cardiac pathophysiology

Question 1

what are the two essential mechanical functions of the heart

Answer 1

1. eject blood into the arteries: systolic performance
2. recieve blood from the veins: diastolic performance

Question 2

what is systolic performance

Answer 2

• generation of high pressure sufficient for organ perfusion
• pulmonary artery and aorta
• ventricles during systole

Question 3

what is diastolic performance

Answer 3

• maintenance of low pressure to avoid congestion
• atria and veins
• ventricles during diastole

Question 4

what are the 5 determinants of cardiac output

Answer 4

1. preload
2. afterload
3. contractility
4. synergy
5. heart rate

Question 5

what is preload

Answer 5

• the stretch of the ventrile just before the onset of contraction (end-diastolic volume)
• achieving an optimal strech of the myocyte causes improved contractility

Question 6

what is afterload

Answer 6

• the load against which the ventricles contracts
• resistance to the ejection of blood from the ventricle (myocardial wall stres)
• determined by: peripheral resistance (blood pressure) & heart size (chamber size/wall thickness)

blood pressure - pressure in order for blood to leave heart

Question 7

what is myocardial contractility

Answer 7

• strength of the cardiac muscle contraction (systolic functioon)
• at the molecular level - it is a load-independent interaction between Ca2+ ions and the contractile proteins

Question 8

what is synergy

Answer 8

atrio-ventricular synchrony

• atrial pump-priming funciton
• contribute roughly 25% of cardiac output

Question 9

what is heart rate

Answer 9

cardiac output = stroke volume x HR

Question 10

what is the modern concept of heart failure

Answer 10

• cardiac injury
• decreased cardiac output and decreased tissue perfusion
• “compensatory” responses
• Na+ and H2O retention, vasocontriction, cardiac and vascular remodeling
• congestion, inc afterload, early myocyte death
• cardiac injury (repeat cycle)

Question 11

what are the frank-starling limitations

Answer 11

• flattened cardiac performance curve
• less improvement in performance for any given inc. in preload
• excessive preload -> congestive signs

Question 12

what are the heart rate limitations

Answer 12

• inverse force-frequency relationship
• impaired diastolic filling due to elevated HR

Question 13

what is cardiac hypertrophy

Answer 13

• one of the primary ways the heart responds to stress or disease
• pressure overload -> concentric hypertrophy
• volume overload -> eccentric hypertrophy

Question 14

why does concentric hypertrophy occur?

Answer 14

• pressure overload = increased afterload
• increased afterload is the same as increased wall stress
• increase in P is offset by increase h (wall thickness), thus restoring normal wall stress

Question 15

what are the limitations of myocardial hypertrophy

concentric

Answer 15

• excessive hypertrophy
• myocardial ischemia
• increased ventricular stiffness and poor diastolic relaxation
• arrhythmias
• diastolic heart failure

Question 16

what are the limitations of myocardial hypertrophy

eccentric

Answer 16

• increased myocardial oxygen demand
• fibrosis, ventricular remodeling

Question 17

what are endocrine responses

Answer 17

• the heart as a target of systemic endocrine substances
• catecholamines (SNS-NE)
• renin-angiotensin-aldosterone-system (RAAS)
• vasopressin (ADH)
• the heart produces natriuretic peptides

Question 18

what triggers RAAS

Answer 18

• decreased renal perfusion due to low cardiac output
• renin release from the macula densa-juxtaglomerular cells (DCT)

Question 19

how does angtiotensin II & aldoseterone work by trying to support circulation by increasing plasma volume and vasoconstriction

Answer 19

1. fluid and Na+ retention in kidney
2. increase ADH
3. vasoconstriction of vascular smooth muscle
4. increase thirst
5. increase SNS/NE
6. increase aldosterone
7. myocardial hypertrophy

Question 20

what are the short term effects of SNS activation

Answer 20

• increase HR
• vasocontriction
• increase contractility
• RAAS activation
• ADH release

Question 21

what are the long term effects of SNS activation

Answer 21

• increase myocardial O2 demand
• increase afterload
• myocyte necrosis
• increase RAAS/ADH -> congestion
• arrhythmias

Question 22

what is the natriuretic peptide system

Answer 22

• heart as endocrine organ
• increased plasma volume causes stretch or sress of myocardial tissue triggers production and release of natriuretic peptides
• atrial natriuretic peptide (ANP): B-type natriuretic peptide (BNP) -> elicits diuresis & vasodilation: counteracts the RAAS and SNS

Question 23

what are the limits of natriuretic peptides

Answer 23

• diminished production by damaged heart tissue
• down-regulation of NPR-A (reduced beneficial biological effect)
• enhanced clearance of ANP/BNP
• NP system is overwhelmed by SNS and RAAS activity in later stages of heart disease

Question 24

what are the clinical aspects of CHF: right vs left

Answer 24

• right: ascites, pleural effusion
• left: pulmonary edema (pleural effusion: cats)
• biventricular failure: both right and left CHF

Question 25

what are the clinical aspects of low output heart failure

Answer 25

low cardiac output leads to hypotension and poor tissue perfusion: weakness, shock, collapse

Question 26

what is preclinical vs symptomatic

Answer 26

• stage A: predisposed
• stage B: preclinical
• stage C: symptomatic
• stage D: end-stage

Question 27

what are the clincial signs of congestion

Answer 27

• jugular distention, pulses
• abdominal distension, ascities
• anorexia, diarrhea, weight loss or gain
• cough, tachypnea
• dyspnea, increased effort
• orthopnea, cyanosis
• pulmonary edema (dogss, cats)
• pleural effusion (cats)

Question 28

what are the clinical signs of low outout

Answer 28

• excersise intolerance
• weakness, fatigue
• collapse, syncope