Marked impairment in myocardial contractile function, 2. Reduced CO, and 3. symptomatic decompensated heart failure.
166
Q

Advanced HF effect on right atrial pressure?

A

RAP is increased. It represents CVP

167
Q

What represents CVP in heart?

A

RAP

168
Q

If RAP elevated, suspect: (2)

A
  1. Volume overload in RV

2. Right sided HF

169
Q

Thrombus in dilated cardiomyopathy? Why and where?

A

Due to localized stagnation of blood.

LV thrombus. In severely dilated LV cavity with systolic dysfunction

170
Q

3 upregulations in dilated cardiomyopathy?

A

Inc. LV compliance
ATII signaling
Expression of beta-myosin heavy chain/upregulation of contractile proteins

171
Q

When dilation of LV cavity what is result for heart wall and function?

A

Increased wall compliance and decreased contractility.

172
Q

S3 normal in …. (2)

A

Age <40; pregnancy

173
Q

Abnormal S3 in …(3)

A

Systolic HF (dilated cardiomyopathy);
Mitral regurgitation;
High-output states

174
Q

S4 normal in….

A

Healthy older adults

175
Q

S4 abnormal in ….. (2)

A 
Diastolic dysfunction (hypertrophic cardiomyopathy);
Younger adults, children
176
Q

Ventricular gallop sound (after S2) in …………..

A

S3

177
Q

Gallop heard during rapid PASSIVE FILLING of ventricles in diastole in gallop …….

A

S3

178
Q

Sudden cessation of filling as ventricle reaches its elastic limit in gallop ………..

A

S3

179
Q

Atrial gallop sound (before S1) in …………

A

S4

180
Q

Heard immediately after ATRIAL CONTRACTION as blood is forced into a stiff ventricle in gallop …………

A

S4

181
Q

…………… (gallop) is …………….. a low-frequency sound occurring immediately after …………

A

S3 is a low-frequency sound occurring immediately after S2.

182
Q

S3 is typically a sign of LV ………………….. (causing exertional dyspnea and paroxysmal nocturnal dyspnea in this patient).

A

A sign of left ventricular (LV) volume overload/failure (causing exertional dyspnea and paroxysmal nocturnal dyspnea in this patient).

183
Q

………….. (gallop) is a low-frequency, ……………… (early/late) ………… (systolic/diastolic) sound on cardiac auscultation that immediately precedes ………….

A

S4 is a low-frequency, late diastolic sound on cardiac auscultation that immediately precedes the first heart sound (S1).

1 STEP Uworld cardio (7 decks)

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