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Pathophysiology 212 > Heart failure & circulatory shock > Flashcards

Heart failure & circulatory shock Flashcards

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1
Q

What is heart failure?

A

Heart Failure is a clinical syndrome that occurs when the heart is unable to pump adequate blood to meet the metabolic demands of the body

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2
Q

Who is at greater risk for heart failure?

A 
Primarily the elderly
Vessel stiffness
ASHD
Hypercholesterolemia
Hyperlipedemia
Decreased estrogen production for women
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3
Q

Evolution of Our Understanding of HF

A

CHF as a disorder of excessive sodium & water retention (cardio-renal model)

CHF as a hemodynamic disorder (reduced CO or AL)

HF as a neurohormonal model

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4
Q

What is preload?

A

“End -diastolic volume”

Determined by venous return to the heart

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5
Q

What is afterload?

A

Amount of force needed to eject filled heart

Determined by SVR and ventricular wall tension

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6
Q

Contractility

A

Performance of cardiac muscle

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7
Q

What is systolic heart failure and its causes?

A
  • Impaired ejection of blood

- Presence of S&S of HF with an EF

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8
Q

Ejection Fraction (EF)

A

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

If the LV has 100ml @ end-diastole, and the stroke volume is 70ml (leaving 30ml still in the LV after systole), then….
70/100 = 70%

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9
Q

What is diastolic heart failure & and its causes?

Who is at risk?

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
    Causes
  • Impaired ventricular stretch pericardial effusion, pericarditis, amyloidosis)
  • Increased wall thickness hypertrophy, myopathy)
  • Delayed diastolic relaxation (aging, CAD)
    Aggravated by tachycardia
    At Risk: women, obesity, HTN, DM
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10
Q

Left-side heart failure (LV dysfunction)

A
  • Decreased CO

- Pulmonary congestion

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11
Q

LV Dysfunction Manifestations (CNS, CVS, Renal)

A
  • Decreased CO
    CNS
  • Fatigue, weakness, confusion, dizziness (worsens over day)
    CVS
  • Hypotension, angina, tachycardia, palpitations, pallor, weak peripheral pulses, cool extremities, S3/S4
    Renal
  • Oliguria (daytime d/t gravity)
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12
Q

LV Dysfunction Manifestations (pulmonary congestion)

A
  • SOB (initially during exertion/orthopnea/PND)
  • Cough, “cardiac asthma” (worse at night)
  • Inspiratory crackles/expiratory wheezes
  • Tachypnea
  • Frothy/pink sputum (pulmonary edema) fluid overload in the alveoli
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13
Q

Right sided failure (RV dysfunction)

A

-systemic congestion

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14
Q

RV Dysfunction Manifestations

A

> Systemic Congestion

  • JVD/elevated CVP
  • Enlarged liver and spleen
  • Dependent edema
  • Ascites
  • Polyuria @ night
  • Weight gain
  • Hepatojugular reflux (HJR) – push down on liver to see if fluid in jugular vein changes
  • BP changes (elevated or decreased)
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15
Q

Compensatory Mechanisms in HF (Frank-Starling Mechanism & Sympathetic Nervous System)

A

> Frank-Starling Mechanism
+ Increased ED volume (preload) will increase stroke volume
- Stretch increases wall tension, increasing oxygen requirements

> Sympathetic Nervous System
+ Increase in circulating catecholamines increase HR, contractility, PVR, SV, CO
- Increased workload

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16
Q

Compensatory Mechanisms in HF (Renin-Angiotension-Aldosterone System)

A

+ Increased concentration of renin, angiotensin ll, & aldosterone d/t decreased renal perfusion
Increased preload, increased workload

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17
Q

Compensatory Mechanisms in HF (Natriuretic Peptide (ANP & BNP))

A

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

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18
Q

Compensatory Mechanisms in HF (Endothelins)

Study These Flashcards
A

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

19
Q

Ventricular Remodeling

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A

>

  • Symmetric hypertrophy
  • Proportionate increase in muscle length & 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 (decreased wall thickness)

20
Q

Late Manifestations of HF

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A

> Cyanosis (late stage failure)
- d/t pulmonary edema, vasoconstriction, decreased oxygen availability
Clubbing of fingers
Cachexia/Malnutrition (end-stage failure)
CNS factors
Liver & GI congestion
Arrhythmias/Sudden Cardiac Death
- Atrial fibrillation/VT/Ventricular fibrillation

21
Q

What is happening in the heart during atrial fibrillation?

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A

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

22
Q

How will your patient present when they have atrial fibrillation?

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A
  • Irregularly irregular HR
  • Pulses will be irregularly irregular with varying strength
  • Low BP
  • Possibility of angina
  • Possibility of thrombiAll other Systems will exhibit the S&S of decreased CO
23
Q

Acute Pulmonary Edema

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A 
> Accumulation of capillary fluid in alveoli
- Impairs gas exchange & limits lung expansion
Manifestations
-SOB, dyspnea, tachypnea
-Tachycardia, moist/cool skin
-Fine to course crackles
-Frothy, blood tinged sputum
-Cyanotic lips, nailbeds
-CNS: confusion, stupor
24
Q

