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Pathophysiology > Class 3 chapter 20 > Flashcards

Class 3 chapter 20 Flashcards

1
Q

What is heart failure?

A 
Clinical syndrome that occurs when the heart is unable to pump adequate blood to meet the metabolic demands of the body
Primary the elderly
Vessel stiffness
ASHD
Hypercholesterolemia
Hyperlipedemia
Decreased estrogen production for women
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2
Q

Contractility

A

Performance of cardiac muscle

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3
Q

Types of heart failure

A

Systolic vs Diastolic
Dilated vs Hypertrophic
Left vs Right
High-output vs Low-output

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4
Q

Systolic HF

A

Impaired ejection of blood

Presence of signs and symptoms of HF with an EF

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5
Q

Ejection fraction

A

The % of blood ejected from the LV during systole (echocardiogram)
Normal EF = 55-70%

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6
Q

Diastolic HF

A

Impaired filling during diastole
Presence of signs and symptoms of HF in the absence of systolic dysfunction (LVEF > 40%)
Myocardium is “stiff” (and often hypertrophied) and does not relax normally after contraction

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7
Q

Diastolic HF risks

A

Women, obesity, htn, DM

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8
Q

LV dysfunction manifestations

A
  1. Decreased CO (fatigue, weakness, confusion, dizziness - worsens over day, hypotension, angina, tachycardia, palpitations, pallor, weak peripheral pulses, cool extremities, S3/S4, oliguria - daytime
  2. Pulmonary Congestion (SOB - initially during exertion/orthopnea/PND, cough - “cardiac asthma” - worse at night, inspiratory crackles/expiratory wheezes, tachypnea, frothy/pink sputum - pulmonary edema)
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9
Q

Compensatory mechanisms in HF

A 
Frank-Starling Mechanism
Sympathetic Nervous System
Renin-Angiotension-Aldosterone System
Natriuretic Peptide (ANP and BNP)
Endothelins
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10
Q

Late manifestations of HF

A

Cyanosis - late stage failure (d/t pulmonary edema, vasoconstriction, decreased oxygen availability)
Clubbing of fingers
Cachexia/Malnutrition - end stage failure
Arrhythmias/Sudden Cardiac Death (atrial fibrillation/VT/ventricular fibrillation)

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11
Q

Why does atrial fibrillation happen?

A

MI/HF

Valvular damage

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12
Q

Acute pulmonary edema

A

Accumulation of capillary fluid in alveoli

Impairs gas exchange and limits lung expansion

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13
Q

Diagnostic methods of HF

A

History, physical assessment (signs and symptoms)
ECG
CXR
Echocardiography (ejection fraction, wall motion, thickness, chamber size, structural defects - valves, tumours)
Blood tests (BNP, CBC)
Central venous pressure/jugular vein distension
Pulmonary artery catheter pressures/volumes

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14
Q

HF treatment

A
  1. Non-pharmacological
    Exercise program, fluid/Na restriction, weight control, dietary counseling
    Non-surgical and surgical medical management
  2. Pharmacological
    Diuretics, ACE inhibitors, cardiac glycoside (digoxin), ARBs, B-blockers
  3. Oxygen Therapy
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15
Q

Circulatory failure - shock

A

Acute failure of the circulatory system to supply tissues and organs with an adequate blood supply resulting in hypoxia

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16
Q

Cardiogenic shock

A

Heart failure, uncompensated

Can be due to other shock situations

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17
Q

Cardiogenic shock causes

A 
Myocardial Infarction
Myocardial contusion
Acute MVR (d/t papillary muscle rupture)
Arrhythmias
Severe dilated cardiomyopathy
Cardiac surgery
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18
Q

Cardiogenic shock manifestations

A 
Similar to extreme HF
Decreased SV, MAP, SBP
Narrow pulse pressure
Normal DBP
Cyanosis (lips, nailbeds, skin)
Elevated CVP/PCWP (pressure inside heart)
Dysrhythmias
Oliguria, anuria
Altered mentation
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19
Q

