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Pathophysiology > Class 3 chapter 20 > Flashcards

Class 3 chapter 20 Flashcards

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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

Study These Flashcards
A

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

24
Q

Neurogenic shock

Study These Flashcards
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
Anaphylactic shock
Immunological mediated reaction of histamine release causing V/d of arterioles and venuoles Increased capillary permeability
26
Anaphylactic shock manifestations
``` Dependent on: Level of sensitivity Rate/quantity of antigen exposure Pruritis, urticaria Angioedema Laryngeal edema/bronchospasm Rapid hypotension; circulatory collapse ```
27
Anaphylactic shock treatment
Remove cause | Epinephrine, oxygen, antihistamines, corticosteroids
28
Septic shock
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
Shock complications
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
Evolution of our understanding of HF
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
Preload
“End-diastolic volume” | Determined by venous return to the heart
32
Afterload
Amount of force needed to eject filled heart | Determined by SVR (systemic vascular resistance) and ventricular wall tension (how well it can contract)
33
Systolic HF causes
``` Muscle issues (CAD, myocarditis, cardiomyopathy, conduction issues) Volume overload (valvular insufficiency, kidney failure) Pressure overload (HTN, valvular stenosis, pulmonary disease) ```
34
Diastolic HF causes
Impaired ventricular stretch (pericardial effusion, pericarditis, amyloidosis) Increased wall thickness (hypertrophy, myopathy) Delayed diastolic relaxation (aging, CAD) Aggravated by tachycardia
35
Left sided failure (LV dysfunction)
Decreased CO | Pulmonary congestion
36
Right sided failure (RV dysfunction)
Systemic congestion (liver distended, edema)
37
RV dysfunction manifestations
``` 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
Frank-Starling Mechanism
+ 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
Sympathetic Nervous System
+ Increase in circulating catecholamines increase HR, contractility, PVR, SV, CO - Increased workload
40
Renin-Angiotension-Aldosterone System
+ 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
Natriuretic Peptide (ANP and BNP)
+ Released in response to stretch, pressure, fluid overload (promote diuresis) Decreases preload, decreased CO
42
Endothelins
+ Responds to pressure changes (v/c, myocyte hypertrophy, ANP & catecholamine release) - Increased workload
43
Ventricular remodelling
+ 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
What is happening in the heart during atrial fibrillation?
Quivering muscle (atria) Poor emptying of atria Poor filling of ventricle resulting in decreased CO
45
How will patient present during atrial fibrillation?
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
Acute pulmonary edema manifestations
``` SOB, dyspnea, tachypnea Tachycardia, moist/cool skin Fine to course crackles Frothy, blood-tinged sputum Cyanotic lips, nailbeds Confusion, stupor ```
47
Cellular response to shock
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
Hypovolemic shock manifestations
``` Tachycardia, weak/thready pulses Skin cool/clammy/mottled Hypotension Decreased CVP ADH release, thirst Altered mentation Tachypnea, deep resps Oliguria, anuria ```
49
Anaphylactic shock causes
Medications Foods Insect venom Latex
50
Septic shock manifestations
Vasodilation (decreased SVR), hypovolemia, hypotension, tachycardia, skin flushed, edema Pyrexia, abrupt change in mentation Oliguria, anuria Leukocytosis, metabolic acidosis, thrombocytopenia
51
Acute Respiratory Distress Syndrome
Rapid onset of hypoxemia unrelieved by supplemental oxygen Ventilation-perfusion mismatch Atelactasis, impaired gas exchange, fluid limits inflation Tx: mechanical ventilation, oxygen
52
Acute Renal Failure
Ischemia/injury of renal tubules > 20 minutes
53
GI Tissue Damage d/t hypoxia
GI bleeding
54
Disseminated Intravascular Coagulation
Widespread activation of coagulation cascade (not the primary disease Tx: anticoagulation, platelets, plasma
55
Multi-Organ Dysfunction Syndrome
Failure of multiple organs such that homeostasis cannot be achieved Body has failed

Pathophysiology (13 decks)

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