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Pathophysiology > unit 6 (other half) > Flashcards

unit 6 (other half) Flashcards

1
Q

Describe Congestive Heart Failure

A
  • describes condition when heart is unable to pump enough blood to meet body’s oxygen demands
  • Often a sequela or complication of another heart condition (ex: myocardial infarction)
  • Usually a chronic condition that will not ‘heal’
  • usually chronic that will not heal
  • Failure may be right or left sided, based upon the ventricle affected (left or right)
  • In heart failure, heart loses effectiveness as a pump
  • Digoxin is a drug that slightly helps the muscle in heart failure to improve stroke volume and cardiac output
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2
Q

Congestive Heart Failure: Etiology

A

Etiology Variable:

  • Dx of the heart itself (ex: MI)
  • Dx aprat from the heart (ex: chronic hypertension or lung dx)
  • Coronary artery dx is the most common cause
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3
Q

Heart Failure Adaptation: The good news

A

Decrease CO in heart disease results in reflex adaptation mechanisms that improve cardiac function

Sympathetic stimulation:

  • Increase HR: increases cardiac output
  • Vasoconstriction –> increase BP
  • Increase contractility –> increase stroke volume

Renin-angiotensin-aldosterone system (RAAS):
-Vasoconstriction –> increase BP
-Na+ retention –> increase BV (–> increase BP)
-H2O retention –> increase BV
(–> increases BP)

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4
Q

Heart Failure Adaptation: The Bad News

A

Compensation may be effective initially but it ultimately stresses the damaged heart muscle

Sympathetic Stimulation:

  • Increase HR –> increase workload + decreases EDV (end diastolic volume) –> decrease CO
  • Vasoconstriction –> increase BP
  • -> increases afterload –> increases workload
  • Increase contractility –> increase SV –> increase workload
  • end diastolic volume is when the ventricles relax and allow the fullest amount of volume

Renin-angiotensin-aldosterone system (RAAS)

  • Vasoconstriction –> increase BP –> afterload –> increase workload
  • Na+ retention –> increases BV –> increase preload –> increases workload
  • H2O retention –> increases BV –> increases preload –> increases workload

More bad news:
Under conditions when ventricles weakens:
-Ventricle cannot eject all the blood in it
-Ventricles dilates

Under conditions of increased workload:

  • Ventricular muscle hypertrophies
  • Larger mass necessitates increased blood flow (problem if heart is damaged)
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5
Q

Forward Consequences of Failing Heart

A
  • Forward consequences are those that occur downstream from the heart muscle (past the heart)
  • Affect those aspects of homeostasis that require normal heart function
  • Failing heart has reduced CO or SV, which leads to: tissue hypoxia, poor cellular function (–> lethargy, weakness), mild metabolic acidosis (–> tachypnea) and reduced venous return
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6
Q

Backup Consequences of Failing Heart

A
  • Backup consequences are those that affect aspects of homeostasis related organs and tissues upstream from heart
  • See congestion (fluid accumulation) in tissues proximal to affected ventricle: therefore, the ventricle unable to pump out (eject) all of venom return, blood backs up behind affected ventricles and blood pressure rises behind affected ventricle
  • Congestion affects different tissues depending upon which ventricle is affected
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7
Q

CHF: signs and symptoms

A

Common to both right and left side failure:

Tissue Hypoxia:

  • weakness
  • fatigue
  • dyspnea (difficult or laboured breathing)

Compensation:

  • Tachycardia (reflex sympathetic stimulation)
  • Weak pulse (reduced cardiac output)
  • Pallor (peripheral vasoconstriction)
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8
Q

Left Side CHF: signs and symptoms

A

Related to issues caused by fluid filling the lungs

Dyspnea/orthopnea: lungs filled with fluid

Paroxysmal nocturnal dyspnea (cardiac asthma)
-actue pulmonary edema

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9
Q

Right Side CHF: signs and symptoms

A
  • Related to issues caused by flooding filling peripheral tissues
  • Swelling in feet, legs and buttocks
  • Hepatomelgaly and splenomegaly: resulting from deem in intestine
  • Ascites: fluid in abdomen
  • Flushed appearance
  • Distended neck veins
  • Vision disturbance
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10
Q

Left Side CHF

A
  • Increase pulmonary capillary pressure –> pulmonary edema
    1. Left ventricle weakens and c cannont empty
    2. Decreased CO to system
    3. Decreased renal blood flow and stimulates renin-angiotensin and aldosterone secretion
    4. Backup of blood into pulmonary vein
    5. High pressure in pulmonary capillaries lead to pulmonary congestion of edam
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11
Q

Right Side CHF

A
  • Increased peripheral capillary pressure –> peripheral edema
    1. Right ventricle weakens and cannot empty
    2. Decreased CO to system
    3. Decreased renal blood flow and stimulates renin-angiotensin and alderstone secretion
    4. Backup of blood into systemic circulation (venae cavae)
    5. Increased venous pressure resulting in edema in legs, liver and abdominal organs
    6. Very high venous pressure causes distended neck vein and cerebral edema
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12
Q

Heart Failure: Treatment

A
  • Ca2+ required for cardiac muscle contractile activity
  • In heart failure, muscle contractility is reduced
  • Enter the plants Digitalis purpurea and digitalis
  • Digoxin is a drug derived from foxglove plant. It causes accumulation of Ca2+ inside CaM cell
  • Increased Ca2+ –> contractility of CaM cell –> CO
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13
Q