HF: Diagnostic Methods

Study These Flashcards
A 
History, physical assessment
Signs and symptoms
ECG
CXR
Echocardiography
-Ejection fraction
-Wall motion, thickness
-Chamber size
-Structural defects (valves, tumors, etc.)
Blood tests: BNP, CBC
Central venous pressure/jugular vein distension
Pulmonary artery catheter pressures/volumes
25
HF: Treatment
> Non-pharmacological - Exercise program, fluid/Na restriction, weight control, dietary counseling - Non-surgical and surgical medical management > Pharmacological - Diuretics, ACE inhibitors, cardiac glycoside (digoxin), ARBs, B-blockers > Oxygen Therapy
26
Circulatory Failure: Shock
Acute failure of the circulatory system to supply tissues and organs with an adequate blood supply resulting in hypoxia
27
Cellular Response to Shock
Anaerobic energy production Cytoplasm uses glucose to create ATP and pyruvate Less efficient Aerobic energy production Oxygen and pyruvate create ATP in mitochondria If no oxygen, pyruvate converts to lactic acid
28
Cardiogenic Shock
``` > Heart failure, uncompensated Can be due to other shock situations! > Causes: -Myocardial Infarction -Myocardial contusion -Acute MVR (mitral valve replacement) d/t papillary muscle rupture -Arrhythmias -Severe dilated cardiomyopathy -Cardiac surgery ```
29
Cardiogenic Shock: Manifestations (CVS, CNS, Renal)
``` > Similar to extreme heart failure CVS: - Decreased SV, MAP, SBP - Narrow pulse pressure - Normal DBP - Cyanosis (lips, nailbeds, skin) - Elevated CVP/PCWP - Dysrhythmias Renal: oliguria, anuria CNS: altered mentation (GCS 15-0) ```
30
Cardiogenic Shock: Treatment
Balance! Fluid volume management Treat cause & symptoms Improve CO, avoid increasing workload of heart Inotropes (dopamine, dobutamine) Intra-aortic balloon pump
31
Hypovolemic Shock
> Any condition which decreases blood volume >15% > External Loss - Hemorrhage, burns, severe dehydration/vomiting/diarrhea > Internal Loss - 3rd spacing, hemorrhage > Immediate compensation - SNS, RAAS, Hypothalamus, fluid shift
32
Hypovolemic Shock: Manifestations (CVS, CNS, Resp, Renal)
``` > CVS - tachycardia, weak/thread pulses - Skin cool/clammy/mottled - Hypotension - Decreased CVP > CNS - ADH release, thirst - Altered mentation > Respiratory: - tachypnea, deep resps > Renal: - oliguria, anuria ```
33
Hypovolemic Shock: Treatment
``` Treat cause Increase oxygen delivery by maintaining adequate vascular volume IV crystalloids (NS, D5W) IV colloids (rbc’s, plasma volume expanders) Vasoactive pharmacology (not usually recommended) ```
34
Obstructive Shock
Mechanical obstruction of blood to or through great veins, heart, lungs ``` Pulmonary embolus Dissecting AA Tamponade Pneumothorax Atrial myxoma Abdominal evisceration ```
35
Obstructive Shock
Mechanical obstruction of blood to or through great veins, heart, lungs - Pulmonary embolus - Dissecting AA - Tamponade - Pneumothorax (collapsed lung) - Atrial myxoma (tumor in the atria) - Abdominal evisceration
36
Distributive Shock
Loss of vascular tone usually d/t loss of sympathetic control Neurogenic Anaphylactic Septic
37
Neurogenic Shock
``` > 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 ```
38
Anaphylactic Shock
``` > Immunological mediated reaction of histamine release causing - v/d of arterioles and venuoles - Increased capillary permeability > Causes - Medications - Foods - Insect venom - Latex ```
39
Anaphylaxis: Manifestations/Treatment
``` Manifestations dependent on: - Level of sensitivity - Rate/quantity of antigen exposure Pruritus, urticarial Angioedema Laryngeal edema/bronchospasm Rapid hypotension; circulatory collapse ``` Treatment - Remove cause - Epinephrine, oxygen, antihistamines, corticosteroids
40
Septic Shock
> Systemic inflammatory response to a severe infection - Neutrophils increase capillary permeability & damage to endothelial cells result - Cytokines, nitric oxide, & coagulation products are released, damaging cells/tissues and causing massive vasodilation
41
Septic Shock: Manifestations (CVS, CNS, Renal, Hemat)
CVS: vasodilation (decreased SVR), hypovolemia, hypotension, tachycardia, skin flushed, edema CNS: pyrexia, abrupt change in mentation Renal: oliguria, anuria Hemat: leukocytosis, metabolic acidosis, thrombocytopenia
42
Shock: Complications (ARDS)
Acute Respiratory Distress Syndrome (ARDS) -Rapid onset of hypoxemia unrelieved by supplemental oxygen -Ventilation-perfusion mismatch -Atelactasis, impaired gas exchange, fluid limits inflation Tx: mechanical ventilation, oxygen
43
Shock: Complications (Acute renal failure & GI tissue damage)
Acute Renal Failure Ischemia/injury of renal tubules > 20 mins GI Tissue Damage d/t hypoxia - GI bleeding
44
Shock: Complications (DIC & MODS)
Disseminated Intravascular Coagulation (DIC) Widespread activation of coagulation cascade (not the primary disease) Tx: anticoagulation, platelets, plasma Multi-Organ Dysfunction Syndrome (MODS) Failure of multiple organs such that homeostasis cannot be achieved

Pathophysiology 212 (18 decks)

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