Cardiac Conditions Flashcards
Hypertension
- Can cause hypertrophy (enlargement/thickening)
- Shee stress on vessels
- Primary (95%; idiopathic) vs Secondary (5%)
- Goal: Decreas both SBP and DBP
HTN and CVD
- Increased BP has an relationship with increased in cardiac events.
- Within DBP 70-110 mm Hg, any reducation will decreased risk of CHD or CVA risk
- Lowering HTN is twice the benefit for older adults.
Lifestyle Changes to reduce HTN (with #s)
- Physical activity 4-9 mmHg
- Weight Loss (10 kg loss) 5-20 mmHg
- Stop Smoking
- Decrease alcohol 4-9 mmHg
- Decrease sodium (if sodium sensitive) 2-8 mmHg
- DASH diet (5-6 fruits and 5-6 veggies each day)
Pharmalogical ways to decrease HTN
Diuretic: Water pill; drop volume, drop level
CCB: Calcium channel blocker
ACEI: Ace inhibitor: often hacking cough
BB: angiotension reg blocker.
HTN and Exercise
- Normal Response: SBP increase, DBP stay the same
- Some HTN patient’s: Increase SBP and DBP
- Exercise Training: Post Ex Hypotension
– Decrease SBP by 4-10 mm Hg
– Decrease DBP slightly less
Guidelines for Ex and HTN
- Resting SBP is >200 mmg or DBP >100 mmHg obtain medical provider clearance pre-exercise
- Discontinue if SBP > 250 mmHg; DBP > 110 mmHg
- Medication effect (may lead to hypotension; chaning position, post-exercise, long term stanfin, in warm water)
This is a guideline NOT an end all be all. Use clinical reasoning.
HTN and PT
- All pt’s - screened for BP every 2 yrs
– However, System Review all pts at eval - Everyone over 35 should routinely have their BP assessed
– Part of your examination - Ask them if they are on medication
– Ask if they are taking it as prescribed
All cardiac condition eventually lead too…
Heart Failure
Heart Failure Definition
- Impaired contraction and relaxation of myocardial tissue
– Decrease CO, Decrease contraction, Decrease stroke volume
First degree HF is caused by
pathology of myocardial tissue
Can be genetic, acquired or both.
Second degree HF results from…
Can be genetic, acquired or both.
systemic disease process
Types of HF
Dialated (Systolic Dysfunction; Ventricles are enlarged; Can be caused by long standing HTN)
Hypertrophic (Diastolic Dysfunction; Muscle is thickened)
Restrictive (Both Systolic and Diastolic; Tissue is stiff or scarred)
Pump effectiveness is influenced by…
Preload and afterload
Preload
- volume of blood in the ventricle just prior to systole
– Depends on venous return and compliance
– Measured by left ventricular end diastolic volume
Afterload
- the force against which the left ventricle must pump
– Clinically, BP is often used to measure it
– Pulmonary artery pressure
Left vs Right Sided HF
Left sides: Blood can’t leave left ventricle. Backs up into the lungs. Hear crackles – fluid backed up in lungs; Pools in bottom of aveoli. Preload is higher when laying flat which leads to paroxysmal nocturnal dyspnea (wake up during sleeping short of breath). Pressure builds up here.
Right Side: Blood leaves heart. JVD, enlarge liver and spleen. Swelling in lower extremities.
Left Sided HF Symptoms
- Paroxysmal noctunal dyspnea
- Cyanosis
- Fatigue
- Exertional dyspnea
- Confusion
- Orthopnea
Right Sided HF Symptoms
- Fatigue
- Ascites (Build up of fluid)
- Enlarged liver and spleen
- JVD
- Weight gain (fluid in abdomin and legs)
- May be secondary to chronic pulmonary conditions
HF Pathogenesis
Initial compensation for impaired contractility:
Frank-Starling mechanism
– Increase EDV (dilation) to increase SV
Neurohumoral activation (medication use)
– Increase HR (tachycardia) to increase CO
Eventual decompensation
– Ventricular remodeling (thickness; less blood flow to portion – ischemia and decrease contractility)
– Myocyte death
– Valvular regurgitation
– Inc. Peripheral Vascular resistance leads to pulmonary and systemic congestion
Compensation vs Decompensation
Compensation: body tries to make things work better.
