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Patho > Heart Failure and Shock > Flashcards

Heart Failure and Shock Flashcards

1
Q

What happens in pulmonary capillary

A

O2 movies into the blood and CO2 leaves
- Goes throught the pulmonary veins to the left atrium then the left ventricle and finaly leaves to the Aorta

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2
Q

What happen in capillary beds

A

O2 leaves the blood and CO2 enters
- Goes to the right atrium then to the right ventricle and finally to the pulmonary arteries

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3
Q

Congestive Heart Failure (CHF)

A

An endpoint of many disorders resulting from heart failure to maintain adequate out-flow
- Normally 60% of ventricular blood leaves during contraction
– In CHF 15-20% is ejected with increased residual volume
- Signs/symptoms of both forward and backward are evident
- Heart cannot generate sufficient output to meet metabolic demand,
– Onset is gradual due to cumulative work overload or loss of myocardium
- CHF can appear abruptly
- May result from either systolic or diastolic dysfunction
- All organs in the body are affected; either by failure of perfusion or congestion of venous system
Disease is progressive and prognosis is poor

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4
Q

Systolic dysfunction

A

Result form inadequate contraction
- Result of MI, Valve stenosis or hypertention
-

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5
Q

Diastolic dysfunction

A

Inability of heart to relax and fill
- Result of left ventricular hypertropy, myocardial fibrosis, pericarditis
CHF lead to increased end diatolic ventricular volumes and elevated end diastolic pressure

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6
Q

High Output Failure

A

Rarely CHF result from excessive requirement of systemic tissues in the presesnce of normal or elevated cardiac output
- Happens in sever hyperthryoidism or sepsis

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7
Q

Left and Right Heart Failure

Picture

A

Look at the screen shot

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8
Q

Short Term Compensation

A
  • Starling mechanism: stretiching of cardiac fibers with consequent increase of contractile forces
  • Activation of neurohumoral system: Release norepinephrine, aldosterone, activation of renin angiotensin system
  • Cardiac muscle hypertrophy and/or ventricular dilation: this lead to an INCREASED cardiac workload which increase the oxygen requirement
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9
Q

Compensated Heart Failure

A

If compensation maintain cardiac output

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10
Q

Decompensated Heart Failure

A

Compensation are inadequate

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11
Q

Left Side Heart Failure

A

Most of CHF begin with functional impairment of left heart
- Most common causes are CHD/MI, hypertension or valve disease
- Eventually, both side of the heart, the lung, and the systemic organs on BOTh arterial and venous citculation will become involved
- Increased cardiac back pressure and decreased tissue perfusion are the ULTIMATE cause of pathology

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12
Q

What causes left side failure

A
  • Coronary artery disease
  • Lose of contractile function due to MI, myocardial disease, physical injury
  • Valve disease: heart can’t keep up with preload
  • Hypertension: Increased workload of heart
  • Cardiac dysrhythmias: Asynchronous contraction
  • Pericarditis: Less flexibility
  • Cardiac tamponade: fluid causing pressure on heart
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13
Q

Backward Left Heart Failure

A
  • Increased preload, dilation of left ventricle
  • Inability to handle blood form lungs with incomplete emptying of pulmonary vasculature
  • Increased pressure in pulmoary capillaries (from 6-9 mmHg to 25-30 mmHg)
  • Development of pulmonary edema and compromised gas exchange
  • Dyspenea (shortness of breath) and hypoxemia
  • Classical dyspenea, exertional dyspnea, paroxysmal nocturnal dyspnea (accumalte fluid in lung), orthopnea
  • Eventually, right heart failure occures
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14
Q

Forward Left Heart Failure

A
  • Failing left heart can’t perfuse systeminc organs
    – Most evident on organs with high O2 demand (brain, kidney, GI track)
  • Kidney: Decreased perfusion => low GFR,
    – Perceived as shot and activates system to increase circulating blood volume
    – This increase cardiac workload in failing heart by increasing the vol of blood to pump
  • Brain perfusin lowered caus cerbral hypoxia
    – patient display fatigue, irritability, inattention, restlessness
    – May develop into stupor and coma
  • GI ischemia may cause ulceration and mcosal necrosis
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15
Q

Right Heart failure

A

Most common cause is left heart failure (this mean anything that cause the left side to fail will cause the right side too)
- Pure right heart failure is rare for example:
– Intrinsic disease of lung vasculature suck as pulmonay embolism (thrombus, air bubble, tumor, fat)
- Cor pulmonale is right ventricular enlargement secondary to pulmonary hypertension caused by disorder of lung ( due to pulmonary embolism or pulmoary fibrosis)
- Chronic obstructive pulmoary disease,
- Cystic fibrosis
- Adult respiratory distess syndrome and chemically induced fibrosis

