Heart Failure and Shock Flashcards
What happens in pulmonary capillary
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
What happen in capillary beds
O2 leaves the blood and CO2 enters
- Goes to the right atrium then to the right ventricle and finally to the pulmonary arteries
Congestive Heart Failure (CHF)
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
Systolic dysfunction
Result form inadequate contraction
- Result of MI, Valve stenosis or hypertention
-
Diastolic dysfunction
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
High Output Failure
Rarely CHF result from excessive requirement of systemic tissues in the presesnce of normal or elevated cardiac output
- Happens in sever hyperthryoidism or sepsis
Left and Right Heart Failure
Picture
Look at the screen shot
Short Term Compensation
- 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
Compensated Heart Failure
If compensation maintain cardiac output
Decompensated Heart Failure
Compensation are inadequate
Left Side Heart Failure
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
What causes left side failure
- 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
Backward Left Heart Failure
- 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
Forward Left Heart Failure
- 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
Right Heart failure
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
Clical Manifestation of Right Heart Failure
- 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
Anasarca
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
High output Heart Failure
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
Heart Drug Therapies
- 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)
CHF in Perspective
- 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)
Shock
A state in which diminished cardiac output lead to reduced effective circulating blood volume which impairs tissue perfusion and lead to cellular hypoxia
Factors that Change Total Blood Volume
- 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
Types of Shock
- 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
Clinical Features of Shock
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
Four Stages of Classical Shock
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)
What do shock begin with
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
What do anaerobic metabolism cause
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
Hypovolemic Shock
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)
Cardiogenic Shock
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
Septic Shock
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
Toxic Shock Syndrome
- 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
Anaphylaxis
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
Neurogenic Shock
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
Positive Feedback Loop in Shock
- 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
Pharmacological Principles of Shock
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
Things to correct in shock
Preload, Contractility, After Load, Oxygen delivery
Multiple Organ Dysfunction Syndrome
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