Cardiogenic shock treatment

A

Balance
Fluid volume management
Treat cause and symptoms
Improve CO, avoid increasing workload of heart (inotropes - dopamine, dobutamine, intra-aortic balloon pump)

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20
Q

Hypovolemic shock

A

Any condition which decreases blood volume >15%
1. External Loss
Hemorrhage, burns, severe dehydration/vomiting/diarrhea
2. Internal Loss
3rd spacing, hemorrhage
3. Immediate compensation
SNS, RAAS, hypothalamus, fluid shift

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21
Q

Hypovolemic shock treatment

A

Treat cause
Increase oxygen delivery by maintaining adequate vascular volume (IV crystalloids - NS and D5 W, IV colloids - RBCs and plasma volume expanders, vasoactive pharmacology - not usually recommended)

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22
Q

Obstructive shock

A 
Mechanical obstruction of blood to or through great veins, heart, lungs (blood goes whereever and not brought back to heart properly)
Pulmonary embolus
Dissecting AA
Tamponade
Pneumothorax
Atrial myxoma
Abdominal evisceration (coming out)
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23
Q

Distributive shock

A

Loss of vascular tone usually d/t loss of sympathetic control
Neurogenic
Anaphylactic
Septic

24
Q

Neurogenic shock

A 
Rare, often transitory depending on the cause
Decreased SNS control of vessel tone
Brain stem defect
Spinal cord injury
Drugs
General anaesthesia
Hypoxia
Insulin reaction
25
Q

Anaphylactic shock

A

Immunological mediated reaction of histamine release causing
V/d of arterioles and venuoles
Increased capillary permeability

26
Q

Anaphylactic shock manifestations

A 
Dependent on:
Level of sensitivity
Rate/quantity of antigen exposure
Pruritis, urticaria
Angioedema
Laryngeal edema/bronchospasm
Rapid hypotension; circulatory collapse
27
Q

Anaphylactic shock treatment

A

Remove cause

Epinephrine, oxygen, antihistamines, corticosteroids

28
Q

Septic shock

A

Systemic inflammatory response to a severe infection
Neutrophils increase capillary permeability and damage to endothelial cells result
Cytokines, nitric oxide, & coagulation products are released, damaging cells/tissues and causing massive vasodilation

29
Q

Shock complications

A
  1. Acute Respiratory Distress Syndrome
  2. Acute Renal Failure
  3. GI Tissue Damage d/t hypoxia
  4. Disseminated Intravascular Coagulation
  5. Multi-Organ Dysfunction Syndrome
30
Q

Evolution of our understanding of HF

A

CHF (congestive HF) as a disorder of excessive sodium and water retention (cardio-renal model)
CHF as a hemodynamic (pressure) disorder (reduced CP or afterload – amount of pressure the heart has to push against to eject blood into system)
HF as a neurohormonal model (getting down to cellular level about why the heart is not functioning the way it should)

31
Q

Preload

A

“End-diastolic volume”

Determined by venous return to the heart

32
Q

Afterload

A

Amount of force needed to eject filled heart

Determined by SVR (systemic vascular resistance) and ventricular wall tension (how well it can contract)

33
Q

Systolic HF causes

A 
Muscle issues (CAD, myocarditis, cardiomyopathy, conduction issues)
Volume overload (valvular insufficiency, kidney failure)
Pressure overload (HTN, valvular stenosis, pulmonary disease)
34
Q

Diastolic HF causes

A

Impaired ventricular stretch (pericardial effusion, pericarditis, amyloidosis)
Increased wall thickness (hypertrophy, myopathy)
Delayed diastolic relaxation (aging, CAD)
Aggravated by tachycardia

35
Q

Left sided failure (LV dysfunction)

A

Decreased CO

Pulmonary congestion

36
Q

Right sided failure (RV dysfunction)

A

Systemic congestion (liver distended, edema)