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16
Q

Clical Manifestation of Right Heart Failure

A
  • Resistance to right ventricular empting=> dilation
  • Venous congestion with peripheral edema/3rd spacing (intestional); fluid accumulation is a major feature of CHF and can be massive
    – May involve liver, spleen, kidney, brain
  • Edema of ankles: distension of jugular vein in neck (ominous sigh)
    – Sign of pericardial effusion and constrictive pericarditis
  • Dyspnea on exertion, fatigue, evidence of pulmonary edema, evidence of underlying cornary artery diseaes, hypertension, or valve disease may all be indicators
  • Right heart failure is characterized by systemic venous congestion but MINIMAL pulmonary congestion
17
Q

Anasarca

A

Fluid accumulate into belly
- Congestive heart failure
- Renal failure
- Fluid overload (full of protein and electroytes)
- Portal hypertension
- Positional effect on respiration due to diaphram shift

18
Q

High output Heart Failure

A

The inability of heart to supply the demand of blood-borne nutrient despite adequate blood volume and normal or Elevated myocardial contractility
- Heart increase cardiac output but metabolic needs are not met
– Anemia: Decreased oxygen carrying capacity of blood
– Septicemia: Vasodilation due to bacterial toxin
– Hyperthrodisim: excessive cellular metabolism, without enough metabolic and oxygen compensation
- Thiamine deficiency: malnutriton seconday to alcoholism, impairs cellular metabolims; contractility

19
Q

Heart Drug Therapies

A
  • Chronotropic Drugs: alter heart rate (Beta Blockers; propranolol)
  • Inotropic Drugs: Increased myocardial contractility; decrease heart rate (glycosides; digitalis)
  • Anti-arrhythmics: Alter electrical propeties of myocardial cells (lidocaine)
  • Diuretics: Promote urinary fluid loss (furosemide)
  • Vasodilators: Relax smooth mucle in arterioles (nitrates)
  • ACE inhibitor: act on renin-angiotensin-aldosterone system and limit cardiocyte hypertrophy (captopril)
  • Cardiac Resynchronization Therapy: Exogenous pacing of both ventricles (avoid heart blocker)
20
Q

CHF in Perspective

A
  • Very common and increasing as population ages
  • Morbidity and mortality appreciable
  • Efficacy of lifestyle interventon is increasingly accepted
  • Preferred treatment of ACE inhibitors and/or Beta blocker(individual treatment is often empiric and multidrug)
21
Q

Shock

A

A state in which diminished cardiac output lead to reduced effective circulating blood volume which impairs tissue perfusion and lead to cellular hypoxia

22
Q

Factors that Change Total Blood Volume

A
  • Antidiuretic hormones (vasopressin-pituitary)
    – Relased by posterior pituitary=>resorption H2O by kidney
  • Renin-angiotensin-aldosterone
    – Relased by kidney: promote angiotensin production which stiumulate aldosterone => which increase H2O retention
  • Aterial natriuretic hormone:
    – released by right atrium if right atrial bp increases=> inhibit ADH=> decreased bp
23
Q

Types of Shock

A
  • Hypovolemic Shock: Low cardiac output and decreasd in circulation volume (due to blood or plasma loss or dehydration)
  • Cardiogenic Shock: Low cardiac output due to collapse of cardiac output: Usually from MI, Fibrillation or CHF
  • Septic Shock: Result from Vasodilation and blood pooling as part of immune reaction to bacterial or fungal infection
  • Anaphylactic Shock: Systemic vasodilation and increased vascular permeability due to mast cell degranulation and relase of inflammatory mediatiors
  • Neurogenic Shock: Sudden loss of vascular tone throughtout the body; generally resut of spinal cord or brain injury. May result from burst of parasympathetic stimulation to heart slowing rate and sympathetic stumulation of vessel (fainting)
  • Burn Shock: massive loss of fluid due to denuding of body surface and release of vasodilatory mediators and increased capillary leakage
24
Q

Clinical Features of Shock

A

Depend on precipitating insult
Hyprovolemic and cardiogenic shock
- Hyportension
- Weak, rapid pulse
- Tachypnea
- Coll, clammy cyanotic skin (caused by vasoconstriction)
- Hypovolemia: good clinal outcome with appropriate treatment
- Cardiogenic shock: depend on severity of heart injury
- Rate of blood loss critical
Septic shock
- Warm, flushed skin
- Vasodilation
- Septic and cardiogenic shock have worse outcome regardless of supportive care
- Morality is 20-30%; 2% of hospital admission