Hypertension

A
  • Affects one in 3 adults
  • Sneaky in onset: may be undiagnosed and untreated until symptoms appear
  • Even if diagnosed, compliance with intervention may be poor until dysfunction occurs
  • Would likely result in left-sided heart failure
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14
Q

Three Categories of Hypertension

A

Primary (‘essential’ hypertension):

  • Idiopathic
  • Majority of cases

Secondary Hypertension:
-Arises as a sequela of another underlying pathology: ex: kidney disease (reduced renal blood flow), hyperaldosteronism (increase Na+, H2O retention)
and pheochromocytoma (adrenalin secreting tumour)
-Better to have secondary because knowing the etiology can help to control it

Malignant Hypertension:
-uncontrollable, severe and rapidly progressive

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15
Q

BP Classification

A

-Normal: 120/80
-Pre-hypertension: 120-139/80-89
Stage 1: 140-159/90-99
Stage 2: >160/>100

*Systolic heart pumping and diastolic heart filling

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16
Q

Essential Hypertension (Primary)

A

Defined as BP constantly above 140/90
-diastolic figure important reflection of cardiac after load

Fundamental issue is increased vasoconstriction:

  • Recall * that peripheral resistance increases dramatically with even modest narrowing of vessels
  • Results in large increase in after load (what the heart is pushing against, over working the heart)

Vicious Cycle Ensues:
-Vasoconstriction (fundamental lesion) –> decrease in renal blood flow –> RAAS activity –> increases BV, increases vasoconstriction –> RAAS activity

17
Q

Effects of Primary

A

Triple A effects:

  • Arteriosclerosis
  • Aneurism
  • Atheroma formation

In areas affected by damaged arteries, schema, necrosis and loss of function may occur:
-Brain, kidneys and retinas

18
Q

Describe Infective Endocarditis

A
  • Inflammation of the endocardium (ends in itis)
  • Distinguished from rheumatic fever: presence of active infection in infective endocarditis
  • Two types of infective endocarditis: subacute and acute
19
Q

Infective Endocarditis Pathophysiology: Subacute and Acute

A

Subacute:

  • affects defective heart valves
  • invasion is by one or several low-virulence bacteria: streptococcus viridans (a normal mouth flora) and HACEK groups (ora commensal organisms) haemohilus, actinobacillus, cardiobacterium, eikenella, kingella

Acute:

  • Affects normal heart valves
  • Invasion by one of several high-virulence organisms (ex: staphylococcus aureus)
  • Causes severe tissue damage
20
Q

Infective Endocarditis Pathophysiology

A
  • Invasion of heart valves by microorganisms during bacteremia
  • Inflammatory response (relatively minimal)
  • Formation of valve cusp vegetations (growth or outgrowth): mass of platelets, fibrin, blood cells and bugs. It may interfere with valve operation
  • Vegetation may embolize: spread infection to distant site and cause infarction
  • Additonal scarring of valve and chordae tendinae
21
Q

Infective Endocarditis: Etiology

A

Involves a combination of risk factors:

  • lowered host resistance (immune response reduced) (ex: corticosteroid rx, AIDS)
  • Abnormal valve tissue, perhaps caused by: congenital defects, rheumatic fever and protheses (valves, catheters, etc)
  • Bacteremia: at risk individuals should pre medicated (standard protocols) before procedures that carry risk of bacteria (ex: dental scaling)
22
Q

Describe Pericarditis

A
  • Inflammation of the pericardium (peri means outside of perimeter, itis =inflammation), which is the sac surrounding the heart
  • Usually occurs as a sequel of a broad range of other conditions
  • Maybe acute or chronic
  • It is an inflammatory process within the sac that causes vasculature around the heart to become more permeable and build up fluid
23
Q

Acute Pericarditis: Pathophysiology/Etiology

A

May be due to simple pericardial inflammation:
-swelling causes chest pain and friction (audible)

May see pericardial effusion (fluid build-up) in pericardial sac:

  • Serous (inflammation)
  • Purulent (infection)
  • Bloody (injury or cancer)

Fluid Compression of the heart prevents expansion:
-heart cannot fill (decreases EDV) –> decrease CO (cardiac tamponade)

Right heart is affected first: Since the heart cant fill properly it results in a

  • lower pressure
  • effects analogous to R-CHF
  • Backup of blood raises pressure in systemic veins: distended neck veins and abdominal discomfort
ETIOLOGY: 
Underlying conditions that may lead to onset of acute pericarditis: 
-Rheumatic fever
-Open heart surgery 
-MI
-Systemic lupus erythematosus 
-Renal failure 
-Cancer 
-Viral infection
24
Q

Chronic Pericarditis: Pathophysiology/ Etiology

A
  • Maybe caused by adhesions between 2 layers of pericardial sac
  • Fibrous scar tissue may form, restricting movement of heart

ETIOLOGY:

  • Tuberculosis infection
  • Mediastinal (center spine of chest) radiation
  • Spread of inflammation or infection to the heart from another region, ex: lungs (pleurisy or pneumonia)
25
Q

Pericarditis Tx

A
  • Resolve underlying causative factors: paracentesis to investigate etiology
  • Aspiration of fluid to prevent tamponade

*paracentesis is taking out the fluid and seeing if it is serous, bloody, etc, to help make a diagnosis

Pathophysiology (9 decks)

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