Decompensated: body fails to compensate. Heart failure is dangerous here.
HF Clinical Manifestations - Decreased CO
- Tachypnea (fast breathing)
- Decrease BP
- Cold/Cyanotix
- Fatigue
- Decrease exercise capacity
– Increase HR and RPE - Sinus Tachycardia
HF Clinical Manifestations - Pulmonary/Venous Congestions
- Paroxysmal nocturnal dyspnea
- Orthopnea
- Crackles
- Dyspnea
HF Clinical Manifestations - Cardiac
- S3 Heart Sounds (acutely)
- Mitral regurgitation
HF Clinical Manifestations - Systemic congestion
- Increased JVD
- Hepatomegaly
- Ascites (fluid in peritoneal/abdomen cavity)
- Peripheral edema (weight gain 3 lbs)
Diagnostic Assessment - HF
- Chest X-ray
- Echocardiogram (US of heart)
- EKG
- Angiography (x ray of coronary arteries with dye inserted to look for blockages)
Heart Failure Criteria
-
Brain Natriuretic Peptide (BNP)
– Amino Acid secreted by heart in response to excessive stretching
– > 700 ng/L; criteria for de-compensated — HF and admission to hospital
– Normal less than 100
– 100-700 = compensated HF - Typically seen with wt gain (2-3 lbs) overnight
Classification of Heart Failure
Class 1: No limitation of PA, Normal PA does not cause symptoms
Class 2: Slight limitation of PA, Comfortable at rest, Normal PA caused symptoms
Class 3: Marked limitation of PA, Comfortable at rest, but less than ordinary activity causes symptoms
Class 4: Severe limitation and discomfort with any PA, symptoms present even at rest.
Risk Factors of HF
- Hypertension
- Myocardial infarction
- Abnormal heart valves
- Cardiomyopathy (enlargement of the heart)
- Family history of heart disease
- Diabetes
Anything that causes CV system can contribute to HF
Complications - HF
- Kidney damage or failure
- Dysfunctional heart valves
- Arrhythmias
- Liver Damage
- Pulmonary conditions
Complications - HF
- Kidney damage or failure
- Dysfunctional heart valves
- Arrhythmias
- Liver Damage
- Pulmonary conditions
Coronary Artery Disease (CAD) - Definition
Plaque accumulates in coronary arteries which causesnarrowing of the arteries(atherosclerosis)
Results in blood, oxygen, and nutrient deprivation to the cardiac muscle cells
Most common form of heart disease in the US
If I have an coronary artery occlusion of 80% am I going to die?
Not necessarily. Depending on if it is a thick or thin lining will tell you if you if you are at risk of rupture. Thin is more dangerous and we can only test by looking inside the arteries.
If I have an coronary artery occlusion of 80% am I going to die?
Not necessarily. Depending on if it is a thick or thin lining will tell you if you if you are at risk of rupture. Thin is more dangerous and we can only test by looking inside the arteries.
Pathogenesis - CAD
Plaque buildup (atherosclerosis) in the coronary arteries starts with damage to the endothelium.
- A clot or spasm may close the vessel, causing a heart attack (MI)
– Vasospasm (Neural input often caused by smoking) – Prinztmetal’s angina - Plaque are either:
– Stable (thick lining)
– Unstable (thin lining); easily exposed and ACS can develop
CAD Modifiable RF
- Hypertension
- Smoking
- Elevated lipids
- Obesity
- Poor control of Diabetes
- Physical inactivity
- Stress
Emerging Risk Factor: Men who spend sitting 5 or more hours out side of work are 34% more likely to develop HF than those who sat 2 hours. Additionally, low to mod PA did not eliminate risk.
CAD Non-modifable RF
Age
– Getting older increases risk
Gender
– Men are at a higher risk
Family history
Race
Clinical Manifestations - MI; Male and Female vs Female
- Male and Female
– Angina
– Dizziness
– Dyspnea - Primarily Female
– Nausea
– Vomiting
– Fatigue
– Jaw pain - Females may have little or no symptoms
Diagnostic - CAD
- EKG
- Stress Test
- Coronary Angiogram
- Echocardiogram (Ultrasound of heart)
Complications of CAD
- Heart Failure (pump dysfunction)
- Electrical problems (arrhythmias)
– Afib, AV blocks - Decreased functional capacity
- Angina
- Myocardial infarction