25
Q

Four Stages of Classical Shock

A

Initial: Low perfusion
- Result in hypoxia and incomplete shift to anaerobic and catabolic metabolism
Compensatory:
- Body emply physilogical mechanism to counter the condition
Progressive (decompensation)
- Failure to compensate lead to progressively worsening injury
Refractory:
- Organ shock occure and treatment is not effective; irreversible (causes clinical despair)

26
Q

What do shock begin with

A

It begins with impairment of oxygen
- without oxygen cells shift from aerobic to anaerobic metabolism
– anaerobic metabolism is less efficient and uses ATP faster than they can be replaced
— This lead to cellular impairment. As without ATP the cell cannot maintain the elctrochemical gradient across cell permeable membrane.
—- Cell eventually get edematous and release lysosomal enzymes that injure the cell and make them leak

27
Q

What do anaerobic metabolism cause

A

it causes acidosis which further impairs the cell and gets more lysomal enzyme
- With low pH, O2 carring capacity decrase. it also blunts vasomotor response; arterioles dilate
- Also cause impaired glucose use leading to lactic acid and acidosis pathway
– when the glycogen stored get used up tgluconeogensis use protein as feul
positive feedback loop contiune to contribute to symptoms

28
Q

Hypovolemic Shock

A

Most common
- Loss of fluid produce a significant loss of preload
- Sympathetic system seek to maintain BP
– Vasoconstriction
– Venoconstriction
– Activation of renin angiotensin
Cuase can be Hemorrhagic (trauma, childbirth) or non hemorrhagic (dhydration due to vomiting, diarrhea, burns)

29
Q

Cardiogenic Shock

A

Primary Pump Failure Always: causes include
- Massive loss of myocardium (eg. post MI necrosis; 40% of heart involve)
- Reduced contractility
- Filling anomalies (mitral stenosis)
- Acute Valve failure
- Dysrhythmais
Serious and frequently fatal even with best care

30
Q

Septic Shock

A

Overwhelming microbial infection (inflammatory and counter inflammatory processes)
- Gram negative sepsis (localized)
- Gram poitive septicemia
- Super antigens (toxic shock syndrome, Polyclonal T cell activators, cytokines release)
(Difficult to treat. Care is supportive, address infection, cautious fluid control)
- Endothelial activation and injury with vascular leaks and DIC (discriminated intravascullar coagulation)
- Metabolic and organ abnormalities
- Mortality is 20-30%; incidence increase due to hospital base infection

31
Q

Toxic Shock Syndrome

A
  • Strep Pyogenes: 50% mortality
  • Staph Aureus: 5% mortality
    Clinically: systolic BP <90, fever 102F, Erythrodermia, involvemnet of 3 or more organ system
  • Superantigens
  • Toxic tampon syndrome
32
Q

Anaphylaxis

A

Happens when exposed to an offending agent; Type I hypersensitivity; IgE, other mediators
- Insect venom
- Medication
- Allergic reaction
Massive vasodilators (systemic) with Low central venous pressure

33
Q

Neurogenic Shock

A

Loss of autonomic control as a result of spinal injury, depressive drug
- Hypotension
- Bradycardia
- Warm dry skin
Lose vascular tone in spite of normal blood volume

34
Q

Positive Feedback Loop in Shock

A
  • Ammonia and urea production: toxic to cell
  • Protein breakdown: Alanine converted to lactive acid
  • Serum albumin metabolism: broken down but needed to help maintain capillary osmotic pressure
  • Muscle wasting: skeletal and cardiac muscle weakened by protein breakdown
  • Waste product buildup: metabolic end products are toxic to cell
    Try to revers with IV fluid to raise BV and vasoactive drugs to raise BP
35
Q

Pharmacological Principles of Shock

A

Morbidity and Mortality are directly related to duration and severity of shock; With survival => renal failure, gastric ulcers, interstinal infarction and or sloughing of skin
- Things to correct include: preload, Contractility, After Load, Oxygen delivery

36
Q

Things to correct in shock

A

Preload, Contractility, After Load, Oxygen delivery

37
Q

Multiple Organ Dysfunction Syndrome

A

Result from uncontrolled inflammatory response to sever illness or injury and systemic ischemia
- Frequenly progresses to organ failure and death
- Sepsis and septic shock are most common cause (any injury or disease activating massive inflammatory reponse as trauma, burn, surgery, necrotic tiissue)
- Mortaility rate is 50-90% if more than one organ involved

Patho (17 decks)

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