37
Q

RV dysfunction manifestations

A 
Systemic Congestion
JVD/elevated CVP (jugular vein distention/central venous pressure)
Enlarged liver and spleen
Dependent edema
Ascites
Polyuria at night 
Weight gain
Hepatojugular reflux (HJR)
BP changes (elevated d/t excess volume or decreased d/t decreased CO)
38
Q

Frank-Starling Mechanism

A

+ Increased ED volume (preload) will increase stroke volume (the more you stretch it, the better output you have)
- Stretch increases wall tension, increasing oxygen requirements (makes you work harder)

39
Q

Sympathetic Nervous System

A

+ Increase in circulating catecholamines increase HR, contractility, PVR, SV, CO
- Increased workload

40
Q

Renin-Angiotension-Aldosterone System

A

+ Increased concentration of renin, angiotensin 2 (vasoconstrictor) and aldosterone d/t decreased renal perfusion
- Increased preload, increased workload (more fluid increases workload of heart)

41
Q

Natriuretic Peptide (ANP and BNP)

A

+ Released in response to stretch, pressure, fluid overload (promote diuresis)
Decreases preload, decreased CO

42
Q

Endothelins

A

+ Responds to pressure changes (v/c, myocyte hypertrophy, ANP & catecholamine release)
- Increased workload

43
Q

Ventricular remodelling

A

+ Symmetric hypertrophy
Proportionate increase in muscle length and width (athletes)
- Pressure overload (hypertension)
Concentric hypertrophy d/t replication of myofibrils, thickening of myocytes
Increase in wall thickness (hypertension)
- Volume overload (dilated cardiomyopathy)
Eccentric hypertrophy d/t replication of myofibrils, disproportionate elongation of muscle cells

44
Q

What is happening in the heart during atrial fibrillation?

A

Quivering muscle (atria)
Poor emptying of atria
Poor filling of ventricle resulting in decreased CO

45
Q

How will patient present during atrial fibrillation?

A

Irregularly irregular HR
Pulses will be irregularly irregular with varying strength
Low BP
Possibility of angina
Possibility of thrombi
All other systems will exhibit the signs and symptoms of decreased CO

46
Q

Acute pulmonary edema manifestations

A 
SOB, dyspnea, tachypnea
Tachycardia, moist/cool skin
Fine to course crackles
Frothy, blood-tinged sputum 
Cyanotic lips, nailbeds
Confusion, stupor
47
Q

Cellular response to shock

A
  1. Anaerobic energy production
    Cytoplasm uses glucose to create ATP and pyruvate
    Less efficient
  2. Aerobic energy production
    Oxygen and pyruvate create ATP in mitochondria
    If no oxygen, pyruvate converts to lactic acid
48
Q

Hypovolemic shock manifestations

A 
Tachycardia, weak/thready pulses
Skin cool/clammy/mottled
Hypotension
Decreased CVP
ADH release, thirst
Altered mentation
Tachypnea, deep resps
Oliguria, anuria
49
Q

Anaphylactic shock causes

A

Medications
Foods
Insect venom
Latex

50
Q

Septic shock manifestations

A

Vasodilation (decreased SVR), hypovolemia, hypotension, tachycardia, skin flushed, edema
Pyrexia, abrupt change in mentation
Oliguria, anuria
Leukocytosis, metabolic acidosis, thrombocytopenia

51
Q

Acute Respiratory Distress Syndrome

A

Rapid onset of hypoxemia unrelieved by supplemental oxygen
Ventilation-perfusion mismatch
Atelactasis, impaired gas exchange, fluid limits inflation
Tx: mechanical ventilation, oxygen

52
Q

Acute Renal Failure

A

Ischemia/injury of renal tubules > 20 minutes

53
Q

GI Tissue Damage d/t hypoxia

A

GI bleeding

54
Q

Disseminated Intravascular Coagulation

A

Widespread activation of coagulation cascade (not the primary disease
Tx: anticoagulation, platelets, plasma

55
Q

Multi-Organ Dysfunction Syndrome

A

Failure of multiple organs such that homeostasis cannot be achieved
Body has failed

Pathophysiology (13 decks)

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